Infectious Diseases of Concern to Wildlife in North America

Infectious Disease Manual Infectious Diseases of Concern to Captive and Free Ranging Wildlife in North America An official publication of the American Association of Zoo Veterinarians Animal Health and Welfare Committee Updated April 2020 Edited by Paige Brock DVM DACZM cVMA Gretchen Cole DVM DACZM DECZM ZHM and Richard Sim DVM DACZM Introduction This publication was designed as a starting reference point for information on the infectious diseases that affect zoo and wild animal species captively housed or freeranging in North America This volume complements a similar dynamic and routinelyupdated version that exists for the same populations in Europe While each sheet has been peerreviewed often by a topic expert these fact sheets are not intended to be used as an exclusive source of information but rather provide quick reference of basic disease properties and concerns These fact sheets also highlight diagnostics laboratories specialists and treatment recommendations for clinicians pathologists and wildlife biologists that encounter an infectious disease This compendium acts as a common resource and point of information for this discipline It is important to remember that these fact sheets are not to replace state or federal regulations As such they are not legally enforceable documents or required standards of care From the Editors We hope that you find the information in this manual helpful There have been some changes made since the last update of the Infectious Disease Manual For example the links to US state reportable diseases have been removed as this information is now easily searchable on the internet We feel that it is impossible to maintain uptodate information on these topics in such a quickly changing world We encourage our readers to contact the specialists listed on each factsheet to obtain the most current information about a disease We would like to thank the many authors and reviewers who have contributed to this updated edition as well as the previous editions of this manual We also thank Melanie Pearson Class of 2021 who assisted with the formattingtechnical editing of many of the updates Without the hard work by so many people this manual would not be possible Please note that we have elected to update this manual in stages so fact sheets have been updated between 2013 through 2020 The date of the most recent update is noted on the first page of each fact sheet We will continue to update this publication regularly as new updates become available If you find any broken links within this document please let us know so that we can attempt to correct the issue If you would like to contribute as a new factsheet author updating author or reviewer we would also love to hear from you We can be reached at drbrockdvmgmailcom Paige Brock GColeokczooorg Gretchen Cole and simrichardrgmailcom Richard Sim Table of Contents Click on the name of each disease to be taken to the disease factsheet Acanthamoebiasis Acanthocephalosis Actinobacillus lignieresii Wooden Tongue Actinomycosis Lumpy Jaw Adenovirus Aeromonas Red Leg African Horse Sickness African Swine Fever Aleutian Disease Virus Anaplasmosis Anatrichosoma Angiostrongylus Anthrax Aspergillosis Avian Bornavirus Avian Influenza Avian Poxvirus Babesia sp Balantidium coli Baylisascaris Bertiellosis Blastomycosis Bluetongue Virus Bordetella Borreiliosis Lyme Disease Botulism toxicosis See Clostridial disease Botulism Bovine Spongiform Encephalopathy Bovine Viral Diarrhea Virus Brucellosis Bovine Marine Mammal Porcine Callitrichid Hepatitis Virus See Lymphocytic Choriomeningitis Virus Campylobacteriosis Canine Distemper Virus formerly Chrysosporium anamorph of Nannizziopsis vriesii Caprine Infectious ArthritisEncephalitis Virus Chagas disease See Trypanosoma cruzi Chimp Coryza See Respiratory Syncytial Virus Chlamydiophila abortus Enzootic Abortion ChlamydiosisChlamydophilosis Chronic Wasting Disease Circovirus See Psittacine Beak and Feather Disease Chytridiomycosis Classical Swine Fever Clostridial disease Botulism toxicosis Tetanus Coccidioidomycosis Contagious Bovine Pleuropneumonia Contagious Ecthyma Orf Coronavirus Cowpox Coxiella burnetti Q Fever Cryptococcosis Cryptosporidiosis Cytauxzoon Cytomegalovirus Dermatophytosis Ringworm Dirofilaria immitis Heartworm Disease Eastern Equine Encephalitis EbolaReston virus Echinococcosis Edwardsiellosis Ehrlichia ruminantium Heartwater Ehrlichiosis Encephalitozoon cuniculi Encephalomyocarditis Virus Enzootic Abortion See Chlamydiophila abortus Equine Infectious Anemia Erysipelas Escherichia colicolibacillosis Feline Calicivirus Feline Immunodeficiency Virus Feline Infectious Peritonitis Feline Leukemia Virus Feline Panleukopenia Foot and Mouth Disease Giardiasis Glanders Hantavirus Heartworm Disease See Dirofilaria immitis Heartwater See Ehrlichia ruminantium Helicobacter Helminths of Ungulates Hemobartonella Hemogregarines of Reptiles Hepatitis A Hepatitis B Herpesviruses Duck viral enteritis Elephant Endotheliotropic Herpesvirus EpsteinBarr Virus Equine Herpesvirus Feline Rhinotracheitis FibropapillomatosisAssociated Herpesvirus Herpes B Hominus and Simplex Types 1 and 2 HumanSimian Varicella Infectious Bovine Rhinotracheitis Koi Herpesvirus Macropod Herpesvirus Malignant Catarrhal Fever Pachecos Disease Herpesvirus in Parrots Pseudorabies Saimariine Herpesvirus Simian Agent 8 SA 8 Cercopithecine Herpesvirus 2 Testudinid Herpesviruses Histoplasmosis Human Metapneumovirus Inclusion Body Disease Virus Infectious Hematopoietic Necrosis Johnes Disease See M avium subsp paratuberculosis Klebsiella Kyasanur Forest Disease Leprosy Leptospirosis Listeriosis Lumpy Jaw See Actinomycosis Lumpy Skin Disease Virus Lung mites Lyme Disease See Borreiliosis Lymphocytic Choriomeningitis Virus Callitrichid Hepatitis Virus Malaria See Plasmodium Marburg Hemorrhagic Fever Measles virus Melioidosis Meningeal Worms See Parelaphostrongylus tenuis Methicillinresistant Staphylococcus aureus MRSA Monkeypox Mycobacteria Atypical Avian In elephants M avium subsp paratuberculosis Johnes Disease Paratuberculosis Nonhuman primates Piscine Ungulates Mycoplasmosis Oesophagostomiasis Ophidian Paramyxovirus Orf See Contagious Ecthyma Oxyuriasis Paratuberculosis See M avium subsp paratuberculosis Parelaphostrongylus tenuis Meningeal Worms Parvovirus Pasteurellosis Peste des Petits Ruminants Phocid Distemper Virus Plague See Yersinia pestis Plasmodium Malaria Pneumococcosis Pneumocystosis Poliovirus Pseudogymnoascus destructans See White Nose Syndrome Pseudotuberculosis See Yersiniosis Psittacine Beak and Feather Disease Circovirus Pythiosis Q Fever See Coxiella burnetti Rabbit Hemorrhagic Disease Rabies Ranavirus Red Leg See Aeromonas Respiratory Syncytial Virus Chimp Coryza Rickettsial tickborne disease Rift Valley Fever Ringworm See Dermatophytosis Rotavirus Salmonellosis Schistosomiasis Screwworm New World Old World Sealpox Sheep and Goat Pox Shigellosis Simian Foamy Virus SFV Simian Hemorrhagic Fever SHF Simian Immunodeficiency Virus SIV Simian Retroviruses SRV Simian TLymphotropic Viruses STLV Spiruroidosis Spring Viremia of Carp St Louis Encephalitis Staphylococcus spp Streptococcus Group C Strongyloidiasis Swine Vesicular Disease Virus Tanapox Toxoplasmosis Tetanus See Clostridial disease Tetanus Trichostrongylosis TrichuriasisCapillariasis Trypanosoma cruzi Chagas disease Tularemia Ulcerative Stomatitis Vesicular Exanthema of Swine Vesicular Stomatitis Virus Vibriosis Viral Hemorrhagic Septicemia Virulent Newcastle Disease Visceral Leishmaniasis West Nile Virus Western Equine Encephalitis WEE White Nose Syndrome Pseudogymnoascus destructans Wooden Tongue See Actinobacillus lignieresii Yabapox Yellow Fever Yersinia pestis Plague Yersiniosis Pseudotuberculosis Authors and Reviewers Dalen Agnew Roberto Aguilar A Alonso Aguirre Copper AitkenPalmer Lowell Anderson Douglas Armstrong Elizabeth ArnettChinn Mark W Atkinson Frank Austin Kay A Backues Laurie A Baeten Anne Ballmann Priya Bapodra Alan Barrett David A Bemis Majorie Bercier Tom Besser Beth Bicknese Troy Bigelow Adam Birkenheuer Peter Black David Blehert Emily L Blizzard Rebecca Bloch Christopher J Bonar Diana Boon Rose Borkowski Walter Boyce Robert W Bradsher Edward B Breitschwerdt Robert E Briggs Ellen Bronson Gayle Brown Kevin Brunner Anne Burgdorf Roy Burns Ronald Mitchell Bush Salomé Cabrera Paul P Calle Joseph Camp Sarah A Cannizzo Carol Cardona Nancy Carpenter Lilian Silva Catenacci Shannon Cerveny Sara ChildsSanford Sathya Chinnadurai Melanie L Church Sarah Churgin Meredith M Clancy Elsburgh Tres Clarke Leigh Ann Clayton Ryan Colburn Gretchen A Cole Heather Cole Ken Conley Victor Cortese Philip Craig Thomas Craig Michael R Cranfield Lara M Cusack Jennifer DAgostino Robert D Dahlhausen Sharon L Deem Kristina M Delaski Tom Deliberto Pauline Delnatte Thomas W deMaar Elizabeth Didier George D Di Giovanni Mark Drew Jitender P Dubey Amanda Duffus Genevieve Dumonceaux Ann E Duncan Richard Eberle M Scott Echols Ginny Emerson James J England Claire ErlacherReid James Evermann A Hossain Farid Charles Faulkner Cara Field Ariana Finkelstein Christine Fiorello John Flanders Deidre Fontenot Ruth FrancisFloyd Patrice Frost Laurie Gage Jackie Gai Kathryn C Gamble Nadia F GallardoRomero Kathryn C Gamble Rae Gandolf Franklyn Garry Dorothy Geale Annette Gendron Tim Georoff Francis Gigliotti Kirsten Gilardi John Gilliam Tony Goldberg Andrea Goodnight Leah Greer Ellis C Greiner Amy Grooters Amanda Guthrie Zoltan S Gyimesi Catherine A Hadfield Holly Haefele Sarah A Hamer Elizabeth E Hammond Christopher S Hanley Kenneth Harkin Craig Harms Julie Harris M Camille Harris Tara M Harrison Kelly Helmick Lawrence Herbst Christie Hicks Clayton Hilton Lauren Howard Zachary Hoy Martin HughJones Donna Ialeggio Charles Innis Ramiro Isaza S W Jack Donald Janssen James G Johnson III Lynelle Johnson Priscilla H Joyner Randy Junge Anne JusticeAllen Malika Kachani John Kaneene Tanit Kasantikul Taranjit Kaur Sarrah Kaye Melissa Kennedy Suzanne KennedyStoskopf Cornelia J KetzRiley Lester Khoo Jennifer Kilburn Eric Klaphake Hilton Klein Stephanie Kottler Kristian J Krause Lana Krol Claude Lacasse Charles Lamien Ana Cristina Leandro Alfred M Legendre Kevin Leiske Karn Lekagul Gregory A Lewbart Michael Lierz Karen Liljebjelke David Lindsay Susan M Lindstedt Erica Wilson Lipanovich Remo Lobetti Samantha Lockwood Guy Loneragan Douglas R Mader Roger Maes Elizabeth Manning AJ Marlar Rachel Marschang Thomas P Meehan Leonel Mendoza Carol U Meteyer Denise McAloose Michael McBride Stephanie McCain David S Miller Michele Miller Vikki Milne Mark Mitchell Christine Molter Benjamin P Monroe Susan Montgomery Andrew Moorhead Gail Miriam Moraru John C Morrill Pat Morris Ulrike Munderloh Hayley Murphy Gwen E Myers Natalie Mylniczenko Yvonne Nadler Julie Napier Eleanor C Manela Newcomb Alisa Newton Tom Nolan Danelle M Okeson June Olds Steve Olsen Kortney A ONeill Francesco C Origgi Mark Papich Dennilyn Parker Lily Parkinson Rosalia Pastor Linda Peddie Kerri Pedersen Allan P Pessier Denise Petty David N Phalen Nicholas Phelps Patrick Pithua Roman Pogranichniy Linda Pote Lauren V Powers Kate Pritchett Kimberly Rainwater Jan Ramer Alex Ramirez Ed Ramsay Katrina Ramsell Bonnie Raphael James M Rasmussen Stephen Raverty Patrick Redig Karen Register Janelle Renschler Christy Rettenmund Jack C Rhyan Bryan J Richards Bruce Rideout Gary Riggs Branson W Ritchie Sam Rivera Heather Robertson Carlos Rodriguez Susan Rohrer Pierre E Rollin Carlos Romero Melinda Rostal James Roth E Marie Rush Carlos R Sanchez Sam Sander Sara Childs Sanford Gene M Scalarone Joni Scheftel Dennis Schmitt Mark Schoenbaum David M Scollard Wynona C Shellabarger Inga F Sidor Tom Sidwa Noelia SilvadelRio Rich Sim Jatinder Singh Cora Singleton Owen M Slater Rebecca Smedley Dale A Smith Joseph A Smith Stephen A Smith Danielle R Graham Snyder Angkana Sommanustweechai Evan Sorley Anna Rovid Spickler Terry Spraker Maria Spriggs Cynthia Stadler David Stallknecht James Steeil Nadia Stegeman Simone Stoute Betsy Stringer Gerardo Suzán Amy Swinford Jane Sykes John Sykes Teresa J Sylvina Ginger L Takle Aubrey M Tauer Sam Telford Jr Julie Ter Beest Karen A Terio Brenda Tesini Charles O Thoen Ian Tizard Kristen J Tobin Alfonso Torres Erika TravisCrook Richard W Truman Thomas N Tully Jr Claude Turcotte Kathryn Tuxbury Steve Unwin John Vacek Marc Valitutto Gediminas Valkiûnas William Van Bonn Arnaud Van Wettere Susan VandeWoude Michelle L Verant Guilherme G Verocai Winston Vickers Raquel Vilela Kurt Volle Allison Wack Ray Wack Thomas Waltzek Jim Watson Lynnette Waugh Genevieve Vega Weaver Scott Weber III Glen C Weiser James Wellehan A Gary West Joe Wheat Brent R Whitaker Douglas P Whiteside Ellen Wiedner Annabel Wise Kimberlee B Wojick Tiffany M Wolf Peregrine Wolff Rasana Wongratanachewin Sarah Woodhouse Arno Wünschmann Janna Wynne Michael J Yabsley Enrique Yarto KyoungJin Yoon Dawn Zimmerman American Association of Zoo Veterinarians Infectious Disease Manual ACANTHAMOEBIASIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primates Dogs Sheep Cattle Horses Kangaroos Birds Reptiles Amphibians Fish Invertebrates Source soil water Gains entry via breaks in skin respiratory tract corneal surface hematogenous spread to central nervous system Cutaneous lesions Sinusitis Pneumonitis Neurologic signs Fever Nausea Vomiting Asymptomatic in immunecompetent individuals Frequently fatal in immunocompromised individuals Pentamidine isethionate Sulfadiazine Flucytosine Fluconazole Itraconazole Amphotericin B Azithromycin Difficult due to ubiquitous nature of the organism Limit exposure to dust soil and water Not directly transmitted Can cause disease in humans Fact Sheet compiled by Laurie Gage Sheet completed on April 14 2011 updated 19 March 2013 Fact Sheet Reviewed by Kimberly Rainwater Ariana Finkelstein Susceptible animal groups Primates dogs sheep cattle horses kangaroos birds reptiles amphibians fish invertebrates Causative organism Opportunistic protozoan parasites Acanthamoeba spp A castellanii A culbertsoni A hatchetti A healyi A polyphaga A rhysodes A astronyxis A divionensis Zoonotic potential May infect cornea of contact lens wearers and cause disseminated infection in immunocompromised individuals Distribution Ubiquitous worldwide It may be found in soil fresh and brackish water bottled mineral water cooling towers of electric and nuclear power plants heating ventilating and air conditioning units humidifiers Jacuzzi tubs hydrotherapy pools in hospitals dental irrigation units dialysis machines dust in the air bacterial fungal and mammalian cell cultures contact lenses and ophthalmic saline flush aural discharge pulmonary secretions feces Incubation period 1 day to 2 weeks Clinical signs Granulomatous amoebic encephalitis depression nausea vomiting lowgrade fever lethargy cerebellar ataxia visual disturbances hemiparesis cranial nerve deficits seizures and coma Cutaneous lesions ulcers nodules and subcutaneous abscesses Respiratory sinusitis and pneumonitis Acanthamoeba keratitis reported in humans only ocular pain photophobia corneal ulceration loss of visual acuity and blindness Post mortem gross or histologic findings Gross Findings multifocal encephalomalacia and cerebral hemorrhage nodular necrosis in the liver kidney lung pancreas multifocal granulomatous pneumonia cutaneous granulomas Histologic Findings Focal areas of necrosis and granulomatous inflammation in affected tissues necrotizing vasculitis resence of cysts 1216 um diameter and trophozoites 1440 um diameter in affected tissues Diagnosis Direct observation of amoebae in tissues stained with hematoxylineosin indirect immunofluorescence staining using rabbit antiamoeba sera polymerase chain reaction to detect amoeba DNA in tissue and cerebrospinal fluid samples computed tomography and magnetic resonance imaging Material required for laboratory analysis Serum cerebrospinal fluid formalinfixed tissue samples fresh tissue samples for culture culture should only be done by accredited laboratories with the proper safety equipment American Association of Zoo Veterinarians Infectious Disease Manual ACANTHAMOEBIASIS Relevant diagnostic laboratories Centers for Disease Control and Prevention Atlanta Georgia Treatment Pentamidine isethionate sulfadiazine and other sulfa drugs flucytosine fluconazole itraconazole amphotericin B and azithromycin Prevention and control Limit exposure to airborne soil particles that may carry cysts to the respiratory system prevent exposure of open wounds to contaminated soil or water preventative measures are especially important for immunocompromised individuals Suggested disinfectant for housing facilities Chlorhexidine isopropyl alcohol 20 hydrogen peroxide Notification Not required Measures required under the Animal Disease Surveillance Plan None required Measures required for introducing animals to infected animal None required Conditions for restoring diseasefree status after an outbreak It is not possible due to ubiquitous nature of this organism Experts who may be consulted Centers for Disease Control References 1 Mehlhorn H 2008 Encyclopedia of Parasitology Volume 1 3rd Ed SpringerVerlag New York Pp 2 2 Schuster FL and GS Visvesvara 2004 Amebae and ciliated protozoa as causal agents of waterborne zoonotic disease Vet Parasitol 126 91120 3 Rutala WA DJ Weber and the Healthcare Infection Control Practices Advisory Committee 2008 Guideline for Disinfection and Sterilization in Healthcare Facilities 2008 httpwwwcdcgovhicpacpdfguidelinesDisinfectionNov2008pdf Accessed 14 April 2011 4 Visvesvara GS H Moura and F L Schuster 2007 Pathogenic and opportunistic freeliving amoebae Acanthamoeba spp Balamuthia mandrillaris Naegleria fowleri and Sappinia diploidea FEMS Immunol Med Microbiol 50 126 American Association of Zoo Veterinarians Infectious Disease Manual ACANTHOCEPHALANS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All vertebrates Requires ingestion of the intermediate host or a paratenic or transport host Ill thrift weight loss anorexia diarrhea abdominal discomfort or colic clinical signs compatible with peritonitis Infections can cause clinical disease and mortality Severity of disease may not be directly correlated with the number of adult parasites present There have been treatment difficulties noted in some species However ivermectin and doramectin have eliminated Macracanthorhynchus species in dogs and swine Albendazole has eliminated Moniliformis clarki from cottontopped tamarins Identify presence of infected animals Removal of intermediate paratenic or transport hosts from environment Yes if there is consumption of an intermediate or transport host Fact Sheet compiled by Peregrine Wolff Sheet completed on updated 9 July 2018 Fact Sheet Reviewed by Rachel Marschang Susceptible animal groups Vertebrate species Causative organism Phylum Acanthocephala are commonly known as thorny headed worms and are highly specialized unsegmented parasites of the digestive tract of mammals birds reptiles amphibians and fish Acanthocephala are characterized by their large size up to 65 cm and the presence of an anterior retractable proboscis that is covered with rings of recurved hooks arranged in horizontal rows in almost all species These hooks are used to attach the parasite to the intestinal mucosa of its final host while it completes its life cycle Acanthocephalans do not possess a digestive tract and absorb all nutrients through their body wall It is believed that over 1300 species of Acanthocephalan parasites exist Within the four orders of Acanthocephalans Neoechinorhynchidea infect turtles amphibians and fish Echinorhynchidea infect primarily fish amphibians reptiles birds and aquatic mammals However a few species are known to infect terrestrial mammals and birds of prey such as Corynosoma reported in free ranging marine mammals and C polymorphus reported in sea ducks Within the order Aporhynchidea the species Apororhynchus is a parasite of birds Gigantorhynchidea contains families and species that infect mammals Macracanthorhynchus suiids carnivores Prosthenorchis primates Moniliformis rodents and Oncicola carnivores and birds Zoonotic potential Yes Human reports of infection with acanthocephalans are rare and are associated with ingestion of the intermediate host or the transport or secondary hosts and most commonly associated with the consumption of raw fish Distribution Worldwide distribution in aquatic and terrestrial vertebrate species Incubation period Adult females lay eggs which contain a fully developed larva called an acanthor which passes into the environment If the acanthor is ingested by a suitable insect eg cockroaches can serve as intermediate insect hosts in zoos or crustacean intermediate host it will first enter the acanthella stage before developing in 612 weeks into the infective stage larva or cystacanth which encysts in the intermediate host American Association of Zoo Veterinarians Infectious Disease Manual ACANTHOCEPHALANS If the intermediate host is ingested by a final host then the cystacanth attaches onto the intestinal lumen and matures into an adult in 812 weeks If the intermediate host is ingested by a transport or paratenic host then the cystacanth will penetrate through the gut and encyst in the tissues or organs of this host only completing its life cycle if the transport host is ingested by a final host In experimental infections in swine Macracanthorhynchus ingens worms were found embedded in the mucosa of the intestine 3 days after the pig was fed cystacanths contained in a gelatin capsule Clinical signs Depending upon the host the species of parasite and the parasite burden there may be sub clinical to severe clinical signs Diarrhea emaciation restlessness abdominal pain often severe and poor weight gain has been described in pigs infected with Macracanthorhynchus hirudinaceus Diarrhea emaciation lethargy and illthrift have been noted in primates infected with Prosthenorchis elegans If the parasite penetrates the serosa of the intestines then clinical signs consistent with peritonitis may be evident Among birds ducks geese swans birds of prey and some species of passerines are most commonly infected Severe disease outbreaks have been reported in common eiders All age classes can become infected Acanthocephalans are actively being studied as bioindicators of pollution Parasites in fish have been found to have concentrations of heavy metals orders of magnitude greater than either the tissues of their hosts or the surrounding water If captive species were fed fish that were heavily parasitized by acanthocephalans with high concentrations of heavy metals perhaps the potential for toxicity exists Post mortem gross or histologic findings Attachment sites of the adult worms may be visible on the serosal surface of the intestine as circular flat areas of discoloration or as raised firm white nodules The proboscis may penetrate the mucosa submucosa muscularis and serosal layers of the intestine with the body of the worm protruding into the lumen Peritonitis occurs secondary to penetration of the parasite through the wall of the small intestine Histological changes at the intestinal site of penetration include thickening of the submucosa muscularis and serosa resulting from cellular infiltration and inflammatory exudates Intestinal villi at and immediately surrounding the site of attachment may be absent the cellular architecture may be disrupted and accompanied by leukocytic infiltration Some species of Acanthocephala may move around the intestine prior to settling on a final attachment site Gross and histological evidence of worm attachment without the presence of a parasite may be evident Some individuals can have worm burdens numbering from hundreds to thousands It is believed that this volume of large parasites within the lumen may cause mechanical blockage contributing to starvation of the host Diagnosis Identification of adults often is based on the pattern of hooks on the proboscis thus it is important that this portion of the worm is preserved and visible If required for identification and no adults are free floating then the worm should be carefully removed from its attachment site within the intestine and placed in water which creates an osmotic turgor forcing the proboscis to evert The worm is then fixed in warm alcohol formaldehydeacetic acid AFA a preservative which consists of 85 parts 85 ethanol 10 parts stock formalin and 5 parts glacial acetic acid Acanthocephalan eggs are large and heavy thus fecal sedimentation techniques utilizing formalinethyl acetate are felt to be superior to flotation techniques for identifying acanthocephalan eggs The eggs are elongated with a thick outer wall and thin inner walls often appearing to have 3 layers Within the egg lies the acanthor larva If the spines at one end of the larva are visible then a positive identification of acanthocephalan can be made Although when laid by the female the eggs are clear eggs of some species will appear brown due to fecal staining as they pass along of the intestinal tract of the host Material required for laboratory analysis Feces to determine presence of eggs are needed and fecal centrifugation techniques are preferred The whole parasite is necessary for species identification Sections of the intestine with the parasite within the lumen or embedded within the wall to determine degree of pathology associated with the attachment site Relevant diagnostic laboratories Before submission confirm with your diagnostic laboratory that they can key out species of adult parasites American Association of Zoo Veterinarians Infectious Disease Manual ACANTHOCEPHALANS Treatment Albendazole 50 mgkg bid x 16 days or 100 mgkg bid x 3 days and then repeated biweekly for a total of 4 treatments has been used to successfully treat captive cottontopped tamarins Saguinus oedipus infected with Moniliformis clarki Swine and dogs have been successfully treated for Macracanthorhynchus species with ivermectin and doramectin at dosages typical for the species Surgical removal of adult Prosthenorchis elegans from captive marmoset and tamarin species has also been an effective treatment Prevention and control All incoming animals should be quarantined and receive comprehensive fecal exams Animals infected with Acanthocephala should be treated Species should not have the opportunity to infect or ingest possible intermediate or transport hosts that could be infected with acanthocephalan species Although one species may shed the parasite another taxonomically unrelated species accidental host may ingest the intermediate host and become infected This transfer can have implications for mixed species exhibits and implementation of an effective pest control program Suggested disinfectant for housing facilities Removal of intermediate host pest control Notification None required Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Introductions should not be done unless no opportunity for introduction of a suitable intermediate host exists Conditions for restoring diseasefree status after an outbreak It is necessary to break the life cycle and remove possible intermediate hosts Experts who may be consulted Most research regarding acanthocephalans revolves around emerging human infections and identification of new species in new hosts Parasitologists at each veterinary university diagnostic laboratory can be consulted for acanthocephalan identification References 1 Amin OM Classification of the acanthocephalan Folia Parasitol 201360273305 2 Bowman DD Georgis Parasitology for Veterinarians 9th ed St Louis MO Elsevier 2009 p 464 3 ITIS Internet Acanthocephala ITIS Report c2017 cited 2019 January 14 Available from wwwitisgovservletSingleRptSingleRptsearchtopicTSNsearchvalue64238null 4 José ZárateRamos JJ GómezGarza MA RodríguezTovar LE Escareño JH ContrerasLozano JA An Alternative Treatment Against Acanthocephala Prosthenorchis elegans in Captive Squirrel Monkeys Saimiri sciureus in Mexico J Parasitol 20181045574575 5 Richardson DJ Brink CD Effectiveness of various anthelmintics in the treatment of moniliformiasis in experimentally infected Wistar rats Vector Borne Zoonotic Dis 201111811516 6 USGS Acanthocephaliasis In Friend M Franson JC eds Field manual of wildlife diseases general field procedures and diseases of birds Washington DC US Fish and Wildlife Service 1999 p 241243 Available from httpwwwfwspubsorgdoisuppl103996082016JFWM 065supplfilefwma080120refs05pdf 7 Weber M Junge R Identification and treatment of Moniliformis clarki Acanthocephala in cotton topped tamarins Saguinus oedipus J Zoo Wildl Med 200031 4503507 8 Yazwinski TA Tucker C Featherston H Johnson Z WoodHuels N Endectocidal efficacies of doramectin in naturally parasitized pigs Vet Parasitol 199770123 American Association of Zoo Veterinarians Infectious Disease Manual WOODEN TONGUE Actinobacillus lignieresii Fact Sheet compiled by Amanda Guthrie Sheet completed on 16 March 2011 updated 5 April 2013 updated 2018 Fact Sheet Reviewed by Mark Drew and Nancy Carpenter Susceptible animal groups Most commonly cattle are affected but can infect sheep horses pigs dogs and rarely chickens Causative organism Actinobacillus lignieresii Gramnegative coccobacillus Zoonotic potential No Distribution Occurs sporadically worldwide preferentially in areas with copper deficiency or pasture with abrasive weeds Incubation period Unknown Clinical signs Disease mainly affects the tongue and the lymph nodes of the head and neck Characteristic lesion is pyogranulomatous inflammation of the tongue with purulent discharge Inability to eat or drink may be noticed as well as excess salivation rapid weight loss and painful and swollen ulcerated tongue With chronicity the tongue becomes fibrous shrunken and immobile Draining lymph nodes in this area may become enlarged and abscessed with purulent discharge rarely granulomas can form in and around the jaw lungs esophagus udder skin or internal organs Sheep frequently are affected by purulent granulomas of the face lips nose jaw and neck Post mortem gross or histologic findings Poor body condition pyogranulomatous lesions containing pus in and around the mouth Oral ulcers and encapsulated abscesses of the local lymph nodes may be noted In chronic cases fibrous connective tissue proliferation of the tongue can be observed Diagnosis Reasonable suspicion based on clinical signs and it may be confirmed with microscopic exam of cytological specimens or by direct culture Purulent discharge contains small brownwhite granules which consist of colonies of Gramnegative rodshaped bacteria Material required for laboratory analysis Smears of pus fine needle aspirate samples Relevant diagnostic laboratories Kansas State University Veterinary Diagnostic Lab 1800 Denison Avenue Manhattan KS 66506 Phone 8665125650 Fax 7855324481 dlabofficevetkstateedu httpwwwvetkstateedudeptsdmpservice Treatment Surgical debridement systemic sodium iodide which is not labeled for use in food animals call FARAD about withdrawal times and antibiotics Streptomycin is considered the antibiotic of choice also tetracyclines erythromycin and tilmicosin are effective but require extended duration Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primarily cattle but also sheep horses pigs dogs and rarely chickens Normal oropharyngeal and rumen flora enters tissues through epithelial damage Granulomas of tongue and lymph nodes of head and neck Variable life threatening without treatment Surgical debridement systemic sodium iodide and longterm antibiotics Early recognition and treatment isolation of affected animals No American Association of Zoo Veterinarians Infectious Disease Manual WOODEN TONGUE Actinobacillus lignieresii Prevention and control Early recognition and treatment and isolation of affected animals is critical Animals with weeping lesions should be isolated and areas should be cleaned routinely as these bacteria only survive for a few days in the environment Lowquality dry stalky feed grass seeds coarse hay and scrub can predispose to disease by causing oral abrasions Tooth eruption may also allow for entry of bacterium into oral epithelium Suggested disinfectant for housing facilities Routine disinfection as organisms only live for a few days outside of an animal host Notification This disease is not reportable Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal None this organism is normal gastrointestinal flora it is not considered very contagious Conditions for restoring diseasefree status after an outbreak None Experts who may be consulted Kansas State University Veterinary Diagnostic Laboratory 1800 Denison Avenue Manhattan KS 66506 8665125650 References 1 Overview of Actinobacillosis Internet MSD Veterinary Manual cited 2018 Feb 13 Available from httpwwwmsdvetmanualcomgeneralizedconditionsactinobacillosisoverviewofactinobacillosis 2 Actinobacillosis Wooden Tongue Internet AHP Disease Manual cited 2018 Feb 13 Available from httplrdspcintextDiseaseManualFinalactinobacillosiswoodentonguehtml 3 Lumpy jaw and wooden tongue in cattle Internet NSW Department of Primary Industries cited 2018 Feb 13 Available from httpswwwdpinswgovauanimalsandlivestockbeefcattlehealthand diseasebacterialdiseaseslumpyjawwoodentongue 4 Carmalt JL Baptiste KE ChirinoTrejo JM Actinobacillus lignieresii infection in two horses J Am Vet Med Assoc 19992158268 5 Kokotovic B Angen O Bisgaard M Genetic diversity of Actinobacillus lignieresii isolates from different hosts Acta Vet Scand 201153 6 Available from httpwwwactavetscandcomcontentpdf17510147536pdf 6 Rycroft AN Garside LH Actinobacillus species and their role in animal disease Vet J 2000159118 36 7 Caffarena RD Rabaza A Casaux L Rioseco MM Schild CO Monesiglio C Fraga M Giannitti F RietCorrea F Natural lymphatic atypical actinobacillosis in cattle caused by Actinobacillus lignieresii J Vet Diagn Invest 2018302218225 American Association of Zoo Veterinarians Infectious Disease Manual ACTINOMYCOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Many mammal species including humans birds Endogenous infection into susceptible tissues or by bite wound Local abscesses chronic draining fistulas bony infections or infections of body cavities Clinical signs referable to the involved area Can be mild if restricted to local infection but can be fatal depending on infection location spread and time to diagnosis Surgical drainage and debridement Appropriate antibiotic therapy continued for several weeks after elimination of clinical signs Ensure good oral care Limit the amount of rough forage fed and limit the number of plant awns in environment Yes but most human infections are endogenous Fact Sheet compiled by Rebecca Bloch Sheet completed on 24 June 2011 updated 21 December 2012 Fact Sheet Reviewed by Amy Swinford John Gilliam Susceptible animal groups Horses cattle small carnivores goats sheep wild ruminants monkeys rabbits squirrels hamsters marsupials humans river otter and birds Causative organism Actinomyces spp including A bovis A hodeovulneris A israelii A naeslundii A pyogenes A suis and A viscosus These organisms are anaerobic to microaerophilic Gram positive rod shaped bacteria that may produce branching filaments The disease process termed lumpy jaw has many bacterial agents that include Fusobacterium necrophorum Bacteroides Streptococcus Staphylococcus Corynebacterium Nocardia and Actinobacillus in addition to Actinomyces species A bovis has been stated as being the causative agent of lumpy jaw in cattle but it has also been suggested that Actinomyces infection in exotic bovids is secondary to a tooth root infection rather than a primary infection J Oosterhuis personal communication If the mandible undergoes a traumatic incident that interrupts the blood supply to a tooth causing it to become devitalized this damage leads to necrosis and then secondary invasion by various bacteria including Actinomyces species Zoonotic potential Generally the disease is not contagious except via bite wounds The only suggested documented zoonotic infection in the literature was caused by Actinomyces pyogenes since reclassified as Arcanobacterium pyogenes Distribution Normal flora of the oral and nasopharyngeal membranes This species is secondarily found in the gastrointestinal tract In humans these organisms are also found in the female genitourinary tract Incubation period This organism requires 2448h for growth in media but infections are endogenous and require introduction of the bacteria into susceptible tissue to initiate infection generally through tissue trauma or less frequently through bite wound Clinical signs Lesions include localized abscesses chronic draining fistulas bone infections or infections of body cavities Drainage from the lesions is serosanguinous and often contains small yellow granules Infection may be associated with fever Clinical signs are referable to the area of involvement In cattle humans and marsupials Actinomyces sp associated with osteomyelitis is characterized by dislodgement of teeth inability to chew and mandibular fractures In several hosts this bacterium can cause soft tissue infections In horses it may manifest as supraatlantal or supraspinous bursitis or sometimes cervical abscesses Actinomyces endopthalmitis has been documented in a dog Actinomyces spp has been associated with plant awn foreign American Association of Zoo Veterinarians Infectious Disease Manual ACTINOMYCOSIS bodies and associated disease such as discospondylitis in small carnivores In humans in addition to other sites of infection actinomycosis can be associated with contraceptive intrauterine devices A bovis is associated with osteomyelitis in cattle typically causing formation of periosteal new bone and fibrosis in the mandible most commonly on the horizontal ramus It can occasionally cause ganulomatous abscesses in the soft tissues of the head esophagus forestomachs and trachea A actinoides is occasionally found in enzootic pneumonia of calves and seminal vasculitis in bulls A hordoevulneris causes localized abscesses and systemic infections such as pleuritis peritonitis visceral abscesses and septic arthritis in dogs Infection is associated with migrating plant awns A israelii is associated with chronic granulomatous infections in humans but has rarely been isolated from pyogranulomatous lesions in pigs and cattle A neslundii has been isolated from suppurative infections in several animal species the most common being aborted porcine fetuses A pyogenes currently Arcanobacter pyogenes is associated with infections in many organ systems in many species of animals Infections include suppurative mastitis suppurative pneumonia septicemia vegetative endocarditits endometritis intracranial abscesses or suppurative meningoencephalitis septic arthritis wound infections and liver abscesses A suis causes pyogranulomatous porcine mastitis Chronic deep seated abscesses may fistulate A viscosus causes chronic pneumonia pyothorax and localized subcutaneous abscesses in dogs Thoracic lesions are pyogranulomatous while cutaneous lesions are granulomatous abscesses often with fistulous tracts Lesions generally develop after a traumatic injury such as a bite wound A denticolens has been reported to cause mandibular lymphadenopathy in horses with possible fever nasal discharge and depression making it clinically similar to strangles Post mortem gross or histologic findings Aggregates of Gram positive filamentous nonacidfast bacteria with associated inflammation in the areas of infection While it is possible to detect Actinomyces sp in tissue sections stained with hematoxylin and eosin sulfur granules are round or oval basophilic masses with a radiating arrangement of eosinophilic terminal clubs special stains such as Gomori methenamine silver paminosalicylic acid McCallenGoodpasture and BrownBenn may be needed Diagnosis Grossly yellowish particles up to several millimeters in diameter in the lesions or tissue may be observed These particles called sulfur granules are suggestive of Actinomyces infection but can also be seen with other types of bacteria Nocardia sp In the case of A viscosus infection soft grayish white granules may be seen in the pus or exudate Clinical presentation Gram stain and histopathologic visualization of the bacteria and granules are supportive of the diagnosis Definitive diagnosis requires culture but is not always possible as this group of organisms is sometimes difficult to grow Material required for laboratory analysis Culture swab or tissue sample from the affected area Relevant diagnostic laboratories Any laboratory capable of running bacterial cultures should be able to culture this organism Although most strains do not require anaerobic incubation they do benefit from increased carbon dioxide concentration Treatment Appropriate surgical drainage or debridement in addition to antimicrobial administration Iodine compounds penicillin and isoniazid have been used to treat bovine cases In small carnivores a penicillin derivative is the drug of choice but penicillins have difficulty penetrating pyogranulomatous lesions which may necessitate prolonged therapy Chloramphenicol and clindamycin can also be used Antibiotic impregnated beads have been used in the treatment of bone infections A published suggestion for treatment of jaw osteomyelitis includes surgical debridement of the lesion followed by surgical fistulation to allow lavage with sterile water hydrogen peroxide 525 sodium hypochlorite and then 2 Betadine Once infection is eliminated or contained surgical repair of the tooth and bony defect can occur Prevention and control Reduce feeding of rough or excessively fibrous plant material that might cause American Association of Zoo Veterinarians Infectious Disease Manual ACTINOMYCOSIS trauma to the oral cavity Reduce any environmental stressors such as overcrowding Good oral care to help prevent food impaction or entry of bacteria in dental caries Suggested disinfectant for housing facilities Since Actinomyces sp are normal flora and generally found in the oral cavity of the animals they effect environmental decontamination of the environment has less importance However the bacteria can reside in the environment in organic material and these organisms can be removed through thorough cleaning of any organic material from the environment followed by disinfection with 10 bleach or any of the commercially available disinfectants mixed to manufacturers instructions Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Since most infections are endogenous unless the infected animal is likely to bite another animal no special measures beyond individual health care need to be taken Conditions for restoring diseasefree status after an outbreak Special attention should be paid to husbandry practices and oral care in the animals of concern Experts who may be consulted Amy K Swinford DVM MS Dipl ACVM Head Diagnostic Bacteriology PO Drawer 3040 College Station TX 77841 aswinfordtvmdltamuedu 9798453414 References 1 Barnes L and B H Grahn 2007 Actinomyces endopthalmitis and pneumonia in a dog Can Vet J 48 11551158 2 Bartlett JG Actinomyces Johns Hopkins Antibiotic Guide httpwwwhopkinsguidescomhopkinsubviewJohnsHopkinsABXGuide540005allActinomyces Accessed 11 July 2013 3 Biberstein EL and DC Hirsh 1999 Pathogenic Actinomycetes Actinomyces and Nocardia In Hirsh DC and YC Zee eds Veterinary Microbiology Blackwell Sciences Inc Malden Massachusetts Pp 250253 4 Britton A P E Zabek and H Schwantje 2011 Pleural actinomycosis in a freeranging river otter Lutra canadensis J Zoo Wildl Dis 427514 5 Davidson W R V F Nettles L E Hayes E W Howerth and C E Couvillion 1990 Epidemiologic features of an intracranial abscessationsuppurative meninogencephalitis complex in whitetailed deer J Wildl Dis 26 460467 6 Fagan DA JE Oosterhuis and K Benirschke 2005 Lumpy jaw in exotic hoofstock a histopathologic interpretation with a treatment proposal J Zoo Wild Med 36 3643 7 Oostman O and RA Smego 2005 Cervicofacial actinomycosis diagnosis and management Curr Infect Dis Rep 7 170174 8 Overview of actinomycosis httpwwwmerckmanualscomvetgeneralizedconditionsactinomycosisoverviewofactinomycosis html Accessed 11 July 2013 9 Smith BP 1996 Actinomycosis In Smith BP ed Large Animal Internal Medicine MosbyYear Book St Louis Missouri Pp 796797 10 Vogelnest L and T Portas 2008 Macropods In Vogelnest L and R Woods eds Medicine of Australian Mammals Csiro Publishing Collingwood Victoria Australia Pp 133225 American Association of Zoo Veterinarians Infectious Disease Manual ADENOVIRUS Fact Sheet compiled by Natalie D Mylniczenko Sheet completed on 29 January 2011 6 October 2012 update 19 April 2018 Fact Sheet Reviewed by Erika TravisCrook Susceptible animal groups Mammals Infectious canine hepatitis canine adenovirus 1 foxes wolves ferrets raccoons skunks ursids black bears Eurasian otter n1 hedgehog n1 and other small carnivores Adenoviral hemorrhagic disease virus cervids Acute hepatic necrosis California sea lion CSLAdV1 Dolphin Simian adenoviruses 130 oncogenic and nononcogenic SA8 baboons infantspneumonia Birds Many avian adenoviruses quail bronchitis virus hemorrhagic enteritis etc Egg drop syndromeduck adenovirus A chickens ducks quail Pigeon adenovirus Reptiles Agamid adenovirus 1 bearded dragon Snake and lizard adenoviruses Amphibian and fish have adenoviruses that are of no known clinical significance at this time Causative organism Adenovirus Nonenveloped DNA virus Zoonotic potential None Distribution Worldwide Incubation period Mammal 810d avian 34d for respiratory 1024 for egg production Clinical signs Mammal blue eye young animals nonspecific gastrointestinal signs Course is typically peracute or acute Birds young birds respiratory disease change in egg qualityproduction Reptiles none to chronic poor doer to death Post mortem gross or histologic findings respiratory gastrointestinal and ocular systems typically affected Mammals Carnivores hemorrhage of stomach and serosal surfaces coagulation impairment hepatic congestion and hepatomegaly Focal hepatic necrosis Cervids pulmonary edema and hemorrhagic enteropathy Birds enteritis splenitis marble spleen disease hepatitis bronchitis pulmonary congestion Reptiles enteritis and hepatitis rarely encephalitis and esophagitis Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Birds Reptiles Vertical Direct contact Fecaloral Venereal Mammal respiratory conjunctivitis liver disease gastro enteritis Avian abnormal eggs and production respiratory disease Reptile none to poor doer to unexplained death Variable asymptomatic to death Usually disease is sporadic and limited to the young and immune compromised Supportive symptomatic Vaccination carnivores however this approach is not common One case of vaccine induced disease No as virus is highly host specific American Association of Zoo Veterinarians Infectious Disease Manual ADENOVIRUS Diagnosis Mammals Antemortem is difficult since signs are nonspecific and rapid Virus isolation immunofluorescence or characteristic intranuclear inclusion bodies in the liver or other lesions Serology is available Birds serology agar gel immunodiffusion fluorescent antibody virus isolation Reptiles polymerase chain reaction or electron microscopy Material required for laboratory analysis Mammals serum swabs tissue from liver and lung Birds serum tissue from lesions Reptiles tissues from lesions or cloacalfecal swabs Relevant diagnostic laboratories Mammals Mammalian tests bovine canine equine porcine llamamany veterinary diagnostic labs Primate httpwwwvrlnet httpzoologixcomprimateindexhtm Birds National Veterinary Services Laboratories USDAAPHISVSNVSL Avian Viruses Section Head Dr Mia Kim Torchetti Phone 515 3377551 Email miakimtorchettiaphisusdagov httpswwwaphisusdagovaphisourfocusanimalhealthlabinfo servicessadiagnostictestsctdiagnostictests Charles River Avian Vaccine Services httpswwwcrivercomproductsservicesavianvaccineservices Penn State Animal Diagnostic Laboratory Wiley Lane University Park PA 16802 Phone 8148630837 Fax 8148653907 adlhelppsuedu httpvbspsuedufacilitiesadlservicestestsavianvirology Reptiles Zoo Medicine Infectious Disease Lab University of Florida 2015 SW 16th Ave Building 1017 Room V2238 Gainesville FL 32610 Contact April Childress Phone 3522944420 childressaufledu httplabsvetmedufledusamplerequirementsmicrobiologyparasitologyserologyzoomedinfections Treatment Supportivesymptomatic Prevention and control Vaccination carnivoresmodified live vaccine for canids American Association of Zoo Veterinarians Infectious Disease Manual ADENOVIRUS Virus shed in urine nasal and conjunctival secretions and feces Virus persists in the kidney and may be shed for months after recovery Do not translocate cervids from affected areas to nonendemic areas Suggested disinfectant for housing facilities Adenoviruses are very stable in the environment but are susceptible to 1 sodium hypochlorite 2 glutaraldehyde and quaternary ammonium compounds Notification Some states require notification with birds and deer Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Vaccination prior to introduction should be considered however incidence rate in most species is low Animals may shed virus in urine and other secretions for up to 6 months Conditions for restoring diseasefree status after an outbreak Outbreaks are not typical Experts who may be consulted See Diagnostic Laboratories References 1 Adenoviridae In Murphy FA Gibbs EPJ Horzinek MC Studdert MJ eds Veterinary Virology 3rd ed Orlando FL Academic Press 1999 p 327334 2 Boyce WM Woods LW Keel MK MacLachlan NJ Porter CO Lehmkuhl HD An epizootic of adenovirusinduced hemorrhagic disease in captive blacktailed deer Odocoileus hemionus Am J Pathol 1978 912259276 3 The Center for Food Safety Public Health Internet 2017 cited 2018 December 27 Available from httpwwwcfsphiastateeduFactsheetspdfseggdropsyndromepdf 4 Hall NH Archer LL Childress AL Wellehan JFX Identification of a novel adenovirus in a cottontop tamarin Saguinus oedipus J Vet Diagn Invest 2012242359363 5 Hess M Detection and differentiation of avian adenoviruses a review Av Pathol 200029195206 6 Katoh H Ogawa H Ohya K Fukushi H A review of DNA viral infections in psittacine birds J Vet Med Sci 201072910991106 7 McFerran JB Smyth JA Avian adenoviruses Rev Sci Tech 2000192589601 8 RubioGuerri C GarcíaPárraga D NietoPelegrín E Melero M Álvaro T Valls M Crespo JL SánchezVizcaíno JM Novel adenovirus detected in captive bottlenose dolphins Tursiops truncatus suffering from selflimiting gastroenteritis BMC Vet Res 201511153 9 Shilton CM Smith DA Woods LW Crawshaw GJ Lehmkuhl HD Adenoviral infection in captive moose Alces alces in Canada J Zoo Wildl Med 20023317379 10 Swenson J Orr K Bradley GA Hemorrhagic and necrotizing hepatitis associated with administration of a modified live canine adenovirus2 vaccine in a maned wolf Chrysocyon brachyurus J Zoo Wildl Med 2012432375383 11 Twomey DF Grierson SS Martelli F Higgins RJ Jeffrey M Enteritis in an alpaca Vicugna pacos associated with a potentially novel adenovirus J Vet Diagn Invest 2012245 10001003 12 Vereecken M de Herdt P Ducatelle R Adenovirus infections in pigeons a review Av Pathol 1998 274333338 13 Woods LW Adenoviral diseases In Williams ES Barker IK eds Infectious Diseases of Wild Mammals 3rd ed Ames IA Iowa State University Press 2001 p 202212 American Association of Zoo Veterinarians Infectious Disease Manual AEROMONAS INFECTIONS Fact Sheet compiled by Douglas P Whiteside Sheet completed on 31 March 2011 updated 17 July 2013 Updated 27 January 2018 Fact Sheet Reviewed by Karen Liljebjelke Stephen Raverty Susceptible animal groups Fish especially salmonids goldfish carp amphibians reptiles waterfowl marine mammals Occasionally isolated from invertebrates Causative organism Aeromonas hydrophila A salmonicida A shigelloides A formicans A sobria and Aeromonas sp of which of the at least seven recognized species four of which are considered more pathogenic It is a Gram negative oxidative positive facultative anaerobic polar flagellated bacterial rod Zoonotic potential Yes but also direct environmental exposure Opportunistic zoonotic pathogen especially in immunocompromised or debilitated individuals Distribution Worldwide distribution Common in fresh brackish and salt water environments particularly with increased detritus or sewage and carried by some invertebrate and vertebrate species Incubation period 2448 hours Clinical signs Fish Acute mortality septicemia erythema exophthalmia hemorrhages in skin fins muscle and oral cavity with skin boils and ulceration Fecal casts or bloody discharge from vents Amphibians Acute mortality septicemia anorexia ventral erythema with cutaneous hemorrhage especially ventral thighs edema in subcutis anasarca hemorrhagic ulcerations of digit tips and jaw May feature digital amputation due to vasoconstriction secondary to septicemia Reptiles Acute mortality septicemia pneumonia ulcerative stomatitis particularly in snakes dermal ecchymoses epidermal ulceration anorexia listless labored respirations harsh respiratory sounds mouth gaping steady decline in status rule out predisposing or underlying environmental or host factors Waterfowl Upper respiratory tract infections salpingitis enteritis septicemia localized abscessation and arthritis Marine mammals Septicemia pneumonia Humans Gastroenteritis watery diarrhea which can be chronic in nature septicemia pustular dermatitis cellulitis necrotizing fasciitis pneumonia peritonitis cholecystitis bacteremia and hepatitis Post mortem gross or histologic findings Fish Cavitating dermal ulceration furuncles and myositis exophthalmus serosanguineous ascites commonly observed Splenomegaly and swollen kidneys are common Multifocal areas of necrosis and hemorrhage in Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Fish Amphibians Reptiles Waterfowl Marine mammals Horizontal transmission close contact with infected individual ingestion of bacterium direct inoculation through wounds especially from contaminated water and detritus Snake mite Ophionyssus natricis capable of transmitting bacteria Acute mortality dermal hyperemia skin wounds pustular dermatitis stomatitis fasciitis muscle cavitations pneumonia gastro intestinal disease Mild to severe depending on immune status and route of infection Antibiotics appropriate wound management supportive care Ubiquitous in environment and may comprise part of the normal intestinal flora Opportunistic infection Prevention through good environmental and personal hygiene practices optimal husbandry UV irradiation or ozonation of water vaccination for Aeromonas salmonicida Yes American Association of Zoo Veterinarians Infectious Disease Manual AEROMONAS INFECTIONS the spleen liver kidney and heart with numerous bacilli Punctate colonies of extracellular bacteria and a lack of associated inflammatory infiltrate are hallmarks of A salmonicida infections in salmonids Carp erythrodermatitis Amphibians Ventral erythema hepatosplenomegaly ascites anasarca pulmonary congestion petechiae and ecchymoses in skeletal muscle coelomic serosa kidneys and spleen Reptiles Dermal hyperemia ulceration stomatitis hepatomegaly exudates in trachea and lungs ascites splenomegaly renomegaly intestinal edema Waterfowl Salpingitis peritonitis arthritis or septicemia Marine mammals Severe pneumonia septicemia ulcerative dermatitis Humans Pustular dermatitis cellulitis necrotizing fasciitis osteomyelitis pyomyositis pneumonia bacteremia peritonitis and meningitis Diagnosis Isolation on routine media heart infusion agar blood agar MacConkey Tryptone soya agar with subsequent identification commercial systems molecular identification amplified fragment length polymorphism AFLP analysis Results must be taken in context of clinical signs and pathologic findings Material required for laboratory analysis Transport media CaryBlair medium is most suitable Transport at roomenvironmental temperature yields greatest recovery Relevant diagnostic laboratories Any laboratory that can perform bacteriological isolation identification and antimicrobial resistance Treatment Antibiotic selection is dependent on susceptibility testing In general these bacteria are susceptible to aminoglycosides carbapenems extended spectrum cephalosporins azithromycin monobactams nitrofurans extended spectrum penicillins piperacillin piperacillintazobactam phenicols fluoroquinolones and tetracyclines with variable susceptibility to potentiated antifolates trimethoprim sulfas Aeromonas spp produce strong Blactamases so they resistant to narrow spectrum penicillins eg amoxicillin ampicillin ampicillinsulbactam ticarcillin oxacillin penicillin and cephalosporins eg cefoxitin sulfamethoxazole erythromycin and clarithromycin Prevention and control In species other than fish infections are often opportunistic or secondary to debilitation or immunosuppression Maintain good environmental hygiene water quality and optimal husbandry conditions ultraviolet irradiation or ozonation of water sources proper food storage and follow safe cooking and thawing recommendation follow all wound care procedures recommended by veterinarian or physician practice good hygiene wash hands often Suggested disinfectant for housing facilities UV irradiation or ozonation of water sources is possible Most disinfectants are effective such as sodium hypochlorite chlorhexidine quaternary ammonium products phenolics accelerated hydrogen peroxide Virkon Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Ubiquitous and opportunistic bacteria Good quarantine procedures Tank water to discharge or if recirculating ensure appropriate treatment and disinfection Ideally isolate infected animals for treatment Conditions for restoring diseasefree status after an outbreak Environmental hygiene povidone iodine disinfection of fish eggs Experts who may be consulted Ruth FrancisFloyd DVM MS DACZM University of Florida IFAS Extension PO Box 100136 2015 SW 16th Ave Gainesville FL 326080136 Phone 3522944197 Fax 3523928289 rffloydufledu American Association of Zoo Veterinarians Infectious Disease Manual AEROMONAS INFECTIONS References 1 Batra P Mathur P Misra MC Aeromonas spp as a causative agent for nosocomial infection in trauma patients J Infect 201570687689 2 Boseret G Mainil JG Aeromonas spp as pathogens for marine mammals in systemic and skin disease In Proc 41st Internat Symp Dis Zoo Wild Anim 2003 p 157160 3 Cipriano RC Bullock GL Furunculosis and other diseases caused by Aeromonas salmonicida National Fish Health Research Laboratory 2001 4 Higgins R Bacteria and fungi of marine mammals a review Can Vet J 200041105116 5 Jacobson ER Bacterial diseases of reptiles In Jacobson ER ed Infectious Diseases and Pathology of Reptiles Boca Raton FL CRC Press 2007 p 463 6 Janda JM Abbott SL The Genus Aeromonas Taxonomy Pathogenicity and Infection Clin Microbiol Rev 20102313573 7 Jauniaux T Petitjean D Brenez C Borrens M Brosens L Haelters J Tavernier T Coignoul F Post mortem findings and causes of death of harbour porpoises Phocoena phocoena stranded from 1990 to 2000 along the coastlines of Belgium and Northern France J Comp Pathol 2002126424353 8 Kaiser L Surawicz CM Infectious causes of chronic diarrhoea Best Practice Research Clinical Gastroenterology 2012265563571 9 Kong RYC Lee SKY Law TWF Law SHW Wu RSS Rapid detection of six types of bacterial pathogens in marine waters by multiplex PCR Water Res 20023628022812 10 Semel JD Trenholme G Aeromonas hydrophila waterassociated traumatic wound infections a review J Trauma 199030324327 11 Taylor SK Green DE Wright KM Whitaker BR Bacterial diseases In Wright KM and Whitaker BR eds Amphibian Medicine and Captive Husbandry Malabar FL Krieger Publishing 2001 p 161 166 12 Thorton SM Nolan S Gulland FM Bacterial isolates from California sea lions Zalophus californicus harbor seals Phoca vitulina and northern elephant seals Mirounga angustirostris admitted to a rehabilitation center along the central California coast 19941995 J Zoo Wildl Med 199829171176 13 Zhou Z Guo Q Dai H Identification of differentially expressed immunerelevant genes in Chinese softshelled turtle Trionyx sinensis infected with Aeromonas hydrophila Vet Immunol Immunopathol 200812512 8291 American Association of Zoo Veterinarians Infectious Disease Manual AFRICAN HORSE SICKNESS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Equidae carnivores camel Infectious non contagious vector borne disease transmitted by Culicoides midge mechanical transmission by biting flies is possible ingestion of virus infected meat Respiratory form fever dyspnea nasal discharge conjunctivitis Cardiac form fever swollen head and neck colic Mixed form combination of respiratory and cardiac form signs Fever form fever Mortality depends on serotype and species affected most severe in horses and mules typically acute or subacute illness with high morbidity and mortality of respiratory cardiac and mixed forms fever form is mild with no mortality No effective treatment but supportive care warranted Vaccinate reduce exposure to vector test and quarantine prior to importation No Fact Sheet compiled by Priscilla H Joyner Sheet completed on 31 March 2011 updated 1 February 2018 Fact Sheet reviewed by John Sykes Susceptible animal groups Equidae carnivores Horses are highly susceptible with a mortality rate as high as 95 with peracute disease while mules are less susceptible African donkeys zebra elephants and camels are generally resistant to disease Antibodies to all 9 serotypes have been reported in elephants and zebra Dogs are susceptible to disease if they ingest virus infected meat Wild African carnivores are less susceptible Causative organism Orbivirus of the family Reoviridae including 9 serotypes 19 Zoonotic potential No However vaccine strains have caused encephalitis and retinitis in humans following transnasal transmission Distribution Endemic in Africa with outbreaks reported in the Middle East and Europe Dependent on climatic factors favoring the Culicoides vector such as warm humid weather and high rainfall Distribution of disease has potential to expand with changes in climate and potential vector distribution Virus transmission is greatly reduced when biting midge activity is reduced following onset of winter and frost Incubation period 314 days depending on form of infection acute respiratory form 35 days cardiac form 12 weeks fever form 414 days Clinical signs The respiratory form can be acute or peracute causing fever 4042 C respiratory distress RR50 paroxysmal coughing nasal discharge congested conjunctiva and abnormal stance Mortality rate may reach 95 The cardiac form causes fever 3941 C swelling of the supraorbital fossa extending to head and neck causing dyspnea and colic Mortality rate may be as high as 50 The most common form is the mixed form A combination of respiratory signs with head and neck swelling is seen with a mortality rate of 70 The fever form is characterized by mild pyrexia with occasional congestion of conjunctiva depression and inappetence but minimal mortality In endemic areas this disease can be confused with equine encephalosis or equine viral arteritis Dogs usually develop the respiratory form of disease Zebra may develop a mild fever Post mortem gross or histologic findings Gross lesions vary based on the form of disease In the respiratory form lesions include pulmonary edema hydrothorax frothy fluid in the trachea bronchi and bronchioles occasional pleural effusion edematous lymph nodes congestion and hyperemia of abdominal viscera and petechiae of the epicardium and endocardium In the cardiac form yellow gelatinous infiltrations of subcutaneous and intramuscular tissues of the head and neck as well as hydropericardium myocarditis with petechiae of the endocardium and epicardium petechiae of the peritoneum and ventral tongue flaccid or slightly edematous lungs and hemorrhagic gastritis may be seen The mixed form of disease produces a combination of lesions characteristic of the respiratory and cardiac forms Diagnosis Virus neutralization is the gold standard test although RTPCR is used for rapid screening samples American Association of Zoo Veterinarians Infectious Disease Manual AFRICAN HORSE SICKNESS from suspected clinical cases Serology ELISA complement fixation virus neutralization lateral flow assay Luminex assay and virus isolation are also available For determination of serotype use virus neutralization or RTPCR Outbreaks should be diagnosed using more than one test when possible Material required for laboratory analysis Serum whole blood Lithium heparin or EDTA blood tubes fresh tissue not frozen spleen lymph node lung formalin fixed tissue 101 Relevant diagnostic laboratories Call prior to sample submission Foreign Animal Disease Diagnostic Laboratory for PCR testing of sick animal samples must be in packages USDAAPHIS FADDL 40550 Route 25 579 Edwards Ave Calverton NY 11933 This is a hold location address and must be included on way bill Orient Point NY 11957 For Friday fed ex shipping must check box 6 on label to ensure Saturday delivery Director Dr Kimberly Dodd Telephone 631 3233256 Fax 631 3233366 Email KimberlyADoddaphisusdagov National Veterinary Services Laboratory for VI ELISA and PCR testing USDAAPHISNVSL PO BOX 844 1920 DAYTON AVENUE AMES IA 50010 Telephone 515 3377514 Treatment None but supportive care is warranted Prevention and control Imported equids should be free of clinical signs on day of export and should not have received AHS vaccine within 40 days infective period prior to export and be quarantined in vector protected facilities for 1440 days prior to export and throughout transportation Importation of equine semen follows the same guidelines Review the OIE website for the most up to date recommendations on exportimport requirements In endemic areas vaccinate susceptible animals using approved vaccines Reduce vector exposure by stabling equids at peak times of vector activity Establish vector control methods During an outbreak quarantine the area stop all equid movement in or out test suspect cases vaccinate susceptible equids and conduct epidemiological investigation Do not feed carcasses from infected individuals to carnivores Suggested disinfectant for housing facilities Commercial chlorine iodine and quaternary ammonia based compounds Notification Reportable to the OIE Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Do not introduce naive animals to infected animals Animals at risk of exposure should be vaccinated prior to introduction to new groups Conditions for restoring diseasefree status after an outbreak Clean areas with appropriate disinfectants Experts who may be consulted Alan Guthrie MMedVet PhD Director Equine Research Centre University of Pretoria Onderstepoort South Africa alanguthrieupacza References 1 USDA APHIS Internet United States Department of Agriculture cited 2018 March 1 Available from httpswwwaphisusdagovaphisourfocusanimalhealth 2 OIE Internet World Organization for Animal Health cited 2018 March 1 Available from American Association of Zoo Veterinarians Infectious Disease Manual AFRICAN HORSE SICKNESS httpwwwoieintanimalhealthintheworldofficialdiseasestatusafricanhorsesickness 3 McKenna T Overview of African Horse Sickness In Aiello SE Moses MA eds The Merck Veterinary Manual 11th ed Kenilworth NJ Merck Co 2016 p 696698 4 Alexander KA Kat PW House J House C OBrien SJ Laurenson MK McNutt JW Osburn BI African horse sickness and African carnivores Vet Microbiol 199547133140 5 Binepal VS Wariru BN Davies FG Soi R Olubayo R An attempt to define the host range for African Horse Sickness virus Orbivirus Reoviridae in East Africa by a serological survey in some Equidae Camelidae Loxodontidae and Carnivore Vet Microbiol 1992311923 6 Guthrie AJ Maclachlan NJ Joone C Lourens CW Weyer CT Quan M Monyai MS Gardner IA Diagnostic accuracy of a duplex realtime reverse transcription quantitative PCR assay for detection of African Horse Sickness virus J Virol Methods 2013189305 7 Mellor PS Hamblin C African Horse Sickness Vet Res 200435445466 8 Shirai J Kanno T Tsuchiya Y Mitsubayashi S Seki RJ Effects of chlorine iodine and quaternary ammonium compound disinfectants on several exotic disease viruses Vet Med Sci 2000628592 American Association of Zoo Veterinarians Infectious Disease Manual AFRICAN SWINE FEVER Fact Sheet compiled by Cora Singleton Sheet completed on 1 March 2011 updated 1 October 2012 Fact Sheet Reviewed by Pat Morris Alex Ramirez Susceptible animal groups Swine Warthogs Phcochoerus aethiopicus bushpigs Potamochoerus porcus and giant forest hogs Hylochoerus meinertzhageni act as reservoir hosts in Africa Ticks of the genus Ornithodoros are considered the natural arthropod host Causative organism African swine fever virus is a large icosahedral DNA virus the only member of the genus Asfivirus in the Asfarviridae family Zoonotic potential No Distribution Africa parts of Europe Spain and Portugal the Caribbean Incubation period 319 days acute form 37 days Clinical signs Acute disease Pyrexia severe depression weak hind legs ocular discharge erythema cyanotic skin blotching extensive hemorrhages diarrhea cough convulsions High mortality Chronic disease Pyrexia depression emaciation joint swelling pneumonia necrotic skin patches abortion Low mortality persistent viremia Post mortem gross or histologic findings Widespread petechial and ecchymotic hemorrhages lymph nodes kidneys skin larynx urinary bladder dark red to purple areas on skin occasional button ulcers in cecum enlarged spleen Diagnosis Agent identification Culture hemadsorption test fluorescent antibody test FAT PCR serology ELISA indirect fluorescent antibody test IFA immunoblotting test counter immunoelectrophoresis OIE prescribed test for international trade ELISA alternative IFA Material required for laboratory analysis Contact regulatory agencies prior to collecting and shipping samples which should include tissues lymph node kidney spleen lung and blood serum and EDTA anticoagulated whole blood Relevant diagnostic laboratories Foreign Animal Disease Diagnostic Laboratory USDAAPHISVSNVSLFADDL 40550 Route 25 for packages Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Domestic and wild pigs and peccaries Direct oral and nasal routes skin wounds Indirect feeding uncooked infected pork products fomites or bites of soft ticks Ornithodoros spp Acute pyrexia weak hind legs cyanotic skin hemorrhages Chronic emaciation joint swelling abortion Inapparent disease to acute death None Prevention no vaccine control soft ticks do not feed uncooked pork Control test slaughter quarantine disinfect No American Association of Zoo Veterinarians Infectious Disease Manual AFRICAN SWINE FEVER Orient Point NY 11957 PO Box 848 for letters Greenport NY 119440848 Director Dr Fernando TorresVelez Phone 631 3233256 Fax 631 3233366 Email FernandoJTorresVelezaphisusdagov Treatment No effective treatment Prevention and control Prevention vaccines are not effective Prevention includes control of pig movements and implementation of serological surveys to detect carrier pigs control of natural reservoirs soft ticks and avoidance of feeding uncooked pork products Control measures include depopulation of infected pigs disinfection of premises area quarantine and control of pig movement Suggested disinfectant for housing facilities Sodium hydroxide hypochlorites formalin sodium carbonate orthophenylphenol iodine compounds Notification Reportable to the USDAAPHIS through the State Veterinarian or the federal Area Veterinarian in Charge The disease is also reportable to the World Organization for Animal Health OIE Measures required under the Animal Disease Surveillance Plan Foreign animal disease reportable Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Infections must be reported to USDAAPHIS for management Experts who may be consulted USDA State Veterinarians or federal Area Veterinarians in Charge References 1 The Center for Food Security and Public Health Iowa State University College of Veterinary Medicine 2010 African swine fever httpwwwcfsphiastateeduDiseaseInfodiseasephpnameafricanswinefeverlangen Accessed 3 September 2013 2 Jackson P G G and P D Cockcroft 2007 Handbook of Pig Medicine Saunders Elsevier London England Pp 184185 3 SanchezVizcaino J J 1999 African swine fever In Straw B E S DAllaire W L Mengeling D J Taylor eds Diseases of Swine 8th ed Iowa State University Press Ames Iowa Pp 93102 4 United States Department of Agriculture Animal Plant and Health Inspection Services 2012 National Animal Health Laboratories Network httpwwwaphisusdagovanimalhealthnahlnlabsshtml Accessed 3 September 2013 5 United States Department of Agriculture Animal Plant and Health Inspection Services 2011 National Veterinary Services Laboratories Diagnostic Tests Available httpwwwaphisusdagovanimalhealthlabinfoservicesdiagnostestsshtml Accessed 3 September 2013 6 World Organization for Animal Health OIE 2013 African swine fever In Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2012 httpwwwoieintfileadminHomeengHealthstandardstahm20801ASFpdf Accessed 3 September 2013 7 World Organization for Animal Health OIE 2013 List of Tests for International Trade In Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2012 httpwwwoieintfileadminHomeengHealthstandardstahm002PRESCRIBED TESTS2012pdf Accessed 3 September 2013 American Association of Zoo Veterinarians Infectious Disease Manual ALEUTIAN DISEASE Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mustelids most common in farmraised mink rarely observed in ferrets over last several years Vertical not reported in ferrets and horizontal transmission air direct contact with urine feces or blood contact with contaminated fomites Chronic wasting weakness reproductive failure melena CNS signs and renal failure The disease can be fatal some pet ferrets are carriers and may not show clinical signs for years No effective therapy although antiinflam matory or immune suppression treatment may minimize organ damage and clinical signs in pet ferrets Biosecurity in facilities test and cull positive animals or minimally isolate in pet situations No Fact Sheet compiled by Gwen E Myers Sheet completed on 1 February 2011 updated 15 August 2013 Fact Sheet Reviewed by A Hossain Farid Katrina Ramsell Susceptible animal groups Mustelids notably mink weasels and ferret Causative organism Parvovirus Zoonotic potential None has been identified However rare reports of a possible relationship between Aleutian mink disease parvovirus AMDV and human infection are noted Two mink farmers with vascular disease and microangiopathy similar to that in mink with Aleutian disease were found to have AMDVspecific antibodies and AMDV DNA These findings raise the suspicion that AMDV may play a role in human disease See article at the end of sheet marked Distribution Worldwide predominantly on mink farm operations uncommonly reported in pet ferrets recently Incubation period Variable but long period inapparent carrier state can occur AMDV can be detected in blood by PCR in most animals within 10 days postinfection Viral replication reached its peak around 10 days post infection thus incubation period is considered short Clinical signs Pathogenesis of this disease is an immune system response of producing a large increase in antibodies resulting in a hypergammaglobulinemia The formed antigenantibody complexes are unable to neutralize the virus but they are deposited and cause damage within various tissues and organ systems including kidneys liver bile ducts respiratory system spinal cord gastrointestinal tract urinary bladder and blood vessels Subsequently inflammation occurs with an elevation in plasmacytes and lymphocytes and significant inflammation will result in disease with the organs affected However ferrets with mild inflammation may have no clinical signs Post mortem gross or histologic findings Gross Hepatomegaly splenomegaly renal changes varying from swelling petechiation to atrophy and pitting and enlarged mesenteric lymph nodes Infected ferrets may have few or no gross lesions Histologic Plasma cell infiltration in the kidneys liver spleen lymph nodes and bone marrow bile duct proliferation membranous glomerulonephritis and fibrinoid arteritis lymphoplasmacytic meningitis Diagnosis Presumptive diagnosis is based on clinical signs and hypergammaglobulinemia Common testing modalities counterimmunoelectrophoresis CEP ELISA and PCR Tissue biopsies usually done postmortem American Association of Zoo Veterinarians Infectious Disease Manual ALEUTIAN DISEASE Material required for laboratory analysis Blood serum for CEPELISA urine saliva feces tissues for PCR Relevant diagnostic laboratories PCR and virus sequencing Weymouth AD Laboratory Weymouth Nova Scotia CIEO Nova Scotia Department of Agriculture Pathology Laboratory Truro Nova Scotia CIEP Dalhousie University Faculty of Agriculture co Hosain Farid PhD Department of Plant Animal Sciences Agricultural Campus PO Box 550 Truro Nova Scotia B2N 5E3 Canada afariddalca 902 8936727 PCR and ELISA testing Blue Cross Animal Hospital Attention Dr Blau CEP tests 401 N Miller Avenue Burley Idaho 83318 Phone 208 6785553 Fax 2086778957 PCR and ELISA University of Georgia Infectious Diseases Laboratory 110 Riverbend Rd Riverbend North Room 150 Athens GA 30602 706 5428092 PCR Wisconsin Veterinary Diagnostic Lab 445 Easterday Lane Madison Wisconsin 53706 608 2625432 Treatment No effective treatment Selective breeding for mink that can tolerate the virus Prevention and control Test and cull on mink farms no vaccine option Strict biosecurity and quarantine in ferret colonies and shelters Ferrets in a seropositive household should have no exposure to ferrets outside of the household although cagemates are considered already exposed Suggested disinfectant for housing facilities Clean environment with 10 bleach solution Steam clean pens and spray with 2 sodium hydroxide Notification None required Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Not recommended infected animals should be isolated or culled Conditions for restoring diseasefree status after an outbreak Following removal of infected animals and American Association of Zoo Veterinarians Infectious Disease Manual ALEUTIAN DISEASE environmental cleaning restocking can be considered Identify the source and route of infection to prevent re infection Experts who may be consulted Hosain Farid PhD Dalhousie University Department of Plant Animal Sciences Agricultural Campus PO Box 550 Truro Nova Scotia B2N 5E3 Canada afariddalca 902 8936727 References 1 Allendar M J Schumacher KV Thomas SL McCain EC Ramsay EW James AG Wise RK Maes and D Reel 2008 Infection with Aleutian disease viruslike virus in a captive striped skunk J Amer Vet Med Assoc 232 742746 2 Farid AH 2013 Aleutian mink disease virus in furbearing mammals in Nova Scotia Canada Acta Vet Scand 55 103 3 Morrisey JK and MS Kraus 1997 Aleutian disease In Quesenberry KE and JW Carpenter eds Ferrets Rabbits and Rodents Clinical Medicine and Surgery Saunders St Louis Missouri Pp 7173 4 Jepsen JR 2009 Aleutian mink disease and humans Emerg Infec Dis 15 20402042 5 Langlois I 2005 Viral diseases of ferrets Vet Clin Exot Anim Pract 8 139160 6 Brown SA 2012 Aleutian disease in ferrets httpwwwveterinarypartnercomContentplxPAA483 Accessed 28 August 2013 7 Ohshima K DT Shen JB Henson and JR Gorham 1978 Comparison of the lesions of Aleutian disease in mink and hypergammaglobulineinia in ferrets Amer J Vet Res 39 653657 8 Williams BH Aleutian disease virus httpmiamiferretorgfhcaleutianhtm Accessed 28 August 2013 American Association of Zoo Veterinarians Infectious Disease Manual ANAPLASMOSIS Fact Sheet compiled by Dorothy Geale and Enrique Yarto Sheet completed on 20 Jan 2019 Fact Sheet Reviewed by Gretchen Cole Susceptible animal groups Group 1 Cattle sheep goats mule deer and other ruminants Group 2 Mammals humans cattle sheep goats camels dromedary donkeys pigs domestic dogs and cats small mammals birds and many wildlife species Infected domestic cattle become persistent carriers after recovery and play an important role in the epidemiology of the disease Due to global warming vector tick distribution and increase in the horse industry horses should be considered as a potential reservoir for A phagocytophilum and cross infectivity should be assessed Causative organism Obligate intracellular bacteria Order Rickettsiales Family Anaplasmataceae Genus Anaplasma Group 1 infect red blood cells A marginale A ovis Group 2 infects white blood cells and platelets A phagocytophilum A bovis A platys Biological transmission by ticks occurs in both groups Iatrogenic mechanical transmission by transfer of infected blood cells occurs in Group 1 by contaminated scalpels needles or tattooing dehorning and castration equipment and in Group 2 in humans by blood transfusions or organ transplants Natural mechanical transmission is effected in Group 1 by biting flies most commonly horse and stable flies For Group 1 transplacental transmission is reported especially with acute infection in the 2nd or 3rd trimester It also occurs in Group 2 but its epidemiological role is not well characterized for either group Group 1 A marginale infects cattle and is the agent of bovine anaplasmosis Major reservoirs are cattle and ticks Less pathogenic is A marginale subspecies centrale which is never reported in North America and used as a live vaccine strain in South Africa Israel and some South American countries A ovis infects sheep goats deer mule deer and reindeer red fox primarily in North America Two groups in Anaplasmataceae Group 1 infects red blood cells Group 2 infects other blood cells Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Group 1 Ruminants Group 2 Wide range of mammals including humans Group 12 Biological transmission via ticks mechanical transmission by infected blood cell transfusion transplacental Group 1 mechanical transmission eg biting flies Group 1 Anemia lethargy pale mucous membranes Group 2 Headache pyrexia chills myalgia anemia Nausea vomiting diarrhea In latter stages bleeding problems respiratory and organ failure death Group 1 Severity increases with age Group 2 typically mild more severe in mature or immuno suppressed animals or with co infections Group 1 Oxytetra cycline chlortetra cycline in feed Group 2 Doxy cycline Group 1 Control ticks and biting flies prevent entry of carriers vaccination prophylactic antibiotics Group 2 control tick exposure insect repellents Group 1 no Group 2 yes American Association of Zoo Veterinarians Infectious Disease Manual ANAPLASMOSIS Group 2 A phagocytophilum previously Ehrlichia phagocytophila E equi and the human granulocytic ehrlichiosis agent infects a wide variety of mammals including ruminants cattle white tailed deer horses rabbits pigs and small rodents eg whitefooted mice wood rats gray squirrels marsupial Virginia opossum skunk hedgehog bears fox and raccoon Additional snakes northern alligator lizard Pacific gopher snake have been reported Red foxes Vulpes vulpes have been identified as hosts of Anaplasma spp A phagocytophilum A ovis A platys and may contribute to the maintenance of A phagocytophilum in Europe Raccoons have Procyon lotor have been reported as hosts for A bovis A phagocytophilum and other Anaplasmacetae playing a role in the maintenance of A phagocytophilum in the USA and Europe In camels age has been identified as a risk factor for the prevalence of A phagocytophilum in a farmed camels C dromedarius in Iran where camels less than 5 yr had a prevalence of 443 while camels older than 5 yr had a prevalence of 254 Anaplasma bovis previously Ehrlichia bovis infects cattle deer and raccoon dogs which are reservoirs in Asia and Africa Anaplasma platys previously Ehrlichia platys is reported in dogs and rarely in cats red fox impala and sheep in Asia Europe and South America and is the only Anaplasma to infect platelets Zoonotic potential Group 1 Anaplasma sp are not infective for humans and therefore not zoonotic A phagocytophilum of Group 2 first described in sheep in Europe has become an emerging pathogen of humans in both Europe and the US It is transmitted by Ixodes ticks as biological vector Blood transfusions or organ transplants also pose a zoonotic risk Additionally red deer and wild boars have been found to be infected with human pathogenic variants of this bacteria Distribution Group 1 A marginale occurs worldwide and in all states of US except Hawaii It is endemic throughout the Gulf Coast states and several of the Midwestern and Western states Outbreaks are often seasonal and coincide with the emergence of arthropod vectors in warmer months spring early summer and early fall Group 2 A phagocytophilum also occurs worldwide and in US primarily in the west upper midwest and northeast but future distribution may change with tick vectors States reporting the highest incidence in 2010 included Minnesota Wisconsin New York New Jersey Rhode Island and Connecticut Norway UK Sweden Switzerland and Germany have reported infections in ruminants dogs and people Infections in camels in Iran is reported with regional variation Infections in wild felids have been reported in Brazil and Africa Incubation period Group 1 ranges from 7 to 60 days A marginale A ovis A marginale subsp centrale depending on dose Rickettsemia doubles every 24 hours with acute clinical disease in 710 days in susceptible species Group 2 ranges from 7 to 14 days in humans sheep and dogs Clinical signs Group 1 Clinical signs are highly variable ranging from subclinical infection in calves under a year to severe peracute disease in adult naïve cattle characterized by significant production losses milk or weight gain bull infertility severe anemia icterus inappetence dehydration constipation dark yellow urine weight loss pyrexia abortion and death The acute form generally occurs in cattle from 13 years old with similar but more moderate clinical signs All recovered animals become persistent carriers and reservoirs of infection for life Group 2 Humans A phagocytophilum Clinical disease is associated with acute parasitemia of which the duration and severity is variable Coinfection with other pathogens results in greater severity of symptoms Genetic variants of A phagocytophilum and be associated with mild or flulike clinical signs or rash in 10 American Association of Zoo Veterinarians Infectious Disease Manual ANAPLASMOSIS of patients The aged and immunosuppressed show more severe signs These signs include headache pyrexia chills myalgia nausea ataxia organ failure susceptibility to opportunistic infections neuritis or respiratory complications The US case fatality rate from 20002010 was 1 with a rise in incidence from 14 to 61 cases per million In 2016 the Centers for Disease Control reported 4151 human cases of anaplasmosis in the US a 14 increase between 2015 and 2016 Dogs A platys A phagocytophilum Most often disease is subclinical or a mild flulike presentation that is selflimiting Animals with an acute infection often have vague signs including pyrexia malaise lethargy anorexia and general muscle pain resulting in reluctance to move A phagocytophilum most commonly causes clinical disease in dogs older than 8 years with joint pain and lameness so it must be distinguished from Lyme disease Gastrointestinal respiratory and neurological signs may also occur Infections may be subclinical or in a carrier state In endemic areas over 40 of dogs may be seropositive while morbidity is low Dogs coinfected with Borrelia burgdorferi and A phagocytophilum are nearly twice as likely to develop clinical disease A platys produces clinical disease related to a cyclic thrombocytopenia typically 20000μl for 12 days then repeats in 12 weeks Although usually mild more severe clinical signs including pyrexia lethargy pale mucus membranes petechial hemorrhages epistaxis and lymphadenopathy occur Other animals A phagocytophilum Sheep may have mild clinical signs of lethargy with abortions in ewes Similarly in endemic areas dairy cattle exhibit abortions drop in milk production and respiratory disease Complications occur due to secondary bacterial infections eg pastuerellosis septicemic listeriosis Other ruminants and cervids may exhibit anorexia dullness fever weight loss coughing abortion and low fertility Horses may have acute onset with older animals developing fever lethargy inappetence limb edema while young animals typically have mild disease A report in maned wolves Chrysocyon brachyurus describes coughing and tachypnea due to severe pulmonary congestion splenomegaly ataxia anorexia lethargy dehydration mild jaundice petechiation leukocytosis anemia hyperfibrinogenemia Post mortem gross or histologic findings Group 1 include anemia jaundice splenomegaly and the liver may be enlarged with a deep orange color Hepatic and mediastinal lymph nodes may appear brown and the gall bladder distended with thick brown or green bile Serous effusions may occur in body cavities edema petechial hemorrhages in the epi and endocardium often accompanied by severe gastrointestinal stasis Reticuloendothelial phagocytosis of erythrocytes may be evident microscopically in various organs most notably in the spleen Group 2 A phagocytophilum is only one of four human neutrophil intracellular organisms forming morulae cytoplasmic vacuole containing multiple coccoid to ellipsoid basophilic rickettsia approximately 15 µm to 25 µm in diameter reported up to 6 µm During acute rickettsemia the organism has been demonstrated in the alveolar macrophages Kupffer cells and other tissue macrophages Sites of persistence inbetween recurrent rickettsemia remain to be established Diagnosis Hematology Group 1 Initially based on clinical signs history of tick exposure and clinical pathology lymphopenia mild to severe thrombocytopenia mild to moderate nonregenerative anemia elevated ALP mild to moderate hypoalbuminemia and hyperfirbrinogenemia may occur In the acute phase the presence of characteristic intracellular inclusions marginal bodies on GiemsaWrightsDiffQstained blood smears buffy coat recommended along the margins of the erythrocyte A marginale or more centrally A marginale subsp centrale Group 2 Neutrophils infected by A phagocytophilum 127 contain distinctive granulocytic morulae which appear in the peripheral blood at 414 days and persist up to 8 days In animals with polyarthritis synovial fluid may exhibit decreased viscosity and an increased leukocyte count 3000 cellsμl American Association of Zoo Veterinarians Infectious Disease Manual ANAPLASMOSIS predominantly neutrophils but 1 may contain morula A platys morulae may be found in circulating platelets Hematology is not reliable for presymptomatic or carriers Antibody serology Group 1 Enzymelinked immunosorbent assay ELISA marketed by VMRD will not differentiate between Anaplasma species as the test is based on major surface protein 5 MSP5 which is highly conserved in the genus The reported A marginale sensitivity 95 and specificity 98 is limited by cross reactivity low early sensitivity and low specificity for true negative cattle after oral chlortetracycline treatment The complement fixation CF and card agglutination tests CAT are no longer considered to be valid and thus not used for diagnosis of bovine anaplasmosis Group 2 ELISA IDEXX SNAP 4Dx for A phagocytophilum sensitivity 994 specificity 100 reportedly detects as early as 8 days postinoculation dogs with Ehrlichia ewingii do not likely crossreact some crossreactivity with A platys The indirect immunofluorescence assay IFA detects a 4fold increase in IgGspecific antibody titer to A phagocytophilum antigen in paired serum samples taken the 1st week of illness and 24 weeks later Note IgM tests are not always specific and that the IgM response may be persistent Seroconversion in dogs may occur as soon as 25 days after morulae appear in the peripheral blood Positive titer 180 most will have titer 1320 Antigen detection Group 1 2 polymerase chain reaction PCR is the most specific method nested PCR theoretically detects 00000001 rickettsemia or 30 infected red blood cells per ml can distinguish between species but poses problems due to nonspecific amplification requiring confirmation of the amplified fragment sequencing Should be repeated if negative in suspect carriers A marginale Other means of diagnosis Group 1 2 Immunohistochemistry can demonstrate Anaplasma antigen in a biopsynecropsy sample The organism can be isolated in cell culture mainly research as it is impractical for clinical cases The gold standard for A marginale is the demonstration of the organism 48 weeks after inoculation of suspect blood into splenectomized calves Material required for laboratory analysis For both Group 1 2 Anticoagulant blood thin and thick blood films At necropsy thin blood films of liver kidney spleen lungs and peripheral blood PCR whole blood EDTA Sample blood prior to starting antimicrobials to avoid false negative test results Relevant diagnostic laboratories Anaplasma sp can be diagnosed at most accredited diagnostic laboratories using ELISA inhouse SNAP 4Dx IDEXX for A phagocytophilum cELISA for A marginale VMRD Antech FastPanel PCR Canine EhrlichiosisAnaplasmosis Profile for A platys and A phagocytophilum crossreacts with Ehrlichia Zoologix PCR A platys also offers tickborne disease PCR panel that includes A platys Treatment Group 1 In acute outbreaks parenteral oxytetracycline cattle is used as recommended by extension specialists The survival rate is high in the early stages of the disease PCV 15 Blood transfusions electrolyte solutions and hematinic drugs may be beneficial in later stages of the disease Convalescent period of up to 3 months Cattle remain immune for life but become persistent carriers Group 2 Treatment may be difficult as clinical signs often do not appear until the disease has progressed Testing for coinfections with other tickborne organisms is recommended Tetracycline antibiotics usually doxycycline in humans and dogs for 1014 days or at least until 3 days after fever subsides A marked improvement is usually seen in 2448 hours American Association of Zoo Veterinarians Infectious Disease Manual ANAPLASMOSIS Prevention and control Group 1 2 organisms need control of tick vectors Additionally for Group 1 strict sanitation with needles and surgicaldehorning instruments remove carriers from herd and chlortetracycline during vector season medicated saltmineral blocks or feed blocks In South Africa Australia Israel and South America live A centrale is used as a vaccine Universal vaccines are not available that are effective for geographically diverse strains for A marginale or A phagocytophilum A conditional killed vaccine made from a Mississippi strain is available in some southern states In California a modified live vaccine Anavac is available for cattle 11 months but lacks efficacy and is rarely used Identification of regional vectors are important to control zoonotic anaplasmosis Use of Environmental Protection Agency EPA registered insect repellents is also recommended Suggested disinfectant for housing facilities No disinfectant Application of acaricides and removal of leaf litterbrush tick habitat can be effective Notification A marginale is a reportable disease in 30 states and tracked nationally through National Animal Health Reporting System USDA in 48 states A phagocytophilum is monitored through National Notifiable Disease System CDC Measures required for introducing animals to infected animal Infected animals become carriers and act as a reservoir of infection for life In endemic areas early infection or vaccination in cattle promotes life long immunity With no killed vaccines available in the US separation of carriers and noninfected introduced mature animals is essential Conditions for restoring diseasefree status after an animal outbreak Group 1 Carriers may relapse when immunosuppressed eg corticosteroids when infected with other pathogens or after splenectomy As a lifelong reservoir of infection they should be removed No anti microbials are approved in the US for eliminating A marginale infections in cattle Allegedly the carrier state may be eliminated with a longacting oxytetracycline treatment but experimental work at Kansas State University in the mid 2000s found chemosterilization inconsistent Although long term oral tetracycline at high extralabel doses had greater success parenteral administration was less so and conflicting results suggests differences in susceptibility of A marginale strains Chemosterilized animals are fully susceptible to reinfection Experts who may be consulted Katherine M Kocan Oklahoma State University Veterinary Pathobiology 004 McElroy Hall Stillwater OK 74078 Phone 405 7447271 Fax 405 7445275 KatherineKocanokstateedu References 1 André MR Diversity of Anaplasma and EhrlichiaN eoehrlichia agents in terrestrial wild carnivores worldwide Implications for human and domestic animal health and wildlife conservation Front Vet Sci20185 2 Atif FA Anaplasma marginale and Anaplasma phagocytophilum Rickettsiales pathogens of veterinary and public health significance Parasitol Res 201511411394157 3 Aubry P Geale DW A review of bovine anaplasmosis Trans Emerg Dis 201158130 4 Bahmari S Hamidinejat H Ganjali Tafresi AR First molecular detection of Anaplasma phagocytophilum in dromedaries Camelus dromedarius J Zoo Wildl Dis 2018494844848 American Association of Zoo Veterinarians Infectious Disease Manual ANAPLASMOSIS 5 The Center for Food Security Public Health Internet Ehrlichiosis and Anaplasmosis Zoonotic Species 2013 cited 2019 February 18 Available from httpwwwcfsphiastateeduFactsheetspdfsehrlichiosispdf 6 Centers for Disease Control and Prevention Internet Anaplasmosis 2019 cited 2019 Febryary 18 Available from httpswwwcdcgovanaplasmosis 7 Di Domenico M Pascucci I Curini V Cocco A DallÄcqua F Pompilii C Camma C Detection of Anaplasma phagocytophilum genotypes that are potentially virulent for human in wild ruminants and Ixodes ricinus in Central Italy Ticks Tick Borne Dis 201675782787 8 Dumler JS Barbet AF Bekker CP Dasch GA Palmer GH Ray SC Rikihisa Y Rurangirwa FR Reorganization of genera in the Families Rickettsiaceae and Anaplasmataceae in the order Rickettsiales unification of some species of Ehrlichia with Anaplasma Cowdria with Ehrlichia and Ehrlichia with Neorickettsia descriptions of six new species combinations and designation of Ehrlichia equi and HGE agent as subjective synonyms of Ehrlichia phagocytophila IntJ Syst Evol Microbiol 20015121452165 9 Dumler JS Madigan JE Pusterla N Bakken JS Ehrlichioses in humans epidemiology clinical presentation diagnosis and treatment Clin Inf Dis 200745 SupplS4551 10 Foley J Human ehrlichiosis a review of clinical disease and epidemiology for the physician Inf Dis Clin Pract 200099398 11 Kocan KM de la Fuente J Guglielmone AA Melendéz RD Antigens and alternatives for control of Anaplasma marginale infection in cattle Clin Microbiol Rev 200316698712 12 Kocan KM de la Fuente J Step DL Blouin EF Coetzee JF Simpson KM Genova SG Boileau MJ Current challenges of the management and epidemiology of bovine anaplasmosis Bov Pract 201044293102 13 Kocan KM Coetzee JF Step DL de la Fuente J Blouin EF Reppert E Simpson KM Boileau MJ Current challenges in the diagnosis and control of bovine anaplasmosis Bov Pract 2012466777 14 Koh FX Panchadcharam C Sitam FT Tay ST Molecular investigation of Anaplasma spp in domestic and wild animals in Peninsular Malaysia Vet Parasitol Reg Stud Rep 201813141147 15 LewTabor AE Internet 2018 cited 2019 February 18 Available from httpswwwmerckvetmanualcomcirculatorysystembloodparasitesanaplasmosis 16 Mghirbi Y Oporto B Khrouf F Hurtado A Bouattour A Anaplasma marginale and A phagocytophilum in cattle in Tunisia Parasit Vectors 201691556 17 Padilla LR Bratthauer A Ware LH Acosta V Hope KL SiegalWillott J Murray S Anaplasma phagocytophilum infection in captive maned wolves Chrysocyon brachyurus at the Smithsonian Conservation Biology Institute In Proc Am Assoc Zoo Vet 2010 p 162 18 Reinbold JB Coetzee JF Hollis LC Nickell JS Riegel C Olson KC Ganta RR The efficacy of three chlortetracycline regimens in the treatment of persistent Anaplasma marginale infection Vet Microbiol 2010145126975 19 Seo MG Ouh IO Choi E Kwon OD Kwak D Molecular detection and phylogenetic analysis of Anaplasma phagocytophilum in horses in Korea Korean J Parasitol 2018566559565 20 Woldehiwet Z The natural history of Anaplasma phagocytophilum Vet Parasitol 2010167108 122 21 Yang J Liu Z Niu Q Luo J Wang X Yin H Molecular detection of Anaplasma phagocytophilum in wild cervids and hares in China J Wild Dis 2017532420423 American Association of Zoo Veterinarians Infectious Disease Manual ANATRICHOSOMA Animal groups affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals primates marsupials rodents carnivores Unknown Cutaneous nasal oral gastric or ocular nodules or ulcers Clinically insignificant to severe ulceration Avermectins benzimidazoles Hygiene and sanitation control of wildlife prophylactic parasite treatments Yes Fact Sheet compiled by Beth Bicknese Sheet completed on 30 April 2011 Last updated 12 Dec 2017 Fact Sheet reviewed by Jennifer DAgostino Susceptible animal groups Mammals Reported in Old World monkeys apes and marmosets under human care wildcaught tree shrews wild American and Australian marsupials wild rodents domestic cats and dogs and humans Severe inflammatory cutaneous lesions in carnivores and some primates including humans suggest these are aberrant hosts Causative organism Anatrichosoma cutaneum and A cynomolgi have been found in nasal and cutaneous lesions in wild caught and captive primates and are the presumed cause of most human and domestic animal cases A buccalis has been found in the oral mucosa of opossums and was suspected in one human case A ocularis A gerbilis and A haycocki have been reported in wild or wildcaught tree shrews gerbilid and murid rodents and Antechinus spp marsupials respectively Adult females tunnel through the epidermis laying embryonated ova which reach the surface through normal exfoliation Ova are then swallowed and passed in feces or released directly into the environment Adult males reside in the dermis Mechanism of infection is unknown Attempts at experimental direct infection have been unsuccessful suggesting an indirect life cycle but no intermediate host has been identified One report found free immature A haycocki in the intestine of Antechinus spp hosts suggesting an enteric route of infection in this species Lesions have recurred after treatment in captive primates suggesting either reinfection or incomplete response to treatment Zoonotic potential Eight human cases reported Japan Vietnam Malaysia Italy USA including one case in Illinois in 2010 and two in Iowa in 2014 all with recent travel to Mexico Exposure route unknown Distribution Documented in wild animals from the Americas the Middle East Africa India and Australia and in humans and domestic animals in the Americas Europe Africa and Asia Incubation period Unknown clinical lesions are associated with migration of adult worms Clinical symptoms Cutaneous A cutaneum A cynomolgi Nodules or tracklike lesions with ulceration apparent predilection for glabrous skin Severe ulcerative pododermatitis in domestic cats Nasal A cynomolgi A cutaneum Nodules or tracks in the nasal mucosa of primates minimal local inflammation Oral A buccalis Nodules or tracks in the oral mucosa Minimal local inflammation in opossums mucosal ulceration in one suspected human case Gastric A gerbilis Nodules or tracks in the gastric mucosa of gerbilid and murid rodents American Association of Zoo Veterinarians Infectious Disease Manual ANATRICHOSOMA Ocular A ocularis Adults visible within the corneal or conjunctival epithelium of tree shrews minimal local inflammation Glandular A haycocki Adults within the tissue of paracloacal glands or encapsulated in the lumen of the cloaca of Antechinus spp minimal local inflammation Post mortem gross or histologic findings Histopathology shows adults and ova embedded in epithelial tissue Diagnosis Mucosal swab skin scraping biopsy fecal flotation for ova Trichurislike bipolar plugged Ova have also been identified by cytology of an otic flush in a dog Material required for laboratory analysis Swab scrape biopsy or flush of lesion feces Relevant diagnostic laboratories None Treatment Avermectins and benzimidazoles have effectively resolved clinical lesions in reported cases recurrence is infrequently reported Primates Fenbendazole 1025 mgkg PO once daily for 310 days Domestic cat Ivermectin 03 mgkg SC weekly for 4 weeks Human Mebendazole 100 mg twice daily for 20 days or albendazole 400 mg once daily for 3 days Prevention and control The mechanism of infection is unknown However control of feral animals and wildlife in exhibit areas sanitation and hygiene with regular removal of feces from enclosures and routine prophylactic deworming are expected to be beneficial Suggested disinfectant for housing facilities None specified expect sensitivity as for Trichuris spp and Capillaria spp Notification None required Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal None specified treat infected animals prior to introduction if possible Conditions for restoring diseasefree status after an outbreak None required treat exposed individuals if possible eliminate feces in enclosure Experts who may be consulted Dwight D Bowman MS PhD ddb3cornelledu Professor of Parasitology C4119 VMC Dept Micro Immunol Cornell University College of Veterinary Medicine Tower Road Ithaca NY 148536401 Dr Heather Stockdale Walden hdstockdaleufledu University of Florida College of Veterinary Medicine Department of Comparative Diagnostic and Population Medicine 1945 SW 16th Ave V2155 Gainesville FL 32608 American Association of Zoo Veterinarians Infectious Disease Manual ANATRICHOSOMA References 1 Bowman DD Hendrix CM Lindsay DS Barr SC Feline Clinical Parasitology 1st ed Ames IA Iowa State University Press 2002 p 346348 Available from httpseurekamagcompdf003003769618pdf 2 Conrad HD Wong MM Studies of Anatrichosoma Nematoda Trichinellida with descriptions of Anatrichosoma rhina sp n and Anatrichosoma nacepobi sp n from the nasal mucosa of Macaca mulatta J Helminthol 1973473289302 3 Eberhard ML Hellstein JW Lanzel EA Zoonotic anatrichosomiasis in a mother and daughter J Clin Microbiol 2014528 31273129 4 Harwell G Dalgard D Clinical Anatrichosoma cutaneum dermatitis in nonhuman primates In Proc Am Assoc Zoo Vet 1979 p 5 5 Kessler MJ Nasal and cutaneous anatrichosomiasis in the freeranging rhesus monkeys Macaca mulatta of Cayo Santiago Am J Primatol 19823145560 6 Kinsella JM Winegarner CE A field study of Anatrichosoma infections in the opossum Didelphis virginiana J Parasitol 1975614779781 7 Noden BH Du Plessis EC Morkel C Tubbesing U Soni M Anatrichosoma sp in the footpads of a cat Diagnosis and pathology of Namibian case Vet Parasit 201319134386389 8 Orihel TC Ash LR Parasites in human tissues Chicago IL ASCP Press 1995 American Association of Zoo Veterinarians Infectious Disease Manual ANGIOSTRONGYLUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic A cantonensis non human primates marsupials horses dogs A vasorum canids red pandas stoats badgers Ingestion of intermediate snails and slugs or paratenic shellfish frogs lizards hosts A cantonensis variety of neurologic signs including ataxia ascending paresis hy peresthesia seizure muscle wasting coma gastrointest inal signs A vasorum cough dyspnea exercise intolerance hemorrhage anorexia weight loss occasional CNS signs A cantonensis causes severe progressive neurologic disease in nonhuman primates often resulting in death or euthanasia A vasorum can be asymptomatic to fatal in canids It appears fatal in red pandas Recovery for both is independent of severity of presenting signs Primary supportive care for both Treatment with anthelmintics fenbendazole milbemycin topical moxidenctin may shorten clinical course of A vasorum infections The use of anthelminthics is controversial in A cantonensis infections Avoidance and removal of intermediate paratenic hosts Monthly topical moxidectin has been recommende d Monthly prophylactic anthelmintics have been used in red pandas A canto nensis has been reported in humans Fact Sheet compiled by Kristina M Delaski Sheet completed on 14 February 2018 Fact Sheet Reviewed by Susceptible animal groups A cantonensis Rats are the definitive hosts Aberrant hosts include several species of nonhuman primates marsupials wallaby bettong opossum ninebanded armadillos Tawny frogmouths cockatoos raptors horses and dogs A vasorum Dogs and red foxes are the definitive hosts Other canids coyote wolf jackal European otter ferrets badgers and red pandas have also been infected and red pandas have been reported to shed infective larvae Causative organism Angiostrongylus cantonensisneurologic disease A vasorumcardiopulmonary disease Zoonotic potential A cantonensis has been extensively studied in humans and is considered a zoonotic disease Transmission is through ingestion of an intermediate or paratenic host usually raw or undercooked seafood in endemic areas Distribution A cantonensis is endemic in the Pacific Islands and Southeast Asia but has spread to the Americas including the US the Caribbean islands and Brazil It is now considered endemic in the southwestern US A vasorum is endemic to Europe Africa and South America It has recently been documented in Newfoundland Canada and in West Virginia American Association of Zoo Veterinarians Infectious Disease Manual ANGIOSTRONGYLUS Incubation period A cantonensis larvae can be seen in the CNS hours to days following ingestion although typical incubation is 23 weeks in humans The prepatent period for A vasorum ranges from 28 to108 days Clinical signs A cantonensis Due to migration of the L3 larvae in central nervous tissue and subsequent eosinophilic inflammation infection can result in a variety of neurologic signs Most common signs include ascending bilateral paresis and muscle wasting urinary bladder paresis hyperesthesia and occasional gastrointestinal signs Seizures cranial nerve palsies and coma have also been reported In humans ocular larva migrans can occur A vasorum Signs can vary and may be absent early in infection or with low parasite burdens Interstitial pneumonia and hemorrhage is most common leading to fibrosis This results in tussis dyspnea exercise intolerance anorexia and weight loss Vascular lesions associated with adult worms can lead to pulmonary hypertension and congestive heart failure Coagulopathy of unknown etiology has been documented and can be the presenting clinical sign This results in anemia melena subcutaneous hematomas and other sequelae depending on location of hemorrhage Central nervous system signs are often related to intracranial hemorrhage but can also be the result of aberrant larval migration Signs vary depending on location of lesions Red pandas were reported with cough dyspnea and exercise intolerance although apparent asymptomatic infections can occur Post mortem gross or histologic findings A cantonensis Cerebral and cerebellar meningitis with varying degrees of malacia Nematodes are often found near the cerebral blood vessels or free in the white matter of the central nervous system with mild to moderate inflammation Similar lesions may occur in the spinal cord Hemorrhage in the central canal of the spinal cord has been reported A vasorum Adult worms present in the lumen of the pulmonary artery and right ventricle They can be differentiated from Dirofilaria immitis by the small size of A vasorum Interstitial pneumonia with hemorrhage granulomas around eggslarvae and fibrosis Adult worms cause thromboarteritis and intimal proliferation in affected vessels Cases with coagulopathy may have intracranial intrathoracic or intraabdominal hemorrhage Due to larval migration L1 larvae may be found in a large variety of tissues at necropsy The presence of undifferentiated eggs and larvae is characteristic Necropsies of infected red pandas have found mineralized fibrous tissue in the lungs with nodules centered on nematode eggs and coiled larvae Granulomas around larvae have also been reported in pulmonary lymph nodes Diagnosis A cantonensis Definitive diagnosis is difficult Fecal analysis is of little value as the infection is only patent in rats Hematology shows eosinophilia and CSF often shows an eosinophilic pleocytosis Occasionally larvae may be seen in CSF samples High field MRI has been able to detect cavitations caused by larval migration in humans but has yet to be useful in canine cases ELISA tests on serum were not very sensitive but those performed on CSF were reported as promising PCR testing is under development Neither ELISA nor PCR testing is available commercially A vasorum Definitive diagnosis in canids is by detection of larvae in feces through Baermann examinations or detection of larvae in bronchoalveolar samples The larvae have a characteristic tail morphology kinked tail and dorsal spine Radiographs may show a bronchoalveolar pattern but are often nonspecific Possible hematologic changes include anemia eosinophilia thrombocytopenia and hypercalcemia Decreased serum fructosamine has been reported in infected dogs PCR testing is available but may not detect chronic infections Combination of fecal PCR and Baermann tests may improve detection Antigen and antibody ELISA tests are under development and may be the most sensitive method of testing Commercial antigendetection kits for Dirofilaria immitis have been reported to crossreact with A vasorum American Association of Zoo Veterinarians Infectious Disease Manual ANGIOSTRONGYLUS Material required for laboratory analysis A cantonensis CSF for cytology and PCR ELISA tests for serum were not very sensitive but those for CSF were reported as promising A vasorum Pooled fecal samples collected over 3 consecutive days for Baermann examination PCR testing is available for fresh feces tracheal lavage fluid and whole blood Antigen and antibody ELISAs are in development for use on serum and a canine patientside antigen test for serum is available through the UK branch of IDEXX Relevant diagnostic laboratories IDEXX offers a PCR test for A vasorum which can be performed on fresh feces tracheal lavage fluid or whole blood in EDTA IDEXX has also developed a rapid patientside antigen test for serum available in the UK It has been reported to crossreact with other species of Angiostrongylus in definitive hosts More information is available here httpangiodetectcouk Treatment Supportive care for both Treatment with anthelmintics fenbendazole milbemycin topical moxidectin is effective for A vasorum in dogs though caution is urged as rapid dieoff of adult worms may cause severe secondary reactions ascites dyspnea in the patient All treated animals are monitored with multiple posttreatment fecal Baermann exams The use of anthelmintics are controversial in A cantonensis infections due to risk of increased damage sustained due to inflammatory reactions in the central nervous system Treatment with prednisolone and albendazole has prevented death in a Geoffroys tamarin but the individual had permanent neurologic deficits Supportive care for A cantonensis consists of fluid support analgesics sedatives and glucocorticoids Prevention and control Prevention is centered on restricting access to intermediate and paratenic hosts A cantonensis is carried by rats so pest control is an important component of prevention Both nematodes can infect a wide range of gastropod intermediate hosts which can then in turn infect paratenic hosts when frogs lizards or shellfish consume the gastropods Chickens have also been reported to be possible paratenic hosts Collection animals should have limited access to these sources of infection Monthly topical moxidectin has been recommended for prevention of A vasorum in dogs Monthly doses of milbemycin have been used as prophylaxis in red pandas in endemic areas but as no trial studies have been conducted these reports are anecdotal Suggested disinfectant for housing facilities 1 bleach 15 glutaraldehyde and cresolbased products are effective disinfectants Notification None Measures required under the Animal Disease Surveillance Plan NA Measures required for introducing animals to infected animal As neither nematode is transmitted directly no special measures are necessary as long as the enclosure has been cleared of intermediate hosts Conditions for restoring diseasefree status after an outbreak Adult A vasorum worms can live in vasculature for up to five years and ova shedding can be intermittent Repeated negative fecal exams and PCR tests would likely indicate lack of infection Experts who may be consulted Gary Conboy DVM PhD Dip ACVM Atlantic Veterinary College Charlottetown PEI Canada conboyupeica References 1 Aguilar RF Topham K Heatley JJ Nichols D Cross J Bauer R and Garner M Neural angiostrongylosis in nonhuman primates diagnosis treatment and control of an outbreak in southern Louisiana In Proc Am Assoc of Zoo Vets 1999 p 272276 2 AlSabi MNS Deplazes P Webster P Willesen JL Davidson RK Kapel CMO PCR detection of Angiostrongylus vasorum in faecal samples of dogs and foxes Parasitol Res 2010107135140 American Association of Zoo Veterinarians Infectious Disease Manual ANGIOSTRONGYLUS 3 Barratt J Chan D Sandaradura I Malik R Spielman D Lee R Marriott D Harkness J Ellis J Stark D Angiostrongylus cantonensis a review of its distribution molecular biology and clinical significance as a human pathogen Parasit 201714310871118 4 Bertelsen MF MeylandSmith F Willensen JL Jefferies R Morgan ER Monrad J Diversity and prevalence of metastrongyloid nematodes infecting the red panda Ailurus fulgens in European zoos Vet Parasit 2010172299304 5 Bourque AC Conboy G Miller LM and Whitney H Pathological findings in dogs naturally infected with Angiostrongylus vasorum in Newfoundland and Labrador Canada J Vet Diagn Invest 20082011 20 6 Burns RE Bicknese EJ Qvarnstrom Y DeLeonCarnes M Drew CP Gardiner CH Rideout BA Cerebral Angiostrongylus cantonensis infection in a captive African pygmy falcon Polihierax semitorquatus in southern California J Vet Diagn Invest 201426695698 7 Canonne AM Roels E Caron Y Losson B Bolen G Peters I Billen F Clercx C Detection of Angiostrongylus vasorum by quantitative PCR in bronchoalveolar lavage fluid in Belgian dogs J Small Anim Pract 201657130134 8 Carlisle MS Prociv P Grennan J Pass MA Campbell GL Mudie A Cerebrospinal angiostrongyliasis in five captive tamarins Sanguinus spp Aust Vet J 199876167170 9 Conboy GA Canine angiostrongylosis the French heartworm an emerging threat in North America Vet Parasit 2011176382389 10 Dalton MF Fenton H Cleveland CA Elsmo EJ Yabsley MJ Eosinophilic meningoencephalitis associated with rat lungworm Angiostrongylus cantonensis migration in two ninebanded armadillos Dasypus novemcinctus and an opossum Didelphis virginiana in the southeastern United States Int J for Parasit 20176131134 11 Deak G Gherman CM Ionica AM Daskalaki AA Matei IA DAmico G Domsa C Pantchev N Mihalca AD Czma V Use of a commercial serologic test for Angiostrongylus vasorum for the detection of A chabaudi in wildcats and A daskalovi in badgers Vet Parasitol 2017233107110 12 Elsheikha HM Holmes SA Wright I Morgan ER Lacher DW Recent advances in the epidemiology clinical and diagnostic features and control of canine cardiopulmonary angiostrongylosis Vet Res 20144592104 13 Houpin E McCarthy G Ferrand M De Waal T ONeill EJ Zintl A Comparison of three methods for the detection of Angiostrongylus vasorum in the final host Vet Parasitol 20162205458 14 Jensen HE Dietz HH Grondahl C Kapel C and Monrad J The pathology associated with Angiostrongylus vasorum infection in the red panda Ailurus fulgens fulgens In Proc Eur Soc of Vet Path 2005 p 7071 15 Kistler WM Brown JD Allison AB Nemeth NM Yabsley MJ First report of Angiostrongylus vasorum and Hepatozoon from a red fox Vulpes vulpes from West Virginia USA Vet Parasitol 2014200216 220 16 Kottwitz JJ Perry KK Rose HH Henddrix CM Angiostrongylus cantonensis infection in captive Geoffroys tamarins Saguinus geoffroyi J Am Vet Med Assoc 2014245821827 17 Lunn JA Lee R Smaller J MacKay BM King T Hunt GB Martin P Krockenberger MB Spielman D Malik R Twenty two cases of canine neural angiostrongylosis in eastern Australia 20022005 and a review of the literature Parasites Vectors 5 2012 Published online 5 April 2012 18 Morgan E Shaw S Angiostrongylus vasorum infection in dogs continuing spread and developments in diagnosis and treatment J Sm Anim Prac 201051616621 19 Mozzer LR Lima WS Gallus gallus domesticus paratenic host of Angiostrongylus vasorum Vet Parasitol 20152078184 20 Pathogen Safety Data Sheet Infectious Substances Angiostrongylus cantonensis Internet Public Health Agency of Canada c2010 cited 2018 February 13 Available from httpwwwphac American Association of Zoo Veterinarians Infectious Disease Manual ANGIOSTRONGYLUS aspcgccalabbiorespsdsftssacantonensisengphp 21 PattersonKane JC Gibbons LM Jefferies R Morgan ER Wenzlow N Redrobe SP Pneumonia from Angiostrongylus vasorum infection in a red panda Ailurus fulgens fulgens J Vet Diagn Invest 200921270273 22 Reece RL Perry RA Spratt DM Neuroangiostrongyliasis due to Angiostrongylus cantonensis in gang gang cockatoos Callocephalon fimbriatum Aust Vet J 201391477481 23 Schnyder M Jefferies R Schucan A Morgan ER Deplazes P Comparison of coprological immunological and molecular methods for the detection of dogs infected with Angiostrongylus vasorum before and after anthelmintic treatment Parasitol 201514212701277 24 Wang QP Wu ZD Wei J Owen RL Lun ZR Human Angiostrongylus cantonensis an update Eur J Clin Microbiol Infect Dis 201231 389395 25 VerzbergerEpshtein I Markham RJF Sheppard JA Stryhn H Whitney H Conboy GA Serologic detection of Angiostrongylus vasorum infection in dogs Vet Parasit 2008151 5360 American Association of Zoo Veterinarians Infectious Disease Manual ANTHRAX Fact Sheet compiled by Thomas W deMaar updated by Vikki Milne Sheet completed on 21 January 2011 updated 4 August 2013 Fact Sheet reviewed by Martin HughJones Mark Drew Susceptible animal groups Domestic and wild ruminants are most commonly affected However humans equids and other mammals such as elephants are susceptible Suids and carnivores may develop subacute to chronic gastrointestinal type disease after eating infected carcasses It has been reported in ostriches and rheas Scavenging birds and mammals primarily carrion feeders are known to pass spores through their digestive system without becoming infected as vegetative cells are killed in their acidic stomachs Causative organism Bacillus anthracis spore forming nonmotile Gram positive rod Zoonotic potential Humans affected via contact with diseased carcasses or via animal products meat bone meal leather wool bristles drum skins from contaminated carcasses Cutaneous gastrointestinal and inhalation forms of disease occur It is considered a potential bioterrorism agent Distribution Worldwide especially in areas with neutral or alkaline calcareous soils Outbreaks can occur after soil disturbance following drought or flood conditions In US it occurs sporadically with limited distribution and is more common in west and midwest US and is enzootic in west Texas North and South Dakota and northwest Minnesota Incubation period Typically 37 days range 114 days OIE standards up to 20 days Spores maybe inactive in lungs for several weeks before causing disease Clinical signs Peracute ruminants sudden death Acute ruminants and horses Abrupt fever and excitement followed by depression respiratorycardiac distress staggering convulsions severe colic and anterior edema cutaneous signs can be seen in cattle and horses with biting fly infections Process can lead to death Chronic pigs and carnivores Oropharyyngeal and gastrointestinal signs of disease usually followed by recovery but death occurs if systemic Death is not uncommon in freeranging African lions Animal Groups Affected Transmission Animal Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals including humans and ratites Ingestion of spores that can come from soil infected carcass soil contaminated forage or blow fly contaminated browse Usually direct transmission possibly biting flies Sudden death fever followed by death excitement followed by stupor respiratory and cardiac distress colic diarrhea and vomiting edema Peracute and acute in ruminants and equids Commonly fatal Subacute and chronic forms in suids and carnivores from carcass consumption Long acting antibiotics given early Multiple classes of antibiotics are effective Vaccination Rapid detection followed by quarantine carcass disposal treatment and movement of adjoining animals removal of contaminated feed or items vaccination and site de contamination Humans affected via contact with diseased carcasses or via animal products meat bone meal leather wool bristles American Association of Zoo Veterinarians Infectious Disease Manual ANTHRAX Post mortem gross or histologic findings Carcass presented with absence of rigor mortis and rapid decomposition Dark blood may ooze from mouth nostrils eyes ears vulva and anus Edema may be apparent Carcass will show lack of blood clotting and hemorrhages of serosal surfaces Organs particularly the spleen will be congested and enlarged Oropharyngitis pharyngeal edema diptheritic membranes or ulcers of tonsils are seen in suids and carnivores Gastrointestinal inflammation and mesenteric lyphadenitis may be seen in suids and carnivores Hemorrhagic lymphadenitis is histopatholgic observation Diagnosis Documentation of Bacillus spores in dried blood sample PCR culture IFA ELISA and Western Blot tests are available Material required for laboratory analysis Whole blood for culture can be taken post mortem from vein due to lack of clotting Dried blood smears from similar source can be obtained or blood dried on a cotton swab Prior to submission laboratory must be notified for suspicion of anthrax Relevant diagnostic laboratories Diagnostic laboratory with microbiological capacity Confirmation is accomplished thru NVSL Treatment Immediate antibiotic therapy Numerous classes of antibiotics are effective oxytetracycline penicillins aminoglycosides fluoroquinolones macrolides and sulfonamides Prevention and control Rapid detection and prevention of disease spread via quarantine and removal of affected animals Vaccination of susceptible animals in enzootic areas Move animals from potential contamination prior to periods of increased exposure Do not use meat or animal products from uninspected or unknown sources cases of sudden death or emergency slaughters Do not open carcasses in suspected cases Do not contaminate soil during necropsy Use protective clothing during necropsy Post exposure antibiotics are recommended after exposure to aerosolized spores Suggested disinfectant for housing facilities Cremation or deep burial of carcasses and contaminated materials Disinfect using formaldehyde oxidizing agents such as peroxides 5 lye quicklime anhydrous calcium oxide and bleach however prolonged contact is required A commercial product Mold Control 500 has been approved Several protocols for large scale premise decontamination have been utilized Formaldehyde 5 can be used on soil if contamination is minimal otherwise soil removal is advised Notification Reportable to USDA National Animal Health Reporting System B051 Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Wait at least 21 days after outbreak is completed and quarantine varies although the recommended time is 21 days before movement is allowed Conditions for restoring diseasefree status after an outbreak Where the disease is known to be endemic diseasefree status will only be granted after an extended period 10 years without cases and with surveillance For normal sporadic cases there should be at least 5 years without cases but with vaccination Experts who may be consulted Ginger Harvey DVM or Kristina Lantz DVM National Veterinary Services Laboratories PO Box 844 Ames IA 50010 USA 51533770705153377083 Fax 5156637073 gingerrharveyaphisusdagov kristinalantzaphisusdagov References 1 wwwbtcdcgovagentanthraxindexasp Accessed 5 August 2013 2 wwwupmcbiosecurityorgwebsitefocusagentsdiseasesfactsheetsanthraxhtml Accessed 5 American Association of Zoo Veterinarians Infectious Disease Manual ANTHRAX August 2013 3 wwwcfsphiastateeduDiseaseInfodiseasephpnameanthraxlangen Accessed 5 August 2013 4 httpwwwoieintindexphpid169L0htmfilechapitre181htm Accessed 5 August 2013 5 wwweurekalertorgpubreleases200704dnlsdf042607php Accessed 5 August 2013 6 wwwsciencenewsorgviewgenericid5581titlePesticideDisposalGoesGreen Accessed 5 August 2013 7 wwwehsocombleachhtm Accessed 5 August 2013 8 httpwwwaphisusdagovanimalhealthemergingissuesdownloadsanthraxpdf Accessed 5 August 2013 9 wwwvetugaeduvppgraybook02indexphp Accessed 5 August 2013 10 wwwaphisusdagovimportexportanimalsoiedownloadstahcsep09tahcanthrax78sep09pdf Accessed 5 August 2013 11 httpwwwwhointcsrresourcespublicationsAnthraxGuidelines2008en Accessed 9 September 2013 12 Bengis RG 2012 Anthrax in freeranging wildlife In Fowler M E and RE Miller eds Zoo and Wild Animal Medicine 7th ed Elsevier Saunders St Louis Missouri Pp 98107 13 Turnbull P ed 2008 Anthrax in humans and animals Fourth edition World Health Organization Geneva Switzerland 208 pp httpwwwwhointcsrresourcespublicationsanthraxwebspdf Accessed 9 September 2013 American Association of Zoo Veterinarians Infectious Disease Manual ASPERGILLOSIS Fact Sheet compiled by Joseph A Smith Sheet completed on 1 February 2011 updated 15 July 2013 Fact Sheet Reviewed by Mark Mitchell Mark Papich Patrick Redig James Wellehan Susceptible animal groups Vertebrates and invertebrates can be affected However it affects primarily immunocompromised individuals eg those young geriatric stressed affected by concurrent disease or undergoing management changes Higher incidence of disease is associated with penguins waterfowl raptors sea birds and galliforms Birds from polar or pelagic environments tend to be more susceptible High environmental load of fungal spores is a predisposing factor for the development of disease but exposure to ambient levels can also result in disease Prolonged corticosteroid and antibiotic use have both been associated with increased risk of disease Causative organism Primarily Aspergillus fumigatus a saprophytic mold occasionally A flavus A nidulans A niger and A terreus A flavus traditionally is more associated with mycotoxin production aflatoxicosis Fungi use a nomenclature inconsistent with the rest of biology as separate names for asexual anamorph stages and sexual teleomorph stages of the same organism exist resulting in multiple species names and paraphyletic taxa The anamorph genus Aspergillus is the same fungus as several teleomorph genera including Neosartorya Eurotium and Emericella Zoonotic potential Aspergillosis is reported in people but the infections usually are acquired from environmental exposure Immunocompromised humans are more susceptible Theoretically any lesions where sporeforming conidia are present eg some air sac granulomas in birds may release spores into the environment which could be inhaled and thus pose some zoonotic potential In immunocompetent humans the most common clinical presentation is fungal sinusitis Distribution Worldwide distribution ubiquitous in the environment The fungus proliferates in soil decaying vegetation and moist environments with poor ventilation Preformed spores can also be easily aerosolized in dry dusty environments Contaminated ventilation systems have been a risk factor for disease Incubation period Highly variable May cause acute disease or prolonged chronic infections Clinical progression depends primarily on immune response and degree of environmental exposure Clinical signs Primarily affects the respiratory system and may cause dyspnea stridor cyanosis coughing vocalization changes and sneezing The most common site of infection in mammals is the upper respiratory tract The organism frequently infects cavities such as sinuses air sacs guttural pouches and similar locations Signs of disseminated disease depend on the organs affected Fungal plaques on large blood vessels may cause rupture and fatal hemorrhage Nonspecific signs of disease such as lethargy weakness and weight loss are common In birds aspergillosis can result in marked leukocytosis Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Vertebrates invertebrates Environment acquired via spores It is not considered contagious Primarily respiratory but can become systemic Occasionally a cutaneous disease May cause severe disease in immune compromised hosts Antifungal drugs polyenes azoles allylamines pyrimidines Minimize environmental accumulation of fungus prevent immune suppression of host prophylactic treatment Only if spore forming conidiospores are present American Association of Zoo Veterinarians Infectious Disease Manual ASPERGILLOSIS Post mortem gross or histologic findings GrossRhinitis sinusitis tracheitis air sacculitis pneumonia disseminated granulomatous lesions in any organ Lesions are yellow to pale pyogranulomatous or granulomatous nodules or plaques In some air sac lesions white or green cottony sporeforming conidiospores can be observed HistologicGranulomatous inflammation with intralesional fungal hyphae measuring 36 µm with parallel walls evenly distributed septa and progressive dichotomous branching at acute angles Angioinvasion with thrombosis Diagnosis Fungal culture combined with cytology or histopathology of affected tissues is the gold standard for a definitive diagnosis The fungus can be cultured from normal tissues without pathologic lesions so it is important to combine culture with microscopic evaluation Fungi can be enhanced with special stains eg periodic acidSchiff PAS Grocotts methenamine silver GMS or immunohistochemical labels to aid in microscopic evaluation Other supportive diagnostics include PCR serology antigen blood tests eg galactomannan endoscopy radiology protein electrophoresis and complete blood counts Because of the ubiquity of this genus serological results correlate poorly with disease Material required for laboratory analysis Swabs or biopsies of affected tissues for culture cytology histopathology and PCR Serum or plasma for serology antigen blood tests and protein electrophoresis Relevant diagnostic laboratories Almost any commercial diagnostic lab can perform fungal cultures cytology or histopathology Aspergillus is readily cultured on a Sabarouds dextrose plate incubated at 37º C for 48 hours An Aspergillus diagnostic panel consisting of ELISA serology galactomannan antigen testing and protein electrophoresis is offered by the University of Miami Avian and Wildlife Laboratory The Fungus Testing Laboratory Department of Pathology Room 329E Mail Code 7750 The University of Texas Health Science Center at San Antonio San Antonio Texas 782293900 2105674131 2105674076 Treatment Antifungal drug classes that have been used to treat aspergillosis include polyenes amphotericin B azoles voriconazole itraconazole ketoconazole allylamines terbinafine and pyrimidines flucytosine Newer echinocandins caspofungin and azoles posaconazole ravuconazole are being used in human medicine The effectiveness of azoles varies widely Most isolates tested are susceptible to voriconazole Terbinafine is synergistic with voriconazole and a terbinafinevoriconazole combination is the current treatment of choice Supportive care treatment of concurrent disease and removing any sources of stress or immunosuppression are also important components of treatment Prevention and control Because clinical disease caused by Aspergillus spp is typically caused by either high environmental exposure with or without immunosuppression methods at prevention and control should be aimed at controlling these predisposing factors Environmental sanitation adequate ventilation and air filtration can all help to reduce environmental fungal spore loads Ensuring that substrates that support fungal growth such as dead plant materials are not present in the enclosure will reduce exposure Enilconazole can be considered when environmental treatment is indicated Commercial formulations of enilconazole eg Clinafarm EC have been developed to disinfect poultry facilities Minimizing stress and concurrent disease can help reduce disease caused by immunosuppression Prophylactic treatment using antifungal drugs eg itraconazole has been used during periods of stress or prolonged antibiotic use for highly susceptible species Animals with aspergillosis should be investigated for other causes of immunosuppression Suggested disinfectant for housing facilities Bleach is the most effective disinfectant Efficacy of other classes of disinfectants is variable and may be species and strain dependent American Association of Zoo Veterinarians Infectious Disease Manual ASPERGILLOSIS Notification Not a reportable disease Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Aspergillosis is not considered a contagious disease However case clusters that mimic outbreaks can be caused by common environmental predisposing factors such as high environmental spore loads or environmental stressors These environmental factors should be considered when introducing animals to the environment of an infected animal Conditions for restoring diseasefree status after an outbreak Not applicable Experts who may be consulted Michael J Dykstra MS PhD mycology North Carolina State University College of Veterinary Medicine 9195136202 michaeldykstrancsuedu Mark G Papich DVM MS clinical pharmacology North Carolina State University College of Veterinary Medicine 9195136221 markpapichncsuedu Patrick T Redig DVM PhD clinical management University of Minnesota redig001umnedu References 1 Burek K 2001 Mycotic diseases In Williams ES and IK Barker eds Infectious Diseases of Wild Mammals 3rd ed Blackwell Publishing Ames Iowa Pp 514531 2 Converse KA 2007 Aspergillosis In Thomas NJ DB Hunter and CT Atkinson eds Infectious Diseases of Wild Birds Blackwell Publishing Ames Iowa Pp 360374 3 Cray C T Watson and KL Arheart 2009 Serosurvey and diagnostic application of antibody titers to Aspergillus in avian species Avian Dis 534 491494 4 Cray C T Watson M Rodriguez and KL Arheart 2009 Application of galactomannan analysis and protein electrophoresis in the diagnosis of aspergillosis in avian species J Zoo Wildl Med 401 6470 5 Disomma A T Bailey C Silvanose and C GarciaMartinez 2007 The use of voriconazole for the treatment of aspergillosis in falcons Falco species J Av Med Surg 21 307311 6 Duncan M 2003 Fungal diseases in all taxa In Fowler ME and RE Miller eds Zoo and Wild Animal Medicine 5th ed Elsevier Science St Louis Missouri Pp 727732 7 Dykstra MJ and K Reininger 2007 Aviary airhandler design and its relationship to fungal spore loads in the air J Zoo Wild Med 38 540547 8 Gupta AK I Ahmad and RC Summerbell 2002 Fungicidal activities of commonly used disinfectants and antifungal pharmaceutical spray preparations against clinical strains of Aspergillus and Candida species Med Mycol 40 201208 9 Kunkle RA 2003 Fungal infections In Saif YM ed Diseases of Poultry 11th ed Iowa State University Press Ames Iowa Pp 883902 10 Pare JA L Sigler KL Rosenthal and DR Mader 2006 Microbiology fungal and bacterial diseases of reptiles In Mader DR ed Reptile Medicine and Surgery 2nd ed Saunders Elsevier St American Association of Zoo Veterinarians Infectious Disease Manual ASPERGILLOSIS Louis Missouri Pp 217238 11 Reidarson TH JF McBain LM Dalton and MG Rinaldi 1999 Diagnosis and treatment of fungal infections in marine mammals In Fowler ME and RE Miller eds Zoo and Wild Animal Medicine Current Therapy 4 WB Saunders Company Philadelphia Pennsylvania Pp 478485 American Association of Zoo Veterinarians Infectious Disease Manual AVIAN BORNAVIRUSES Animal Groups Affected Transmission Clinical Signs and Lesions Severity Treatment Prevention and Control Zoonotic Captive psittacine birds Canaries finches Wild free ranging goose swan duck and gull species Rare proven examples of broad species jumps consistent histopathologic findings have been reported sporadically in a variety of avian species Primarily direct transmission initial assumption of urofecaloral route has been challenged by experimental work suggesting that tissue inoculation may be required Viral shedding in urine feces choanal secretions and possibly feathers Some evidence for vertical transmission to egg not proven to live hatchlings Cause of psittacine proventricular dilatation disease PDD From asymptomatic to severe gastrointestinal signs andor neurological signs leading to death Gross PM classic lesions are emaciation dilation of crop proventriculus or ventriculus ventricular muscle atrophy duodenal distension No lesions may be present with primarily neurological forms Histology non suppurative inflammation in peripheral central andor autonomic nervous systems Birds infected with ABV may or may not show clinical disease Once clinical signs develop avian bornaviral infection is generally considered a progressive disease which ultimately becomes fatal Acute outbreaks with high mortality have been described in psittacine aviaries No specific treatment Suppressing T lymphocyte function may improve clinical signs eg cyclosporin Inconsistent results with the use of various COX II NSAIDs Antiviral drugs inadequately investigated Supportive and symptomatic treatment and good husbandry can prolong life Possibility of complete cure is not certain No vaccine Avoid introducing infected birds into new flocks Excellent husbandry practices strict quarantine protocols including determining the disease and ABV status of all newly introduced birds Isolate infected or exposed birds Standard disinfection protocols should be effective enveloped virus No Fact Sheet compiled by Pauline Delnatte Dale A Smith Sheet completed on September 1 2018 Fact Sheet Reviewed by Michael Lierz Ian Tizard Susceptible animal groups affected by different viral genera Psittacine birds Infection by Psittaciform 1 and 2 orthobornaviruses has been reported in more than 80 species of captive psittacine birds in at least 33 different genera Certain species such as African grey parrots blue and gold macaws cockatoos and Amazon parrots seem most frequently affected Passerine birds Passeriform 1 and 2 orthobornaviruses have been described from captive canaries Serinus canaria a BengaleseSociety finch Lonchura striata domestica and 3 estrildid finches Anseriformes Laridae Waterbird 1 orthobornavirus infection was initially recognized in North America in freeranging mute Cygnus olor and trumpeter swans Cygnus buccinator and in Canada geese Branta canadensis This and related viruses have since been identified in a range of wild goose and duck species as well as in several species of gulls Investigations in Europe have identified Waterbird 1 orthobornavirus infections in three additional species of geese in Denmark and a Eurasian oystercatcher Haematopus ostralegus in Germany Single reports of what are interpreted as broad breaks in fidelity of a given virus for a given host group have American Association of Zoo Veterinarians Infectious Disease Manual AVIAN BORNAVIRUSES been reported thus molecular sequencing of bornaviruses from avian host groups or species not listed above is highly recommended Causative organism The first avianassociated bornavirus ABV was identified in 2008 as the cause of PDD in psittacine birds Bornaviruses are enveloped singlestranded RNA viruses in the family Bornaviridae There are currently five species of bornaviruses affecting birds Passeriform 1 orthobornavirus canary bornaviruses 13 Passeriform 2 orthobornavirus estrildid finch bornavirus Psittaciform 1 orthobornavirus parrot bornaviruses 14 7 Psittaciform 2 orthobornavirus parrot bornavirus 5 and Waterbird 1 orthobornavirus aquatic bird bornaviruses 12 Parrot bornaviruses 2 and 4 are the most commonly identified viruses in psittacine birds Additional viruses await formal classification Zoonotic potential None reported Distribution Parrot bornaviruses PDD the originallyrecognized clinical syndrome of ABV infection in psittacine birds was first identified in the late 1970s in the United States ABV infection and associated disease have been described in captive psittacines around the world Worldwide dissemination is assumed to have resulted from the trade in captive birds While there is some evidence for the presence of exposure of wild parrots to an ABV in South America a reservoir in wild psittacine birds has not been confirmed Canary bornaviruses Reports suggest these viruses are prevalent in captive European canaries Aquatic bird bornaviruses Infection initially recognized as widespread in North America has also been reported from freeranging wild birds in Denmark and Germany A lack of reports from other parts of the world likely reflects a lack of dedicated investigation Incubation period Poorly investigated but appears extremely variable Reports suggest a minimum of 11 days under experimental conditions up to months or years under natural conditions There is a suggestion of an acute form birds die within days or weeks after acute onset of symptoms and of a persistent form birds are able to live for years without clinical impairment likely this simply reflects a continuum Clinical signs Descriptions of PDD in psittacine birds predate the discovery of ABV Birds infected with ABV may or may not develop clinical disease Clinical signs result from pathology in the autonomic central andor peripheral nervous systems and vary in nature severity and duration Nonspecific signs include depression lethargy weight loss muscle atrophy abdominal enlargement polyuria and polydipsia as well as sudden death Classic gastrointestinal signs associated with myenteric plexus dysfunction include dysphagia crop stasis regurgitation impaction maldigestion passage of undigested seeds and progressive loss of body condition Central and peripheral nervous system signs include changes in awareness and demeanor tremors seizures erratic head movements torticollis headpressing opisthotonos abnormal gait and posture inability to perch proprioceptive and motor deficits ataxia paralysis status epilepticus and ophthalmologic abnormalities dilated pupils anisocoria chorioretinitis retinal degeneration and blindness Change in behaviour has also been noted The factors that govern the development of clinical disease in ABV positive birds are not known but are likely related to features of the host immune status as well as of the infecting virus Affected birds can develop secondary opportunistic infections that increase mortality Post mortem gross or histologic findings Consistency among clinical signs and gross and histologic findings is not always present Gross lesions include mild to severe emaciation atrophy of the pectoral proventricular and ventricular muscles proventricular and ventricular dilatation and duodenal distension Proventricular rupture and resulting peritonitis have been rarely reported One report described accumulation of fluid in the subarachnoid space Occasionally no gross lesions are observed Microscopic lesions consist of nonsuppurative inflammation in peripheral central and autonomic nervous tissues Similar infiltrates may also be present in adrenal glands and myocardium Cerebellar Purkinje cell necrosis neuronophagia myelin degeneration gliosis and axonal swelling can accompany the inflammatory lesions Diagnosis PDD as a clinical entity and infection with ABV are not synonymous Histological lesions in biopsy or postmortem samples remain the gold standard for diagnosis of PDD Detection of virusviral RNAviral antigen or antibodies against ABV provides evidence of infection or exposure but does not differentiate among patients with clinical PDD asymptomatic shedders and previously exposed birds There is no standardized American Association of Zoo Veterinarians Infectious Disease Manual AVIAN BORNAVIRUSES screening protocol for PDD andor ABV infection in psittacine flocks but screening programs involving separation of birds based on a combination of repeated RTPCR assessment of choanal andor cloacal swabs feather sampling has also been recommended and serology have been used to derive flocks clear of ABV infection Clinical signs and pathologic lesions ABV infection should be considered as a differential diagnosis for clinical signs referable to the digestive andor nervous systems Prior to the identification of the avian bornaviruses techniques for the antemortem diagnosis of PDD included plain and contrast radiography contrast fluoroscopy and crop biopsy Crop biopsy has a variable and often low sensitivity Detection of virus RNA or antigen Reverse Transcriptase Polymerase Chain Reaction RTPCR Both gelbased and real time RTPCR have been developed using primers for various segments of the ABV genome particularly the N and M genes Not all primers will detect all bornaviruses that affect avian species Immunohistochemistry IHC IHC can be used to identify ABV antigen in formalin fixed biopsy or necropsy specimens Moderately intense diffuse intracytoplasmic staining accompanied by intranuclear staining in neurons and certain epithelial cells is considered positive for viral antigen presence Virus culture Various genotypes of ABV have been successfully grown in a range of avian cell lines Cytopathic effects do not occur thus virus must be demonstrated by Western blot immunohistochemistry indirect immunofluorescence or RTPCR Sequence analysis The recognition of an increasing number of bornaviral species and genotypes makes genome sequencing a critical component in the diagnosis of ABV infection and of PDD Detection of antibodies Indirect immunofluorescence using infected cell cultures which present multiple antigens Western blot and indirect ELISA assays using various sources of monoclonal primary antigen have been used in psittacine birds and waterfowl Several private laboratories offer serologic testing which is also used as a research tool Test specificity and sensitivity are difficult to determine and compare due to the absence of a gold standard for diagnosis and the relatively poor correlation between the presence of antibodies fecal shedding of ABV and the presence of pathologic lesions andor clinical disease Considerable research is required before we will understand which viral proteins are the most immunogenic and the role of antibodies in resistance to infection and to the development of clinical signs Material required for laboratory analysis Antemortem Crop tissue histology IHC RTPCR choanal and cloacal swabs feces less sensitive than cloacal swabs and possibly calami of plucked chest contour feathers RTPCR plasma or serum serology Pooling multiple cloacal swabs or droppings from a single bird over several days or samples from multiple birds in an aviary increases test sensitivity as shedding of virus is frequently intermittent Postmortem Brain proventriculus ventriculus adrenals and vitreous of the eye most consistently infected tissues RTPCR sequencing brain proventriculus ventriculus histology IHC As lesions vary in location and severity submission of a full suite of tissues is highly recommended RTPCR can also be performed on formalinfixed paraffin embedded FFPE tissues in some laboratories Relevant diagnostic laboratories Histopathologic assessment can be performed by any veterinary pathology diagnostic service RTPCR testing can be carried out by any molecular laboratory with appropriate primers Information on test validation and primer selection should be requested Animal Health Laboratory University of Guelph Guelph Ontario Canada AAVLD accredited httpwwwguelphlabservicescomahl Diagnostic Services Faculté de médecine vétérinaire University of Montréal St Hyacinthe Quebec Canada AAVLD accredited httpservicedediagnosticcom American Association of Zoo Veterinarians Infectious Disease Manual AVIAN BORNAVIRUSES Infectious Disease Laboratory University of Georgia Athens Georgia USA httpwwwvetugaeduidlindex Veterinary Molecular Diagnostics Inc Milford Ohio USA wwwvmdlabscom Commercially available RTPCR and ELISA testing offered as a panel Animal Genetics Inc USA Tallahassee Florida USA Europe Cornwall England httpanimalgeneticscom RTPCR Realtime RTPCR Serology Sanitation of flocks located in Europe Clinic for Birds Reptiles Amphibians and Fish JustusLiebig University Giessen Germany httpswwwunigiessendefbzfb10instituteklinikumklinikumkvraf email kvrafvetmedunigiessende Treatment No specific treatment exists Supportive and symptomatic therapy may prolong life for months to years Nonsteroidal antiinflammatory drugs Celecoxib tepoxalin and meloxicam have been recommended but evidence of effectiveness has been inconsistent A study in cockatiels suggested that the use of meloxicam would actually be detrimental to birds affected with PDD Immunosuppressive protocols May be of therapeutic benefit especially selective Tcell elimination Cyclosporine appears to hold the most promise based on limited research Antiviral drugs Have been described as beneficial by some authors eg amantadine but have been reported as having no apparent effect on fecal shedding of virus by others Ribavirin reduces viral replication in tissue culture but does not appear to have a measurable effect on viral shedding in vivo Most recent research suggests favipiravir may be able to eliminate Borna disease virus 1 and parrot bornavirus 4 from infected cultured cells In vivo studies have not been carried out Prevention and control Preventive measures are intended to avoid introduction of an ABV into new flocks and include excellent husbandry and sanitation practices and strict quarantine protocols Screening of birds in quarantine should include a combination of PCR and serologic testing see Diagnosis above The interpretation of test results can be challenging as diagnostic test protocols vary among laboratories and an understanding of the biology of the disease is necessary for interpretation eg intermittent shedding asymptomatic carriers testing of nonpsittacine species etc The possibility of vertical transmission of ABV complicates the management of infected aviaries Pairing ABV positive birds incubating their eggs artificially and handraising the chicks separately until their ABV status is determined may be a viable option for critically endangered species There is currently no vaccine against ABV infection Recent studies have suggested that serum antibodies are not protective and that persistent infection is a result of ABV escaping recognition by the innate immune system Early research on vaccine development has been published with reduction of infection and hence clinical disease in one study and prevention of clinical disease but not infection in another Suggested disinfectant for housing facilities Although there are no data on environmental survival of the ABVs or sensitivity to disinfectants they are assumed to have the same stability as other enveloped RNA viruses of similar size and structure Disinfection with phenols formaldehyde or hypochlorites is thus recommended Notification None legally required information regarding the infection and exposure status of birds being transferred between institutions is recommended Measures required under the Animal Disease Surveillance Plan Not applicable Measures required for introducing animals to infected animal The mixing of infected and noninfected birds is not recommended There is no known strategy to prevent viral transmission between incontact birds Excellent hygiene appears to prevent spread within a facility containing infected and uninfected birds Conditions for restoring diseasefree status after an outbreak American Association of Zoo Veterinarians Infectious Disease Manual AVIAN BORNAVIRUSES There is no system of ABVfree certification Clearing infection from a flock requires a rigorous program of repeated cycles of testing using both PCR and serology separation of birds positive for virus or antibodies and retesting Reliance on PCR testing when serologic testing is not available makes recognition of infected birds more difficult Some populations of captive birds appear to have a very high prevalence of infection Experts who may be consulted Dr Dale A Smith Professor Department of Pathobiology Ontario Veterinary College University of Guelph Canada dalesmituoguelphca Schubot Exotic Bird Health Centre Department of Veterinary Pathobiology Texas AM University USA Contact research group through Dr Ian Tizard Professor ITIZARDcvmtamuedu Dr Monika Rinder Clinic for Birds University of Munich Oberschleissheim Germany Dr Michael Lierz Clinic for Birds Reptiles Amphibians and Fish Faculty of Veterinary Medicine Justus Liebig University Giessen Giessen Germany References 1 Amarasinghe GK Aréchiga Ceballos NG Banyard AC Basler CF Bavari S Bennett AJ Blasdell KR Briese T Bukreyev A Caì Y Calisher CH Campos Lawson C Chandran K Chapman CA Chiu CY Choi KS Collins PL Dietzgen RG Dolja VV Dolnik O Domier LL Dürrwald R Dye JM Easton AJ Ebihara H Echevarría JE Fooks AR Formenty PBH Fouchier RAM Freuling CM Ghedin E Goldberg TL Hewson R Horie M Hyndman TH Jiāng D Kityo R Kobinger GP Kondō H Koonin EV Krupovic M Kurath G Lamb RA Lee B Leroy EM Maes P Maisner A Marston DA Mor SK Müller T Mühlberger E Ramírez VMN Netesov SV Ng TFF Nowotny N Palacios G Patterson JL Pawęska JT Payne SL Prieto K Rima BK Rota P Rubbenstroth D Schwemmle M Siddell S Smither SJ Song Q Song T Stenglein MD Stone DM Takada A Tesh RB Thomazelli LM Tomonaga K Tordo N Towner JS Vasilakis N VázquezMorón S Verdugo C Volchkov VE Wahl V Walker PJ Wang D Wang LF Wellehan JFX Wiley MR Whitfield AE Wolf YI Yè G Zhāng YZ Kuhn JH Taxonomy of the order Mononegavirales update 2018 Arch Virol Internet 2018163822832294 Available from doi101007s007050183814x 1 de Araujo JL Rech RR Heatley JJ Guo J Giaretta PR Tizard I RodriguesHoffmann A From nerves to brain to gastrointestinal tract A timebased study of parrot bornavirus 2 PaBV2 pathogenesis in cockatiels Nymphicus hollandicusPloS one 20171211 pe0187797 2 Delnatte P Ojkic D DeLay J Campbell D Crawshaw G Smith DA Pathology and diagnosis of avian bornavirus infection in wild Canada geese Branta canadensis trumpeter swans Cygnus buccinator and mute swans Cygnus olor in Canada a retrospective study Avian Path 20134211428 3 Heckmann J Enderlein D Piepenbring AK Herzog S HeffelsRedmann U Malberg S Herden C Lierz M Investigation of different infection routes of parrot bornavirus in cockatiels Avian Dis 20176119095 4 Hoppes S Tizard I Shivaprasad HL Avian bornavirus and proventricular dilatation disease diagnostics pathology prevalence and control Vet Clin North Am Exot Anim Pract 201316339355 5 Lierz M Avian bornavirus and proventricular dilation disease In Speer BL ed Current therapy in avian medicine and surgery St Louis MO Elsevier 2016 p 2846 6 Payne SL Delnatte P Guo J Heatley JJ Tizard I Smith DA Birds and bornaviruses Anim Health Res Rev 201213145156 7 Rubbenstroth D Schmidt V Rinder M Legler M Twietmeyer S Schwemmer P Corman VM Phylogenetic analysis supports horizontal transmission as a driving force of the spread of avian bornaviruses PloS one 2016118e0160936 8 Thomsen AF Nielsen JB Hjulsager CK Chriel M Smith DA Bertelsen MF Aquatic Bird Bornavirus 1 in Wild Geese Denmark Emerg Infect Dis 20152122013 9 Tokunaga T Yamamoto Y Sakai M Tomonaga K Honda T Antiviral activity of favipiravir T705 against mammalian and avian bornaviruses Antivir res 201714323745 American Association of Zoo Veterinarians Infectious Disease Manual AVIAN INFLUENZA Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Birds predominantly carried by waterfowl and shorebirds various mammals Fecaloral and fecalcloacal ie contaminated water airborne and direct contact through mucous membranes ingestion of infected tissues fomites and mechanical vectors LPAI typically asymptomatic HPAI Respiratory digestive or nervous system signs sudden death Asymptomatic to fatal in all animals affected Antiviral drugs in humans Preparedness protocol including guidelines for facility during an outbreak surveillance techniques and biosecurity protocols Minimize contact between captive birds and wild birds Quarantine new birds for at least 30 days Yes Fact Sheet compiled by Rae Gandolf Sheet completed on 1 January 2011 updated 1 November 2012 Fact Sheet Reviewed by Carol Cardona Walter Boyce Susceptible animal groups Avian influenza viruses can infect a wide variety of species Whereas aquatic birds typically exhibit few signs of infection once the virus spreads to poultry it can become more virulent and can potentially cause severe disease in mammalian species that may come in contact with them Aquatic birds migratory waterfowl Anseriformes and shore birds Charadriiformes act as the major natural reservoir species infection is typically asymptomatic in ducks infected with the low pathogenicity viruses LPAI wild birds have only rarely been infected with high pathogenicity viruses HPAI Poultry other gallinaceous birds typically mild clinical signs or subclinical with LPAI some viruses of the H5 or H7 subtypes may mutate to HPAI while circulating in a flock potentially resulting in very high mortality Mammals and other avian species HPAI H5N1 exhibits a wide and growing host range including humans LPAI viruses may infect mammals and other avian species but infections are typically undetected because they are asymptomatic Examples of species with confirmed HPAI include primates suids felids domestic house cats and several nondomestic species pinnipeds canids raccoon dogs rarely in domestic dogs viverids palm civets mustelids ferrets stone martens mink lagormorphs pikas rabbits rodents whales and a broad range of avian species including psittacines Causative organism Influenza A an enveloped RNA virus in the family Orthomyxoviridae Influenza A viruses are classified according to subtypes based on two surface proteins hemagglutinin H and neuraminidase N Avian influenza viruses are further classified according to their virulence in chickens American Association of Zoo Veterinarians Infectious Disease Manual AVIAN INFLUENZA HPAI or LPAI Although they are classified as LPAI in chickens some isolates can still cause disease in other species Disease significance Appearance and spread of HPAI H5N1 in poultry has increased the risk of spillover into human and non human hosts Poultry farms can sustain very high mortality and morbidity leading to high costs and trade restrictions on poultry products Zoonotic infections of humans may lead to the development of viruses with pandemic potential especially HPAI H5N1 LPAI and HPAI viruses may emerge and cause disease in captive and freeranging wildlife species Zoonotic potential Yes Distribution LPAI viruses occur worldwide in migrating birds and poultry Infections have been confirmed in Africa Asia Australia Europe North America and South America New HPAI viruses emerge periodically in poultry and HPAI H5N1 has become established in several Asian and African countries Incubation period Highly variable Humans typically 27 days up to 17 days poultry 17 days wild birds typically 17 days However the actual incubation period of a given virus in any species ie 9000 species of birds will vary based on host and virus Clinical signs This virus can infect the respiratory digestive or nervous systems alone or in combination depending on the host Signs correlate with the location of the infection and vary depending on viral subtype environmental factors age health status and species LPAI birds asymptomatic to conjunctivitis and mild respiratory symptoms freeranging and domestic species decreased egg production documented in domestic poultry may apply to other species HPAI birds sudden death of large numbers of birds especially in poultry may also see any of the following marked depression sinusitis lacrimation cyanosis of the head edema of the head green to white diarrhea coughing sneezing bloodtinged oral and nasal discharges podothecal ecchymoses neurologic disease decreased egg production loss of egg pigmentation and deformed or shellless eggs HPAI mammals pyrexia and difficulty breathing or rapid breathing are typically the initial symptoms and may be followed by conjunctivitis coughing mucosal bleeding diarrhea vomiting abdominal pain neurologic signs multiorgan failure DIC and death Morbidity and mortality are variable Among zoo animals fatal cases were reported among captive tigers and leopards in Thailand but captive leopards tigers Asiatic golden cats and lions at a wildlife rescue center in Cambodia all recovered after an illness lasting 57 days Post mortem gross or histologic findings Highly variable in birds ranging from no lesions in peracute deaths to subcutaneous edema on the head and neck edema and subcutaneous hemorrhages on the feet fluid in the nares and oral cavity conjunctivitis hemorrhagic tracheitis lung hemorrhage and congestion petechiae throughout the abdominal fat over serosal surfaces and peritoneum congested kidneys sometimes plugged with urate deposits hemorrhagic or degenerated ovaries with areas of necrosis yolk from ruptured ova within the peritoneal cavity yolk peritonitis and air sacculitis It is important to note that the occurrence of peritonitis tracheitis edema of the wattles or neck or petechial hemorrhages in the proventriculus may be particularly suggestive of an HPAI infection Findings in mammals infected with HPAI are also broadranging and may include pulmonary congestion and edema conjunctivitis multiorgan congestion widespread internal hemorrhages encephalitis and myocarditis Diagnosis Virus isolation andor RTPCR assays can identify avian influenza viruses in clinical samples These tests can also distinguish some viral subtypes American Association of Zoo Veterinarians Infectious Disease Manual AVIAN INFLUENZA Viral antigens and antibodies can also be detected with ELISAs including rapid tests As of 2008 the World Organization for Animal Health OIE recommended that antigen detection tests be used to identify avian influenza only in flocks and not in individual birds Serologic tests including agar gel immunodiffusion hemagglutination inhibition and ELISAs are useful as supplemental tests Blocking or competitive ELISAs are species independent and can be very useful for detecting prior exposure to AI virus in wild birds AGID may be insensitive in some avian species and HI requires the proper viral antigen to be useful Serology is not useful in the diagnosis of HPAI in susceptible species because they will die before they seroconvert Material required for laboratory analysis Oropharyngeal tracheal or cloacal swabs or in small birds or for surveillance feces may be used in live birds additionally organ samples trachea lungs air sacs intestine spleen kidney brain liver and heart can be tested in dead birds Links to sample collection protocols for the National Wildlife Health Center lab may be found on the USGS avian influenza page httpwwwnwhcusgsgovdiseaseinformationavianinfluenza Relevant diagnostic laboratories Diagnostic testing for avian influenza is generally performed by specialized county state regional or national laboratories such as the USDAapproved laboratories in the National Animal Health Laboratory Network NAHLN NAHLNaphisusdagov 5156637731 Authorities should be consulted regarding regulations for sending samples to authorized diagnostic laboratories Treatment Four antiviral drugs amantadine rimantadine zanamivir and oseltamivir are active against selected human influenza viruses Studies suggest that these drugs may also be helpful in avian influenza infections in humans although many currently circulating strains are resistant to amantadine and rimantadine In poultry HPAI is managed primarily by flock eradication but LPAI may be managed with vaccination eradication or quarantine Prevention and control Each institution should have general preparedness protocol including advance communication with regulatory officials regarding potential courses of action guidelines concerning the operation of the facility during an outbreak surveillance techniques for captive animals and wildlife on the premise preventative measures to protect public health vaccination planning and biosecurity protocols hand washing disinfecting quarantine etc Additionally Staff should be provided with information regarding human health precautions and trained for proper use of personal protective equipment Case definition criteria for avian influenza should be established for captive species in order to identify the disease early and institute the biosecurity protocol A testing plan should be established and a laboratory where the testing will be done should be identified The entire collection should be catalogued as influenza susceptible or resistant based on the likelihood of infection in the event of exposure The expected clinical appearance of infection of the susceptible birds and mammals in the collection should be recorded to prepare for a possible outbreak Minimize contact between captive birds and wild birds Quarantine new birds for at least 30 days In the face of an outbreak captive birds could potentially be vaccinated 25000 captive birds were vaccinated with a H5N2 inactivated vaccine in European zoological facilities since 2005 Most birds seroconverted following the second booster vaccination and semiannual to annual vaccination is recommended A negative correlation exists between antibody response and increasing mean body weight Some species pelicans and owls may fail to respond to vaccination Different species may have differing responses to vaccination including duration of immunity which may require regular serologic monitoring and additional booster vaccinations Approval for zoological institutions to administer vaccinations to birds American Association of Zoo Veterinarians Infectious Disease Manual AVIAN INFLUENZA in the US will be conditional and overseen by a federally accredited veterinarian Restrictions on transporting vaccinated birds or releasing them back into the wild may be imposed Suggested disinfectant for housing facilities Avian influenza viruses are relatively unstable in the environment and are inactivated by extremes in pH heat and dryness The virus may persist for a long time in cool aquatic environments The virus may survive over 100 days in cool fresh water and indefinitely when frozen In the presence of organic matter AI virus can be inactivated by aldehydes After removal of organic matter several classes of disinfectants are effective at destroying avian influenza virus phenolics One Stroke Environ quaternary ammonium compounds Roccal oxidizing agents Virkon dilute acids eperacetic acid and bleach Notification Any suspect cases should be reported to the state veterinarian or USDA Veterinarian USDA Veterinary Services18665367593 Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak No official diseasefree status offered Experts who may be consulted Carol J Cardona DVM PhD DACPV Ben Pomeroy Chair in Avian Health College of Veterinary Medicine University of Minnesota 1971 Commonwealth Saint Paul MN 55108 612 6255276 phone 612 6255203 fax Walter M Boyce DVM PhD Professor Department of Pathology Microbiology and Immunology School of Veterinary Medicine UC Davis CoDirector Wildlife Health Center Wildlife Health Center TB 128 2105 Haring Hall 530 7521401 wmboyceucdavisedu References 1 Cattoli G and I Capua 2007 Diagnosing avian influenza in the framework of wildlife surveillance efforts and environmental samples J Wildl Dis 43 s35s39 2 Furger M R Hoop H Steinmetz U Eulenberger and JM Hatt 2008 Humoral immune response to avian influenza vaccination over a sixmonth period in different species of captive wild birds Avian Dis 522228 3 Kelly TR MG Hawkins CE Sandrock and WM Boyce 2008 A review of highly pathogenic avian influenza in birds with an emphasis on Asian H5N1 and recommendations for prevention and control J Avian Med Surg 22116 4 Lécu A C De Langhe T Petit F Bernard and H Swam 2009 Serologic response and safety to vaccination against avian influenza using inactivated H5N2 vaccine in zoo birds J Zoo Wildl Med 4073143 5 Martin V S Von dobschuetz A Lemenach N Rass W Schoustra and I Desimone 2007 Early warning database and information systems for avian influenza surveillance J Wildl Dis 43 s71s76 American Association of Zoo Veterinarians Infectious Disease Manual AVIAN INFLUENZA 6 Philippa JD 2008 Avian Influenza In Fowler ME and RE Miller Zoo and Wild Animal Medicine Current Therapy 6th edition W B Saunders Co Philadelphia Pennsylvania Pp 7987 7 The Center for Food Security and Public Health at Iowa State University Highly pathogenic avian influenza httpwwwcfsphiastateeduFactsheetspdfshighlypathogenicavianinfluenzapdf Accessed 11 July 2013 8 USDAAPHIS Interagency Strategic Plan for Avian Influenza Surveillance in Migratory Birds 2006 httpwwwaphisusdagovwildlifedamagenwdppdfwildbirdstrategicplanpdfpdf Accessed 11 July 2013 9 Redrobe S P 2007 Avian influenza H5N1 a review of the current situation and relevance to zoos Int Zoo Yb 41 96109 10 Siembieda J CK Johnson WM Boyce C Sandrock and C Cardona 2008 Risk for avian influenza virus exposure at humanwildlife interface Emerg Infect Dis 14 11513 11 Yoon H OK Moon SJ More CK Park JY Park YJ Lee SD Lee JK Ha SK Jeong JK Jeong and SJ Lee 2010 An outbreak of highly pathogenic avian influenza at a public animal exhibit in seoul Korea during 2008 Zoonoses Pub Health 571425 American Association of Zoo Veterinarians Infectious Disease Manual AVIAN POXVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Avian Mechanical spread by invertebrate vectors Direct contact between birds or indirect contact with contaminated surfaces Cutaneous or dry form skin nodules Diptheritic or wet form internal lesions in upper alimentary or respiratory tracts Systemic infection Small focal skin lesions to widespread severe lesions respiratory difficulties to peracute death in certain species Treat secondary bacterial infections May need to provide supportive fluids and food Vector control and good hygiene No Fact Sheet compiled by Sharon L Deem Sheet completed on updated 31 July 2018 Fact Sheet Reviewed by Kristi Delaski Susceptible animal groups Avians Over 275 species of birds in 23 orders are known to be susceptible Causative organism Avipoxvirus in the family Poxviridae Large up to 400 nm doublestranded enveloped DNA 17 types of Avipoxvirus spp have been identified to date Zoonotic potential No Distribution Worldwide with exception of no published reports from the Arctic or Antarctic Incubation period Variable with approximate range of 4 days up to several months Clinical signs The signs vary with virulence of the virus susceptibility of the host distribution and type of lesions in an infected bird and other complicating factors Manifestations are cutaneous dry diphtheritic wet systemic or some combination of the three Cutaneous lesions are characterized by the appearance of nodular lesions on featherfree regions of the body in editors experience often in nongallinaceous species these lesions occur as single nodules which may resemble a proliferative neoplasm Diphtheritic lesions are moist necrotic lesions on the mucous membranes of the mouth and upper respiratory tract Septicemic form is associated with acute depression anorexia dyspnea and death and has been most frequently reported in certain passerine species eg canary Infected birds can have peracute infections death or may become latent carriers Also note that when stressed eg during transfer intra and interzoo other illness it has been suggested that birds may recrudesce and develop new lesions which may first appear as redswollen areas Any bird with these developing lesions should be immediately separated from other birds and caged individually while avian pox is or is not confirmed Post mortem gross or histologic findings Gross lesions are proliferations of epithelial cells Diphtheritic form may appear as white opaque slightly elevated nodules to coalescing yellowish caseous necrotic material with the appearance of a pseudomembrane Diagnosis Gross lesions in cutaneous infections are often highly suggestive of pox infection but are not definitively avian pox Diphtheritic infections are often harder to diagnosis on gross observations due to differential diagnoses eg trichomonosis Histologic evaluation for Bollinger bodies eosinophilic intracytoplasmic epidermal inclusions on light microscopy is acceptable for diagnosis Virus isolation on the chorioallantoic membrane of embryonated chicken eggs or in cell cultures of avian origin may be used PCR techniques are also available for detection of avian pox DNA from DNAextracted direct from lesion or extracted virus culture PCR targeting the 4b core protein has been widely used for construction of avian poxvirus phylogenies and virus strain differentiation Material required for laboratory analysis Biopsy of cutaneous nodules and diphtheritic mucous membranes for detection of the pathognomonic Bollinger bodies American Association of Zoo Veterinarians Infectious Disease Manual AVIAN POXVIRUS Relevant diagnostic laboratories State or university veterinary diagnostic laboratories in most states can perform diagnostic testing National Wildlife Health Center 6006 Schroeder Road Madison WI 537116223 Phone 608 2702400 Fax 608 2702415 National Animal Disease Center PO BOX 70 1920 Dayton Avenue Ames IA 50010 Treatment No direct treatment for virus infection itself exists However secondary bacterial infections should be treated Supportive care may be needed to provide supplemental food and water for those birds that cannot see or eat properly Prevention and control Mechanically transmitted virus therefore control of vectors eg mosquitoes flies and fomites is very important Perch design and cage structure important to minimize cross infections and to decrease abrasions that allow entry of the virus Suggested disinfectant for housing facilities Any strong disinfectant including bleach Notification None required Measures required under the Animal Disease Surveillance Plan None required Measures required for introducing animals to infected animal Keep birds with pox lesions in quarantine until no clinical signs are present Conditions for restoring diseasefree status after an outbreak Clean with common disinfectants eg bleach and keep mosquitoes and other mechanical vectors to a minimum Experts who may be consulted Charles van Riper III ST Research Ecologist USGSSBSCSonoran Desert Research Station 1110 E South Campus Dr Room 123 mail Room 121A Building 33 office University of Arizona Tucson Arizona 857210033 520 626 7027 Cell 520 491 0721 Fax 520 670 5001 httpcharlesvanripercom Charlesvanriperusgsgov References 1 Bolte AL Meurer J Kaleta EF Avian host spectrum of avipoxviruses Av Pathol 199828415432 2 Jarmin S Manvell R Gough RE Laidlaw SM Skinner MA Avipoxvirus phylogenetics identification of a PCR length polymorphism that discriminates between the two major clades J Gen Virol 20068721912201 3 Lawson B Lachish S Colvile KM Durrant C Peck KM Toms MP Sheldon BC Cunningham AA Emergence of a novel avian pox disease in British tit species PLOS ONE 2012711 e40176 Available from doi101371journalpone0040176 4 Parker PG Buckles EL Farrington H Petren K Whiteman NK Ricklefs RE Bollmer JL Jiménez American Association of Zoo Veterinarians Infectious Disease Manual AVIAN POXVIRUS Uzcátegui G 110 years of Avipoxvirus in the Galapagos Islands PLOS ONE 2011 6 e15989 5 Ritchie BW Poxviridae In Avian Viruses Function and Control Lake Worth FL Wingers Publishing Inc 1995 p 285311 6 Thiel T Whiteman NK Tirape A Maquero MI Cedeno V Walsh T Jimenez G Parker PG Characterization of canarypoxlike viruses infecting endemic birds in the Galapagos Islands J Wildl Dis 200541342353 7 van Riper C Forrester DJ Avian Pox In Thomas NJ Hunter DB Atkinson CT eds Infectious Diseases of Wild Birds Ames IA Blackwell Publishing 2007 p 131176 American Association of Zoo Veterinarians Infectious Disease Manual BABESIOSIS Animal group s affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Ubiquitous in wildlife wherever there are tick infestations Variety of mammal species birds humans Numerous species of Ixodid ticks some evidence for direct bloodblood contact transmission of Entopolypoides in primate colonies Severe hemolytic anemia hemoglobinemia hemoglobinuria fever possible neurologic signs anorexia slight jaundice or subclinical Majority of infections in wildlife are subclinical May be severe with acute clinical presentation and death Clinical disease often less severe in free ranging animals than domestic animals Imidicarb tick control Tick control is primary means of preventing Babesia infection host immunity through exposure Babesia microti carried by wild rodents has caused human infection Fact Sheet compiled by Tiffany M Wolf Sheet completed on December 16 2012 updated February 27 2013 updated January 9 2018 Fact Sheet Reviewed by Arno Wünschmann Ulrike Munderloh Sam Telford Susceptible animal groups Most mammal orders not in marine mammals Cetacea Pinniped several avian species humans Causative organism Babesia bovis bigemina and odocoilei ungulates B caballi and B equi horses renamed Theileria equi B canis gibsoni annae canids B lotori raccoons B mephitis striped skunk B microti rodents currently there are 14 distinct avian Babesia species Babesia sp found outside of North America may be encountered in the zoological setting in animals that are directly imported from other countries Additionally Entopolyploides macaci which is closely related to B microti is often identified in colonies of research primates such as rhesus macaques African monkeys and baboons and will infect other species of primates Zoonotic potential Illness caused by B microti in humans is typically mild or inapparent but B microti does infect and can cause significant illness in immuneintact persons though illness tends to be more severe in immunecompromised persons Other species such as B divergenslike MO1 and B duncani are known to cause disease mainly in immunocompromised people More severe and often fatal babesiosis occurs in splenectomized people Distribution Typically follows that of the tick vector B bovis and B bigemina are transmitted by Rhipicephalus microplus and R annulatus respectively and found in Mexico and occasionally southern Texas and California B odocoilei is transmitted by Ixodes scapularis and I pacificus which are found in eastern half of US and Canada I scapularis and Pacific coast of US and Canada I pacificus B caballi and B equi was eradicated from the US and is absent in Canada B canis and B gibsoni are transmitted by R sanguineus and found throughout most of the US and southeastern Canada B lotoris tick vector is unknown but found in eastern US Texas and California B annae has been reported from raccoons and foxes in Massachusetts B mephitis has been reported in skunks in Maryland B microti is transmitted by I scapularis and found in northeastern and upper Midwest US The geographic distribution of avian Babesia species is not fully understood American Association of Zoo Veterinarians Infectious Disease Manual BABESIOSIS Incubation period B bovis and B bigemina incubation is generally 23 weeks posttick infestation and from 5 days to 3 weeks postblood inoculation depending on dose of inoculum Ticks must feed for 23 days for successful transmission of B canis Incubation period for humans is reported as 16 week from beginning of tick feeding Chronic infections may recrudesce if an animal is stressed or becomes immunocompromised for any reason Clinical symptoms Nonspecific clinical signs include fever anorexia depression and lethargy lymphadenopathy Erythrocyte destruction by the parasite and host immune response results in mild to severe hemolytic anemia icterus hemoglobinemia hemoglobinuria splenomegaly In rare cases where Babesiainfected erythrocytes obstruct brain capillaries neurologic signs may be noted Post mortem gross or histologic findings Pathologic findings may include icterus generalized lymph node enlargement hepatomegaly and splenomegaly due to red pulp hyperplasia abomasal mucosal ulcerations hemorrhage into the intestinal tract and dark red kidneys hemoglobinuric nephrosis Edema and hemorrhage of tissues such as the cardiac muscle intestinal serosa and lymph nodes may be observed as well as fluid in the body cavities and pericardial sac The bladder is frequently distended with dark red urine For fulminating ruminant infections Giemsastained brain crush smears are helpful to detect parasitized erythrocytes in brain capillaries Also the spleen often contains large numbers of parasitized cells which may be appreciated on impression smears taken from cross sections of the spleen Diagnosis Microscopic visualization of piroplasms within erythrocytes in Giemsa Wrights or DiffQuickstained thin or thick whole blood smears Piroplasms become more difficult to find on blood smears after the acute phase of infection passes Serologic tests cELISA IFA CFT nucleic acid probes and PCR are also available Gross splenomegaly is a common finding particularly in naïve or unnatural hosts Impression smears of spleen may be made for the identification of parasitized cells Material required for laboratory analysis Whole blood EDTA for smears and PCR serum for serological testing Relevant diagnostic laboratories Several veterinary diagnostic laboratories offer serologic and PCR testing for B bovis B bigemina B caballi B equi B canis and B gibsoni Research labs with Babesia expertise are good options to work up samples Treatment Treatment is most successful in the early phase of the disease Chemotherapy may not completely eliminate infection and may be unsuccessful in the later stages of the disease Imidocarb dipropionate 1mgkg IM diminazene aceturate 3mgkg IM phenamidine diisethionate 813 mgkg and amicarbalide diisethionate 10 mgkg IM have been used to treat babesiosis in artiodactylids Similarly imidocarb diminazene and phenamidine have also been utilized to treat B canis and B gibsoni Primaquine phosphate is preferred treatment in felids and birds Quinine and clindamycin or atovaquone and azithromycin are used to treat zoonotic babesiosis and might be tried for nonhuman primate infections In addition to specific therapy supportive care with fluids blood transfusions iron and antibiotics may be important as well Supportive therapy may be contraindicated in severely anemic animals that are easily stressed with handling Prevention and control Freeranging animals sharing zoo habitats are often already infected with Babesia as well as vector ticks The primary means of controlling outbreaks is through control of the tick vector Elimination or reduction of tick American Association of Zoo Veterinarians Infectious Disease Manual BABESIOSIS infestation may be accomplished via application of acaricides prophylactic use of chemotherapeutics range burning prolonged pasture rest and repellents Additionally care should be taken to prevent accidental transmission through the transfer of infected blood between animals via routine surgical or vaccination procedures Vaccines of noninfectious material have been developed and although they do not prevent infection they do ameliorate the severity of disease Additionally differences in strain antigenicity limit cross protection by the vaccine Suggested disinfectant for housing facilities Disinfectants are generally not effective in preventing the spread of babesiosis However standard measures should be taken to prevent the transfer of infected blood between animals R sanguineus the vector for canine babesiosis is typically found indoors in kennels and other housing situations such facilities should be treated with appropriate acaricides Notification Babesiosis caused by B bovis B bigemina B equi and B caballi are reportable diseases and state and federal authorities must be notified immediately of infection Public health officials may need to be notified if zoonotic infection has occurred or is suspected Measures required under the Animal Disease Surveillance Plan Equine piroplasmosis is considered a foreign animal disease in the US therefore any equids imported must be serologically screened by the National Veterinary Services Laboratory using the competitive enzymelinked immunosorbent assay cELISA prior to importation Current information regarding the USDAs requirements for disease surveillance can be found at httpswwwaphisusdagovaphisourfocusanimalhealthmonitoring andsurveillance Measures required for introducing animals to infected animal Animals that have been treated for and survive infection should be considered chronic carriers The most important means of preventing transmission is through vector control A premunition approach may be an alternative strategy for introducing naïve animals into endemic areas for conservation purposes Conditions for restoring diseasefree status after an outbreak Diseasefree status may not be realistic particularly where wildlife is involved in the maintenance of endemnicity Experts who may be consulted Sam Telford III Department of Infectious Diseases and Global Health Tufts Cummings School of Veterinary Medicine References 1 Ayoob AL Prittie J Hackner SG Feline babesiosis J Vet Emerg Crit Care 2012201 9097 2 Babesiosis Internet Center for Disease Control cited 2018 May 21 Available from httpwwwcdcgovbabesiosis 3 Barriga OO A review on vaccination against protozoa and arthropods of veterinary importance Vet Parasitol 19945512 2955 4 Bovine Babesiosis Internet The Center for Food Security and Public Health College of Veterinary Medicine Iowa State University cited 2018 May 21 Available from httpwwwcfsphiastateeduFactsheetspdfsbovinebabesiosispdf 5 Chalmers WSK Overview of new vaccines and technologies Vet Microbiol 200611712531 6 Cogswell FB Malaria and piroplasms of nonhuman primates In Bowman DD ed Companion and Exotic Animal Parasitology International Veterinary Information Service wwwivisorg 2000 American Association of Zoo Veterinarians Infectious Disease Manual BABESIOSIS Document No A03040600 7 Equine Piroplasmosis Internet The Center for Food Security and Public Health College of Veterinary Medicine Iowa State University cited 2018 May 21 Available from httpwwwcfsphiastateeduFactsheetspdfsequinepiroplasmosispdf 8 Kocan AA Waldrup KA Piroplasms Theileria spp Cytauxzoon spp and Babesia spp In Samuel WM Pybus MJ and Kocan AA eds Parasitic Disease of Wild Mammals Ames IA Iowa State University Press 2001 p 524536 9 Krause PJ Babesiosis Med Clin North Am 2002862361373 10 Lopez M Figueroa JV Ramos JA Mosqueda JJ Rojas E Vega CA Alvarez JA Infection and seroconversion of susceptible animals introduced into a babesiosis endemic area Ann NY Acad Sci 20081149131131135 11 McEnroe WD Human babesiosis Science 19771954277506507 12 Nijhof AM Penzhorn BL Lynen G Mollel JO Morkel P Bekker CPJ Jongejan F Babesia bicornis sp nov and Theileria bicornis sp nov tickborne parasites associated with mortality in the black rhinoceros Diceros bicornis J Clin Microbiol 200341522492254 13 Taboada J Babesiosis In Greene CE ed Infectious Diseases of the Dog and Cat Philadelphia PAWB Saunders Company 1998 p 473480 14 Telford SR Gorentflot A Brasseur P Spielman A Babesial infections of humans and wildlife In Kreier JP Baker JR eds Parasitic Protozoa Vol 5 2nd edition New York NY Academic Press 1993 p 147 15 Yabsley M Greiner E Tseng F Garner M Nordhausen R Ziccardi MH Borjesson DL Zabolotzky S Description of novel babesia species and associated lesions from common murres Uria aalge from California J Parasitol 20099551183 16 Zaugg JL Babesiosis In Smith BP ed Large Animal Internal Medicine 4th ed St Louis MO Mosby Elsevier 2009 p 115760 American Association of Zoo Veterinarians Infectious Disease Manual BALANTIDIUM COLI Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Suids Primates especially captive great apes and humans Fecaloral Contact with infected suids or primate or water contaminated by same environmental transmission Asymptomatic Mild cases present recurrent watery and mucoid diarrhea abdominal pain Acute severe typhlitis ulcerative colitis with anorexia dysentery lethargy vomiting diarrhea Ranges from asymptomatic carriers to severe diarrhea in susceptible species Invasive form of the disease is considered fatal and occasionally can be extra intestinal Paromomycin metronidazole tetracyclines iodoquinol supportive care Avoid contact with infected suids or carriers or waterfood contaminated with their feces Environmental and personal hygiene measures Yes Fact Sheet compiled by Kathryn C Gamble Sheet completed on 26 September 2013 updated 16 February 2018 Fact Sheet Reviewed by Kay Backues Tony Goldberg Susceptible animal groups The parasite most commonly infects suids and great apes including humans In great apes freeranging populations appeared to present exceptionally low to no prevalence infection or were unaffected by these limited B coli burdens while greater than 50 of captive groups and those in closer proximity to humans were infected B coli has been reported in other nonhuman primates eg macaques and lemurs in cercopithecine monkeys the parasite is observed in both captive and freeranging populations Additionally the parasite is reported in artiodactylids cows camels and rarely in laboratory rodents eg guinea pig and rat and dogs Since the last update it also has been reported in freeranging South American sea lions Otaria flavescens and fin whales Balaenoptera physalus but its significance is not yet clear in these newly identified host taxa Causative organism Balantidium coli a cosmopolitan holotrichous ciliated protozoan and largest ciliate to infect humans Other Balantidium species can be observed as commensals in tortoises Zoonotic potential Yes both trophozoites and cysts can initiate infection Occupational exposure to suids poor hygiene or foreign travel have been associated with human infections although disease as a result of infect in humans is not considered common Distribution Worldwide but higher prevalence in tropical and subtropical regions Incubation period 45 days Clinical signs Clinical signs are consistent with gastrointestinal irritation and typically are watery mucoid diarrhea Following ingestion of the cysts excystation occurs in the small intestine then the trophozoites excysted or ingested colonize the large intestine and cecum If invasion occurs through the mucosa extraintestinal disease has been reported including to the liver lung and bone Suids are mostly asymptomatic unless the parasite invades the mucosa and this only occurs when prior mucosal damage enables its entry Similarly cercopithecine monkeys are rarely symptomatic In great apes American Association of Zoo Veterinarians Infectious Disease Manual BALANTIDIUM COLI chimpanzees are typically asymptomatic or present mild clinical signs of diarrhea which may be simply unformed feces Asymptomatic chimpanzees may recrudesce with diarrhea when stressed by other illnesses B coli may compete with commensal protozoa such that perturbation of the normal gastrointestinal microflora may facilitate infection or recrudescence In gorillas ulcerative colitis severe diarrhea and potential abdominal abscessation or colonic fistulation have been noted Postmortem gross or histologic findings Ulcerative colitis with large numbers of characteristic B coli organisms invading the colonic mucosa Diagnosis Direct examination of feces by saline smear allows diagnosis While flotation can be utilized cysts are the only form detected routinely by this method and sedimentation may assist in concentration of the organism Iodine staining may assist in identification of the organism Detection of trophozoites 30150 x 25120 µm in diarrhea is most common this stage is a distinctive ovoid with an elongated end peripheral short cilia and containing a large cytostome This stage also has a distinctive spiraling motility with uniform ciliate beating The infective form cyst 4565 µm is usually found in formed feces is round and contains the ciliated organism within a transparent double wall Both forms have a large kidneyshaped nucleus At necropsy scrapings of the colonic and cecal mucosa can be performed for evaluation and staining with HE Material required for laboratory analysis Feces Relevant diagnostic laboratories Any diagnostic laboratory with routine parasitologic capabilities should be able to diagnose this infection The required diagnostic methods such as fecal flotation are readily available inhouse in any laboratory performing routine fecal exams Treatment Antiprotozoals eg tetracyclines iodoquinol metronidazole and paromomycin are recommended in clinical cases Symptomatic treatment of clinical disease will be necessary in severe cases Starchrich diets support of the organisms replication and may account for the increased susceptibility of captive as opposed to freeranging great apes Prevention and control Carrier animals should be managed separately from susceptible animals For example cohousing of cercopithecine monkeys with great apes should be considered cautiously Excellent sanitation should be practiced between carrier animal enclosures and susceptible animals as this parasite has a direct life cycle and requires no intermediate host That said this approach should include pest control as some roach species have been demonstrated to carry the protozoan within their gastrointestinal tract Treatment of carrier animals to reduce environmental contamination should be considered Suggested disinfectant for housing facilities The B coli trophozoite cannot survive for in a dry environment and generally is expected not to survive beyond 48 hours Regular removal of feces assists with reduction of environmental contamination Cysts can survive outside body for two weeks or more at ambient temperatures and are highly resistant to disinfection Bleach sodium hypochlorite at routine disinfection concentrations is not sufficient to destroy the organism Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Treatment of carrier animals to reduce their burden prior to introductions to naïve animals should be considered Introduction stressors might produce clinical disease in carrier animals Testing of relevant species for this organism during quarantine periods is advisable Conditions for restoring diseasefree status after an outbreak As a carrier state exists diseasefree state is difficult to attain Effective management of carriers and treatment of ill individuals is more realistic American Association of Zoo Veterinarians Infectious Disease Manual BALANTIDIUM COLI Experts who may be consulted Veterinary Advisors for Great Ape Species Survival Plans Chimpanzee Kathryn C Gamble DVM MS Dipl ACZM Dip ECZM ZHM Kay Backues DVM Dipl ACZM Lincoln Park Zoo Tulsa Zoo 2001 N Clark St 5701 East 36th Street N Chicago IL 60614 Tulsa OK 74115 3127427722 918 6696243 Fax 3127427823 Fax 918 6696888 kgamblelpzooorg kbackuestulsazooorg Gorilla Pam Dennis DVM PhD Hayley Murphy DVM Cleveland Metroparks Zoo Zoo Atlanta 4200 Wildlife Way 800 Cherokee Ave SE Cleveland Ohio 44109 Atlanta Georgia 30315 Phone 216 6352520 Phone 4046245801 Fax 216 6353318 Fax 4046245959 pmdclevelandmetroparkscom hmurphyzooatlantaorg Thomas P Meehan DVM Brookfield Zoo 3300 Golf Road Brookfield Illinois 60513 Phone 708 6888501 Fax 708 6887501 tommeehanCZSorg References 1 Acha PN Szyfres B Balantidiasis In Zoonoses and communicable diseases common to man and animals Volume 3 Parasitoses Washington DC Pan American Health Organization 2003 p 2022 2 Centers for Disease Control and Prevention Internet Parasites Balantidiasis also known as Balantidium coli Infection c2019 cited 2018 February 8 Available from httpwwwcdcgovparasitesbalantidium 3 Government of Canada Internet Pathogen Safety Data Sheets Infectious Substances Balantidium coli c2014 cited 2019 September 21 Available from httpswwwcanadacaenpublic healthserviceslaboratorybiosafetybiosecuritypathogensafetydatasheetsrisk assessmentbalantidiumcolipathogensafetydatasheethtml 4 Hamu H Debalke S Zemene E Birlie B Mekonnen Z Yewhalaw D Isolation of intestinal parasites of public health importance from cockroaches Blatella germanica in Jimma Town Southwestern Ethiopia J Parasit Res Internet 2014 cited 2018 February 12 Available from httpdxdoiorg1011552014186240 5 Hassell JM Blake DP Cranfield MR Ramer J Hogan JN Noheli JB Waters M Hermosilla C Occurrence and molecular analysis of B coli in mountain gorilla Gorilla beringei beringei in the Volcanoes National Park Rwanda J Wildl Dis 20134910631065 American Association of Zoo Veterinarians Infectious Disease Manual BALANTIDIUM COLI 6 Labes EM Hegglin D Grimm F Nurcahyo W Harrison ME Bastian ML Deplazes P Intestinal parasites of endangered orangutans Pongo pygmaeus in Central and East Kalimantan Borneo Indonesia Parasit 2010137112335 7 Mbaya AW Udendeye UJ Gastrointestinal parasites of captive and freeroaming primates at the Afi Mountain Primate Conservation Area in Calabar Nigeria and their zoonotic implications Pak J Biol Sci 201114709714 8 McLennan MR Hasegawa H Bardi M Huffman MA Gastrointestinal parasite infections and self medication in wild chimpanzee surviving In degraded forest fragments within an agricultural landscape mosaic in Uganda PLoS ONE Internet 2017 cited 2018 February 12127 Available from httpsdoiorg101371journalpone0180431 9 Neafie RC Andersen EM KlassenFischer MK Balantidiasis In Meyers WM Firpo A Wear DJ eds Balantidiosis Topics on the Pathology of Protozoan and Invasive Arthropod Diseases Washington DC Armed Forces Institute of Pathology Internet 2011 cited 2018 February 12 Available from httpwwwdticmildocscitationsADA547528 10 Neva FA Brown HW Basic Clinical Parasitology 6th ed Norwalk CT Appleton Lange 1994 650p 11 Pomajbíková K Petrželková KJ Profousová I Petrášová JModrý D Discrepancies in the occurrence of Balantidium coli between captive and African great apes J Parasitol 2010 9611391144 12 Ryan SJ Brashaes JS Walsh C Milbers K Kilroy C Chapman CA A survey of gastrointestinal parasites of olive baboons Papio anubis in human settlement areas of Mole National Park Ghana J Parasitol 2012 98885888 13 Schuster FL RamirezAvila L Current world status of Balantidium coli Clin Microbiol Rev 200821626638 14 Swenson B Great ape neonatology In Fowler ME Miller RE eds Zoo and Wild Animal Medicine Current Therapy Volume 4 Philadelphia PA WB Saunders Company 1999 p 386 15 Zanani SA Gazzonis AL Epis S Manfredi MT Study of the gastrointestinal parasitic fauna of captive nonhuman primates Macaca fascicularis Parasitol Res 2016115307312 American Association of Zoo Veterinarians Infectious Disease Manual BAYLISASCARIASIS Fact Sheet compiled by Emily L Blizzard Sheet completed on 27 May 2011 updated 1 October 2012 updated 01 January 2018 Fact Sheet Reviewed by Laurie A Baeten Kerri Pedersen Michael J Yabsley Susceptible animal groups avian mammal including human Causative organism Recognized species of Baylisascaris Parasite Primary Definitive Hosts B ailuri Red Panda B columnaris Skunks B devosi Martens fishers and wolverines B laevis Groundhogs marmots ground squirrels rodents B melis Badgers B potosis Kinkajous possibly other procyonids eg olingo B procyonis Raccoons and other procyonids eg kinkajou B schroederi Giant pandas B transfuga Bears B tasmaniensis Tasmanian devils quolls native cats B venezuelensis South American spectacled bear Zoonotic potential Yes for B procyonis Other species unknown Distribution Baylisascaris procyonis the most studied species is a common ascarid parasite of raccoons Proycon lotor and has a widespread distribution throughout the United States Canada and Costa Rica and has been introduced to Japan China and several countries in Europe In the US the highest prevalence rates occur in the Midwestern Northeastern and Western states In the Southeastern US infections are most common in mountainous regions Tennessee Kentucky and North Carolina although isolated areas of high prevalence have been detected in regions of Texas Georgia Florida and North Carolina In Canada B procyonis is found in British Columbia Nova Scotia Ontario Prince Edward Island and Quebec Accurate distribution maps are unavailable for the majority of Baylisascaris species since they are relatively rarely studied Although humans are considered accidental hosts for B procyonis over 50 cases of baylisascariasis have been documented Documented cases resulted in severe permanent neurologic andor ocular deficits or death Moreover recent studies utilizing improved serological detection assays for B procyonis suggest that subclinical infections are common in areas of parasite endemicity Within the US and Canada B columnaris B melis and B transfuga may pose a zoonotic risk to humans and are probably found throughout the range of their natural hosts Incubation period Once Baylisascaris spp eggs are shed by a definitive host into the environment eggs develop into an infectivestage larva within 1014 days depending upon environmental conditions Following ingestion by a susceptible host larvae hatch from the egg and can migrate through numerous tissues Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Avian mammals including humans Ingestion of embryonated eggs or infected carrier hosts Depression lethargy agitation tremors head or body tilt circling ataxia lateral recumbency coma Asymptomatic to fatal Early aggressive treatment with albendazole and high dose corticosteroids have shown to be effective ocular larva migrans can be killed using laser treatment Personal environmental hygiene wear gloves and additional PPE when working with potentially infected animals equipment Yes American Association of Zoo Veterinarians Infectious Disease Manual BAYLISASCARIASIS depending on the Baylisascaris spp involved including the central nervous system CNS as early as 3 days post infection In susceptible species clinical disease or death can be observed 910 days postinfection In more resistant host species or if low numbers of larvae are ingested CNS symptoms may not appear until 2 4 weeks postinfection Clinical signs Clinical signs in paratenic hosts including humans vary based on number of larvae ingested the tissues through which larvae migrate and host Pathogenicity varies among Baylisascaris species Baylisascaris procyonis and B melis are the most pathogenic followed by B columaris but little is known about other Baylisascaris species Clinical signs and symptoms associated with baylisascariasis are often nonspecific but may include although not limited to depression lethargy tremors partial paralysis head or body tilts ataxia circling cognitive deficits easy agitation irritability and death Post mortem gross or histologic findings Many infected animals will have no gross lesions However inflammation and traumatic damage may be observed through the liver lungs and other organs of animals infected with large numbers of larvae In these hosts granulomas may be grossly visible in many tissues such as the liver lungs heart diaphragm pancreas spleen kidneys mesentery mesenteric lymph nodes intestinal wall skeletal muscles brain and eyes Histologically extensive inflammatory tracts and larvae may be observed Diagnosis Humans Suspect Baylisascaris infections may be diagnosed using serologic methods such as ELISA recombinant antigenbased and Western blotting Ocular examinations may identify the presence of nonspecies specific larval nematode ocular migrans Neural larva migrans may be identified using neuroimaging and encephalography although additional testing will be needed to identify the species involved Animals Postmortem necropsies of suspected animals are the most conclusive way to diagnose Baylisascaris infections In suspected intermediate hosts clinical signs history of exposure serology post mortem necropsies PCR and recovery andor identification of larvae can be used to diagnose Baylisascarisis To determine the species of Baylisascaris present PCR and sequence analysis should be performed Fecal floats or necropsy and examination of small intestine can be used to diagnose infection in definitive hosts Material required for laboratory analysis Adult nematode specimens may be examined microscopically and identified morphologically although adult males are needed to determine species Genetic identification may be needed for larva migrans found in intermediate hosts andor immature nematodes in definitive hosts Relevant diagnostic laboratories Veterinary clinics can run routine fecal exams to diagnose infection in definitive hosts In intermediate hosts veterinary diagnostic laboratories capable of PCR analysis andor histology should be able to perform diagnostic testing on suspected animal cases Human cases should be referred to the Health Department or the CDC for testing Treatment Aggressive treatment with albendazole 2550 mgkg per day orally for 1020 days combined with high doses of corticosteroids is recommended in humans Treatment appears to be successful when administered quickly following exposure If albendozole is not available mebendazole or ivermectin may be used Ocular larva migrans can be killed using lasers followed by a regime of antiinflammatory drugs and steroids to aid in the possible recovery of any remaining visual acuity Intestinal infections in various definitive hosts such as raccoons other procyonids skunks domestic dogs and bears can be successfully treated with common antihelmintics such as pyrantel pamoate 20 mgkg ivermectin 1 mgkg moxidectin 1 mgkg albendazole 50 mgkg x 3 days fenbendazole 50 mgkg x 3 days and flubendazole 22mgkg x 3 days Animals should be monitored regularly after treatment to ensure complete clearance of worms Prevention and control Continued education of the public human health wildlife and veterinary professionals should be made a priority Recent research using anthelmintic baits combined with the removal of latrine sites has shown to decrease prevalence rates among intermediate hosts Further research is needed to determine the exact distribution potential for spread transmission dynamics and impacts on wildlife Suggested disinfectant for housing facilities Areas should be cleaned immediately to avoid accidental ingestion of eggs by children or pets Personnel should wear appropriate personal protective equipment and avoid contaminating hands and clothes with potentially contaminated materials Eggs are not immediately American Association of Zoo Veterinarians Infectious Disease Manual BAYLISASCARIASIS infectious and must develop in the environment for a period of time 1014 days up to several months depending on environmental conditions before becoming infective Frequent sanitation will limit the buildup of eggs on these surfaces However eggs will continue to accumulate in the surrounding environment and once the eggs embryonate they can remain viable for several years Currently few methods are available for decontaminating areas infested with B procyonis eggs Highly concentrated caustic chemicals such as a 5050 mixture of xylene and absolute alcohol boiling lye or boiling Lysol may be used to decontaminate potentially infected areas The most effective way of decontaminating an area is flaming Although burning is the most effective way to kill eggs it is not feasible for flammable areas such as roofs decks etc In the laboratory exposing infectious eggs to water heated to 62C for 1 minute has been shown to inactivate larvae Notification Baylisascariasis in humans is reportable in some states check your local requirements Infection in animals is not reportable except in Washington State where infections in animals other than raccoons is reportable Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Animals displaying neurologic symptoms are not infective to other intermediate hosts However impaired intermediate hosts are likely to become prey for various carnivore or omnivore species If ingested by an appropriate definitive host the parasite cycle within a system could be perpetuated Definitive hosts known to harbor infections should be quarantined placed on an anthelmintic regime and monitored regularly for infection Before placing susceptible animals in cages that had contact with infected animals the cages should be decontaminated Conditions for restoring diseasefree status after an outbreak None Experts who may be consulted Centers for Disease Control and Prevention Division of Parasitic Diseases Local Health Departments USDA APHIS Wildlife Services State Agencies References 1 Baylisascariasis httpcdcgovparasitesbaylisascarisindexhtml Accessed 2017 December 23 2 Blizzard EL Davis CD Henke S Long DB CHall CA Yabsley MJ Distribution prevalence and genetic characterization of Baylisascaris procyonis in select areas of Georgia J Parasitol 20109611281133 3 Kazacos KR Baylisascaris procyonis and related species In Samuel WM Pybus MJ Kocan AA eds Parasitic Diseases of Wild Mammals Ames IA Iowa State University Press 2001 p 301 341 4 MurrayW Human infections caused by the raccoon roundworm Baylisascaris procyonis Clin Microbiol Newsletter 2002241 5 Page K Beasley JC Olson ZH Smyser TJ Downey M Kellner KF McCord SE Egan II TS Rhodes Jr OE Reducing Baylisascaris procyonis roundworm larvae in raccoon latrines Emerg Infect Dis 2011179093 6 Parzansky MC Baylisascaris Spp In Nonraccoon Procyonid Hosts and Assessment of Potential Risk of Human Exposure Purdue University MS Thesis 2015 7 Prez Mata A Perez HG and Para GJ Morphological and molecular description of Baylisascaris venezuelensis n sp from a natural infection in the South American spectacled bear Tremarctos ornatus Cuiver 1825 in Venezuela Neotrop Helminthol 20161085103 8 Sapp SGH Gupta P Martin MK Murray MH Niedringhaus KD Pfaff MA Yabsley MJ Beyond the raccoon roundworm The natural history of nonraccoon Baylisascaris species in the New World Int J Parasitol Parasites Wildl 201768599 9 Sapp SGH Rascoe LN Wilkins PP Handali S Gray EB Eberhard ML Woodhall DM Montgomery SP Bailey KL Lankau EW Yabsley MJ Baylisascaris procyonis Roundworm Seroprevalence among Wildlife Rehabilitators United States and Canada 20122016 Emerg Infect Dis 20172221282131 American Association of Zoo Veterinarians Infectious Disease Manual BAYLISASCARIASIS 10 Tokiwa T Nakamura S Taira K Une Y Baylisascaris potosis n sp a new ascarid nematode isolated from captive kinkajou Potos flavus from the Cooperative Republic of Guyana Parasitol Int 201463591596 11 Wise ME Sorvillo FJ Shafir SC Ash LR Berlin OG Severe and fatal central nervous system disease in humans caused by Baylisascaris procyonis the common roundworm of raccoons a review of current literature Microbes and Infect 20057317323 American Association of Zoo Veterinarians Infectious Disease Manual BERTIELLOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Nonhuman primates Dermopterans Rodents Australian marsupials Humans Via accidental ingestion of intermediate host oribatid mites containing cysticercoids Typically none In humans it has caused intermittent diarrhea abdominal pain anorexia and weight loss Low Natural infection does not pose a serious health hazard for wild animals Praziquantel Screen and treat captive animals avoid ingestion of soil in endemic areas Yes Fact Sheet compiled by Sara ChildsSanford Sheet completed on 15 November 2012 Fact Sheet Reviewed by Lily Parkinson Susceptible animal groups Old World primates including Papio ursinus Papio cynocephalus Cercopithecus mona mona Cercopithecus ascanius Cercopithecus pygerythrus Cercopithecus schmidti Piliocolobus tephrosceles Colobus guereza Colobus angolensis Pan troglodytes verus Pan troglodytes schweinfurthii Macaca fascicularis Pongo pygmaeus Pongo abelii New World primates including Callicebus personatus nigrifons Callicebus oenanthe Cebus paella fatuellus Cebus capucinus Callithrix saguinus Alouatta caraya Alouatta guariba clamitans Dermopterans including Cynocephalus volans Cynocephalus variegates rodents including Rattus spp Uromys spp Australian marsupials including Trichosurus vulpecula humans Causative organism Bertiella spp cestode family Anoplocephalidae In nonhuman primates Old World primates Bertiella studeri B satyri New World primates B mucronata Lemurs B lemuriformis Dermopterans B elongata B plastica B rauschi B musasabi Rodents B anapolitica Australian marsupials B trichosuri Humans B studeri B mucronata Zoonotic potential Yes Human infection via accidental ingestion of the intermediate host can occur in those having close contact with the environment of definitive hosts especially primates and is most common in children Distribution Africa Asia South America AustraliaNew Zealand Incubation period Unknown Clinical signs Typically none Humans have been reported to experience intermittent diarrhea abdominal pain anorexia and weight loss Increased leaf swallowing behavior has been reported in wild chimpanzees Post mortem gross or histologic findings The adult tapeworm may be found in the small intestine Diagnosis Identification of eggs or gravid proglottids in feces identification of adult worm at necropsy Free eggs from gravid segments or feces are 4046µm long and 3640µm wide in B mucronata and 48 60µm long and 4060µm wide in B studeri Should be considered as a diagnosis when fecals continue to be tapeworm positive after treatment with fenbendazole or albendazole Material required for laboratory analysis Feces Relevant diagnostic laboratories Any veterinary diagnostic laboratory with a parasitologist on staff Treatment Praziquantel American Association of Zoo Veterinarians Infectious Disease Manual BERTIELLOSIS Prevention and control Wild Avoid contact with soil in proximity of definitive hosts Proper hygiene practices and food safety in endemic areas Captivity quarantine screen all animals for infection and treat accordingly Suggested disinfectant for housing facilities Commonly used disinfectants are generally not effective in killing tapeworm eggs or larvae Recent research has demonstrated that sodium hypochlorite is effective in killing Taenia spp eggs but its effectiveness against Bertiella spp eggs is currently unknown Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Eliminate infection in positive animals prior to introduction to other animals Conditions for restoring diseasefree status after an outbreak Repeated negative fecals Experts who may be consulted While no specific researchers are currently reporting expertise in this parasite parasitology staffs at veterinary colleges would be a good option it would be prudent to consider Australian veterinary colleges due to parasite location References 1 Beveridge I Species of Bertiella Cestoda Anoplocephalidae in dermopterans and squirrels from Southeast Asia Sys Parasit 1989141115 2 Conder GA Roehm PA Duprey DA Johnson SS Pagano PJ Treatment of bertiellosis in Macaca fascicularis with praziquantel J Helminthol Soc Wash 199158128 3 Denegri G Bernadina W PerezSerrano J RodriguezCaabiero F Anoplocephalid cestodes of veterinary and medical significance a review Folia Parasitol 19984518 4 Foitova I Masova S Tenora F Koubkova B Hodova I Vyskocilova M Barus V Nurcahyo W Rediscription and resurrection of Bertiella satyri Cestoda Anoplocephalidae parasitizing the orangutan Pongo abelii in Indonesia Parasitol Res 20111093 68997 5 de Sousa Junior JC Goulart JAG Varnier S Denegri G da Silva Filho HH Hirano ZMB de Aliva Pires FD Bertiellosis in Brazilian nonhuman primates natural infection in Alouatta guariba clamitans Cabrera 1940 Primates Atelidae in Aanta Catarina State Brazil Revista de Patologia Tropical 2008371 4856 6 Huffman MA Chapman CAeds Primate Parasite Ecology The Dynamics and Study of Host Parasite Relationships New York NY Cambridge University Press 2009 548 p 7 Kooriyama T Hasegawa H Shimozuru M Tsubota T Nishida T Iwaki T Parasitology of five primates in Mahale Mountains National Park Tanzania Primates 2012534365375 8 McLennan MR Huffman MA High frequency of leaf swallowing and its relationship to intestinal parasite expulsion in village chimpanzees at Bulindi Uganda Am J Primatol 2012747642650 9 Rasambainarivo FT Junge RE Lewis RJ Biomedical evaluation of Verreauxs sifaka Propithecus verreauxi from Kirindy Mitea National Park in Madagascar J Zoo Wildl Med 2014452247255 10 Sharma S Menon J Lal S Thapa BR Bertiella studieri infectionA rare cause of chronic abdominal pain in a child from north India J Trop Pediatr 2018644 348351 11 Stankiewicz M Heath DD Cowan PE Internal parasites of possums Trichosurus vulpecula from Kawau Island Chatham Island and Stewart Island N Z Vet J 1997456 24750 12 Valadares V dos Santos HA da Silva A Gontes G Vieira GL Ferreira AC da Silva ES First case of human infection by Bertiella studeri in Brazil Rev Inst Med Trop Sao Paulo 2015575447450 13 Wrangham RW Goodall J Chimpanzee use of medicinal leaves In HeHne PG Marquardt LA eds Understanding Chimpanzees Cambridge MA Harvard University Press 1989 p 2237 American Association of Zoo Veterinarians Infectious Disease Manual BLASTOMYCOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Canids primates marine mammals felids horses bats ursids mustelids Inhalation of airborne conidia from disturbed endemic soil Fever anorexia coughing dyspnea ocular and nasal discharge loss of body condition draining cutaneous lesions lameness ocular disease characterized by anterior uveitis or retinal disease Disease severity may range from asymptomatic to fatal fulminant respiratory failure Clinical signs may persist for weeks to months before disease progresses in severity Itraconazole is currently treatment of choice in dogs Amphotericin B is rarely used due to nephrotoxicity Fluconazole is a lower cost alternative to itraconazole Treatment duration in dogs usually 36 months There are no standards for prevention or control due to origin of the organism in the soil Normally not zoonotic Human infection is a result of exposure to a shared environmental source Fact Sheet compiled by Tiffany Wolf Sheet completed on August 4 2010 updated December 23 2012 updated January 18 2018 Fact Sheet Reviewed by Arno Wünschmann Joni Scheftel Robert W Bradsher Gene M Scalarone Alfred M Legendre Janelle Renschler Susceptible animal groups Blastomycosis has been reported in canids primates felids equids marine mammals ursids mustelids and bats Causative organism Blastomyces dermatitidis Zoonotic potential Human infection is generally a result of exposure to a shared environmental source rather than transmission from another mammalian host Although very rare there are reports of zoonotic transmission associated with dog bites cat scratches animal necropsies and a kinkajou bite Care should be taken to avoid accidental inoculation with contaminated objects such as needles knives etc One report of a localized Blastomyces infection in a veterinarian from an inadvertent needlestick following aspiration of a draining lesion Distribution Endemic in MississippiOhio river basin and central Atlantic states of the US and northern Ontario and Manitoba Canada It is believed to be a soil saprophyte associated with acidic sandy soil often in close proximity to a water source Incubation period Usually 26 weeks but clinical signs may appear as long as several months to years after infection Clinical signs Blastomycosis is typically a primary pulmonary disease as infection often occurs via the inhalation of aerosolized fungal spores from a soil source Primary cutaneous disease does occur although rarely Infections are often disseminated and clinical signs are associated with distribution of lesions Fever anorexia coughing dyspnea loss of body condition and draining cutaneous lesions are common clinical signs Bone or joint involvement can result in lameness Ocular involvement is also relatively common dogs and may be exhibited by anterior uveitis and subretinal effusion which can lead to retinal detachment and blindness Post mortem gross or histologic findings With pulmonary involvement lesions are often distributed throughout the lungs and consist of multifocal to coalescing whitegrey granulomas sometimes with central abscessation Regional lymph nodes are typically involved and characterized by granulomas abscesses or caseous lesions Similar granulomatous lesions will be seen with disseminated disease in any involved tissues American Association of Zoo Veterinarians Infectious Disease Manual BLASTOMYCOSIS The distribution of disease throughout the body often includes but is not limited to the lungs skin eyes bones joints lymph nodes and central nervous system Microscopically organisms appear as spherical thickwalled yeasts of 820um in diameter with broadbased budding Organisms can usually be identified cytologically from lymph node aspirates or impression smears from draining skin lesions Pyogranulamotous inflammation is frequently observed on cytology or histopathology specimens Organisms may be infrequent in more chronic infections Histologically hematoxylin and eosin HE stains may result in poor visualization of fungal elements therefore special stains such as Periodic AcidSchiff PAS stain or Gomoris methenamine silver GMS stain should be used in addition to HE Diagnosis Tracheal wash bronchoalveolar lavage impression smears or aspirates of enlarged lymph nodes skin lesions or draining exudates are appropriate for cytological examination Biopsy of granulomatous lesions can be submitted for histopathology Urine andor serum can be submitted for antigen concentrations Serum can be sampled for antibody testing with AGID but this is less sensitive than the urine antigen early in the course of the disease Material required for laboratory analysis Many commercial and state veterinary laboratories can provide cytologic histopathologic and serologic diagnostic services Serum samples for itraconazole concentrations can be sent to The Fungus Testing Lab University of Texas Health Science Center San Antonio Texas or MiraVista Diagnostics Indianapolis Indiana Mira Vista Diagnostics can also perform the antigen test for Blastomycosis Relevant diagnostic laboratories Many commercial and state veterinary laboratories can provide cytologic histopathologic and serologic diagnostic services Serum samples for itraconazole concentrations can be sent to The Fungus Testing Lab University of Texas Health Science Center San Antonio Texas or MiraVista Diagnostics Indianapolis Indiana Mira Vista Diagnostics can also perform the antigen test for Blastomycosis Treatment Itraconazole is currently the treatment of choice for blastomycosis given its ease of administration per os and lower toxicity Itraconazole blood levels should be measured 1421 days after beginning therapy and dosage should be increased if below 30 ugmL Given the high cost of itraconazole fluconazole is a lowercost alternative but generally requires a longer treatment duration Duration is typically 4 months with itraconazole and 6 months with fluconazole Antigen level may be used to monitor therapy Treatment should be continued until antigen levels are below 1 ugmL Amphotericin B is nephrotoxic and requires intravenous administration but may be an excellent option for animals presenting with serious disease or not responding to itraconazole therapy Absorption of compounded itraconazole is inconsistent and may account for treatment failures Treatment relapse is not uncommon within 1 year of treatment Prevention and control Blastomyces dermatitides originates from the soil and will grow in shaded sandy acidic soil with close proximity to water Although sterilization of soil is not realistic restriction of access by animals to areas where other cases are thought to have originated may reduce risk Alteration of the environment to eliminate the growth conditions of the organism may be beneficial Suggested disinfectant for housing facilities Replacing soil or gravel based outdoor housing facilities with concrete floors will reduce the presence of the organism in the housing area Disinfectants with antifungal spectrum of action may be used on impervious environmental surfaces according to the manufacturers directions however there is no proven method of disinfecting the environment to eliminate Blastomyces organisms Notification Human and animal cases may be reportable in certain states Ask local public health and animal health officials for direction in your area A national surveillance program does not currently exist in the American Association of Zoo Veterinarians Infectious Disease Manual BLASTOMYCOSIS United States Measures required under the Animal Disease Surveillance Plan None currently Measures required for introducing animals to infected animal Blastomycosis is generally not considered a contagious disease that is directly transmitted Conditions for restoring diseasefree status after an outbreak Diseasefree status can only be achieved after a minimum of 6090 days to 180 days of therapy accompanied by complete resolution of clinical signs and lesions Given the relatively common occurrence of relapse patients should be monitored for return of clinical signs or lesions in the following 1215 months Increasing urine or serum antigen levels may indicate a possible relapse Experts who may be consulted Gene M Scalarone PhD Department of Biological Sciences Idaho State University References 1 The Fungus Testing Lab University of Texas Health Science Center San Antonio Texas httppathologyuthscsaedustrlfungusindexshtml 2 Mira Vista Diagnostics Indianapolis Indiana httpwwwmiravistalabscom 3 Blastomycosis Internet Center for Disease Control cited 2018 May 20 Available from httpswwwcdcgovfungaldiseasesblastomycosisindexhtml 4 Baker R Lumsden JH Infectious agents In Lumsden JH ed Color Atlas of Cytology of the Dog and Cat St Louis MO Mosby Inc 2000 p 2338 5 Harris JR Blaney DD Lindsley MD Zaki SR Paddock CD Drew CP Johnson AJ Landau D Vanderbush J Baker R Blastomycosis in man after kinkajou bite Emerg Infect Dis 201117268 6 Legendre AM Blastomycosis In Greene CE ed Infectious Diseases of the Dog and Cat St Louis MO WB Saunders 2011 p 569576 7 Krizan P Blastomycosis in a free ranging lone wolf Canis lupus on the north shore of Lake Superior Ontario The Canadian FieldNaturalist 2000114491 8 Morris PJ Legendre AM Bowersock TL Brooks DE Krahwinkel DJ Shires GMH Walker MA Diagnosis and treatment of systemic blastomycosis in a polar bear Ursus maritimus with itraconazole J of Zoo Wildl Med 198920336 9 Ramsey DT Blastomycosis in a veterinarian J of the Am Vet Med Assoc 19942057968 10 Spector D Legendre AM Wheat J Bemis D Rohrbach B Taboada J Durkin M Antigen and antibody testing for the diagnosis of blastomycosis in dogs J Vet Intern Med 200822839843 11 Stewart AJ Fungal infections of the equine respiratory tract In Smith BP ed Large Animal Internal Medicine 4th ed St Louis MO Mosby Elsevier 2009 p 522533 12 Storms TN Clyde V Munson L Ramsay E Blastomycosis in nondomestic felids J Zoo Wildl Med 200334231 13 Thiel RP Mech LD Ruth GR Archer JR Kaufman L Blastomycosis in wild wolves J Wildl Dis 198723321 14 Zwick L Briggs M Tunev S Lichtensteiger C Murnane R Disseminated blastomycosis in two california sea lions Zalophus californianus J of Zoo Wildl Med 20003122114 American Association of Zoo Veterinarians Infectious Disease Manual BLUETONGUE VIRUS BTV EPIZOOTIC HEMORRHAGIC DISEASE VIRUS EHDV Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic BTV All ruminants are susceptible camelids other mammals positive on serological tests without disease recent evidence of possible BTV disease in carnivores EHDV primarily white tailed deer but also elk prong horn mule deer cattle rarely camelids but likely all ruminants can be infected Insect vector primarily biting midges of genus Culicoides C sonorensis principally in US iatrogenic in utero possibly oral in carnivores Pyrexia oral and nasal ecchymoses and ulcerations facial edema conjunctivitis rhinorrhea ptyalism BTV Hoof slough and wool loss in sheep EHDV Hoof slough in deer BTV variable dependant on species isolate geographic location sheep white tailed deer and pronghorn most likely to be severely affected EHDV variable whitetailed deer and pronghorn most likely affected In cattle EHDV BTV uncommon generally mild however more severe disease associated with specific subtypes or outbreaks reported Symptomatic Insect control which is realistically difficult potential to vaccinate for some strains of BTV no vaccines available for EHDV No Fact Sheet compiled by Allison Wack Sheet completed on 25 January 2011 updated 19 March 2013 Fact Sheet Reviewed by David Stallknecht Holly Haefele American Association of Zoo Veterinarians Infectious Disease Manual BLUETONGUE VIRUS BTV EPIZOOTIC HEMORRHAGIC DISEASE VIRUS EHDV Susceptible animal groups BTV Ruminants sheep goats cattle bison deer antelope bighorn sheep North American elk camelids greater kudu muntjac topi perinatal infection in Grants gazelle gemsbok sable buffalo ibex hartebeest addax Many other ungulates serologically positive without evidence of disease Clinical signs common in sheep occasional in goats and rare in cattle Whitetailed deer pronghorn and desert bighorn sheep may have severe disease Abortions caused by BTV contaminated vaccine in dogs Seropositivity in a variety of large African carnivores Report of infection and death in 2 Eurasian lynx fed ruminant fetuses and stillborns EHDV Ruminants whitetailed deer most severely affected less frequently in mule deer and pronghorn Blacktailed deer red deer wapiti roe deer fallow deer bison black and white rhinoceros black bear have been found seropositive Rare outbreaks in cattle sheep experimentally infected but rarely develop clinical signs Causative organisms Family Reoviridae Genus Orbivirus BTV 26 serotypes worldwide 15 identified in US 2 10 11 13 17 considered endemic 13 5 6 912 14 19 22 24 sporadically in domestic or wild ruminants EHDV 7 serotypes 3 endemic to US 1 2and 6 EHDV6 was first identified in 2006 Zoonotic potential None one anecdotal unconfirmed report of BTV infection in a laboratory worker Distribution BTV Worldwide where vectors are present generally between latitudes of 40N and 35S although may be moving north Mostly southern and western also southeastern US EHDV Disease in North America Australia Asia Africa seropositive animals in South America Incubation period BTV 510 days in domestic sheep typically infectious to insect vector for several weeks EHDV 510 day incubation in deer May remain viremic for up to 2 months Clinical signs BTV Variable and species dependent Sheep pyrexia ptyalism depression dyspnea panting hyperemia and edema of muzzle lips tongue ears ulcerations and erosions in mouth sloughing of hooves abortion loss of wool 34 weeks post infection Recrudescence possible severity partially dependant on serotype Cattle pyrexia rarely hyperemia vesicles or ulcers in mouth hyperemia of coronary band dermatitis hydranencephaly or cerebral cysts in calves Pronghorn and whitetail deer hemorrhage and sudden death EHDV Three distinct syndromes in deer Peracute fever anorexia weakness swelling of head and neck respiratory distress death within 836 hours Acuteclassical multiorgan hemorrhage ptyalism rhinorrhea oral and GI ulcerations mortality may be high Chronic ill for several weeks with gradual recovery may have hoof damageslough or enough scarring from rumen ulcerations to cause emaciation Typically subclinical in cattle but clinical signs include fever oral ulcers salivation lameness associated with coronitis and weight loss Fetal resorption and hydranencephaly possible death uncommon in North America although lameness and unthriftiness may be prolonged Post mortem gross or histologic findings BTV and EHDV Clinical signs similar in affected animals but both highly variable Sheep edema of face and ears crusty exudates on nostrils hyperemia of coronary bands ulcers and erosions of oral cavity necrosis and cyanosis hyperemia hemorrhage and edema throughout internal organs possible Hemorrhage at base of pulmonary artery American Association of Zoo Veterinarians Infectious Disease Manual BLUETONGUE VIRUS BTV EPIZOOTIC HEMORRHAGIC DISEASE VIRUS EHDV EHDV In deer gross findings differ with form of disease consistent with clinical presentation Histologic findings include widespread vasculitis with thrombosis endothelial swelling hemorrhages degenerative changes and necrosis in many organs Diagnosis Serologic tests are only diagnostic with paired serum BTV AGID ELISA CF PCR VI VN EHDV AGID PCR VI VN Material required for laboratory analysis Serum for AGID ELISA CF VN Whole blood or spleen for PCR Whole blood spleen or lung for VI ELISA if pre and post serum available PCR VI may be most useful clinically positive serology does not correlate well with viremia Relevant diagnostic laboratories NVSL httpwwwaphisusdagovanimalhealthlabinfoservicesdownloads AmesDiagnosticTestingCatalogpdf TVMDL httptvmdltamueduschedule2php Treatment Symptomatic analgesics and antiinflammatories may help address clinical signs Prevention and control BTV Limiting vector exposure number and habitat Pyrethroids or organophosphates effective against Culicoides Vaccination for sheep available in some areas typically serotype specific MLV Serotype 10 available throughout US combo of serotypes 10 11 17 in CA 17 available in Texas Vaccination recommended in spring prior to vector season in endemic areas contraindicated in pregnant ewes and during outbreaks Quarantine of imported animals serologic screening and vector control during transport are important for preventing introduction into bluetonguefree areas EHDV Limiting vector exposure as above No vaccines available Suggested disinfectant for housing facilities Primarily vector borne unlikely to contaminate environment However sodium hypochlorite or 3 sodium hydroxide are effective if disinfection is warranted Notification Required in certain states check with AVIC or state veterinarian Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Seronegative animals two negative test results 28 days apart with no vector exposure between vaccinated animals or naturally immune animals positive serologic test for all applicable serotypes 60 days prior pose minimal risk for introduction Introduction of an actively infected animal to a naïve populationarea should be avoided A viremic animal should become negative on PCR or VI prior to being introduced which should take no longer than 60 days During that time the viremic animal should be kept without vector access and treated with insecticides both animal and environment Conditions for restoring diseasefree status after an outbreak Seasonal in endemic areas unlikely to be eradicated once established in vector population OIE has firm guidelines for being classified as a BTV free country Infection by one serotype of either virus usually offers lasting immunity for that serotype though may not be protective against others Experts who may be consulted NVSL OIE state veterinarian References 1 httpwwwcfsphiastateeduFactsheetspdfsbluetonguepdf Accessed 5 July 2013 2 httpwwwcfsphiastateeduFactsheetspdfsepizootichemorrhagicdiseasepdf Accessed 5 July American Association of Zoo Veterinarians Infectious Disease Manual BLUETONGUE VIRUS BTV EPIZOOTIC HEMORRHAGIC DISEASE VIRUS EHDV 2013 3 httpwwwoieintfileadminHomeengHealthstandardstahm20103BLUETONGUEpdf Accessed 5 July 2013 4 httpwwweazanetactivitiestdfactsheets00720Bluetonguedocpdf Accessed 5 July 2013 5 httpwwwaphisusdagovimportexportanimalsoiedownloadstahcsep11tahcbluetonguech83u o80sep11pdf Accessed 7 July 2013 6 Committee on bluetongue and related Orbiviruses 2009 Annual Report Proc USAHA Pp 182205 7 Howerth EW Stallknecht DE and PD Kirkland 2001 Blue tongue epizootic hemorrhagic disease and other orbivirusrelated diseases In William ES and IK Barker eds Infectious Diseases of Wild Mammals 3rd ed Manson Publishing Ltd London UK Pp 7797 8 Jauniaux TP De Clercq KE Cassart DE Kennedy S Vandenbussche FE Vandemeulebroucke EL Vanbinst TM Verheyden BI Goris NE and FL Coignoul 2008 Bluetongue in Eurasian lynx Emerg Infect Dis 14 14961497 9 Maclachlan NJ 2011 Bluetongue history global epidemiology and pathogenesis Prev Vet Med 1022 107111 10 Savini G Afonso A Mellor P Aradaib I Yadin H Sanaa M Wilson W Monaco F and M Domingo 2011 Epizootic hemorrhagic disease Res Vet Sci 91 1 117 American Association of Zoo Veterinarians Infectious Disease Manual BORDETELLOSIS Fact Sheet compiled by Kortney A ONeill updated by David A Bemis Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Dogs Cats Birds turkeys Swine domestic Rodents Rabbits Horses Seals Humans rarely non human primates Aerosol oronasal Aerosol oronasal Contaminated water direct contact Direct contact aerosol Direct contact Aerosol Direct contact aerosol Direct contact aerosol Direct contact Direct contact aerosol Paroxysmal coughing Sneezing pyrexia nasal discharge occasional cough Sinusitis with clear nasal discharge foamy eyes character istic snick or cough Nonprogressive atrophic rhinitis as sole pathogen pneumonia Nasal discharge sneezing snuffling rales dyspnea Snuffling pneumonia Nasal discharge pneumonia Tracheitis pneumonia Paroxysmal cough runny nose sneezing pyrexia Mild to severe Antibiotics supportive care Quarantine affected animals Only in immune compromised people American Association of Zoo Veterinarians Infectious Disease Manual BORDETELLOSIS Sheet completed on 30 April 2011 updated 5 August 2013 Fact Sheet Reviewed by Claude Lacasse Karen Register Susceptible animal groups Reported in canids felids ursids suids lagomorphs rodentia aves primates human and nonhuman insectivores mustelids ovids pinnipeds equids and koalas Causative organism Bordetella bronchiseptica most animal cases rare human cases Bordetella pertussis humans nonhuman primates Bordetella parapertussis humans ovids Bordetella avium birds and B hinzii birds rodents rabbits and rare human cases Zoonotic potential B bronchiseptica B hinzii usually reported in immunocompromised people Distribution Worldwide Incubation period 314 days Clinical signs Disease may be present in asymptomatic carriers Paroxysmal cough is most notable sign in dogs and humans and sneezing oculonasal discharge rhinitis pyrexia or pneumonia may be developed Sudden death may occur Post mortem gross or histologic findings Bronchopneumoina suppurative bronchitis tracheitis mucopurulent rhinitis The disease rarely causes mortality in animals unless concurrent infection with virus or other bacterial component Diagnosis Bacterial culture PCR Material required for laboratory analysis Oropharyngeal or nasopharyngeal culture swab Relevant diagnostic laboratories Any diagnostic lab with capability to perform bacterial culture Treatment If the sole infectious agent the disease may be selflimiting However antibiotics decrease course of shedding Supportive care antitussives humidification expectorants etc can be applied Prevention and control Isolation of any suspected upper respiratory infection animals during active disease Adequate ventilation and air exchanges 1220hr within holding areas Vaccination of susceptible species can be utilized Suggested disinfectant for housing facilities Thorough cleaning and disinfection most cleansers are effective against Bordetella spp sodium hypochlorite chlorhexidine or benzalkonium solution Notification Pertussis is reportable in some states Measures required under the Animal Disease Surveillance Plan None currently Measures required for introducing animals to infected animal Infected animals should be quarantined for 26 weeks until clinical signs resolve Conditions for restoring diseasefree status after an outbreak Clean and decontaminate environment Experts who may be consulted David A Bemis PhD DACVM Honorary Department of Comparative Medicine University of Tennessee Knoxville TN 865 9745576 bemisutkedu References 1 Aiello SE and A Mays eds 1998 The Merck Veterinary Manual 8th edition Merck Co Inc Philadelphia Pennsylvania Pp 11001102 1320 1390 19771979 2 Blanshard W and K Bodley 2008 Koalas In Vogelnest L and R Woods eds Medicine of Australian mammals CSIRO Publishing Collingwood Victoria Pp 272275 3 Cullinane LC MR Alley RB Marshall and BW Manktelow 1987 Bordetella parapertussis from lambs New Zealand Vet J 3510 175 American Association of Zoo Veterinarians Infectious Disease Manual BORDETELLOSIS 4 Ettinger SJ and B Kantrowitz 2005 Diseases of the trachea In Ettinger SJ and EC Feldman eds Textbook of Veterinary Internal Medicine 6th edition Elsevier Inc Saint Louis Missouri Pp 12211222 5 Finger H and CHW von Koenig 1996 Bordetella In Baron S ed Medical Microbiology 4th edition University of Texas Medical Branch at Galveston Galveston Texas httpwwwncbinlmnihgovbooksNBK7813 Accessed 26 August 2013 6 Fowler ME and RE Miller eds 2003 Zoo and Wild Animal Medicine 5th ed Elsevier Science Saint Louis Missouri Pp 9798 193 311 380 385 466 507508 7 GarciaCantu MC FA Hartmann CM Brown and BJ Darien 2000 Bordetella bronchiseptica and equine respiratory infections a review of 30 cases Eq Vet Educ 12 4550 8 Greene CE ed 2006 Infectious Diseases of the Dog and Cat 3rd ed Elsevier Inc Saint Louis Missouri Pp 5461 145155 1058 9 Hammond EE D Sosa R Beckerman and RF Aguilar 2009 Respiratory disease associated with Bordetella bronchiseptica in a Hoffmanns twotoed sloth Choloepus hoffmanni J Zoo Wildl Med 402 369372 10 Lacasse C and KC Gamble 2006 Tracheitis associated with Bordetella bronchiseptica in a polar bear Ursus maritimus J Zoo Wildl Med 372 190192 11 Leissinger M K Pescosolido and A Royal 2013 What is your diagnosis Equine transtracheal wash fluid Vet Clin Pathol httponlinelibrarywileycomdoi101111vcp12077full Accessed 23 September 2013 12 McKenzie RA AD Wood and PJ Blackall 1979 Pneumonia associated with Bordetella bronchiseptica in captive koalas Aust Vet J 559 427430 13 Raffel TR KB Register SA Marks and L Temple 2002 Prevalence of Bordetella avium infections in selected wild and domesticated birds in the eastern USA J Wildl Dis 38 4046 14 Register K 2006 Letter to the Editor Vet Pathol 43 1041 15 Register KB and RA Kunkle 2009 Strainspecific virulence of Bordetella hinzii in poultry Avian Dis 53 5054 16 Register KB 2013 Development of a PCR for identification of Bordetella hinzii Avian Dis 57 307 310 17 Register KB RE Sacco and G Foster 2000 Ribotyping and restriction endonuclease analysis reveal a novel clone of Bordetella bronchiseptica in seals J Vet Diagn Invest 12 535540 18 Rijks JM FL Read MW van de Bildt HG van Bolhuis BE Martina JA Wagenaar K van der Meulen AD Osterhaus and T Kuiken 2008 Quantitative analysis of the 2002 phocine distemper epidemic in the Netherlands Vet Pathol 45 516530 19 Staveley CM KB Register MA Miller SL Brockmeier DA Jessup and S Jang 2003 Molecular and antigenic characterization of Bordetella bronchiseptica isolated from a wild southern sea otter Enhydra lutris nereis with severe suppurative bronchopneumonia J Vet Diagn Invest 15570 4 American Association of Zoo Veterinarians Infectious Disease Manual LYME DISEASE caused by BORELLIA BURGDORGERI Fact Sheet compiled by Elizabeth E Hammond Sheet completed on 6 Sept 18 Fact Sheet Reviewed by Anne Burgdorf Tara Harrison Kristen J Tobin Susceptible animal groups all mammals dogs horses but cattle appear less susceptible some birds birds are usually asymptomatic and may be a reservoir host Causative organism Borrelia burgdorferi sensu lato sl sensu stricto ss gramnegative spirochete B burgdorferi ss is the cause of Lyme disease in the US but B mayonii has recently been identified as the cause of Lyme disease in the Midwest US different strains may explain varied clinical signs depending on region tick vector Ixodes sp I scapularisI ricinus I pacificus nymph life stage responsible for transmission Zoonotic potential Yes tick bite only tick must attached for at least 24hr Distribution temperate areas worldwide Incubation period 6090d Clinical symptoms shifting leg lameness joint swelling arthritis kneeelbow most common lymphadenopathy anorexia fever myocarditis CNS signs renal syndrome dogs uveitis and neuroborelliosis horses in humans there is often a rash erythema migrans aka bulls eye rash at the site of tick attachment Post mortem gross or histologic findings perivascular lymphoplasmacytic infiltrates in kidneys that can lead to glomerulonephritis dogs liver cerebrum meninges and lungs synovitis with inflammatory cells and fibrin deposits Diagnosis serology ELISA IFA EIA modified Western blot Western immunoblot can differentiate between vaccine titer and natural infection based on band pattern dogs PCR or culture of organism from urinary bladder difficult kidney spleen skin and other organs with evidence of clinical signs of disease history of exposure and response to treatment also xenodiagnosis feeding uninfected tick larvae on a host and evaluating for signs of infection Material required for laboratory analysis serum whole blood tissue Animal groups affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals especially dogs occasionally horses some birds birds are usually asymptomatic andor are reservoirs Tick vector Ixodes sp White tailed deer and rodent reservoir hosts including white footed mouse Peromyscus leucopus in N America Apodemus sp in Eurasia General Shifting leg lameness arthritis fever myocarditis CNS signs Humans erythema migrans bulls eye rash Dogs renal syndrome Horses uveitis neuroborreliosis Varies can be mild lameness or chronic illness Doxycycline x 30d azithromycin minocycline ceftriaxone amoxicillin recrudescence is possible Prevent tick attachment Remove ticks as soon as possible vaccine available for dogs Yes tick bite only American Association of Zoo Veterinarians Infectious Disease Manual LYME DISEASE caused by BORELLIA BURGDORGERI Relevant diagnostic laboratories Standard diagnostic laboratories can test for serologic evidence of Lyme disease patientside ELISA SNAP test 4Dx Plus IDEXX Westbrook ME 04092 USA available for dogs culture of organism requires special growth media Treatment Doxycycline x 30d contraindicated in young animals or minocycline x28d minocycline has better nervous system penetrationcommon in horses azithromycin ceftriaxone especially for neurologic disease amoxicillin recrudescence is possible better chance of resolution if treatment initiated early Prevention and control Tick prevention remove ticks within 48hr minimum time needed to transmit the organism Lyme disease killed and recombinant subunit vaccines are available for dogs human vaccine is no longer available Suggested disinfectant for housing facilities standard disinfectants such as 1 sodium hypochlorite 70 ethanol heat and UV light are appropriate Borrelia sp cannot survive freeliving in the environment Notification reportable in humans US but not in animals Measures required under the Animal Disease Surveillance Plan none Measures required for introducing animals to infected animal tick control Conditions for restoring diseasefree status after an outbreak none Experts who may be consulted Adam Birkenheuer DVM PhD DACVIM NCSU ajbirkenncsuedu References 1 Brown RN and Burgess EC Lyme Borreliosis In Williams ES and Barker IK eds Infectious disease of wild mammals Ames IA Iowa State University Press 2001 p435454 2 The Center for Food Security and Public Health Internet Lyme Disease 2019 cited 2018 July 31 Available from httpwwwcfsphiastateeduDiseaseInfodiseasephpnamelymediseaselangen 3 Centers for Disease Control and Prevention Internet Lyme disease 2018 cited 2018 July 31 Available from httpwwwcdcgovlyme 4 Centers for Disease Control and Prevention Internet New Lymediseasecausing bacteria species discovered 2016 cited 2019 January 23 Available from httpswwwcdcgovmediareleases2016p0208lymediseasehtml 5 Companion Animal Parasite Council Internet Lyme disease 2019 cited 2018 September 9 Available from httpswwwcapcvetorgguidelineslymedisease 6 Cook RA and Karesh WB Emerging diseases at the interface of people domestic animals and wildlife In Miller RE and Fowler ME eds Zoo and wild animal medicine Current therapy 6th ed St Louis MO Saunders Elsevier 2008 p 5565 7 Divers TJ Gardner RB Madigan JE et al Borrelia burgdorferi Infection and Lyme Disease in North American Horses A Consensus StatementJ Vet Intern Med 2018322617632 8 Fritz CL and Kjemtrup AM Lyme Borreliosis JAVMA 2003 223912611270 9 Greene CE Appel MJG Straubinger RK Lyme borreliosis In Greene CE ed Infectious diseases of the dog and cat 2nd ed Philadelphia PA WB Saunders 1990 p 282293 10 Lymeinfo Internet Lyme Info 2016 cited 2018 September 9 Available from httpwwwlymeinfonet 11 Stoebel K Schoenberg A Streich WJ The seroepidemiology of Lyme borreliosis in zoo animals in Germany Epidemiol Infect 2003 131 975983 12 Vogt NA Sargeant JM MacKinnon MC Versluis AM Efficacy of Borrelia burgdorferi vaccine in dogs in North America A systematic review and metaanalysis J Vet Intern Med 2019332336 American Association of Zoo Veterinarians Infectious Disease Manual BOVINE SPONGIFORM ENCEPHALOPATHY BSE Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Naturally affected Cattle Bos taurus and B indicus captive exotic ungulates of Bovidae felines both domestic and captive exotic domestic goats Ingestion of BSE contaminated feed ie meat and bone meal or infected carcasses Apprehension nervousness andor aggression tremoring incoordination especially hindlimb ataxia and difficulty in rising hyperesthesia Average incubation period is 28 years The clinical duration is usually several weeks to 6 months The disease is invariably progressive and fatal None Prohibit the feeding of most ruminant or mammalian proteins to ruminants Yes Fact Sheet compiled by Linda A Detwiler Sheet completed on 27 September 2013 Fact Sheet Reviewed by Noelia SilvadelRio Meredith M Clancy Susceptible animal groups Ruminants such as cattle Bos taurus and B indicus sheep and goats captive exotic ungulates eland gemsbok Arabian and scimitarhorned oryx nyala and greater kudu and American bison Bison bison Felines both domestic cats and captive exotic cats cheetah lion Asian leopard cat ocelot puma and tiger have been reported as Feline Spongiform Encephalopathy FSE Experimentally nonhuman primates also have been infected via the oral and intracranial routes American Association of Zoo Veterinarians Infectious Disease Manual BOVINE SPONGIFORM ENCEPHALOPATHY BSE Causative organism The etiological agent has not been fully characterized Understanding of the causative agent remains imperfect but a wealth of accumulating evidence has led to the conclusions that i a misfolded form of the protein PrPTSE known as a prion acts as a template to induce normal protein molecules to cascade into the same misfolded configuration ii infectivity is associated with an aggregate or polymer of 1428 misfolded protein molecules iii an as yet unidentified host molecule chaperone ganglioside noncoding RNA is probably necessary as a cofactor in replication iv the degree of similarity in the primary structure of the protein in different species influences the ease with which the protein can induce interspecies disease and v in some species the entire process appears to occur spontaneously in the sporadic form of disease but can be initiated ie transmitted by the introduction of tissue from a diseased to a healthy host as would have happened when humans consumed BSEcontaminated meat products Until 2004 it appeared that a single strain caused all cases of BSE It is now known that there are at least two additional strains called LType and HType atypical BSE Little is known about atypical BSE The origin and natural routes of transmission if any have yet to be determined Almost all cases have been in older cattle usually 8 years of age that have shown little resemblance to the clinicpathological picture seen in classical disease It has been suggested that the disease may be sporadic or be caused by a genetic mutation but no convincing evidence has been found to support either of these ideas The correct answer will probably only come by study of the future annual incidence curves of both types of disease Regardless of the origin of atypical BSE the possibility of recycling the disease in cattle and other ruminants as well as the potential for transmission to humans mandate a continuation of feed and specifiedrisk materials SRM bans together with diagnostic testing programs for some time to come Zoonotic potential BSE is the cause of the fatal human disease variant CreutzfeldtJakob Disease vCJD Epidemiological evidence indicates that transmission is through the consumption of meat products contaminated with BSE agent which is found primarily in CNS tissue and distal ileum During the incubation period it appears that humans may transmit vCJD to other humans via blood transfusions Distribution The first cases of BSE were recognized in the United Kingdom in 1986 and because of recycling of offals into animal feed the disease rapidly became epidemic in the UK and spread to most other European countries via the trade of contaminated meat and bone meal and infected animals that entered slaughter channels Worldwide the number of cases at the end of 2012 was approximately 190000 all but 6000 of which were within the UK In addition to the officially reported and confirmed cases it is estimated that as many as 35 million animals were infected and may have entered the food and feed chains in the UK without being detected BSE has also been detected in Brazil atypical Canada Falkland Islands import Israel Japan Oman import and the US import and atypical Implementation of feed controls has all but eliminated classical BSE as there were only 21 total cases reported worldwide in 2012 This number includes both classical and atypical BSE The UK found only 3 cases in 2012 Statistics regarding the occurrence of BSE may be found at httpwwwoieintenanimalhealthintheworldbsespecificdata It should also be noted that the absence of reported cases over an extended time in a country might not indicate so much the absence of disease as a lack of adequate surveillance Naturally occurring cases of BSE in species other than cattle have been very limited and have been linked to exposure to contaminated feed or infected carcasses The majority of cases originated in the UK and like BSE in cattle have declined with the implementation of feed controls None of the exotic animals were infected in the wild Incubation period The incubation period for BSE is measured in years and in cattle can range from 28 years American Association of Zoo Veterinarians Infectious Disease Manual BOVINE SPONGIFORM ENCEPHALOPATHY BSE Clinical signs Affected animals develop a progressive degeneration of the nervous system They may display changes in temperament abnormalities of posture and movement and changes in sensation including signs of apprehension nervousness or aggression incoordination especially hindlimb ataxia tremor and difficulty in rising and hyperesthesia to sound and touch In addition many animals have decreased milk production and loss of body condition despite continued appetite Only a small proportion of affected cattle exhibit what would be considered typical mad cow signs BSE can be mistaken for other conditions or go unnoticed due to subtlety of the signs The TSE cases in exotic ruminants had a younger onset age and a shorter clinical duration compared to that in cattle with BSE Clinical signs in the exotic ungulates are similar to those seen in cattle and include ataxia and wasting FSE is characterized by progressive nervous signs including ataxia hyperreactivity and behavioral changes and is fatal Clinical pathological gross and histopathological findings No gross pathological lesions are found in animals affected with BSE and histological changes appear to be confined to the CNS The primary lesions found are noninflammatory vacuolation of neuronal perikarya and greymatterneuropil and are usually bilaterallysymmetric Astrocytosis may also be observed Infected animals may not manifest these lesions until end stage disease Histological changes that are seen in cattle are similar to those seen in the other affected animal species Diagnosis No live animal test for BSE is available Historically the diagnosis of BSE relied on the occurrence of clinical signs of the disease confirmed by postmortem histopathological examination of brain tissue The current diagnostic tests target the detection of PrPTSE the misfolded form of the prion protein deposits in the CNS Immunohistochemistry andor Western blots are usually used as confirmatory tests In addition a number of rapid immunoassays have been developed and approved by governments for use as screening tests These include enzymelinked immunosorbent assays ELISAs automated immunoblotting Western blotting and lateral flow devices LFD Material required for laboratory analysis Clinically suspect cases should be subjected to a standard neuropathological approach in which the whole brain is sampled and a range of representative areas examined BSE sampling is dependent upon the test methods approved and used by the national veterinary services For example in the US brain stem including the obex should be submitted as fresh tissue Countries using immunohistochemistry as the primary diagnostic test may require samples submitted in formalin Relevant diagnostic laboratories USDAAPHIS National Veterinary Services Laboratory 1920 Dayton Ave for packages PO Box 844 for letters Ames IA 50010 515 3377266 Fax 515 3377397 Treatment None American Association of Zoo Veterinarians Infectious Disease Manual BOVINE SPONGIFORM ENCEPHALOPATHY BSE Prevention and control Given that the primary if not sole route of BSE transmission is through the feeding of contaminated meatand bonemeal MBM to cattle countries with any risk factors need to implement feed controls The level of restriction is usually dependent upon the amount of contamination thought to be in the system Three main factors can increase the stability of a national feed production system i Feed bans these regulations can range from the basic prohibition of feeding ruminant MBM back to ruminants to prohibiting most animal proteins from being fed to all animals used for food production including fish ii Specified Risk Materials SRMs ban this ban requires that high infectivity tissues such as bovine brain and spinal cord be removed from both the food and feed chain and be destroyed The intent of this control is to remove the primary source of infectivity from the entire system to prevent the possibility of crosscontamination iii Regulation of rendering although no rendering process can completely remove all detectable infectivity some are more effective than others The best procedure identified to date requires 133C at 3 bars of pressure for 20 minutes Experience in countries that have spent considerable effort to eliminate BSE has underlined the need for an extremely high level of compliance with feed controls in order to remove the agent from the system and prevent new infections in cattle No complacency can be tolerated Bovine products and byproducts are widely used for both food and pharmaceuticals and hence require the highest level of safety Because of the hardy nature of the BSE agent and its high potential for crosscontamination the most effective approach to protect bovine products and bovinederived materials for human use from contamination by BSE is to ensure that infected animals or carcasses never enter processing plants Because there are presently no diagnostic tools sensitive enough for detection of the disease during its long preclinical incubation governments must rely on measures to prevent exposure through feed see above or prohibit high risk tissues SRMs from being used for food or pharmaceuticals Suggested disinfectants BSE is not known to spread laterally between cattle or other animals hence it is not necessary to disinfect a premise where infected cattle have been Regarding BSE the need for disinfection may arise in diagnostic laboratories food processing and pharmaceutical manufacturing plants The agent of BSE shares with other TSE agents the property of unusual resistance to destruction None of the standard disinfection methods is effective including irradiation or exposure to various chemical disinfectants Even harsher conditions that are capable of inactivating all other known pathogens including bacterial spores such as heating under pressure at 121C exposure to dry heat at 600C or immersion in 01 N NaOH or 05 bleach cannot assure complete inactivation Currently the only procedures known to completely eliminate detectable infectivity are exposure to dry heat at 1000C immersion in either 1 N NaOH or fresh undiluted bleach and steam heating under pressure at 132C The preferred method is a sequential exposure to both NaOH and steam autoclaving inactivation treatments Notification BSE is a reportable disease in the US Measures required for introducing animals to infected animal This approach is not applicable American Association of Zoo Veterinarians Infectious Disease Manual BOVINE SPONGIFORM ENCEPHALOPATHY BSE Conditions for restoring diseasefree status after an outbreak As BSE is not known to be laterally transmitted no remediation for farms or zones within a country is needed After a case of BSE has been detected within a country certain measures must be taken to regain negligible risk status As per the World Organization for Animal Health OIE countries detecting BSE must perform a risk assessment to identify historical and existing risk factors The country must demonstrate that appropriate specific measures have been taken for the relevant period of time defined below to manage each identified risk EITHER a If there has been a case every case of BSE has been demonstrated to have been imported and has been completely destroyed and it has been demonstrated through an appropriate level of control and audit including that of cross contamination that for at least eight years neither meatandbone meal nor greaves derived from ruminants has been fed to ruminants OR b If there has been an indigenous case every indigenous case was born more than 11 years ago and the below points have been complied with for 7 years An education program is in place for those involved in the livestock industry to report all suspected cases of BSE BSE is reportable and all suspect cases are investigated Diagnostics are carried out in accordance with the OIE laboratory manual AND i it has been demonstrated through an appropriate level of control and audit including that of cross contamination that for at least eight years neither meatandbone meal nor greaves derived from ruminants has been fed to ruminants ii All BSE cases as well as all cattle which during their first year of life were reared with the BSE cases during their first year of life and which investigation showed consumed the same potentially contaminated feed during that period or if the results of the investigation are inconclusive all cattle born in the same herd as and within 12 months of the birth of the BSE cases if alive in the country zone or compartment are permanently identified and their movements controlled and when slaughtered or at death are completely destroyed Experts who may be consulted Linda A Detwiler DVM Clinical Professor Department of Pathobiology and Population Medicine College of Veterinary Medicine Mississippi State University 7325809391 Fax 732 7417751 ldetwilerbelle terrecom American Association of Zoo Veterinarians Infectious Disease Manual BOVINE SPONGIFORM ENCEPHALOPATHY BSE References 1 Baron T P Belli JY Madec F Moutou C Vitaud and M Savey 1997 Spongiform encephalopathy in an imported cheetah in France Vet Rec 141 270271 2 Bolton DC MP McKinley and SP Prusiner 1982 Identification of a protein that purifies with the scrapie prion Sci 218 13091311 3 Brown P and LA Detwiler 2013 Bovine spongiform encephalopathy consequences for human health In Doyle MP and RL Buchanan eds Food Microbiology Fundamentals and Frontiers 4th ed ASM Press Washington DC Pp 651672 4 Brown P RG Will R Bradley DM Asher and L Detwiler 2001 Bovine spongiform encephalopathy and variant CreutzfeldtJakob disease background evolution and current concerns Emerg Infect Dis 7 616 5 Cunningham AA JK Kirkwood M Dawson YI Spencer RB Green and GAH Wells 2004 Distribution of bovine spongiform encephalopathy in greater kudu Tragelaphus strepsiceros Emerg Infect Dis 10610449 6 Kirkwood JK GA Wells JW Wilesmith AA Cunningham and SI Jackson 1990 Spongiform encephalopathy in an Arabian oryx Oryx leucoryx and a greater kudu Tragelaphus strepsiceros Vet Rec 127 418429 7 Kirkwood JK 1993 Spongiform encephalopathy in a herd of Greater kudu Tragelaphus strepsiceros epidemiological observations Vet Rec 133 360364 8 Kirkwood J K and AA Cunningham 1994 Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles Vet Rec 135 296303 9 OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals Bovine Spongiform Encephalopathy httpwwwoieintfileadminHomeengHealthstandardstahm20406BSEpdf Accessed 7 October 2013 10 OIE Terrestrial Animal Health Code Bovine Spongiform Encephalopathy httpwwwoieintindexphpid169L0htmfilechapitre1115htm Accessed 7 October 2013 11 United Kingdom Department for Environment Food and Rural Affairs Bovine Spongiform Encephalopathy httpwwwdefragovukahvlaendiseasecontrolnotifiablebse Accessed 7 October 2013 12 United States Department of Agriculture USDA Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy httpwwwaphisusdagovnewsroomhotissuesbseind exshtml Accessed 30 September 2013 13 United States Food and Drug Administration Bovine Spongiform Encephalopathy httpwwwfdagovanimalveterinaryguidancecomplianceenforcementcomplianceenforcementbovines pongiformencephalopathydefaulthtm Accessed 7 October 2013 14 Wells GAH AC Scott CT Johnson RF Gunning RD Hancock M Jeffrey M Dawson and R Bradley 1987 A novel progressive spongiform encephalopathy in cattle Vet Rec 121 419420 15 Wells GAH T Konold ME Arnold AR Austin SAC Hawkins M Stack MM Simmons YH Lee D GavierWidén M Dawson and JW Wilesmith 2007 Bovine spongiform encephalopathy the effect of oral exposure dose on attack rate and incubation period in cattle J Gen Virol 88 13631373 16 Wilesmith JW GAH Wells MP Cranwell and JBM Ryan 1988 Bovine spongiform American Association of Zoo Veterinarians Infectious Disease Manual BOVINE SPONGIFORM ENCEPHALOPATHY BSE encephalopathy epidemiological studies Vet Rec 123 638644 17 Will RG JW Ironside M Zeidler SN Cousens K Estibeiro A Alperovitch S Poser M Pocchiari A Hofman and PG Smith 1996 A new variant of CreutzfeldtJakob disease in the UK Lancet 347 921925 18 Willoughby K DF Kelly DG Lyon and GA Wells 1992 Spongiform encephalopathy in a captive puma Felis concolor Vet Rec 131 431434 19 World Organization for Animal Health OIE httpwwwoieint Accessed 7 October 2013 20 Wyatt J M GR Pearson TN Smerdon TJ GruffyddJones GA Wells and JW Wilesmith 1991 Naturally occurring scrapielike spongiform encephalopathy in five domestic cats Vet Rec 129 233 American Association of Zoo Veterinarians Infectious Disease Manual BOVINE VIRAL DIARRHEA VIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Artiodactyla Horizontal Primarily from a persistently infected animal PI but also from transiently infected animals In PI virus is shed heavily and continuously in all bodily secretions Virus also transmitted by fomites Vertical Infection of dam during first trimester can produce PI Horizontal Sub clinical respiratory disease diarrhea mucosal ulcers fever hemorrhagic syndrome secondary infections peracute death and reproductive failure Vertical Infertility abortion stillbirths weak calves and PI Species and viral strain dependent Infections can be sub clinical or cause severe disease and death Supportive care for transiently infected animals Testing identification and elimination of PI Vaccination with MLV is common in cattle and has been reported to prevent infection in alpacas without ill effects No Fact Sheet compiled by Peregrine Wolff Sheet completed on 2018 Fact Sheet Reviewed by Beth Bicknese Susceptible animal groups Ungulates belonging to the order Artiodactyla including Bovidae Suidae Caprinae Camelidae Antilocapridae Tragulidae and Cervidae Causative organism Single stranded RNA viruses belonging to the genus Pestivirus and Family Flaviviridae Two species BVDV1 11 subgenotypes and BVDV2 2 subgenotypes have different profiles In the US the three commonly isolated subgenotypes from cattle are BVDV1a 1b and 2a Within the genotypes or strains two 2 biotypes of BVDV classification are based on their effects on cell culture cytopathic CP or noncytopathic NCP Infections with NCP strains are the most common and it is the NCP strains that result in PI animals Because BVDV is an RNA virus it readily mutates resulting in genetic antigenic and pathogenic variation Zoonotic potential This disease is not considered to have zoonotic potential at this time However the virus can infect human cell lines Distribution Worldwide distribution The principal reservoirs of BVDV are persistently infected PI domestic cattle Numerous wildlife species both captive and freeranging have been shown to be serologically positive for BVDV Persistently infected individuals have been identified in captive and free ranging wildlife primarily cervid species Incubation period Experimental infection in mule deer whitetail deer and cattle indicates that virus may be isolated from white blood cells serum plasma or nasal secretions as early as two days post infection Clinical signs Infections can be transient with no apparent clinical signs or severe with pronounced morbidity and mortality Both genotypes BVD1 and BVDV2 can cause the full spectrum of clinical presentations BVDV is lymphotrophic and immunosuppressive so diseased animals have an increased susceptibility to infectious diseases Hematology may show mild to severe lymphopenia and neutropenia depending on the virulence of the strain to the host Acute Transient or Primary disease syndromes are described from horizontal transmission American Association of Zoo Veterinarians Infectious Disease Manual BOVINE VIRAL DIARRHEA VIRUS which include Respiratory Oculonasal discharge Due to BVDV immunosuppressive effects clinical signs may be indicative of disease caused by other respiratory pathogens Gastrointestinal Diarrhea and clinical signs resulting from lesions which are primarily ulcerous or erosive and which may involve any region of the GIT Mixed infections with other common gastrointestinal organisms are not uncommon Hemorrhagicthrombocytopenic Thrombocytopenia bloody diarrhea prolonged bleeding times petechial and ecchymotic hemorrhages epistaxis death Mucosal disease MD Seen only in PI animals that become super infected with a CP strain of BVDV Clinical signs are secondary to severe ulcerative and erosive lesions throughout the gastrointestinal tract and potentially including lameness secondary to lesions associated with inter digital ulcerations From vertical transmission disease syndromes include Reproductive and fetal Early fetal losses mummified fetuses abortions stillbirths and congenital defects poor doer during neonatal period Persistently infected animals Persistently infected animals result if the dam becomes infected during the first trimester of gestation In cattle infection must occur between 45125 days with a noncytopathic strain of BVDV In whitetail deer infection occurring between days 4552 of gestation resulted in a PI fawn The fetus becomes infected and is immunotolerant to the infecting strain of BVDV and will shed high amounts of virus from all bodily fluids throughout its life The PI animal may mount an immune response to heterologous strains of BVDV Persistently infected individuals may exhibit runtiness immunosuppression and secondary infections but clinically normal animals have been documented Post mortem gross or histologic findings There are no pathognomonic lesions for BVDV Pathological diagnosis may be made based on virus isolation or demonstration of the virus within tissues Transiently infected animals will have gross and histopathological lesions consistent with their clinical syndrome Persistently infected but healthy animals may have few postmortem and histopathological lesions Lymphoid depletion has been reported in both PI cattle and experimentally infected fawns Diagnosis Primary goal is to identify the PI animal Virus isolation is the gold standard However antigen capture ELISA ACE immunohistochemistry and RT PCR are commonly utilized tests as they are rapid sensitive affordable and repeatable amongst diagnostic laboratories Many tests do not differentiate between BVDV1 and 2 and other pestiviruses such as classical swine fever virus border disease virus endemic worldwide pronghorn virus HoBilike isolated in South America and Southeast Asia Bungowannah isolated in Australia and giraffe isolated in Africa Most tests cannot differentiate between an acute and a persistent infection The standard for diagnosis of PI infection is two positive tests on samples collected at least two weeks apart Material required for laboratory analysis Antemortem Haired skin sample ear notch or caudal tail fold or whole blood buffy coat collected in EDTA are preferred samples Postmortem Haired skin and lymphoid tissue mesenteric lymph nodes thymus tonsils spleen and brain These tissues should be collected for culture or immunohistochemistry fresh and formalin fixed Archived formalin fixed tissue blocks can be tested for BVD via PCR however detection rates drop after 3 months 1 year Relevant diagnostic laboratories Check with your local veterinary diagnostic lab to see what tests they perform and the limitations of these tests for the species you are testing Treatment Supportive care of transiently infected animals Persistently infected individuals should be eliminated from the herd Prevention and control Identification and removal of PI individuals All incoming artiodactyls particularly domestic cattle sheep and goats should be quarantined and tested for the presence of BVDV virus American Association of Zoo Veterinarians Infectious Disease Manual BOVINE VIRAL DIARRHEA VIRUS 1 Animals that can only be handled once and with risk of exposure to BVDV Combination of Antigencapture ELISA ACE on haired skin combined with PCR on whole blood buffy coat collected in EDTA and antibody detection via serum neutralization will have the greatest likelihood of identifying PI that may be transiently infected An animal that is positive on both ELISA ACE on haired skin as well as RTPCR on whole blood but is negative on serology is considered highly suspicious of being PI and should undergo follow up testing in 46 weeks Animals that that are positive on RTPCR and have serum titers are most likely transiently infected individuals 2 Pregnant females that have a serum antibody titer to BVDV These animals may have been exposed to the virus within the first trimester of pregnancy and be carrying a PI fetus They should be quarantined until the offspring is born The offspring should then be tested for persistent infection via whole blood buffy coat RTPCR in combination with ELISA ACE or immunohistochemistry on a haired skin sample This will differentiate presence of virus in the face of maternal antibodies if the offspring is sampled post nursing 3 Animals with viremia should not be introduced to other artiodactyls that may be in the first trimester of gestation 4 Individuals utilizing reproductive manipulation techniques should be alerted that BVDV has been isolated from commercial fetal calf serum 5 Vaccination has not been well studied in wildlife Alpacas are reported to be protected with no negative effects when vaccinated with a MLV Vaccination in cattle is primarily focused on the prevention of fetal infections Suggested disinfectant for housing facilities BVDV is an enveloped virus and susceptible to the following classes of disinfectants when used per recommended protocols hypochlorites chlorhexadine alcohol iodine and iodophores quaternary ammonium compounds phenolic disenfectants and aldehydes Notification None Required Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Pregnant animals should not be exposed to animals that are viremic PI animals should be identified and removed from the herd Conditions for restoring diseasefree status after an outbreak dentify and remove PI individuals Any offspring born to dams that were pregnant during the outbreak should be tested to insure that they are not PI and all new additions that may be at risk for infection with BVDV should undergo testing and quarantine prior to introduction to any artiodactyl species Experts who may be consulted Shollie Falkenberg National Animal Disease Center Agricultural Research Service USDA 1920 Dayton Avenue PO Box 70 Ames IA 50010 Phone 515 3377338 office 515 3377372 lab Fax 515 3377402 ShollieFalkenbergarsusdagov References 1 Control of pestivirus infections in the management of wildlife populationsResearch Topic 11 articles internet Front Microbiol 2016 cited 2018 March 10 Available from httpswwwfrontiersinorgresearchtopics2980controlofpestivirusinfectionsinthemanagement ofwildlifepopulationsarticles 2 Nelson DD Duprau JL Wolff PL Evermann JF Persistent bovine viral diarrhea virus infection in domestic and wild small ruminants and camelids including the mountain goat Oreamnos americanus Front Microbiol 2016761415 cited 2018 March 10 Available from httpswwwfrontiersinorgarticles103389fmicb201501415full American Association of Zoo Veterinarians Infectious Disease Manual BOVINE VIRAL DIARRHEA VIRUS 3 Duncan C Ridpath JF Palmer MV Driskell E Spraker T Histopathologic and immunohistochemical findings in two whitetailed deer fawns persistently infected with bovine viral diarrhea virus J Vet Diagn Invest 2008 20289296 4 Kottwitz JK Ortiz M Bovine viral diarrhea virus in zoos A perspective from the veterinary team Front Microbiol 201661496 cited 2018 March 10 Available from httpswwwfrontiersinorgarticles103389fmicb201501496full 5 Passler T Ditchkoff SS Given MD Brock KV DeYoung RW Walz PH Transmission of bovine virus diarrhea virus amongst whitetail deer Odocoileus virginianus Vet Res 20104120 6 Passler T Walz PH Bovine viral diarrhea virus in heterologous species Anim Health Res Rev 201011191195 7 Van Campen H Frölich K Hoffmann M 2001 Pestivirus Infection InWilliam ES Barker IK eds Infectious Diseases of Wild Mammals 3rd ed Ames IA Blackwell Publishing 2001 p 232244 8 Walz PH Grooms DL Passler T Ridpath JF Tremblay R Step DL Callan RJ MD Givens MD Control of bovine viral diarrhea virus in ruminants J Vet Intern Med 201024476486 American Association of Zoo Veterinarians Infectious Disease Manual BOVINE BRUCELLOSIS Fact Sheet compiled by SW Jack updated by Frank Austin Sheet completed on 3 May 2011 updated 30 July 2013 April 2018 Fact Sheet Reviewed by Steve Olsen Julie Ter Beest Jim Watson Susceptible animal groups Ungulates cattle bison buffalo elk goats sheep reindeer camel etc swine carnivores rodents pinnipeds cetaceans horses and humans Causative organism Brucella species generally have a preferred natural host but will frequently infect other hosts Brucella abortus cattle and humans is the primary causative agent However there are other Brucellae that include B melitensis small ruminants and cattle although it is not present in US this organism has been seen in humans in the US from imported nonpasteurized dairy products B ovis small ruminants B suis swine reindeer biovarian 4 cattle B canis dogs B neotomae rodents B microti voles and foxes B ceti cetaceans B pinnipedialis pinnipeds and B inopinata humans Brucellae are gram negative non enteric facultative intracellular coccobacilli Zoonotic potential Relatively high Distribution Worldwide although regionally it is limited in North America Greater Yellowstone Area B abortus in bison and elk Brucella suis transmitted from feral swine is increasingly occurring in cattle housed in the southeast US Increasingly B melitensis is occurring in cattle in central Asia and the Middle East Incubation period Quite variable 2 weeks to 1 year or longer Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Ungulates cattle bison buffalo elk goats sheep camel etc swine carnivores rodents voles pinnipeds cetaceans humans Usually ingestion of materials contaminated by birthing or abortion products fluids placenta fetus direct contact with afore mentioned materials or semen ingestion of unpasteurized milk or dairy products Fomites and mechanical vectors can transmit the organism The organism can pass abraded skin or intact mucous membranes and persists in the environment for up to 60 days especially at low temperatures or high organic material Venereal transmission also can occur with B suis B ovis and B canis Abortion mid to late term stillborn or weak calves neonatal death placentitis endometritis epididymitis seminal vesiculitis orchitis testicular abscess spondylitis or arthritis Many times no other outward clinical signs Chronically infected animals may have decreased milk production or possible hygromas High morbidity in naïve herds Generally a mild disease in animals except abortion with chronically infected herds stabilizing at 3050 sero prevalence Produces undulant fever in humans that is chronic and debilitating but not generally life threatening however B melitensis and B suis tend to induce myocarditis which can be associated with fatality Antibiotics in humans none in animals Avoidance quarantine incoming animals Test and slaughter of serologic reactors Long term antibiotics for humans But antibiotics are of questionable value in animals Use of personal protective equipment adequate gloves protective clothing respiratory and mucosal membrane protection for vocational exposure in humans Yes American Association of Zoo Veterinarians Infectious Disease Manual BOVINE BRUCELLOSIS Clinical signs Abortion weak calves neonatal death placentitis endometritis epididymitis seminal vesiculitis orchitis testicular abscess and spondylitis may occur Often no other outward clinical signs Chronically infected animals may be poor doers In horses infection may produce fistulous withers In humans severe flulike signs fatigue headache fever chills night sweats joint pain backache weight and appetite decreases spontaneous improvement but recrudesces undulant fever In cattle B suis does not appear to cause abortions in cattle but does colonize the mammary gland with subsequent high CFU within milk Post mortem gross or histologic findings Aborted fetus autolysis common intrauterine death subcutaneous edema serosanguineous fluid in body cavities peritoneum pericardium and pleura possible spleno and hepatomegaly pneumonia Placentitis inflamed or necrotic cotyledons leathery intercotyledonary zones Adults granulomatous to purulent inflammation of reproductive tract hygromas draining tracts Diagnosis Serology agglutination screening FPA and CF confirmatory ELISA available Milk ring Test BRT perhaps bacterial isolation newer PCR tests are available Confirmatory tests Culture of the organism is the Gold Standard for diagnosis Confirmatory tests include standard tube test Rivanol test complement fixation test CF fluorescence polarization assay FPA particle concentration fluorescence immunoassay PCFIA semen plasma test and standard plate test 9 CFR Ch I Part 78 Material required for laboratory analysis Microscopic examination of abortion products Stamps modification of ZiehlNeelsen method for presumptive diagnosis low yield procedure Culture of fetal membranes fetal stomach contents many fetal organs vaginal secretions milk semen arthritis or hygroma fluids not often successful Serology antemortem or postmortem AGID ELISA most common procedures Relevant diagnostic laboratories Samples are to be tested for brucellosis only in cooperative StateFederal brucellosis laboratories or by persons who are authorized by Program officials to conduct the tests See Brucellosis Eradication Uniform Methods and Rules by the USDA APHIS Treatment None in cattle Prevention and control All states are free of disease in commercial herds except for the Greater Yellowstone Park Area Test and slaughter in domestic cattle Bulk Milk test Brucella Ring Test for herd individual tests include blood agglutination andor the CARD test Animals that are positive are quarantined and only able to move to slaughter samples are collected for culture Market Cattle Identification back tags on sale barn animals to allow trace back in the event of a seropositive reactor Cattle vaccines are available eg strain 19 old and RB51 Personal protective equipment PPE for humans is good preventive measure especially with exposure to birthing fluids Regarding vaccination in zoo and wildlife species Abortions have been associated with Brucella abortus strain 19 live vaccination in bison this vaccine offers limited protection against infection and abortion in bison and elk Brucella abortus strain RB51 is a live vaccine for use in cattle that protects at least as well strain 19 does not cause abortion and induces antibodies that can be distinguished from antibodies induced by natural infection Calfhood vaccination of bison with strain RB51 vaccination may reduce transmission of brucellosis the vaccine is not however recommended in elk or reindeer American Association of Zoo Veterinarians Infectious Disease Manual BOVINE BRUCELLOSIS Suggested disinfectant for housing facilities Most disinfectants are effective eg 25 hypochlorite 70 ethanol formalin glutaraldehyde xylenes iodophors phenolics 20 slaked lime 23 caustic soda 10 minutes boiling Notification Contact state veterinarian andor AVIC Measures required under the Animal Disease Surveillance Plan Brucellosis Eradication Program see Uniform Methods and Rules Bulk Milk testing Brucella Ring Test Serum testing at sale barns blood agglutination test Fluorescence polarization assay CARD test cow side rapid diagnostics Market Cattle Identification back tags Currently in the US sampling surveillance is performed at large slaughter plants or in states with high risk for exposure Measures required for introducing animals to infected animal Infected animals are quarantined and should not be introduced to other animals Conditions for restoring diseasefree status after an outbreak Brucellosis Eradication Program see Uniform Methods and Rules 12 consecutive months without seropositive evidence of disease is required Experts who may be consulted Federal and state veterinary authorities AVIC and state veterinarian respectively international OIE References 1 Center for Food Security Public Health Iowa State University Internet Brucellosis 2018 cited 2019 September 21 Available from httpwwwcfsphiastateeduFactsheetspdfsbrucellosispdf 2 Centers for Disease Control and Prevention Internet Brucellosis 2019 cited 2019 September 21 Available from httpwwwcdcgovbrucellosis 3 Forbes L Brucellosis in specialized livestock Youngquist RS Threlfall WR eds Current Therapy in Large Animal Theriogenology St Louis MO 2nd Ed WB Saunders 2007 p 10141029 4 Robinson A Guidelines for coordinated human and animal brucellosis surveillance Food and Agricultural Organization FAO Internet 2003 cited 2019 September 24 Available from httpwwwfaoorgdocseimsupload215249y4723e00pdf 5 United States Department of Agriculture Animal and Plant Health Inspection Service Internet Facts about Brucellosis cited 2013 August 1 Available from httpwwwaphisusdagovanimalhealthanimaldiseasesbrucellosisdownloadsbrucfactspdf 6 United States Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Internet National Brucellosis Surveillance Strategy December 2010 2010 cited 2013 August 1 Available from httpwwwaphisusdagovanimalhealthanimaldiseasesbrucellosisdownloadsnatlbrucsurvstrate gypdf 7 United States Department of Agriculture Animal and Plant Health Inspection Service Internet Brucellosis and Yellowstone Bison cited 2019 September 21 Available from httpwwwaphisusdagovanimalhealthanimaldisspeccattledownloadscattlebisonpdf 8 United States Department of Agriculture Animal and Plant Health Inspection Service Internet Brucellosis Eradication Uniform Rules and Methods effective October 1 2003 2003 cited 2013 August 1 Available from httpwwwaphisusdagovanimalhealthanimaldiseasesbrucellosisdownloadsumrbovinebrucpdf American Association of Zoo Veterinarians Infectious Disease Manual MARINE MAMMAL BRUCELLA Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Marine mammals humans Experimental disease has been demonstrated in cattle and guinea pigs suggesting other terrestrial animals are likely susceptible Unknown but likely similar to terrestrial species including in utero vertical transmission ingestion of milk or contaminated fish mucous membrane exposure sexual contact or contact with infected placenta or birthing fluids Lungworms appear to serve as vectors of marine brucellae Variable depending on affected organ system and strain of bacteria Nonapparent disease to stranding abortion placentitis infertility including orchitis and epididymitis neurologic signs cutaneous lesions osteomyelitis and arthritis cardiovascular disease and respiratory distressdisease have been reported in cetaceans Variable serologic evidence of exposure without clinical disease is common Cetaceans may exhibit inapparent acute or chronic disease states Except for a single placenta sample demonstrating placentitis in a Northern fur seal pathology in pinnipeds has not yet been reported A single case of successful treatment of a pulmonary abscess including intralesional amikacin and oral doxycycline and rifampin has been reported WHO reported that human disease may respond to similar antibiotic treatment including rifampin and doxycycline Not well defined serological tests can be used for screening PCR or culture may identify animals actively shedding bacteria General biosecurity and quarantine protocols Yes Fact Sheet compiled by Claire ErlacherReid Sheet completed on updated on 30 May 2018 Fact Sheet Reviewed by Sarah Churgin Kirsten Gilardi Susceptible animal groups Cetaceans pinnipeds sea otters and polar bears also humans There are no known reports of isolation or seropositivity in manatees or dugongs Causative organism Small 15 µm by 07 µm facultative intracellular gramnegative coccobacilli Brucella species typically have different host preferences virulence and zoonotic potential despite 9799 similarity at genome level Marine mammal Brucella spp are currently identified as B ceti cetaceanorigin strains and B pinnipedialis pinnipedorigin strains Molecular characterization suggests two major Brucella ceti clades one group primarily associated with porpoise isolates and another primarily associated with dolphin isolates Distinctive genetic variations in B ceti isolates appear to correlate with oceanic distribution and preferred host Zoonotic potential Yes Outside of laboratoryassociated infection the route of exposure is not known but foodborne exposure ie raw seafood is suspected Typing of human isolates suggests increased zoonotic potential associated with a single genotype ST27 Clinical signs reported in humans include fever headache lethargy myalgia sinusitis arthritis fatigue and neurological disease in rare cases Distribution Globally distributed in wild species of cetaceans including Phocoenidae Delphinidae Monodontidae Balaenidae and Balaenopteridae and pinnipeds including Phocidae Otariidae and Odobenidae Seroprevalance fluctuates in wild populations over time Incubation period Not defined Clinical signs Variable depending on affected organ system and strain of bacteria Although bacterial strains are hostassociated crossspecies infections occur frequently and may affect expression of disease American Association of Zoo Veterinarians Infectious Disease Manual MARINE MAMMAL BRUCELLA Seropositivity and bacterial isolation are reported in pinnipeds without overt disease suggesting hostadapted or lowpathogenic strains Stranding inanition infertility abortion neurologic signs cutaneous and pulmonary abscessation and musculoskeletal disorders have been reported in cetaceans Chronic severe osteoarthritis has been reported in a sea otter Post mortem gross or histologic findings A single Northern fur seal placenta sample demonstrated severe placentitis in association with positive PCR testing and immunostaining for Brucella Otherwise pathology has not been previously reported in pinnipeds In cetaceans lesions are primarily seen in reproductive tract orchitisepididymitis necrotizing placentitisendometritis reticuloendothelialhemolymphatic systems lymphadenitis splenic necrosis central nervous system meningoencephalitis musculoskeletal system discospondylitis osteomyelitis and arthritis and lung interstitial pneumonia pulmonary abscesses and granulomas and lungworm associated pneumonia Additional findings have included blubber abscesses visceral necrosis steatitis mastitis hepatomegaly and vegetative endocarditis Chronic granulomatous osteoarthritis and myelitis were noted in a sea otter with marine Brucella Diagnosis Diagnosis can be divided into direct identification and indirect screening methods of detection Bacterial isolation in culture from infected materials CSF brain lymph node and lung are most commonly used remains the gold standard however this method is difficult at best Farrells media or Brucellaagar with 5 horse blood may be used and incubated with 510 CO2 for up to 14 days Molecular characterization by polymerase chain reaction PCR methods include outer membrane protein polymorphisms infrequent restriction sitederivative PCR insertion sequence IS711 profiling multilocus sequence typing MLST and multiple loci variable number tandem repeat analysis MLVA Detection of Brucella from a blowhole swab utilizing realtime PCR appears to correlate well with detection of Brucella in internal lung tissue Realtime PCR may be used to screen for the presence of Brucella DNA in live cetaceans via blowhole swabs blood andor fecal samples Immunohistochemical staining can identify the presence of bacteria in tissues but has not proved to be as sensitive as other methods for surveillance A number of serologic methods are available for screening ie Rose Bengal test and buffered plate agglutination test the complement fixation test enzyme linked immunosorbent assays ELISA or the fluorescence polarization assay FPA but sensitivity and specificity are variable and seropositivity does not correlate with active disease or bacterial shedding Material required for laboratory analysis Fresh or frozen tissue especially aborted fetuses stomach contents spleen and lung fetal membranes vaginal secretions swabs reticuloendothelial system lymph nodes and spleen brainspinal cordCSF liver and kidney or other gross lesions In live animals bacteria have been recovered from feces blood blow hole swabs fine needle aspirates and lungworms Relevant diagnostic laboratories Clinicians with susceptible populations of marine animals should inquire about routine bacteriologic testing through their local or regional veterinary or medical diagnostic laboratories For culture and bacterial typing USDAAPHIS National Veterinary Services Laboratories Mycobacteria and Brucella Section National Reference Laboratory 1920 Dayton Ave Ames Iowa 50010 515 3377388 Routine culture Marine Mammal Diagnostic Laboratory UC Davis One Health Institute School of Veterinary Medicine 1089 Vet Med Drive VM3B Davis CA 95616 5307524167 American Association of Zoo Veterinarians Infectious Disease Manual MARINE MAMMAL BRUCELLA PCR for Brucella spp Athens Veterinary Diagnostic Laboratory College of Veterinary Medicine University of Georgia 501 DW Brooks D Athens GA 306027383 706 5425568 wwwvetugaedudlab Marine mammal cELISA and qPCR Mystic Aquarium Institute for Exploration Dept of Research and Veterinary Services Tracy Romano 55 Coogan Blvd Mystic CT 063551997 860 5725955 Treatment A single successful treatment of pulmonary abscess was reported in a captive dolphin The treatment included intralesional amikacin followed by six to eight weeks of oral doxycycline and rifampin Prevention and control Surveillance using serological tests can be used for screening population exposure Blowhole andor fecal PCR may identify animals actively shedding bacteria General biosecurity and quarantine protocols are recommended for marine mammal rehabilitation and aquarium facilities Suggested disinfectant for housing facilities General measures for cleaning and disinfection should reduce environmental bacterial contamination as Brucella bacteria are readily killed by common disinfectants and do not appear to live long outside the host cells Notification Marine strains of Brucella are not currently reportable to State Provincial or Federal bodies Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal These measures are not yet defined in marine species Paired serology may be recommended for animals planned to be introduced including use of appropriate quarantine protocols Conditions for restoring diseasefree status after an outbreak Not defined in marine species Experts who may be consulted Inga F Sidor DVM New Hampshire Veterinary Diagnostic Laboratory University of New Hampshire 129 Main St Durham NH 03824 ingasidorunhedu References 1 Cassle S Jensen E Smith C Meegan J Johnson S Lutmerding B Ridgway S FrancisFloyd R Diagnosis and successful treatment of a lung abscess associated with Brucella species infection in a bottlenose dolphin Tursiops truncatus J Zoo Wildl Med 2013442 495499 2 Colville J Berryhill D Brucellosis In Handbook of Zoonoses Identification and Prevention St Louis MO Mosby Elsevier 2007 p 3843 3 Davis D Brucellosis in wildlife In Nielsen K Duncan J eds Animal Brucellosis Boca Raton FL CRC Press 1990 p 321334 4 Duncan C Tiller R Mathis D Stoddard R Kersh G Dickerson B Gelatt T Brucella placentitis and seroprevalence in northern fur seals Callorhinus ursinus of the Pribilof Islands Alaska J Vet Diagn Invest 2014264507512 5 Dunn JL Buck JD Robeck TR Bacterial diseases of cetaceans and pinnipeds In Dierauf LA Gulland FMD eds CRC handbook of marine mammal medicine 2nd ed Boca Raton FL CRC Press 2001 p 312314 American Association of Zoo Veterinarians Infectious Disease Manual MARINE MAMMAL BRUCELLA 6 Foster G MacMillan A Godfroid J Howie R Ross H Cloeckaert A Reid R Brew S Patterson I A review of Brucella sp infection of sea mammals with particular emphasis on isolates from Scotland Vet Microbiol 2002 90563580 7 Foster G Bjorn S Osterman S Godfroid J Jacques I Cloeckaert A Brucella ceti sp nov and Brucella pinnipedialis sp nov for Brucella strains with cetaceans and seals as their preferred hosts Int J Syst Evol Micro 20075726882693 8 Gee J De B Levett P Whitney A Novak R Popovic T Use of 16S rRNA gene sequencing for rapid confirmatory identification of Brucella isolates J Clinic Microbiol 20044236493654 9 GuzmanVerri C GonzalezBarrientos R HernandezMora G Morales J BaqueroCalvo E Chaves Olarte E Morena E Brucella ceti and brucellosis in cetaceans Front Cell Inf Microbiol 20122122 10 HernandezMora G PalaciosAlfaro J GonzalezBarrientos R 2013 Wildlife reservoirs of brucellosis Brucella in aquatic environments Rev Sci Tech Off Int Epiz 201331189103 11 HernandezMora G GonzalezBarrientos R Morales JA ChavesOlarte E GuzmánVerri C Baquero Calvo E DeMiguel MJ Marín CM Blasco JM Moreno E Neurobrucellosis in stranded dolphins Costa Rica Emerg Infect Dis 20081414301433 Erratum 141825 12 Maratea J Ewalt D Frasca S Dunn J DeGuise S Szkudlarek L St Aubin D French R Evidence of Brucella sp infection in marine mammals stranded along the coast of southern New England J Zoo Wildl Med 200334256261 13 Meegan J Field C Sidor I Romano T Casinghino S Smith C Kashinsky L Fair P Bossart G Wells R Dunn J Development validation and utilization of a competitive enzymelinked immunosorbent assay for the detection of antibodies against Brucella species in marine mammals J Vet Diagn Invest 201022 85662 14 Miller G Adams L Ficht T Cheville N Payeur J Harley D House C Ridgway S Brucellainduced abortions and infections in bottlenose dolphins Tursiops truncatus J Zoo Wildl Med 199930100110 15 Miller M Burgess T Dodd E Rhyan J Jang S Byrne B Gulland F Murray M ToyChoutka S Conrad P Field C Sidor I Smith W Isolation and characterization of marine Brucella from a southern sea otter Enhydra lutris nereis California USA J Wildl Dis 2017532215224 16 Nymo I Tryland M Godfroid J A review of Brucella infection in marine mammals with special emphasis on Brucella pinnipedialis in the hooded seal Vet Res 20114293 113 17 Sidor I Dunn J Tsongalis G Carlson J Frasca S Jr A multiplex realtime polymerase chain reaction assay with two internal controls for the detection of Brucella species in tissues blood and feces from marine mammals J Vet Diagn Invest 20132517281 18 SuarezEsquivel M Baker K RuizVillalobos N HernandezMora G BarqueroCalvo E Gonzalez Barrientos R CastilloZeledon A JimenezRojas C ChaconDiaz C Cloeckaert A ChavesOlarte E Thomson N Moreno E GuzmanVerri C Brucella genetic variability in wildlife marine mammals populations relates to host preference and ocean distribution Genome Biol Evol 20179719011912 19 The Merck Veterinary Manual Brucellosis in large animals In Kahn C ed The Merck Veterinary Manual Whitehouse Station NJ Merck Co Inc 2011 p 12381241 20 Whatmore A Dawson C Muchowski J Perrett L Stubberfield E Koylass M Foster G Davison N Quance C Sidor I Field C St Leger J Characterisation of North American Brucella isolates from marine mammals PLoS One 2017129 21 Whatmore A Dawson C Groussaurd P Koylass M King A Shankster S Sohn A Probert W McDonald W Marine mammal Brucella genotypes associated with zoonotic infection Emerg Infect Dis 200814517518 22 Wu Q Conway J Phillips K Stolen M Durden W Fauquier D McFee W Schwacke L Detection of Brucella spp in bottlenose dolphins Tursiops truncates by a realtime PCR using blowhole swabs Dis Aquat Org 2016120 241244 American Association of Zoo Veterinarians Infectious Disease Manual PORCINE BRUCELLOSIS Brucella suis Fact Sheet compiled by Cora Singleton Sheet completed on updated 8 August 2018 Fact Sheet Reviewed by Suzanne KennedyStoskopf Susceptible animal groups Biovars 1 and 3 domestic and wild swine Biovar 2 wild swine European hare Biovar 4 reindeer and caribou maintain the infection moose cattle Arctic fox and wolves can also be infected Biovar 5 wild rodents in former USSR Causative organism Brucella suis a small Gramnegative coccobacillus with five biovars Zoonotic potential Yes Human brucellosis biovars 1 3 and 4 is mainly an occupational risk seen in farmers veterinarians and abattoir workers Biovar 2 is zoonotic but rarely reported in humans Distribution Biovar 1 and 3 worldwide Biovar 2 Europe Biovar 4 Arctic regions including Alaska and Canada and Russia Biovar 5 former USSR Incubation period Bacteremia usually develops within 1 to 7 weeks mean 2 weeks after exposure Bacteremia can last up to 90 days Clinical signs Infection can be asymptomatic Clinical problems include reproductive disease infertility abortion weak or stillborn piglets orchitis epididymitis metritis and pyrexia with less common signs of lameness with swollen joints and tendon sheaths due to bursitis synovitis arthritis posterior paralysis spondylitis and abscess formation in organs Death is rare Post mortem gross or histologic findings Lesions are variable and may include abscess formation in affected organs including the liver spleen kidneys reproductive tract placenta lymph nodes joint capsules tendon sheaths and bones Diagnosis Agent identification bacterial culture PCR Serology Buffered Brucella antigen tests such as buffered plate agglutination test and Rose Bengal test ELISA fluorescent polarization assay complement fixation test Serologic tests are more useful for identifying infected herds than infected individuals Buffered antigen tests often preferred USDA presumptive tests Buffered acidified plate antigen test standard card test USDA confirmatory tests Standard tube test particle concentration fluorescence immunoassay Material required for laboratory analysis Bacterial culture lymph node reproductive organs vaginal swab products of abortion synovial fluid semen blood Serologic tests Serum Relevant diagnostic laboratories State and federal laboratories that have been specifically approved for conducting swine brucellosis serology Treatment No treatments have been proven effective and economically feasible Prevention and control The United States maintains a federal program for eradication of brucellosis from domestic livestock Porcine brucellosis is controlled through serologic testing and carcass inspection at slaughter with traceback investigations of any suspicious cases Pigs are not vaccinated against brucellosis Disease can be prevented by testing and quarantining new animals eliminating contact with feral swine and practicing good sanitation Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Domestic and wild swine European hare reindeer and caribou wild rodents Direct contact with infected animals or body discharges ingestion of infected materials venereal transmission fomites Can be asymptomatic Reproductive disease lameness posterior paralysis pyrexia Mild to severe death is rare None No vaccine Test and quarantine new animals limit contact with wild swine isolate or eliminate infected animals decontaminate premises Yes American Association of Zoo Veterinarians Infectious Disease Manual PORCINE BRUCELLOSIS Brucella suis Suggested disinfectant for housing facilities Hypochlorite solutions 70 ethanol isopropanol iodaphores phenolic disinfectants formaldehyde glutaraldehyde xylene Notification B suis is considered eradicated from domestic swine in the United States Infections are reportable to the USDAAPHIS through the State Veterinarian or the federal Area Veterinarian in Charge The disease is also reportable to the World Organization for Animal Health OIE Measures required under the Animal Disease Surveillance Plan Reportable to USDAAPHIS Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Perform the necessary tests to determine presence or absence of brucellosis in individualsherd and report results Quarantine or depopulate infected or exposed animals Clean and disinfect premises vehicles and equipment Experts who may be consulted Iowa State University College of Veterinary Medicine Department of Veterinary Diagnostic and Production Animal Medicine Phone 5152941950 Fax 5152953564 httpvetmediastateeduvdpam References 1 Olsen SC Boggiatto P Nol P Samartino L Swine Brucellosis In Zimmerman JJ Karriker LA Ramirez A Schwartz KJ Stevenson GW Zhang J eds Diseases of Swine 11th ed Ames IA WileyBlackwell 2018 in press 2 Spickler Anna Rovid Internet Brucellosis Brucella suis 2018 cited 2018 August 08 Available from httpwwwcfsphiastateeduFactsheetspdfsbrucellosissuispdf 3 Thorne ET Brucellosis In Williams ES Barker IK eds Infectious Diseases of Wild Mammals 3rd ed Ames IA Iowa State University Press 2001 p 372395 4 United States Department of Agriculture Animal Plant and Health Inspection Services Internet All National Animal Health Laboratories Network NAHLN Laboratory List 2018 cited 2018 August 08 Available from httpwwwaphisusdagovanimalhealthnahlndownloadsallnahlnlablistpdf 5 United States Department of Agriculture Animal Plant and Health Inspection Services Internet Diagnostic Testing at the National Veterinary Services Laboratories 2015 cited 2018 August 08 Available from httpwwwaphisusdagovaphisourfocusanimalhealthlabinfo servicessadiagnostictestsctdiagnostictests 6 United States Department of Agriculture Animal and Plant Health Inspection Service Internet Swine Brucellosis ControlEradication StateFederalIndustry Uniform Methods and Rules APHIS 9155 042 1998 cited 2018 August 08 Available from httpwwwaphisusdagovanimalhealthanimaldisspecswinedownloadssbruumrpdf 7 World Organization for Animal Health OIE Internet Brucellosis Brucella abortus B melitensis and B suis In Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2018 2016 cited 2018 August 08 Available from httpwwwoieintfileadminHomeengHealthstandardstahm20104BRUCELLOSISpdf American Association of Zoo Veterinarians Infectious Disease Manual CAMPYLOBACTERIOSIS Fact Sheet compiled by Teresa J Sylvina previously published as Taranjit Kaur Sheet completed on 13 April 2011 updated 22 July 2013 Fact Sheet Reviewed by Jatinder Singh Michael R Cranfield Susceptible animal groups Mammals including humans birds reptiles fish and mollusks Causative organism Campylobacter sppvarious Zoonotic potential Yes Distribution Surfaces wet cutting boards or utensils where raw or partially cooked meat particularly poultry is prepared surface waters and mountain streams exposed to feces from cattle and wild birds surfaces in contact with feces from infected agricultural animals pets wild zoo and lab animals Incubation period 25 days and may be up to one week Clinical signs Clinical signs are hostspecific crossinfection is possible and range from none to severe Diarrhea tends to be watery or may be bloody fever abdominal cramps nausea and vomiting may also be present other illnesses such as abortion stillbirths or infertility may occur in cattle and sheep Post mortem gross or histologic findings Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals including humans birds reptiles fish and shellfish Food or waterborne fecaloral spread direct contact with contaminated surfaces or contact with infected animals Hostspecific none to severe diarrheal disease watery or bloody possibly with fever abdominal cramps nausea and vomition other illnesses such as abortion and infertility and periodontal disease Mild to life threatening gastroenteritis with possible sepsis and disseminated infections children immune compromised individuals and the elderly may be at greater risk Longterm consequences such as arthritis or GuillainBarré occur rarely in people Extra fluids to remain hydrated as long as diarrhea persists Recovery often occurs without antibiotics although they may be used to shorten the duration of clinical signs if administered early in course of disease Practice sanitary food preparation use good personal and environmental hygiene wear gloves when working with infected animals or surfaces in contact with their feces wash hands with soap and water To reduce venereal transmission use strict hygiene artificial insemination and vaccination tetracycline may prevent abortion in ewes Yes American Association of Zoo Veterinarians Infectious Disease Manual CAMPYLOBACTERIOSIS Enteric campylobacteriosis Biopsy specimens from people have shown acute colitis with inflammatory infiltrates of the lamina propria and crypt abscesses Organisms can stably colonize the small and large intestine although most animals show cecal and colonic lesions with typhlocolitis marked inflammation of lamina propria dominated by neutrophilic polymorphonuclear and mononuclear cells that sometimes extend into submucosa crypt abscesses and damage to the crypt epithelium is common a compromised epithelial surface also been observed in most species Bovine and ovine genital campylobacteriosis Abortion occurs most frequently in late pregnancy with occasional infertility Liver shows typical gray necrotic foci 12 cm in diameter fetuses usually edematous and body cavities contain reddish fluid fetal membranes edematous and cotyledons pale and necrotic but lesions do vary Curved bacteria in stains of cotyledon impressions or fetal abomasal fluid Gram negative organisms found in wet preps of abomasal fluid examined by darkfield or phasecontrast microscopy Diagnosis Bacterial culture of fresh feces darkfield examination of abomasal contents or culture of placenta or abomasal contents or in uterine discharge Material required for laboratory analysis Fresh fecal samples in enteric transport kit and storage at 4C Relevant diagnostic laboratories Laboratories capable of bacteriologic culturing on selective culture media incubated under microaerobic conditions and temperatures allowing growth of nonthermotolerant species Campylobacter species are difficult to isolate and suboptimal conditions for isolation will yield falsenegative results Variations in laboratory practices have been reported also suggesting variations in specimen handling and processing which likely influence recovery and detection of Campylobacter species Treatment Usually no medical treatment is necessary Rehydrating levels of fluids should be administered during diarrheal disease Appropriate antibiotics such as erythromycin may be a consideration in some cases Suspected genital campylobacteriosis should be confirmed by isolation of organisms from herd bulls selected infertile nonpregnant cows or aborted fetuses or cotyledons Prevention and control Raw poultry meat should not be prepared on a cutting board then used unwashed for other food items especially when not cooked after handling Appropriate hygiene in food preparation should include separate cutting boards for proteins and produce Unpasteurized milk and untreated surface water and mountain streams should be avoided Wash hands using soap and running water after contact with animals their enclosures and other surfaces that are in contact with feces from animals Animals infected with genital campylobacteriosis should not be utilized for breeding Suggested disinfectant for housing facilities After cleaning gross contamination diluted bleach 15ml in one quart of water applied to dry or wiped dry after 10 minutes Other disinfectants may be used check disinfectant label to verify its effectiveness against Campylobacter spp Notification Report cases to the local health department if zoonotic transmission occurs depending on the state Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Maintain infected animal in a quarantine situation until the infection is cleared Do not house infected animals with immune compromised animals Conditions for restoring diseasefree status after an outbreak Improvements in personal and environmental hygiene can be directed at animal husbandry and health staff Education efforts can be directed toward proper food handling techniques and toward avoiding consumption of potentially contaminated food milk or water Experts who may be consulted James G Fox DVM MS DACLAM Professor and Director Comparative Medicine Massachusetts Institute of Technology American Association of Zoo Veterinarians Infectious Disease Manual CAMPYLOBACTERIOSIS Cambridge MA 02139 617 2531757 jgfoxmitedu References 1 httpwwwcdcgovhealthypetsdiseasescampylobacteriosishtm Accessed 8 July 2013 2 Debruyne L T Broman S Bergström B Olsen S L W On and P Vandamme 2009 Campylobacter volucris sp nov isolated from blackheaded gulls Larus ridibundus Int J Syst Evol Microbiol 60 18701875 3 Dingle K E M J Blaser Z C Tu J Pruckler C Fitzgerald M A P van Bergen A J Lawson R J Owen and J A Wagenaar 2010 Genetic relationships among reptilian and mammalian Campylobacter fetus strains determined by multilocus sequence typing J Clin Microbiol 483 977 980 4 Fox J G K O Maxwell N S Taylor C D Runsick P Edmonds and D J Brenner 1989 Campylobacter upsaliensis isolated from cats as identified by DNA relatedness and biochemical features J Clin Microbiol 2710 23762378 5 Gossling J W J Loesche and G W Nace 1982 Large intestine bacterial flora of nonhibernating and hibernating leopard frogs Rana pipiens Appl Environ Microbiol 441 5966 6 Harvey S and J R Greenwood 1985 Isolation of Campylobacter fetus from a pet turtle J Clin Microbiol 212 260261 7 Hollamby S J G Sikarskie and J Stuft 2003 Peafowl Pavo Cristatus for potential pathogens at three Michigan Zoos J Zoo Wildl Med 344 375379 8 Kahn C and S Line eds 2010 The Merck Veterinary Manual 10th ed Whitehouse Station NJ Merck and Co Inc Pp 171174 1227 9 Kaur T J Singh M A Huffman K J Petrželková N S Taylor S Xu F E Dewhirst B J Paster L Debruyne P Vandamme and J G Fox 2011 Campylobacter troglodytis sp nov isolated from feces of humanhabituated wild chimpanzees Pan troglodytes schweinfurthii in Tanzania Appl Environ Microbiol 777 23662373 10 Misawa N S Shinohara H Satoh H Itoh K Shinohara K Shimomura F Kondo and K Itoh 2000 Isolation of Campylobacter species from zoo animals and polymerase chain reactionbased random amplified polymorphism DNA analysis Vet Microbiol 71 59 68 11 Mikanatha N M L A Dettinger A Perry P Rogers S M Reynolds and I Nachamkin 2012 Culturing Stool Specimens for Campylobacter spp Pennsylvania USA Emerg Infect Dis 183 484487 American Association of Zoo Veterinarians Infectious Disease Manual CANINE DISTEMPER VIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All terrestrial families in the order Carnivora Also known cases in marmots phocids primates tamandua tayassuids and sloths Highly contagious Aerosol of respiratory exudate is primary mode but other body excretions and secretions may be infective Vaccinal or vaccine induced distemper possible Respiratory gastrointestina l integumentary ophthalmic CNS Hyperkeratosi s of footpads and myoclonus Variable Inapparent to peracute death Secondary infections Supportive care Vaccination Keep infected animals isolated Exclusion of potential reservoirs eg domestic dogs raccoons No However evidence of correlation of CDV with some human diseases Fact Sheet compiled by Sharon L Deem Sheet completed on updated 31 July 2018 Fact Sheet Reviewed by AJ Marlar Cara Field Susceptible animal groups Species within all terrestrial families of the order Carnivora Canidae Mustelidae Procyonidae Mephitidae Hyaenidae Ursidae Viverridae Herpestidae and Felidae Phocids also infected with CDV Pinnipeds sea otters and cetaceans susceptible to closely related viruses eg PDV PMV and DMV Additionally CDV disease has been confirmed in primates marmots tayassuids tamandua and sloths Mustelids are exquisitely susceptible with mortality approaching 100 Causative organism Canine distemper virus Singlestranded enveloped RNA virus within the family Paramyxoviridae subfamily Paramyxovirinae and genus Morbillivirus Related to measles rinderpest and peste des petits ruminants Zoonotic potential No Some correlation with human diseases and growing concern with the mutability and changing epidemiology of CDV Distribution Worldwide Incubation period 718 days in domestic dogs Variable with species and across individuals but estimated 1 week to 1 month Clinical signs Signs associated with respiratory gastrointestinal integumentary ophthalmic and the central nervous systems are commonly seen Which systems isare affected depends on species as well as strain virulence and environmental conditions Animals are often depressed with mucopurulent oculonasal exudates Nasal and digital hyperkeratosis hard pad and involuntary muscle twitching are characteristic in domestic dogs Acute conjunctivitis and occasionally uveitis but in less severe cases keratoconjunctivitis sicca and chorioretinal lesions are common Differential diagnoses must include rabies and other viral encephalitides respiratory infections toxoplasmosis canine parvovirus lead poisoning and bacterial enteritides Post mortem gross or histologic findings Most significant gross lesions are pneumonia depletion of lymphopoietic organs and hyperkeratosis of the nose foot pads and eyelids Common histologic findings are hyperkeratosis of the nose foot pads and eyelids Eosinophilic inclusion bodies are present in many organs most commonly cytoplasmic but occasionally intranuclear including the CNS urinary bladder and bronchial epithelium Cytoplasmic inclusion bodies in the gastric mucosa and bile ducts and diffuse interstitial giant cell pneumonia often followed by suppurative bronchopneumonia Often lymphoid depletion diffuse interstitial pneumonia and perivascular lymphoplasmacytic infiltration in areas of demyelination and neuronal degeneration of the CNS Syncytial giant cells in the lungs and CNS white matter anterior uvea and lymph nodes may also be present In contrast to histologic lesions identified in the domestic dog lungs of large felids may show diffuse alveolar type 2 cell hyperplasia with intracytoplasmic and intranuclear viral inclusion American Association of Zoo Veterinarians Infectious Disease Manual CANINE DISTEMPER VIRUS bodies Additionally feline brain histopathology may lack the typical canid pattern of demyelination with astrocytosis and vascular cuffing Most cats have had mild patchy CNS lesions compared with those of canids Diagnosis Clinical signs especially hyperkeratosis of foot pads and nose and myoclonus are highly suggestive of CDV Clinical pathologic changes including absolute lymphopenia thrombocytopenia regenerative anemia decreased albumin and increased alpha and gamma globulin concentrations may be present Cytologic evaluation andor immunofluoresence of conjunctival scrapes buffy coat smears CSF skin or foot pads may also demonstrate intracytoplasmic inclusion bodies Paired sera by viral neutralization or the indirect fluorescent antibody test to show a fourfold rise in antibody titer may be of value although often unrewarding as many animals die before building measurable antibody titers Antibodies in CSF may be more diagnostic than serum Newer ELISAs have been developed to detect IgM and IgG antibodies allowing determination of recent infection or vaccination Material required for laboratory analysis Unfixed lung liver lymph nodes brain and spleen of dead animals with suspected CDV infection should be collected for viral isolation fluorescent antibody andor RT PCR RTPCR assays are the test of choice for antemortem testing on oral swabs blood skin biopsies or urine samples Immunohistocytochemistry on formalinfixed tissues or FA on frozen sections provides definitive evidence of CDV infection Vaccine virus may be differentiated from street virus by different target cell susceptibility but sequencing of PCR products is the most definitive test to differentiate between vaccine and wild type viruses Relevant diagnostic laboratories In the US the Animal Health Diagnostic Center at Cornell Michigan State Diagnostic Laboratory and Colorado State Diagnostic Laboratory all routinely perform diagnostic tests for CDV In Canada biomaterials can be sent to Ontario Veterinary College Other provincial laboratories in Canada should also be able to run CDV diagnostics Treatment No specific therapy for animals with clinical canine distemper is available Nonspecific treatment is supportive and includes fluids antibiotics for secondary bacterial infections and medications to minimize CNS inflammation and seizure activity Prevention and control Vaccination is the mainstay of prevention In nondomestic species recombinant vaccines are the safest Exclusion of reservoir species from zoo sites whenever possible is important Quarantine all animals suspected of being infected with CDV Paired CDV titers should be used to monitor potentially naïve carnivores particularly when in quarantine before putting with others or with breeding females to enhance pup titers Suggested disinfectant for housing facilities CDV being an enveloped virus is fairly labile in the environment Extremely susceptible to ultraviolet light heat desiccation and common disinfectants eg formaldehyde ether chloroform phenolic compounds and quaternary ammonium compounds Notification None required Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Maintain infected animal in a quarantine situation until asymptomatic May be necessary to cull animals with residual CNS complications Conditions for restoring diseasefree status after an outbreak Clean infected environment with any of the common disinfectants Vaccination of susceptible species is imperative Vaccines available are modified live MLV killed and recombinant MLV in species safe to vaccinate and probably promotes lifelong immunity but many vaccinal or vaccineinduced infections have resulted from MLV vaccines in wildlife species Currently the Purevax Canine Distemper Merial recombinant vaccine is recommended for nondomestic carnivore species but other products Recombitek C3 by Merial have been used in zoological species but often multivalent and use may not be indicated in some species Experts who may be consulted Edward J Dubovi PhD Animal Health Diagnostic Center Director Virology Section American Association of Zoo Veterinarians Infectious Disease Manual CANINE DISTEMPER VIRUS College of Veterinary Medicine at Cornell Ithaca NY 14853 Phone 6072533923 Cell 6075920575 ejd5cornelledu Jean Paré DMV DVSc DACZM Global Health Program Wildlife Conservation Society 2300 Southern Boulevard Bronx New York 10460 Phone 7187411174 Fax 7182207126 jparewcsorg References 1 Deem SL Spelman LH Yates RA Montali RJ A review of canine distemper virus in terrestrial mammals J Zoo Wildl Med 2000 31441451 2 Greene CE Appel MJ Canine Distemper In Greene CE ed Infectious diseases of dogs and cats Philadelphia PA WB Saunders 1998 p 922 3 Kennedy S Morbillivirus infections in aquatic mammals J Comp Pathol 1998 119201225 4 Lunardi M Molinari Darold G Mendes Amude A Arlington Headley S Sonne L Cristiane Ito Yamauchi K Marques Boabaid F Fernandes A Alcindo Alfieri A Canine distemper virus active infection in order Pilosa family Myrmecophagidae species Tamandua tetradactyla Vet Micro 2018220 711 5 Meli ML Simmler P Cattori V Martínez F Vargas A Palomares F LópezBao JV Simón MA López G LeónVizcaino L HofmannLehmann R Lutz H Importance of canine distemper CDV in freeranging Iberian lynxes Lynx pardinus Vet Microbiol 2010146 132137 6 Origgi FC Plattet P Sattler U Robert N Casaubon J Mavrot F Pewsner M Wu N Giovannini S Oevermann A Stoffel MH Gaschen V Segner H RyserDegiorgis MP Emergence of canine distemper virus strains with modified molecular signature and enhanced neuronal tropism leading to high mortality in wild carnivores Vet Path 201249691329 7 Origgi FC Sattler U Pilo P Waldvogel AS Fatal combined infection with canine distemper virus and orthopoxvirus in a group of Asian marmots Marmota caudate Vet Path 2013505914920 8 Qiu W Zheng Y Zhang S Fan Q Liu H Zhang F Wang W Liao G Hus R Canine distemper outbreak in rhesus monkeys China Emerg Inf Dis 20111715411543 9 RoelkeParker ME Munson L Packer C Kock R Cleaveland S Carpenter M OBrien SJ Pospischil A HofmannLehmann R Lutz H Mwamengele GLM Mgasa MN Machange GA Summers B Appel MJG A canine distemper virus epidemic in Serengeti lions Panthera leo Nature 1996379441445 10 Sheldon JD Cushing AC Wilkes RP Anis E Dubovi E Serologic response to canine distemper vaccination in captive Linnaeuss twotoed sloths Choloepus didactylus after a fatal canine distemper virus outbreak J Zoo Wildl Med 201748412501253 11 Williams ES Canine distemper In Williams ES Baker IK eds Infectious Diseases of Wild Mammals Ames IA Iowa State University Press 2001 p 5059 American Association of Zoo Veterinarians Infectious Disease Manual Chrysosporium anamorph of Nannizziopsis vriesii Nannizziopsis Paranannizziopsis and Ophiodiomyces ophidiicola Under reclassification Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Reptiles Direct Indirect via fomites and environmental contamination Variable dermatitis Cellulitis and edema may be present Internal organ invasion with O ophidiicola Mild to severe but high mortality is possible Itraconazole Voriconazole Terbinafine nebulization SQ implants injection Proper disinfection of housing areas avoid contaminated fomites prevent contact with infected animals No direct transmission from animals reported but humans can be infected Fact Sheet compiled by E Marie Rush Sheet completed on updated 1 May 2018 Fact Sheet Reviewed by Bonnie Raphael Tim Georoff Susceptible animal groups Reptiles Causative organism Nannizziopsis spp Ophidiomyces spp Paranannizziopsis spp Formerly this grouping was Chrysosporium anamorph of Nannizziopsis vriesii CANV fungus Recent taxonomic publications have identified new epidemiological information about these fungi grouped under the CANV appellation While Nannizziopsis vriesii does produce a Chrysosporium anamorph in culture all CANVlike isolates differ so that an overarching CANV appellation is discouraged For example the CANV isolates that caused fatal disease in tentacled snakes have been reclassified as two species of Paranannizziopsis which has not been isolated from other reptile species Paranannizziopsis includes four species that infect squamates and tuataras Ophidiomyces belonging to the Order Onygenales is a potent pathogen of snakes and associated with Snake Fungal Disease but it has not yet been recovered from ill lizards or crocodiles so may not be a threat to these taxa Nannizziopsis guarroi is the main causative agent of Yellow Fungus Disease a common infection in bearded dragons green iguanas and other lizards Classically dermatomycoses in reptiles are linked with stress and substandard husbandry in captive animals however experimental challenge of veiled chameleons Chamaeleo calyptratus with Nannizziopsis dermatitidis confirmed the organism can act as a primary pathogen Zoonotic potential While it is not directly transmitted from animals to humans infection has been reported in two human cases where preexisting immunosuppression was present There are multiple subspecies of reptile infective organisms Human species of these organisms have not been recovered in reptiles Distribution Worldwide Incubation period 25 weeks Clinical signs Infection is often through a breach in the skin Ophidiopmyces is the likely causative agent of Snake Fungal Disease however the two have not always been found in tandem Slow progression occurs from dry hyperkeratotic plaques or vesicles to exudative lesions with excessive crusting that may later darken and slough Snakes with Ophidiomyces may have increased ecdysis frequency abnormal resting in areas of the enclosure and anorexia Skin may have fissures or thickening and upon pressure or incision into these areas exudate may be expelled Cellulitis can present concurrently In advanced disease general debilitation of the animal may be noted and deeper tissues including muscle and bone become affected Hemogram and chemistry panels may be normal during this infection In pygmy rattlesnakes corticosterone levels were proportionately increased in direct correlation with severity of clinical SFD recapture decreased reproduction in females and decreased body condition score Clinical signs correlated American Association of Zoo Veterinarians Infectious Disease Manual Chrysosporium anamorph of Nannizziopsis vriesii Nannizziopsis Paranannizziopsis and Ophiodiomyces ophidiicola Under reclassification with decreased environmental temperatures have been established for SFD Paranannizziopsis australasiensis has been reported in a tuatara with clinical signs and positive testing on PCR Post mortem gross or histologic findings Initially there will be hyphae proliferating in the epidermis stratum corneum with subsequent deeper invasion in most cases Progression to liquefactive necrosis of the epidermis with or without granulomatous inflammation of the dermis is noted over time Terminal chains of arthroconidia may be seen on hyphae and with Ophidiomyces granulocytic change at sites of microinvasion Diagnosis Clinical signs are suggestive Fungal culture of the organism on Mycosel Agar with incubation at 2528C Histopathology can be performed PAS stained sections of tissues will reveal hyphae in the keratin layer epidermis dermis and occasionally skeletal muscle layers depending on severity of disease Fungus can be identified by PCR Although Taqman RT PCR and PCR are considered the most sensitive and specific of the diagnostic tests not all tissues may be positive even if grossly visible lesions are present In a study with O ophiodiicola 98 of culture positive and 40 of culture negative snakes were found to be positive on RTPCR Of these snakes 20 showed clinical signs and 16 had no clinical signs of infection This study suggests that some asymptomatic snakes 6 may harbor low levels of fungus and PCR paired with histopathology is recommended for definitive diagnosis Massasaugas in Illinois with Ophiodiomyces showed changes in WBC counts lymphocytes and basophils noted retrospectively over peak years Material required for laboratory analysis Frozen and formalinfixed representative tissue samples from multiple organ systems including skin muscle and bone of necropsy specimens Biopsies from live animals should be divided and submitted chilled for culture and fixed for histopathology Relevant diagnostic laboratories Most diagnostic laboratories are capable of culturing of this organism Preemptive contact with microbiologist prior to sample submission greatly increases the chance of diagnosis Treatment Itraconazole and voriconazole can be used systemically Terbinafine 10mgkg PO SID x 7 days pulse repeat Q3wk until oneweek past resolution of signs pulsed with itraconazole or voriconazole In a study with timber rattlesnakes and massasaugas voriconazole via SQ pump led to adequate levels in timber rattlesnakes but not massasaugas Levels post injection in cottonmouths were maintained for 1224 hours Cloacal administration in cottonmouths did not reach adequate levels and several snakes died after a single injection without further treatment In cottonmouths terbinafine reached peak concentrations at 054 hours post nebulization and on day 1using subcutaneous implants which maintained therapeutic levels for over 6 weeks Although topical disinfection of skin lesions with chlorhexidine solution may be helpful alone it is not likely to be successful so combined approach is needed Cutaneous lesions can be debrided aggressively along with topical antifungal and antibacterial dressings Mycetomas should be considered for surgical excision in addition to systemic treatment Prognosis for deeper structure involvement eg bone is guarded to poor Prevention and control Optimization of husbandry conditions is critical for most reptiles to prevent disease as the problem is exacerbated by suboptimal husbandry Housing areas should be thoroughly disinfected between individuals and any porous material from the enclosures should be discarded if unable to be sterilized or properly disinfected ie substrate drift wood furniture etc Proper quarantine measures for new animals should be followed Separation of infected animals from healthy animals should be done until infection is completely cleared based on biopsies and culture Suggested disinfectant for housing facilities Bleach and chlorhexidine for CANV For Ophidiomyces 3 bleach for at least 2 minutes 70 ethanol 016 RoccalD for 10 minutes Lysol products CLR bath and kitchen cleaner 510 lactic acid Process NPD or Formula 409 household cleaners Chlorhexidine Simple Green and spectracide are NOT effective for Ophidiomyces Ten minutes of contact time is recommended for most cleaners to reach optimal spore removal Notification None required American Association of Zoo Veterinarians Infectious Disease Manual Chrysosporium anamorph of Nannizziopsis vriesii Nannizziopsis Paranannizziopsis and Ophiodiomyces ophidiicola Under reclassification Measures required under the Animal Disease Surveillance Plan None required Measures required for introducing animals to infected animal It is not recommended to introduce non infected animals to infected animals until confirmation that infection is completely cleared based on culture of biopsy of the originally affected areas Conditions for restoring diseasefree status after an outbreak It must be assured no residual carrier animals in remaining group of animals Experts who may be consulted Jean A Paré DMV DVSc DACZM Associate Veterinarian Global Health Program Wildlife Conservation Society 2300 Southern Boulevard Bronx NY 10460 USA Tel 7187411174 Fax 7182207126 Email jparewcsorg Matt Allender DVM MS PhD Dipl ACZM Director Wildlife Epidemiology Lab Assistant Professor College of Veterinary Medicine University of Illinois 3846 VMBSB 2001 S Lincoln Ave Urbana IL 61802 Tel 2172650320 Email mcallendillinoisedu References 1 Abarca ML Martorell J Castellá G Ramis A Cabañes FJ Cutaneous hyalohyphomycosis caused by a Chrysosporium species related to Nannizziopsis vriesii in two green iguanas Iguana iguana Med Mycol 200846349354 2 Allender MC Hileman ET Moore J Tetzlaff S Detection of Ophidiomyces the causative agent of snake fungal disease in the eastern massasauga Sistrurus catenatus in Michigan USA 2014 J Wildl Dis 20165236948 3 Allender MC Phillips CA Baker SJ Wylie DB Narotsky A Dreslik MJ Hematology in an eastern massasauga Sistrurus catenatus population and the emergence of Ophidiomyces in Illinois USA J Wildl Dis 201652225869 4 Bertelsen MF Crawshaw GJ Sigler L Smith DA Fatal cutaneous mycosis in tentacled snakes Erpeton tentaculatum caused by the Chrysosporium anamorph of Nannizziopsis vriesii J Zoo Wildl Med 200536 8287 5 Bohuski E Lorch JM Griffin KM Blehert DS TaqMan realtime polymerase chain reaction for detection of Ophidiomyces ophiodiicola the fungus associated with snake fungal disease BMC Vet Res 20151195 6 Bowman MR Paré JA Sigler L Naeser JP Sladky KK Hanley CS Helmer P Phillips LA Brower A Porter R Deep fungal dermatitis in three inland bearded dragons Pogona vitticeps caused by the Chrysosporium anamorph of Nannizziopsis vriesii Med Mycol 200745 371376 7 Eatwell K Suspected fatal Chrysosporium anamorph of Nannizziopsis vriesii CANV dermatitis in an albino boa constrictor Constrictor constrictor J Small Anim Pract 2010515290 American Association of Zoo Veterinarians Infectious Disease Manual Chrysosporium anamorph of Nannizziopsis vriesii Nannizziopsis Paranannizziopsis and Ophiodiomyces ophidiicola Under reclassification 8 Franklinos LH Lorch JM Bohuski E Fernandez JR Wright ON Fitzpatrick L Petrovan S Durrant C Linton C Baláž V Cunningham AA Emerging fungal pathogen Ophidiomyces ophiodiicola in wild European snakes Sci Rep 2017191713384 9 Guthrie AL Knowles S Balimann AE Lorch JM Detection of snake fungal disease due to Ophidiomyces ophiodiicola in Virginia USA J Wildl Dis 20165211439 10 Hellebuyck T Baert K Pasmans F Van Waeyenberghe L Beernaert L Chiers K De Backer P Haesebrouck F Martel A Cutaneous hyalohyphomycosis in a girdled lizard Cordylus giganteus caused by the Chrysosporium anamorph of Nannizziopsis vriesii and successfully treated with voraconizole Vet Derm 2010214429433 11 Hill AJ Leys JE Bryan D Erdman FM Malone KS Russell GN Applegate RD Fenton H Niedringhaus K Miller AN Allender MC Common cutaneous bacteria isolated form snakes inhibit growth of Ophidiomyces ophiodiicola Ecohealth 2018151109120 12 Humphrey S Alexander S Ha HJ Detection of Paranannizziopsis australasiensis in tuatara Sphenodon punctatus using fungal culture and a generic fungal PCR N Z Vet J 2016645298 300 13 Johnson RS Sangster CR Sigler L Hambleton S Paré JA Deep fungal dermatitis caused by the Chrysosporium anamorph of Nannizziopsis vriesii in captive coastal bearded dragons Pogona barbata Aust Vet J 20118912515519 14 Johnson DH An emerging dermatomycosis and systemic mycosis syndrome in bearded dragons Exotic DVM 2004637577 15 Kane LP Allender MC Archer G Leister K Rzadkowska M Boers K Souza M Cox S Pharmacokinetics of nebulized and subcutaneously implanted terbinafine in cottonmouths Agkistrodon piscivorus J Vet Pharmacol Ther 2017405575579 16 Last LA Fenton H GonyorMcGuire J Moore M Yabsley MJ Snake fungal disease caused by Ophidiopmyces ophiodiicola in a freeranging mud snake Farancia abacura J Vet Diagn Invest 2016286709713 17 Lind CM McCoy CM Farrell TM Tracking outcomes of snake fungal disease in freeranging pygmy rattlesnakes Sistrurus miliarius J Wildl Dis 2018542352356 18 Lind C Moore IT Akçay Ç Vernasco BJ Lorch JM Farrell TM Patterns of circulating corticosterone in a population of rattlesnakes afflicted with snake fungal disease stress hormones as a potential mediator of seasonal cycles in disease severity and outcomes Physiol Biochem Zool 2018912765775 19 Lindemann DM Allender MC Rzadkowska M Archer G Kane L Baitchman E Driskell EA Chu CT Singh K Hsiao SH and Sykes IV JM Pharmacokinetics efficacy and safety of voriconazole and itraconazole in healthy cottonmouths Agkistrodon piscivorus and massasauga rattlesnakes Sistrutus catenatus with snake fungal disease J Zoo Wildl Med 2017483757766 20 Lorch JM Knowles S Lankton JS Michell K Edwards JL Kapfer JM Staffen RA Wild ER Schmidt KZ Ballmann AE Blodgett D 2016 Snake fungal disease an emerging threat to wild snakes Philos Trans R Soc Lond B Biol Sci 20163711709 21 Lorch JM Lankton J Werner K Falendysz EA McCurley K Blehert DS Experimental infection of snakes with Ophidiomyces ophiodiicola causes pathological changes that typify snake fungal disease MBio 201566 22 McCoy CM Lind CM Farrell TM Environmental and physiological correlates of the severity of clinical signs of snake fungal disease in a population of pygmy rattlesnakes Sistrurus miliarus Conserv Physiol 201751 23 Mitchell MA Walden MR Crysosporium anamorph Nannizziopsis vriesii an emerging fungal pathogen of captive and wild reptiles Vet Clin North Am Exot Anim Pract 201316365968 American Association of Zoo Veterinarians Infectious Disease Manual Chrysosporium anamorph of Nannizziopsis vriesii Nannizziopsis Paranannizziopsis and Ophiodiomyces ophidiicola Under reclassification 24 Nichols DK RS Weyant EW Lamirande L Sigler and RT Mason 1999 Fatal mycotic dermatitis in captive brown tree snakes Boiga irregularis J Zoo Wildl Med 30 111118 25 Ohkura M RR Fitak JH Wisecaver et al 2017 Genome sequence of Ophidiomyces ophiodiicola an emerging fungal pathogen of snakes Genome Announc Jul 27530 26 Ohkura M JJ Worley JE HughesHallett et al 2016 Ophidiomyces ophiodiicola on a captive black racer Coluber constrictor and a garter snake Thamnophis sirtalis in Pennsylvania J Zoo Wildl Med Mar4713416 27 Paré JA and L Sigler 2016 An overview of reptile fungal pathogens in the Genera Nannizziopsis Paranannizziopsis and Ophidiomyces J Herp Med Surg 26124653 28 Paré J and ER Jacobson 2007 Mycotic diseases of reptiles In Jacobson ER ed Infectious Diseases and Pathology of Reptiles CRC Press Boca Raton Florida Pp 527570 29 Paré JA KA Coyle L Sigler AK Maas III and RL Mitchell 2006 Pathogenicity of the Chrysosporium Anamorph of Nannizziopsis vriesii for veiled chameleons Chamaeleo calyptratus Med Mycol 44 2531 30 Paré JA L Sigler KL Rosenthal and DR Mader 2006 Microbiology fungal and bacterial diseases of reptiles In Mader DR ed Reptile Medicine and Surgery 2nd ed Saunders Elsevier St Louis Missouri Pp 217238 31 Paré JA L Sigler KL Rypien and CFC Gibas 2003 Cutaneous mycobiota of captive squamate reptiles with notes on the scarcity of Chrysosporium anamorph of Nannizziopsis vriesii J Herpetol Med Surg 13 1015 32 Paré JA L Sigler DB Hunter RC Summerbell DA Smith and KL Machin 1997 Cutaneous mycoses in chameleons caused by the Chrysosporium anamorph of Nannizziopsis vriesii Apinis Currah J Zoo Wildl Med 28 443453 33 Picquet P KO Heckers E Kolesnik A Heusinger and RE Marchang Detection of Ophidiomyces ophiodiicola in two captive Bocourt water snakes Subsessor bocourti and one captive Pueblan mild snake Lampropeltis trangulum campbelli 2018 J Zoo Wildl Med Mar491219222 34 Robertson J SK Chinnadurai DB Woodburn MJ Adkesson and JA Landolfi 2016 Disseminiated Ophidiomyces ophiodiicola infection in a captive eastern Massasauga Sistrurus catenatus catenatus J Zoo Wildl Med Mar47133740 35 Rzadkowska M MC Allender M ODell and C Maddox 2016 Evaluation of common disinfectants effective against Ophidiomyces ophiodiicola the causative agent of snake fungal disease J Wildl Dis Jul52375962 36 Sigler L S Hambleton S and JA Paré Molecular characterization of reptile pathogens currently known as members of the Chrysosporium anamorph of Nannizziopsis vriesii complex and relationship to some human associated isolates 2013 J Clin Microbiol Oct5110333857 37 Steininger C J van Lunzen K Tintelnot I Sobottka H Rohde M Ansver Horstkotte and HJ Stellbrink 2005 Mycotic brain abscess caused by opportunistic reptile pathogen Emerg Infect Dis 11 349350 38 Thomas A D L Sigler S Peucker JH Norton and A Nielan 2002 Chrysosporium anamorph of Nannizziopsis vriesii associated with fatal cutaneous mycoses in the saltwater crocodile Crocodylus porosus Med Mycol 40 143151 39 Toplon DE SP Terrell L Sigler and ER Jacobson 2013 Dermatitis and cellulitis in leopard geckos Eublepharis macularius caused by the Chrysosporium anamorph of Nannizziopsis vriesii Vet Pathol 504 5859 40 Van Waeyenberghe L K Baert F Pasmans P van Rooij P T Hellebuyck L Beernaert P de Backer F Haesebrouck and A Martel 2010 Voriconazole a safe alternative for treating infections American Association of Zoo Veterinarians Infectious Disease Manual Chrysosporium anamorph of Nannizziopsis vriesii Nannizziopsis Paranannizziopsis and Ophiodiomyces ophidiicola Under reclassification caused by the Chrysosporium anamorph of Nannizziopsis vriesii in bearded dragons Pogona vitticeps Med Mycol 486 880885 American Association of Zoo Veterinarians Infectious Disease Manual CAPRINE ARTHRITISENCEPHALITIS Fact Sheet compiled by Andrea Goodnight Sheet completed on 15 April 2011 updated 21 July 2013 Fact Sheet Reviewed by Kimberly Rainwater Eric Klaphake Susceptible animal groups Domestic goats and more common in dairy goat breeds Domestic sheep may be infected and nonclinical but possibly carriers Causative organism Caprine arthritisencephalitis virus CAEV is a small ruminant Lentivirus in the family Retroviridae that is related closely to OPP and MaediVisna viruses of sheep and diagnostically difficult to differentiate Zoonotic potential None Distribution Worldwide more prevalent in herds with animals imported from longestablished dairy herds US Canada Europe up to 80 seroprevelance especially in longestablished dairy herds Southern Africa relatively free of CAE Incubation period Seroconversion occurs in 28 weeks but disease may be clinically latent for years Once an animal is infected it remains infected for life Clinical signs Five syndromes Arthritis Chronic goats 6 mo of age progressive lameness Swelling of carpal joints most common and preferentially may affect hocks stifles hips and atlantooccipital joints Radiographs show soft tissue swelling and periarticular calcification Leukomyeloencephalitis Typically kids 14 mo of age but may be seen in adults ataxia progressing to tetraparesis blindness head tilt facial paralysis opisthotonos may occur Clinical course 12 weeks Very poor prognosis for recovery Interstitial pneumonia chronic more common in adults Mastitis interstitial hard udder hypogalactia or agalactia around parturition in young does Chronic wasting poor body condition rough hair coat Post mortem gross or histologic findings Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Goats Vertical Infected colostrum or milk Possibly in utero or during parturition Horizontal Aerosolization Unsanitary milking practices Possible venereal transmission Progressive lameness Neurologic signs Interstitial pneumonia Mastitis Chronic weight loss animals may have one or more forms of the disease Asymptomatic carrier state to chronic debilitating arthritis Rapidly progressing neurologic disease Supportive care Analgesics Antibiotics for 2o infections Quarantine or cull infected animals Serologic testing of herd every 6 months beginning at 6 months of age No American Association of Zoo Veterinarians Infectious Disease Manual CAPRINE ARTHRITISENCEPHALITIS Arthritis thickened joint capsule periarticular mineralization chronic proliferative synovitis with subsynovial mononuclear infiltrates Leukomyeloencephalitis increased protein concentration in CSF with mononuclear pleocytosis Asymmetrical foci of discoloration in the brain andor spinal cord Widespread perivascular infiltration by mononuclear cells Coagulative necrosis and demyelination of white matter Interstitial pneumonia nodular lymphoid aggregates proliferation of smooth muscle massive infiltration of the alveolar walls by lymphoid cells Mastitis Inflammatory cell foci within interstitium Extensive nodular lymphoid proliferation can be observed around the alveolar ducts In chronic cases inflammatory cells and connective tissue replace the normal parenchyma Diagnosis Clinical signs CAEV history in herd Serology ELISA or AGID PCR synovial fluid analysis redbrown color with low viscosity increased cell count with the majority mononuclear cells lymphocytes synovial biopsy for histopathology Positive test results in kids 90 days old usually reflect colostral antibody transfer However negative test results do not reliably rule out CAE virus infection because the time for postinfection seroconversion is variable and occasional goats have a very low titer that may not be detectable Low antibody titers are common in late pregnancy Material required for laboratory analysis ship samples cool on ice serum 2 ml whole blood in EDTA 5 mL Relevant diagnostic laboratories National Veterinary Services Laboratories NVSL ELISA and AGID 1920 Dayton Avenue Ames Iowa 50010 USA Tel 515 3377266 Email NVSLConcernsaphisusdagov Website httpwwwaphisusdagovanimalhealthlabinfoservicesdiagnostestsshtml Washington Animal Disease Diagnostic Laboratory WADDL cELISA Bustad Hall Room 155N Pullman Washington 99164 USA Tel 509 3359696 Email waddlvetmedwsuedu Website httpwwwvetmedwsuedudeptswaddlindexaspx Colorado State University Veterinary Diagnostic Laboratory PCR AGID cELISA 200 West Lake Street 1644 Campus Delivery Fort Collins Colorado 80526 USA Tel 970 2970320 Email dlabcolostateedu Website httpwwwdlabcolostateeduwebdocsservicesindexhtm Treatment Supportive care with analgesics NSAIDs physical therapy antibiotics and antifungas for secondary infections Antiviral medications may lessen severity and slow progression of disease but are not routinely used Frequent proper foot trimming soft bedding good pasture management Prevention and control Quarantine or cull affected and seropositive animals Remove kids from affected dams immediately after parturition and feed heattreated 56oC colostrum and feed kids pasteurized goats milk milk from CAEVnegative goats or milk replacer Caesarean section may help prevent vertical transmission Chemical disinfection of equipment Serologic testing of herd recommended every 6 mo beginning with kids at 6 mo of age American Association of Zoo Veterinarians Infectious Disease Manual CAPRINE ARTHRITISENCEPHALITIS Suggested disinfectant for housing facilities Phenolic and quaternary ammonium compounds Notification Reportable for disease monitoring to the World Organisation for Animal Health OIE USDA APHIS and many state veterinarians Measures required under the Animal Disease Surveillance Plan None required Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak No seropositive animals remaining in herd after two successive testing periods Testing performed twice yearly Hand raise newborn kids on colostrummilk from unadulterated source Experts who may be consulted Dr James Evermann Washington Animal Disease Diagnostic Lab Pullman Washington 99164 USA Tel 509 3353044 Email jfevetmedwsuedu Dr Donald P Knowles Animal Diseases Research Unit USDAARS College of Veterinary Medicine Washington State University 3003 ABBF Pullman Washington 99164 USA Tel 509 3356001 Email dknowlesvetmedwsuedu Dr Stephen Valas Laboratoire de Niort Laboratoire détude et de recherches caprines 60 rue du Pied de Fond BP 3081 79000 Niort FRANCE Tel 33 05 49796128 Fax 33 05 49794219 Email stephenvalasansesfr References 1 Bertoni G 2007 Caprine arthritis encephalitis complex In Tempesta M Ed Recent Advances in Goat Diseases International Veterinary Information Service Ithaca NY http wwwivisorg Accessed 15 April 2011 2 Cebra C and Cebra M 2002 Caprine arthritisencephalitis virus infection In Pugh D G ed Sheep and Goat Medicine WB Saunders Co Philadelphia Pennsylvania Pp 388389 3 Logan S H L Tarpley K S and Lattimer 2004 Caprine arthritisencephalitis virus httpwwwvetugaeduVPPclerkloganindexphp Accessed 15 April 2011 4 Reilly L K A N Baird and D G Pugh 2002 Caprine arthritisencephalitis In Pugh D G ed Sheep and Goat Medicine WB Saunders Co Philadelphia Pennsylvania Pp 239240 5 Rowe J D and N E East 1997 Risk factors for transmission and methods for control of caprine arthritisencephalitis virus infection Vet Clin North Am Food Anim Pract 13 3553 6 Smith M C and D M Sherman 2009 Caprine arthritis encephalitis In Goat Medicine 2nd ed WileyBlackwell Ames Iowa Pp 8803 American Association of Zoo Veterinarians Infectious Disease Manual CAPRINE ARTHRITISENCEPHALITIS 7 Washington Animal Disease Diagnostic Lab 2011 Caprine Arthritis Encephalitis CAE Virus httpwwwvetmedwsuedudeptswaddlcaefaqaspx Accessed 3 March 2013 8 httpwwwaphisusdagovanimalhealthemergingissuesdownloadsprcaevinfosheetpdf Accessed 16 July 2013 9 httpwwwmerckmanualscomvetgeneralizedconditionscaprinearthritisandenchph alitisoverviewofcaprinearthritisand encephalitishtml Accessed 3 March 2013 American Association of Zoo Veterinarians Infectious Disease Manual ENZOOTIC ABORTION OF EWESOVINE ENZOOTIC ABORTION Chlamydophila abortus Fact Sheet compiled by Denise McAloose Sheet completed on 13 January 2011 updated 26 March 2013 Fact Sheet Reviewed by Bonnie Raphael Carlos Rodriguez Susceptible animal groups Sheep goat Causative organism Chlamydophila abortus previously Chlamydia psittaci serotype 1 is the causative Gram negative intracellular bacterium and has two genera and 9 species Antigenic strains in sheep and goat appear to be related Antigenic type 1 is implicated in abortion stillbirth and the birth of weak offspring Zoonotic potential Yes and it can cause serious infection in pregnant women and lead to miscarriage Pregnant women are discouraged from having contact with the flock during lambingkidding season In non pregnant humans infection can produce flulike symptoms Distribution Worldwide distribution Incubation period Infection occurs through ingestion Organisms colonize the intestinal tract invade the bloodstream and subsequently infect the placenta and developing fetus Incubation can be as short as 2 weeks although typically proliferation of the organism occurs at about day 90 of gestation Infection is latent in lambs and nonpregnant ewes and becomes activated at conception Clinical signs Nonspecific malaise in dam may be seen Abortion stillbirth or birth of weak offspring does occur Final trimester abortions occur in ewes infected at 56 weeks gestation abortion in the subsequent pregnancy occurs in ewes that were infected after this time Abortion can occur at any time during gestation for goats In both species retained placenta can occur The infection in rams may cause orchitis Post mortem gross or histologic findings Gross Placental tissues contain multifocal to coalescing areas of red discoloration and edema tissues can have a leathery appearance Changes are typically diffuse but more significant changes may be noted in the Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Sheep and goat less commonly cattle pigs horses and deer Oral transmission Organism shed in aborted fetuses placenta vaginal secretions during estrus and up to 9 days prior to and weeks to months post abortion and in infected semen Birds ie pigeons and sparrows may be reservoirs Can see nonspecific malaise in pregnant animals Late term abortions stillbirths and birth of weak offspring Can see high rate of abortion 30 in naïve flock or yearly rates up to 5 in enzootic form Abortion storms can be seen in intensively managed flocks Tetracycline or oxytetracycline Supportive care for complications of infection such as retained placenta metritis pneumonia or kerato conjunctivitis Remove infected or contaminated materials Keep feed sources free of fecal material Separate first lambing ewes from rest of flock Animals that abort develop natural immunity 3 year duration Vaccination Yes American Association of Zoo Veterinarians Infectious Disease Manual ENZOOTIC ABORTION OF EWESOVINE ENZOOTIC ABORTION Chlamydophila abortus cotyledonary than intercotyledonary areas The aborted fetus is often well preserved although can be autolyzed it may have multifocal areas of hemorrhage in muscle lymphoid tissues and the subcutis andor pinpoint yellow areas of discoloration on the surface of the liver Histology Placental changes are characterized by fibrinoid vascular necrosis thrombosis and severe neutrophilic placentitis with superficial necrosis of the chorion Trophoblasts often contain numerous intracytoplasmic organisms that distend the cells are difficult to see with routine hematoxylineosin staining and are positive with special staining using a modified ZiehlNeelsen Gimenez or Giemsa stain Changes in the aborted fetus are few and characterized by foci of coagulative necrosis in the liver and spleen that may be associated with peripheral mononuclear cell inflammation Mild subacute inflammation can also be seen in the lungs and mild meningoencephalitis has also been reported Diagnosis History of abortion provides suspicion to perform testing Serology Complement fixation tests can present some cross reactivity and doesnt distinguish between vaccination and natural infection so should be paired at 23 weeks apart High and rising titers in ewes and fetal serum antibodies aid in diagnosis of disease Tissue sections Histology electron microscopy Special staining Positive staining of organisms with modified ZiehlNeelsen Gimenez or Giemsa in cytologic preparations or placentitis confirmed histologically with intralesionalintracellular positive organisms alternatively can try to id organism on cytology of vaginal swab Immunologic tests ELISA IHC FA Definitive diagnosis PCR and realtime PCR PCR microarray hybridization indirect inclusion fluorescent antibody test immunohistochemical staining tissue culture or egg inoculation Material required for laboratory analysis Placenta preferred or fetus Fresh tissue for cytologic preps 10 neutral buffered formalin fixed paraffin embedded FFPE tissue for histology or immunohistochemical staining fresh or FFPE for PCR contact laboratory for tissue storagefixation for fluorescent antibody test Vaginal swab For cytology or culture Serum C abortus antibodies are confirmatory in the fetus paired titers used diagnostically in adults Relevant diagnostic laboratories Any laboratory capable of bacteriologic culturing is capable of diagnosing C abortus National Veterinary Services Laboratories NVSL PO Box 844 1920 Dayton Ave Ames IA 50010 5153377514 Treatment C abortus is sensitive to tetracyclines although sensitivity testing on cultured organism may aid treatment strategy In face of outbreak recommendations include treating all pregnant females during final 46 weeks of gestation For disease prevention two week treatment with tetracycline in feed 400 to 500 mgheadday in fiberproducing animals or injection of longacting oxytetracycline 20 mgkg IM or SC every 1014 days or twice a week treatment in the last 46 weeks gestation in dairy herds has been reported alternately can treat with one injection of longacting oxytetracycline 6 to 8 weeks prior to parturition and 3 weeks post parturition Prevention and control As high numbers of organisms are shed in aborted or stillborn fetuses and in infected placental tissues or uterine discharge and organisms remain viable for several days or longer in cold or freezing American Association of Zoo Veterinarians Infectious Disease Manual ENZOOTIC ABORTION OF EWESOVINE ENZOOTIC ABORTION Chlamydophila abortus temperatures isolate aborting dams and separate first lambing ewes from rest of flock Animals that abort develop natural immunity of 3 year duration Infected or contaminated materials should be removed and feed sources kept free of fecal material Pest control should be practiced as transmission can occur via rodent and birds Vaccination Live and inactivated vaccines are available for use in areas where vaccination is permitted vaccination reportedly can prevent abortion and reduce excretion can assist in control but will not eradicate it From Terrestrial Animal Health Code httpwwwoie Chapter 145 Prevention For importation for breeding International veterinary certificate ensuring 1 animal has been housed for previous two years or since birth in facility with no EAE positive tests for previous two years 2 no clinical signs of EAE on day of shipment 3 was test negative for EAE within 30 days of shipment For importation of semen International veterinary certificate ensuring donor animals 1 are from facilities that have been EAE test negative for previous two years and have not been in contact with animals of lower health status and were test negative for EAE for 23 weeks post semen collection and 2 an aliquot of the semen for export was culture negative for C abortus Control Separate first lambing ewes from rest of flock Segregate aborting animals from herd for minimum of 3 weeks burn or bury aborted materials disinfect the area Prevent contamination of food and water Control can also include culling of live kids born to infected dams Ewes that abort develop natural immunity to infection after the first abortion wanes after 3 years Vaccine is available and licensed in some countries One recommendation is for IM or SC vaccination 8 weeks prior to breeding and once again 4 weeks later though immunity is thought to be protective for 3 years annual boosters prior to breeding season are suggested Animals that abort develop natural immunity 3 year duration Note Immune or vaccinated animals can shed organism Suggested disinfectant for housing facilities Susceptible to disinfection with quaternary ammoniums Notification Reportable to State and Federal agencies in United States and to OIE Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak The following are requirements of the Terrestrial Animal Health Code httpwwwoie Chapter 14 1 Sheep flock or goat herd is under official veterinary surveillance 2 No sheep or goats have shown clinical evidence of infection for past 2 years 3 A statistically appropriate number of sheep goats 6 months of age were test negative for EAE within past 6 months 4 All sheep goats are permanently identified 5 No sheep goat additions since 30 days prior to test in 3 unless EITHER the additions were isolated from other animals in flockherd in the flockherd of origin for a minimum of 30 days and then were test negative for EAE prior to entry in the new flockherd OR the animal originated from a flockherd of equal health status Experts who may be consulted US Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Emergency Management 4700 River Road Unit 41 American Association of Zoo Veterinarians Infectious Disease Manual ENZOOTIC ABORTION OF EWESOVINE ENZOOTIC ABORTION Chlamydophila abortus Riverdale MD 207371231 Phone 3017348073 Fax 3017347817 References 1 Foster R 2007 Female reproductive system In Pathologic Basis of Veterinary Disease 4th ed Mosby Elsevier St Louis Mo Pp 1296 2 Matthews J 1999 Abortion In Diseases of the Goat 2nd ed Blackwell Science Ltd Osney Mead Oxford Pp 2236 3 Mobini S A M Heath and D G Pugh 2002 Theriogenology of Sheep In Sheep and Goat Medicine 1st ed Saunders Philadelphia Pennsylvania Pp 129186 4 Schlafer D H and R B Miller 2007 Female genital system In Maxie G ed Jubb Kennedy and Palmers Pathology of Domestic Animals 5th ed Elsevier Saunders Philadelphia Pennsylvania Pp 429564 5 World Organization for Animal Health 2012 Terrestrial Animal Health Code Chlamydophila Abortus Infection httpwwwoieintindexphpid169L0htmfilechapitre1145htm Accessed 23 July 2013 American Association of Zoo Veterinarians Infectious Disease Manual AVIAN CHLAMYDIOSISCHLAMYDOPHILOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Birds humans other mammals uncommon Inhalation of aerosolized fecal matter and nasal discharges primarily also oral secretions and feathers Fomites Mechanical transmission may occur rodents and insects Vertical transmission is infrequent Nonspecific oculonasal discharge respiratory signs conjunctivitis diarrhea weight loss anorexia depression green to yellow green urates Some birds may have subclinical infections Morbidity and mortality rates vary with the affected species condition of infected individual and straingenotype involved For most avian species Doxycycline for 3060 days See treatment section for details Screen and quarantine new birds Good hygiene practices PCR testing for antigen testing See Diagnosis section for details on other testing Yes Fact Sheet compiled by Danelle M Okeson Sheet completed on 22 July 2010 updated 8 October 2012 Fact Sheet Reviewed by Thomas N Tully Jr Robert D Dahlhausen Susceptible animal groups Birds reported in more than 30 orders of birds but more common in Psittaciformes and Columbiformes doves and pigeons It is sometimes seen in ducks and turkeys but rarely in chickens Some wild bird species may act as reservoirs and egrets and gulls can be subclinical carriers for strains that are highly virulent for other birds Humans and less commonly other mammals such as occasionally in dogs cats horses cattle sheep and muskrats Causative organism Chlamydophila Chlamydia psittaci Zoonotic potential Yes Distribution World wide Incubation period Birds 3 days to several weeks Some birds may remain subclinical until stressed Some birds may shed the infectious organism 10 days before clinical signs are observed Clinical signs Birds lethargy ruffled feathers anorexia oculonasal discharge conjunctivitis diarrhea weight loss Some birds may manifest respiratory signs ranging from sneezing to respiratory distress Neurologic signs such as tremors torticollis or leg paresis may be found in subacute to chronic cases Infected carriers may not have overt clinical signs Humans fever chills myalgia malaise nonproductive cough sometimes with chest tightness andor breathing difficulty sometimes a nonspecific rash and enlarged spleen are also present Other mammals linked to abortions in horses cattle and sheep variety of clinical disease presentations in dogs including respiratory and reproductive signs American Association of Zoo Veterinarians Infectious Disease Manual AVIAN CHLAMYDIOSISCHLAMYDOPHILOSIS Post mortem gross or histologic findings Nasal inflammation pneumonia fibrinous air sacculitis hepatomegaly with multifocal hepatic necrosis splenomegaly pericarditis Infected birds exhibiting no signs of illness often have no gross lesions Diagnosis Based on clinical signs a combination of antigen and antibody tests and clinical tests including hemogram chemistry panel and radiographs The Compendium of Measures to Control C psittaci lists case definitions for suspect probable and confirmed cases PCR testing may be performed on whole blood samples andor swabs of the choana or swabs of both the choana and cloaca Sensitivity is improved if both blood samples and swabs are tested Serology is available but results must be interpreted appropriately A positive serologic test result is evidence that the bird may have been exposed to C psittaci in the past but does not prove the bird is currently infected Conversely a negative serologic test result is not proof that the bird is free of infection The Direct Compliment Fixation test has been historically the most commonly used serology assay Material required for laboratory analysis Varies with type of testing see Diagnosis section Relevant diagnostic laboratories Several stateuniversity and private labs offer testing a few are listed below see individual labs for types of tests offered Diagnostic Center for Population and Animal Health Michigan State University wwwdcpahmsuedu Comparative Pathology Laboratory University of Miami Miami Florida wwwpathologymedmiamiedu Infectious Diseases Laboratory University of Georgia College of Veterinary Medicine wwwvetugaedusamsidl Texas Veterinary Medical Diagnostic Laboratory College Station Texas httptvmdlwebtamuedu Veterinary Molecular Diagnostics Inc Milford Ohio httpwwwvmdlabscom Treatment Recommended treatment period for most avian species has traditionally been 45 days with doxycycline however some birds may require treatment for as long as 60 days Birds should be rechecked by swab and blood PCR two weeks after cessation of treatment Treatment protocols of 30 days length can be effective in budgerigars However no single protocol ensures safe treatment or complete elimination of infection in every bird Therefore treatment for avian chlamydiosis should be supervised by a licensed veterinarian after consultation with an experienced avian veterinarian Compendium of Measures to Control C psittaci Prevention and control Quarantine for at least 30 days and test birds entering the existing bird collection avoid obtaining birds from multiple sources quarantine any sick birds screen birds with frequent public contact practice preventative husbandrygood hygiene No test or combination of tests can declare a bird disease free of C psittaci Subclinical carriers exist Intermittent shedding of the organism may also complicate testing Further details outlined in the Compendium of Measures to Control C psittaci see references updated yearly and available online Suggested disinfectant for housing facilities The organism is susceptible to many detergents and disinfectants as well as heat However it is resistant to acid and alkali Effective disinfectants include 1 Lysol a 11000 dilution of quaternary ammonium compounds eg Roccal Zephiran or freshly prepared 132 dilution of household bleach ½ cupgallon Notification Reportable disease under USDAAPHISVS National Animal Health Reporting System Psittacosis in humans is a Nationally Notifiable Disease and most states require physicians to report to appropriate local or state health authorities Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Infected birds should be isolated and treated Other birds should not be introduced until treatment is completed and the infected birds facility is American Association of Zoo Veterinarians Infectious Disease Manual AVIAN CHLAMYDIOSISCHLAMYDOPHILOSIS thoroughly cleaned and disinfected Conditions for restoring diseasefree status after an outbreak Infected pet birds or other valuable birds and their contacts may be isolated and treated Poultry may be euthanized rather than treated often due to economic constraints Premises should be thoroughly cleaned and disinfected New birds entering a facility can be tested for the disease but cannot truly be declared diseasefree Experts who may be consulted Consult the list of contributors to the Compendium of Measures to Control Chlamydophila psittaci wwwnasphvorgDocumentsPsittacosispdf References 1 Center for Food Security Public Health Iowa State University Avian Chlamydiosis wwwcfsphiastateeduFactsheetspdfschlamydiosisavianpdf Accessed 2 July 2013 2 Centers for Disease Control and Prevention CDC Psittacosis wwwcdcgovncidoddbmddiseaseinfopsittacosisthtm Accessed 2 July 2013 3 Compendium of Measures to Control Chlamydophila psittaci Infection Among Humans and Pet Birds 2010 by the National Association of State Public Health Veterinarians NASPHV wwwnasphvorgDocumentsPsittacosispdf 4 Dahlhausen B and CS Radabaugh 1997 Detection of Chlamydia psittaci infection in pet birds using a molecular based diagnostic assay Proc Assoc Avian Vet Pp 191198 5 Eidson M 2002 Zoonosis update Psittacosisavian chlamydiosis J Am Vet Med Assoc 22117101712 6 Phalen D 2006 Preventative medicine and screening In Harrison G J and TL Lightfoot eds Clinical Avian Medicine Spix Publishing Inc Palm Beach Florida Pp 573585 American Association of Zoo Veterinarians Infectious Disease Manual CHRONIC WASTING DISEASE Fact Sheet compiled by Roy Burns Sheet completed on 22 March 2011 updated 23 August 2013 Fact Sheet Reviewed by Terry Spraker Mark Drew Bryan J Richards Susceptible animal groups Natural infection mule deer Odocoileus hemionus whitetailed deer Odocoileus virginianus Rocky mountain elk Cervus elaphus nelsoni red deer Cervus elaphus elaphus moose Alces alces and sika deer Cervus nippon Experimental infection intracerebral inoculation variable transmission success across experimentally susceptible species muntjac Muntiacus sp domestic cattle Bos taurus sheep Ovis aries fallow deer Dama dama domestic ferrets Mustela putorius furo mink Mustela vison hamsters mice squirrel monkeys Saimiri sciureus and voles of the genera Mictotus and Myodes Causative organism A transmissible spongiform encephalopathy produced by a prion protein infectious agent Two prevalent strains with divergent biochemical characteristics have been identified and strain variation may occur Zoonotic potential To date no strong evidence of CWD transmission to humans has been reported Several epidemiologic studies provide evidence that to date CWD has not been transmitted to humans Specific studies have focused on identifying human prion disease in hunter population presumed at increased risk for exposure to potentially CWDinfected deer or elk meat In the last 60 or so years in regions where CWD is present and such exposure is known no evidence of an increase in any neurodegenerative disease condition of humans has been identified CWD prions have been found in muscle meat as well as other tissues of cervids and could enter the food supply Although the evidence so far suggests that CWD probably does not affect humans the possibility that it could be zoonotic has not been eliminated although may be increasing over time Distribution Maps of the current distribution of CWD in captive and free roaming herds suggest gradual Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Natural infection mule deer Odocoileus hemionus whitetailed deer Odocoileus virginianus Rocky mountain elk Cervus elaphus nelsoni and moose Alces alces Direct animal to animal contact and contact with contaminated environment Agent shed in feces saliva urine perhaps milk Contagious among susceptible species but mechanism unclear Early subtle and non specific Progressive emaciation abnormal behavior excessive salivation and ending in mortality Progressive and fatal None Early detection and removal of infected individuals Depopulation of infected captive herds unless regular ante mortem testing of remaining animals is possible Regulation of international and interstate movements of cervids and cervid tissues No evidence of transmission to humans under natural conditions Human health advisory to avoid consumption of food derived from any animal with evidence of CWD or containing potentially infectious cervid tissues American Association of Zoo Veterinarians Infectious Disease Manual CHRONIC WASTING DISEASE spread has occurred from original identification in Colorado httpwwwnwhcusgsgovdiseaseinformationchronic wastingdisease As of this update Wild herds and captive facilities infected Colorado Kansas Minnesota Missouri Nebraska New York Pennsylvania South Dakota Wisconsin Alberta Saskatchewan Wild herds only infected Illinois Maryland North Dakota New Mexico Texas Utah Virginia West Virginia Wyoming Captive facilities only infected Iowa Michigan Montana Oklahoma South Korea Incubation period Infected deer and elk can appear robust and healthy in the early stages of CWD and may take two or more years before they show clinical signs of the disease Minimum incubation time in experimental infection 15 mo but can exceed 25 months in deer and 60 months in elk Genetic polymorphisms influence the incubation time in both deer species and in elk and probably in moose Direct animalanimal contact and contact via ingestion and inhalation of contaminated material from the environment is the primary route of transmission Agent shed in feces saliva urine other mechanisms eg nasal secretions milk also are possible Contaminated environments soil feces offal carcass may be infective for years Clinical signs Early clinical signs are subtle and nonspecific behavior changes response to handling interaction with conspecifics somnolence periods of repetitive behavior vacant facial expression During period few weeks to several months prior to death emaciation abnormal behavior progressive weight loss stumbling tremors lack of coordination blank facial expressions excessive salivation loss of appetite excessive thirst and urination listlessness teeth grinding abnormal head posture and drooping ears are observed Later esophageal dilation difficulty in swallowing resulting in pneumonia caused by aspiration of food or saliva into the lungs Disease is progressive and always fatal Post mortem gross or histologic findings At necropsy postmortem findings of emaciation and pneumonia is are found In suspected clinical cases histologic spongiform change with degeneration and loss of neurons and identification of PRP cwd using IHC staining of the obex For preclinical diagnosis IHC on lymph nodes tonsils retropharyngeal lymph nodes or mucosaassociated lymphoid tissue Diagnosis Antemortem IHC staining for PrP cwd of biopsied lymphoid tissue tonsil rectal mucosa Postmortem Detection of PrP cwd via IHC in brain obex specifically parasympathetic vagal nucleus in the dorsal portion of the medulla oblongata at the obex all species later stages of disease For detecting preclinical infections IHC on lymph nodes tonsils retropharyngeal lymph nodes While ELISA Western Blotting and PMCA testing is available IHC is the only assay currently accepted officially by USDA Material required for laboratory analysis Cervid post mortem brain obex and lymph tissues preferably tonsils medial retropharyngeal lymph nodes Relevant diagnostic laboratories USDAAPHISVSNVSL 1920 Dayton Ave for packages PO Box 844 for letters Ames IA 50010 NVSL IHC for PRP Brain obex and medial retropharyngeal lymph node 515 3377266 Fax 515 3377397 USDANAHLN IHC and ELISA 515 3377731 American Association of Zoo Veterinarians Infectious Disease Manual CHRONIC WASTING DISEASE Fax 515 3377397 httpwwwaphisusdagovanimalhealthanimaldiseasescwddiagnosticsshtml Colorado State University Diagnostic Laboratory College of Veterinary Medicine 300 West Drake Road Colorado State University Fort Collins Colorado 80526 Treatment While no therapeutic cures supportive therapy may prolong course but it is not advisable in the context of control Prevention and control Free Ranging Testing hunter harvested and road kill cervids local population reduction in infected areas bans on feeding wild cervids restrictions on transporting hunterkilled carcasses from enzootic regions and transportation restrictions and monitoring of captive cervid operations will reduce transmission Cooking or heat does not inactivate prions Educational efforts is critical as management once disease has entered area has been very ineffective so prevention is paramount Captive Routine surveillance and testing of cervids all species held in zoo collections Early detection and removal of infected individuals Depopulation of infected captive herds is recommended unless regular antemortem testing of remaining animals is possible and strict biocontainment is followed Regulation of international and interstate movements of cervids and restricted importation of captive cervids Consider antemortem testing of animals prior to movements Prevent entrance of freeranging cervids from zoo grounds Post mortem sampling of freeranging and captive cervids that die or are euthanized on zoo grounds Although not shown to be food borne rendered ruminant meat or bone meal should not be fed to cervids No effective vaccine at present Suggested disinfectant for housing facilities Environmental contamination is a major concern in eradication and prevention in new cases Prions are extremely resistant to heat pH ultraviolet and disinfectants Sodium hypochlorite household bleach greater than 2 free chlorine at 280 ml in 720 ml of water at room temperature for one hour Sodium hydroxide caustic soda soda lye at 38g in one litre of water at room temperature for one hour Notification Responsible state agency should be contacted State and Federal regulations are dynamic and responsive to disease status Some states have adopted regulations limiting or prohibiting whole carcass transportation or particular cervid tissue transportation out of CWD areas Measures required under the Animal Disease Surveillance Plan USDAAPHIS established a national voluntary CWD Herd Certification program published in the Federal Register on 13 June 2012 Many states already have CWD monitoring or certification programs for captive herds Guidelines for Chronic Wasting Disease CWD Surveillance in captive cervids in zoos AAZVAZA Animal Health Committee 2003 Measures required for introducing animals to infected animal See measures required under the Animal Disease Surveillance Plan Conditions for restoring diseasefree status after an outbreak See measures required under the Animal Disease Surveillance Plan Experts who may be consulted Numerous experts are identified at httpwwwcwdinfoorg References 1 Chronic Wasting Disease Alliance httpwwwcwdinfoorg Accessed 23 August 2013 2 USDA APHIS AH httpwwwaphisusdagovanimalhealthanimaldiseasescwd Accessed 23 American Association of Zoo Veterinarians Infectious Disease Manual CHRONIC WASTING DISEASE August 2013 httpwwwaphisusdagovanimalhealthnahlndownloadscwdscrapielablistpdf Accessed 23 August 2013 httpwwwaphisusdagovanimalhealthlabinfoservicesapprovedlabsshtml Accessed 23 August 2013 httpwwwaphisusdagovanimalhealthanimaldiseasescwdfarmedshtml Accessed 23 August 2013 3 USGS National Wildlife Health Center httpwwwnwhcusgsgovdiseaseinformationchronicwastingdiseaseindexjsp Accessed 23 August 2013 4 Angers RC H Kang D Napier S Browning T Seward C Mathiason A Balachandran D Kenzie C Joaquin C Soto J Jewell C Graham E Hoover and G Telling 2010 Prion strain mutation determined by prion protein conformational compatibility and primary structure Sci 328 11541158 5 AZA Guidelines for Chronic Wasting Disease CWD Surveillance httpwwwazaorgchronic wastingdisease Accessed 23 August 2013 6 Barria MA GC Telling P Gambetti JA Mastrianni and C Soto 2011 Generation of a new form of human PrPSc in vitro by interspecies transmission from cervid prions J Biol Chem 2867490 7495 7 Miller MW 2008 Chronic wasting disease of cervid species In Fowler ME and RE Miller eds Zoo and Wildlife Medicine Current Therapy 6 W B Saunders Co Philadelphia Pennsylvania Pp 430437 8 Williams ES MW Miller TJ Kreeger RH Kahn and ET Thorne 2002 Chronic wasting disease in deer and elk a review with recommendations for management J Wildl Managem 663 551563 9 Williams ES 2005 Chronic wasting disease Vet Pathol 42530549 American Association of Zoo Veterinarians Infectious Disease Manual CHYTRIDIOMYCOSIS DISEASE Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Amphibians Contact with contaminated water moist or wet substrates or infected animals Crayfish may act as carriers Erythematous skin excessive skin shedding abnormal behavior sudden death Outcome of infection ranges from subclinical to fatal Itraconazole or chloramphenicol baths elevated temperatures Isolate affected amphibians No Fact Sheet compiled by Cynthia Stadler Sheet completed on updated 12 January 2019 Fact Sheet Reviewed by Kathryn Tuxbury Susceptible animal groups Amphibians Causative organism Batrachochytrium dendrobatidis Bd a nonhyphal zoosporic fungus Zoonotic potential No Distribution Worldwide wherever amphibian populations are present Chytridiomycosis has been implicated as the cause of massive amphibian population declines Incubation period 1470 days Clinical signs Erythematous or discolored skin abnormal posture neurologic signs excessive skin shedding behavior changes Clinical signs may not be apparent prior to acute death Post mortem gross or histologic findings Gross lesions are often not present but may include increased sloughing of the skin discolored skin erosions Histologic lesions involve focal hyperkeratosis and epidermal hyperplasia with sloughing of the keratin layer Fungal zoosporangia are found within the keratin layers The fungal lesions are not evenly distributed on the skin surface Predilection is noted for the digits ventral aspect of the hind limbs inguinal and pelvic regions and in tadpoles mouth parts Diagnosis PCR skin swab best histopathology Cytology requires experience PCR is best for detecting subclinical infection whereas histopathology and cytology are most useful for clinically significant infection Material required for laboratory analysis Shed skin skin scraping skin swab or skin sample preferably from the ventral pelvic patch from adults Mouthpart swabs from live tadpoles mouthparts from deceased tadpoles Using finetipped swabs not woodenhandled gently swab skin 2030 times Break swab 23 cm from tip and place in screwtop tube avoiding contact with outside of tube Allow to airdry for 5 minutes Samples can be kept at room temperature or 4 degrees C for 1 2 weeks or frozen for longerterm storage Avoid exposure to high temperatures and direct sunlight Relevant diagnostic laboratories For histopathology any laboratory that routinely examines amphibian tissues For PCR Amphibian Disease Laboratory 15600 San Pasqual Valley Road Escondido CA 92027 760 2915472 760 2915470 amphibianlabsandiegozooorg httpswwwsandiegozooglobalorgNewsAmphibianDiseaseLaboratory Pisces Molecular 1600 Range Street Suite 201 Boulder CO 80301 3035469300 infopiscesmolecularcom httppiscesmolecularcom American Association of Zoo Veterinarians Infectious Disease Manual CHYTRIDIOMYCOSIS DISEASE Research Associates Laboratory 14556 Midway Road Dallas TX 75244 Phone 972 9602221 Fax 972 9601997 httpvetdnacom Zoologix Laboratories 9811 Owensmouth Avenue Ste 4 Chatsworth CA 913113800 Phone 8187178880 Fax 8187178881 infozoologixcom httpzoologixcom Treatment Itraconazole 0005 50 mgliter diluted with 06 saline or amphibian Ringers solution used as a 5 minute bath applied once daily for 610 days Lower concentration of 00025 25 mgliter also has been successful at eliminating the organism Efficacious treatments can vary among species and life stages Hygiene is essential during treatment and animals should be returned to a clean disinfected container after EACH treatment Previously recommended higher concentration of 001 itraconazole is toxic to tadpoles and recently metamorphosed amphibians Other treatments include chloramphenicol baths and elevated environmental temperatures of 37oC for 16 hrs in those species that are thermotolerant Also terbinafine baths and topical voriconazole have been used with variable results to date Animals with clinical chytridiomycosis may have issues from hyponatremia and hypokalemia so electrolyte replacement may be helpful Prevention and control Newly acquired amphibians should undergo a minimum of 30 days in quarantine preferably 60 days Skin swab PCR testing or prophylactic itraconazole baths should be implemented prior to release from quarantine All animals that die in quarantine should be necropsied and submitted for histopathology Enclosures and equipment should be disinfected routinely However it is prudent to wear disposable gloves and use separate equipment for different enclosures Suggested disinfectant for housing facilities Bleach Virkon and quaternary ammonium compounds can be used for enclosures For surgical instruments 70 ethanol glutaraldehyde and benzalkonium chloride can be used Notification Office International des Epizooties OIE notifiable disease Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Introductions are not recommended until numerous negative PCR tests have been completed Conditions for restoring diseasefree status after an outbreak It is recommended to test amphibians by PCR to confirm the fungus is no longer present For diseasefree status there should be serial negative PCR tests over the course of 6 months to 1 year Experts who may be consulted Allan Pessier DVM Dipl ACVP Washington Animal Disease Diagnostic Laboratory Department of Veterinary Microbiology and Pathology College of Veterinary Medicine Washington State University Pullman WA 991647034 apessierwsuedu References 1 Amphibian Ark Internet Chytrid fungus 2018 cited 2019 January 12 Available from httpwwwamphibianarkorgthecrisischytridfungus 2 Whittaker K Vredenburg V Internet An Overview of Chytridiomycosis 2011 cited 2019 January 12 Available from httpamphibiaweborgchytridchytridiomycosishtml American Association of Zoo Veterinarians Infectious Disease Manual CHYTRIDIOMYCOSIS DISEASE 3 Wildlife Health Australia Internet Amphibian chytrid fungus in Australia Fact sheet 2014 cited 2019 January 12 Available from httpswildlifehealthaustraliacomauFactSheetsaspx 4 World Organization for Animal Health Internet OIE Manual of diagnostic tests for aquatic animals Chapter 211 2018 cited 2019 January 12 Available from httpwwwoieintindexphpid2439L0htmfilechapitrebatrachochytriumdendrobatidishtm 5 World Organization for Animal Health Internet OIElisted diseases infections and infestations in force in 2019 2019 cited 2019 January 12 Available from httpwwwoieintenanimalhealthinthe worldoielisteddiseases2019 6 Berger L Speare R Kent A Diagnosis of chytridiomycosis in amphibians by histological examination Zoos Print J 200015184190 7 Bishop PJ Speare R Poulter R Butler M Speare BJ Hyatt A Olsen V Haigh A Elimination of the amphibian chytrid fungus Batrachochytrium dendrobatidis by Archeys frog Leiopelma archeyi Dis Aquat Org 200984915 8 Bowerman J Rombough CR Weinstock SR PadgettFlohr GE Terbinafine hydrochloride in ethanol effectively clears Batrachochytrium dendrobatidis in amphibians J Herp Med Surg 20102012428 9 Brannelly LA RichardsZawacki CL Pessier AP Clinical trials with itraconazole as a treatment for chytrid fungal infections in amphibians Dis Aquat Org 201210195104 10 Brannelly LA Skerratt LF Berger L Treatment trial of clinically ill corroboree frogs with chytridiomycosis with two triazole antifungals and electrolyte therapy Vet Res Commun 201539179 187 11 Forzan MJ Gunn H Scott P Chytridiomycosis in an aquarium collection of frogs diagnosis treatment and control J Zoo Wildl Med 2008393406411 12 Jones MEBD Paddock D Bender L Allen JL Schrenzel MS Pessier AP Treatment of chytridiomycosis with reduceddose itraconazole Dis Aquat Org 201299 243249 13 Pessier AP Amphibian chytridiomycosis In Miller RE Fowler ME eds Fowlers Zoo and Wild Animal Medicine Current Therapy Vol 6 St Louis MO Elsevier Saunders 2008 p 137143 14 Pessier AP Diagnosis and control of amphibian chytridiomycosis In Miller RE Fowler ME eds Fowlers Zoo and Wild Animal Medicine Current Therapy Vol 7 St Louis MO Elsevier Saunders 2012 p 217223 15 Pessier AP Mendelson JR eds A Manual for Control of Infectious Diseases in Amphibian Survival Assurance Colonies and Reintroduction Programs Conservation Breeding Specialist Group Apple Valley MN 2010 229 pp 16 Rifkin A Visser M Barrett K Boothe D Bronson E The pharmacokinetics of topical itraconazole in Panamanian golden frogs Atelopus zeteki J Zoo Wild Med 2017482344351 17 Roberts AA Berger L Robertson SG Webb RJ Kosch TA McFadden M Skerratt LF Glass BD Motti CA Brannelly LA The efficacy and pharmacokinetics of terbinafine against the frogkilling fungus Batrachochytrium dendrobatidis Med Mycol 2019572204214 18 Tamukai KY Une Y Tominaga A Suzuki K Goka K Treatment of spontaneous chytridiomycosis in captive amphibians using itraconazole J Vet Med Sci 201173155159 19 Woodhams DC Alford RA Marantelli G Emerging disease of amphibians cured by elevated body temperature Dis Aquat Organ 2003556567 20 Young SR Speare R Berger L Skerratt LF Chloramphenicol with fluid and electrolyte therapy cures terminally ill green tree frogs Litoria caerulea with chytridiomycosis J Zoo Wildl Med 2012432 330337 American Association of Zoo Veterinarians Infectious Disease Manual CLASSICAL SWINE FEVER hog cholera Fact Sheet compiled by Cora Singleton Sheet completed on 1 March 2011 updated 31 October 2012 updated 8 August 2018 Fact Sheet Reviewed by Sarrah Kaye Susceptible animal groups Domestic and wild swine endemic in wild boar in parts of Europe Causative organism Classical swine fever virus CSFV is an RNA virus in the genus Pestivirus within the family Flaviviridae Strains can range from low to high virulence Related to bovine viral diarrhea virus and border disease virus of sheep Also known as hog cholera Zoonotic potential No Distribution CSFV is present in SouthEast Asia the Caribbean Africa South and Central America and parts of eastern Europe Areas considered free of CSF in domestic pigs include North America US Canada and Mexico some countries in South America New Zealand Australia Asia and many countries in western and central Europe Incubation period 219 days Clinical signs Acute disease high virulence strains Sudden death depression pyrexia anorexia ataxia constipation followed by diarrhea and vomiting ocular discharge cutaneous cyanosis necrosis of ear tips muscle tremors convulsions Chronic disease low virulence strains Dullness anorexia failure to thrive diarrhea dermatitis Congenital disease Stillbirth fetal mummification cerebellar hypoplasia congenital tremors failure to thrive Piglets infected with lowvirulent strains in 1st trimester can be born viremic and healthy serve as subclinical shedders with delayed onset of disease Similar to BVD it sounds like this is an important source of transmission Post mortem gross or histologic findings Petechial hemorrhages in kidney urinary bladder and larynx enlarged hemorrhagic lymph nodes splenic infarcts encephalitis button ulcers in cecum chronic disease cerebellar hypoplasia congenital disease Diagnosis Agent identification Virus culture fluorescent antibody test immunoperoxidase procedure ELISA RTPCR Serology Neutralization peroxidaselinked assay fluorescent antibody virus neutralization ELISA Material required for laboratory analysis Tissues tonsil lymph node spleen kidney distal ileum blood serum Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Swine Direct contact with body secretions feeding uncooked infected pork products mechanical vectors flies vehicles people in utero Acute sudden death ataxia cutaneous cyanosis or hyperemia petechiation necrosis of ear tips Chronic failure to thrive dermatitis Congenital fetal mummification cerebellar hypoplasia congenital tremors Highly contagious Can range from mild disease in chronic infections to severe disease and sudden death in acute infections None Prevention Vaccination utilized in some countries control pig movements serosurveys do not feed uncooked pork Control test slaughter quarantine disinfect No American Association of Zoo Veterinarians Infectious Disease Manual CLASSICAL SWINE FEVER hog cholera Relevant diagnostic laboratories Foreign Animal Disease Diagnostic Laboratory Plum Island 40550 Route 25 for packages Orient Point NY 11957 PO Box 848 for letters Greenport NY 119440848 631 3233256 Fax 631 3233366 Treatment No effective treatment Prevention and control Prevention USDAAPHIS has a surveillance program to prevent reintroduction of the disease Vaccination is utilized in some countries Control pig movements and implement serological surveys to detect carrier pigs Do not feed uncooked pork products Control Depopulation of infected pigs disinfection of premises quarantine of the area and control of pig movement Suggested disinfectant for housing facilities 2 sodium hydroxide considered most suitable 1 formalin sodium carbonate strong iodophors Notification Reportable to the USDAAPHIS through the State Veterinarian or the federal Area Veterinarian in Charge The disease is also reportable to the World Organization for Animal Health OIE Measures required under the Animal Disease Surveillance Plan Report suspicious cases to the USDAAPHIS Area Veterinarian in Charge who will dispatch a Foreign Animal Disease Diagnostician to investigate the case and collect samples for testing Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Infections must be reported to USDAAPHIS for management Experts who may be consulted USDA State Veterinarians or federal Area Veterinarians in Charge References 1 Jackson PGG Cockcroft PD Handbook of Pig Medicine London England Saunders Elsevier 2007 p 182184 2 Kirkland PD Le Potier MF Vannier P Finlaison D Pestiviruses In Zimmerman JJ Karriker LA Ramirez A Schwartz KJ Stevenson GW Zhang J eds Diseases of Swine 11th ed Ames IA WileyBlackwell 2018 in press 3 Spickler Anna Rovid Internet Classical swine fever 2015 cited 2018 August 08 Available from httpwwwcfsphiastateeduFactsheetspdfsclassicalswinefeverpdf 4 United States Department of Agriculture Animal and Plant Health Inspection Service Internet Classical Swine Fever Surveillance 2016 cited 2018 August 08 Available from httpwwwaphisusdagovaphisourfocusanimalhealthanimaldiseaseinformationswinedisease informationctclassicalswinefeversurveillance 5 United States Department of Agriculture Animal Plant and Health Inspection Services Internet National Animal Health Laboratories Network NAHLN Laboratories approved for CSF Surveillance Testing 2018 cited 2018 August 08 Available from httpwwwaphisusdagovanimalhealthnahlndownloadscsflablistpdf 6 United States Department of Agriculture Animal Plant and Health Inspection Services Internet National Animal Health Laboratories Network NAHLN Laboratories approved for ASF Preparedness and Surge Testing 2018 cited 2018 August 08 Available from httpwwwaphisusdagovanimalhealthnahlndownloadsasflablistpdf 7 World Organization for Animal Health OIE Internet Classical swine fever In Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2018 2014 cited 2018 August 08 Available from httpwwwoieintfileadminHomeengHealthstandardstahm20803CSFpdf American Association of Zoo Veterinarians Infectious Disease Manual CLOSTRIDIAL DISEASE BOTULISM TOXICOSIS Fact Sheet compiled by Danielle R Graham Snyder Sheet completed on 17 January 2011 updated 18 October 2012 Fact Sheet Reviewed by Melissa Kennedy Stephanie Kottler Susceptible animal groups Most mammalian and avian species are susceptible to this problem Wild fowl and mink have a high incidence of clinical disease Causative organism Clostridium botulinum bacteria Types AG gram positive slightly curved to straight motile sporeforming saprophytic anaerobic rod Type C is the most common in animal species and Types A B and E most common in humans Zoonotic potential No Distribution Soil fresh water and sea sediments the intestinal tracts of mammals and birds and foods such as homecanned foods sausages meat products canned vegetables and seafood products These toxin contaminated sources can be either ingested or contaminate a wound Incubation period Normally 1236 hrs but can be as much as a week if a small amount is ingested Clinical signs Humans Three types of botulism foodborne wound and infant Foodborne botulism is caused by consumption of toxintainted food In these infections signs can include gastrointestinal issues such as nausea vomiting and abdominal pain symmetric descending flaccid paralysis and drooping palpebrae and dry mouth slurred speech and muscle weakness Descending paralysis of the respiratory muscles potentially fatal arms and legs may occur within 24 hours in severe cases Wound botulism is caused by a wound that is contaminated usually from toxins in the soil Signs are consistent with foodborne illness but usually without gastrointestinal signs Infant botulism is seen only in infants less than one year of age and caused by spores germinating in the intestinal tract Signs include constipation poor suckling reflexes peripheral weakness floppy baby syndrome and in severe cases respiratory distress and death Animals Clinical signs are mostly neurologic and caused by muscle paralysis A symmetrical ascending weakness starting from the rear limbs and progressing to the forelimbs is typical Cranial nerve deficits are usually present and may include decreased palpebral reflex decreased gag or swallowing reflex ptyalism decreased jaw tone mydriasis and sluggish pupillary responses Respiratory or cardiac paralysis can occur and usually causes death Post mortem gross or histologic findings Most post mortem or histologic findings are the result of muscle paralysis Mammals with wound botulism may have lesions but the wounds are generally not obviously or grossly infected Diagnosis History of exposure and clinical signs The toxin can be hard to find in feed or in tissues so most Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals including humans birds Ingestion of toxin contaminated food or tissues Wound contamination Mostly neurologic involving flaccid paralysis Gastrointestinal signs Dose related severity of mild to lethal Supportive care antitoxin when appropriate Proper food preparation and storage Avoid wound contamination No American Association of Zoo Veterinarians Infectious Disease Manual CLOSTRIDIAL DISEASE BOTULISM TOXICOSIS diagnosis is done by eliminating out other differentials Cultures from wounds or tissues can be taken to potentially isolate the organism The toxin can also be isolated from serum feces vomitus or samples of food that were ingested ELISA testing can detect neurotoxin but each subtype of toxin must be evaluated individually Mouse inoculation Serum or an extract of contaminated material is injected alone and in combination with a typespecific antitoxin into the mice Survival of the group of mice protected with antitoxin and death of the other group from signs consistent with botulism confirms the presence of botulism toxin This test is considered the standard and most reliable method of identifying botulism toxin Material required for laboratory analysis Serum feces vomitus stomach or intestinal contents contaminated food or culture of tissues if wound botulism is suspected Relevant diagnostic laboratories National Botulism Reference Laboratory at New Bolton Center University of Pennsylvania National Veterinary Services Laboratories NVSL Ames Iowa Treatment Supportive care is most important Hospitalization may be necessary Therapeutic monitoring involves intensive care of recumbent animals Wounds or abscesses should be cleaned and debrided where possible Selective padding and respiratory support is essential to avoid complications of recumbency Antitoxins can be effective to improve survival rates depending on the toxin involved and the host species Type C antitoxin seems to work well in some birds and mink Antibiotics are only used in cases of wound botulism or to treat secondary infections due to the paralysis Recovery typically takes 14 24 days Prevention and control Vaccines are available for humans and animals with high risk of exposure To ensure food is properly stored and prepared botulism toxin is destroyed by heating food to 80oC for 30 minutes or to 100oC for 10 minutes Wounds should be kept clean and avoid contamination as much as possible For wildlife prompt removal of carcasses that could be infected is critical as decaying carcasses are known to support toxin production Maggots feeding on decaying carcasses are sources of infection for many waterfowl as the maggots are unaffected by the toxin but effectively concentrate it Waterfowl consume the maggots and become infected Stagnant water should be avoided as this creates an environment for Clostridium botulinum bacteria to grow and for spores to germinate Suggested disinfectant for housing facilities Clean areas with diluted bleach when possible Sunlight inactivates the toxins within 13 hours Adding chlorine to water if possible will destroy toxins as well Notification Notification for animals is not necessary at this time Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Infected animals should be kept in a hospital or other stable environment until they are fully recovered Conditions for restoring diseasefree status after an outbreak Removal of decaying vegetable matter and carcasses should be carried out and areas should be cleaned with diluted bleach if possible Experts who may be consulted Julie A Coffield DVM PhD Dept of Physiology and Pharmacology University of Georgia CVM coffieldugaedu Raymond Sweeney VMD Professor of Medicine Director National Botulism Reference Laboratory University of Pennsylvania CVM American Association of Zoo Veterinarians Infectious Disease Manual CLOSTRIDIAL DISEASE BOTULISM TOXICOSIS rsweeneyvetupennedu References 1 httpwwwcdcgovnczveddivisionsdfbmddiseasesbotulism Accessed 8 July 2013 2 httpnabcksueducontentfactsheetscategoryBotulism Accessed 8 July 2013 3 Barsanti JA 1998 Botulism In Greene C E ed Infectious Diseases of the Dog and Cat 2nd ed WB Saunders Co Philadelphia Pennsylvania Pp 263267 4 Hartmann K and Greene CE 2006 Diseases caused by systemic bacterial infections In Ettinger SJ and EC Feldman eds Textbook of Veterinary Internal Medicine 3rd ed St Louis Elsevier Saunders Pp 389394 5 Gyles CL 2008 Clostridial disease In Kahn CM ed The Merck Veterinary Manual 9th ed Merck Co Inc Whitehouse Station New Jersey Pp 286287 6 US Department of the Interior and US Geographical Survey 1999 Avian botulism In Friend M and J C Franson eds Field Manual of Wildlife Diseases 1st rev US Geographical Survey National Wildlife Health Center Reston Virginia Pp 271281 7 Sobel J 2009 Diagnosis and treatment of botulism a century later clinical suspicion remains the cornerstone Clin Infect Dis 48 16741675 8 Rideout BA 2003 Clostridial diseases in all taxa In Fowler ME and RE Miller eds Zoo and Wild Animal Medicine 5th ed Saunders St Louis Missouri Pp 716717 American Association of Zoo Veterinarians Infectious Disease Manual CLOSTRIDIAL DISEASE TETANUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Equidae bovidae cervidae primates elephant macropods and rodents Contamination of wounds from bacteria in soil Muscle rigidity and spasm localized or generalized Up to 80 mortality in clinically ill animals Penicillin tetanus anti toxin supportive care to reduce signs and support of airway Vaccination with tetanus toxoid No Fact Sheet compiled by Ann E Duncan Sheet completed on 18 January 2011 updated 11 July 2013 Fact Sheet Reviewed by Dalen Agnew Sarah Woodhouse Susceptible animal groups The disease is infrequent in animals All warmblooded animals are potentially susceptible Horses and man are most susceptible followed by cattle and sheep Goats pigs dogs elephants kangaroos and rodents also have been infected Cases can occur postpartum and after surgical procedures Neonatal tetanus is seen in animals born without passive immunity usually through infection of the umbilical stump Carnivores and birds are resistant Causative organism Clostridium tetani is a slender grampositive anaerobic rod that may develop a terminal spore giving it a drumstick appearance C tetani is found in the soil and intestinal tracts of animals and man In the presence of oxygen it forms a protective capsule and may live in the soil in spore form for months to years In an anaerobic wound the spores germinate and multiply producing a potent toxin known as tetanospasmin Toxin is disseminated via blood and lymphatics and binds in the central nervous system interfering with neurotransmitter release and blocking inhibition impulses This reaction to the toxin leads to unopposed muscle contraction and spasm Zoonotic potential Tetanus is acquired through contact with spores in the environment and is not transmitted from animal to animal or person to person Distribution Worldwide Found in soil dust and animals waste Enzootic areas exist mainly in the tropics Incubation period Varies from 3 to 21 days after contamination of a deep wound that provides anaerobic conditions Clinical signs It may start with localized contraction of muscles in region of infected wound In generalized tetanus trismus neck stiffness protrusion of the nictitans and difficulty swallowing are often seen initially Generalized rigidity spasms of skeletal muscle and exaggerated reflexes follow Animals often assume a sawhorse stance with ears erect tail stiff and extended In some cases pyrexia sweating and tachycardia are seen Mortality of 80 is expected Post mortem gross or histologic findings No lesions seen It may be possible to see secondary aspiration pneumonia Diagnosis Prior existence of a wound and characteristic signs are the basis for diagnosis Direct microscopic examination of wound material may be useful Attempting to culture Clostridium tetani from the wound is generally not successful Mouse protective bioassays were historically used but they are no longer available Material required for laboratory analysis None Relevant diagnostic laboratories None Treatment Wounds should be cleaned and debrided Antibiotic therapy with high doses of penicillin is American Association of Zoo Veterinarians Infectious Disease Manual CLOSTRIDIAL DISEASE TETANUS effective against C tetani If tetanic spasms are occurring supportive care should be provided and an adequate airway maintained Treatment may include muscle relaxants tranquilizers and barbiturate sedatives Animals who have previously received toxoid should be given a booster Tetanus antitoxin is hyperimmune serum generated by either a horse or human to bind and destroy the tetanus toxin Antitoxin can be used to neutralize unbound circulating toxin but cannot remove toxin already bound to nerve endings Substantial risk of anaphylactic reaction is present when using a blood product from another species Skin testing is used to test for reactivity to antitoxin before use Antitoxin can be given under the skin or intraperitoneally but can take up to 3 days to reach a therapeutic level Intravenous administration is more rapid but more likely to induce anaphylaxsis For passive protection tetanus antitoxin effects will persist for about two weeks Prevention and control Active immunization with tetanus toxoid is recommended in susceptible species due to ubiquitous presence in environment Two doses of tetanus toxoid should be given 48 weeks apart with boosters given one year later and every 25 years thereafter Vaccination is not contraindicated in pregnant animals Passive immunization with antitoxin should be reserved for cases with highrisk wounds and no previous active immunization unvaccinated patients who must undergo surgical procedures and neonates in highrisk situations Procedures such as umbilical cord severing dehorning and castration should be done in the most aseptic conditions possible and antiseptics should be applied to surgical wounds Suggested disinfectant for housing facilities None Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal None Conditions for restoring diseasefree status after an outbreak None Experts who may be consulted None identified References 1 httpwwwcdcgovvaccinespubspinkbookdownloadstetanuspdf Accessed 25 September 2013 2 httpwwwcdcgovvaccinesvpdvactetanusdefaulthtm Accessed 25 September 2013 3 Acha PN and B Szyfres Tetanus 2001 Zoonoses and Communicable Diseases Common to Man and Animals 3rd ed vol I Bacterioses and Mycoses Pan American Health Organization Washington DC Pp 265271 4 Burkitt JM BK Sturges KE Jandrey and PH Kass 2007 Risk factors associated with outcome in dogs with tetanus 38 cases 19872005 J Am Vet Med Assoc 230 7683 5 Lindsay WA E Wiedner R Isaza HGG Townsend M Boleslawski and DP Lunn 2010 Immune responses of Asian elephants Elaphas maximus to commercial tetanus toxoid vaccine Vet Immunol Immunopathol 133 287289 6 Ramsay WR 1960 Tetanus in the kangaroo Aust Vet J 3610 412 7 Rings DM 2004 Clostridial disease associated with neurologic signs tetanus botulism and enterotoxemia Vet Clin N Am Food Anim Prac 202 379391 8 Springer DA K PhillippiFalkenstein and G Smith 2009 Retrospective analysis of wound characteristics and tetanus development in captive macaques J Zoo Wildl Med 401 95102 American Association of Zoo Veterinarians Infectious Disease Manual COCCIDIOIDOMYCOSIS Fact Sheet compiled by Maria Spriggs Sheet completed on 3 August 2011 updated 27 September 2012 Fact Sheet Reviewed by Joe Wheat Tiffany Wolf Susceptible animal groups Mammals including humans reptiles rare published in Sonoran gopher snake exoticzoo cases published in black rhino Indochinese tiger Przewalskis horse ringtailed lemur California sea lion bottlenose dolphin chimpanzees river otter tapir llama bighorn sheep koala Causative organism Disease is also known as Valley Fever Causative agents Coccidioides immitis California and Coccidioides posadasii Arizona Zoonotic potential No direct transmission however fomites bandages cultures should be handled carefully People exposed to C immitis develop asymptomatic infection or mild transient respiratory signs but rarely severe disease In endemic areas 1015 of people are skintest positive Organ transplantation in humans has been reported as rare route of transmission Distribution Disease is found only in the western hemisphere specifically in Southwestern US CA AZ NM UT NV TX Mexico and Central and South America Prevalence increases in years after high rainfall as arthrospores return to surface after rain then are dispersed by wind Incubation period 13 weeks respiratory signs 4 months disseminated disease Clinical signs Clinical disease in dogs is most common in young males Primary pulmonary form chronic dry or moist cough fever anorexia weight loss Disseminated form lameness due to osteomyelitis of appendicular skeleton draining skin tracts especially in domestic cats regional lymphadenopathy CNS signs cardiac signs ocular lesions Primary localized skin lesions rare from penetrating wounds contaminated with organism Post mortem gross or histologic findings Pyogranulomatous inflammation seen in affected tissues Gross lesions may be either disseminated or limited to lungs mediastinum and thoracic lymph nodes The lungs are often involved even in disseminated disease where the primary complaint is not respiratory Diagnosis Clinical pathology Nonregenerative anemia leukocytosis monocytosis hyperglobulinemia hypoalbuminemia Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Inhalation of arthroconidia Wound contamination rare Intrauterine transmission rare reports in horses humans Dogs wet or dry cough fever anorexia weight loss lameness Cats skin lesions fever anorexia weight loss cough and lameness rare Zoo species various signs reported Subclinical infection most common Untreated disseminated disease can be fatal Oral antifungal ie fluconazole Avoid endemic areas reduce animal exposure to dusty conditions Not directly but humans can contract American Association of Zoo Veterinarians Infectious Disease Manual COCCIDIOIDOMYCOSIS Radiography Diffuse interstitial lung pattern hilar lymphadenopathy bone lesions in distal diaphysis of long bones which are more proliferative than lytic Serology IgM and IgG rising titers confirm active infection UC Davis Lab and Greenes text have further interpretation information Cytology and culture Demonstration of organism by cytology is difficult Extracellular spherules are most commonly found in lymph node aspirates fluid from draining masses or pleural fluid and pericardial fluid Periodic AcidSchiff PASstained smears more suitable than dry mount Antigen detection Sensitivity lower in dogs than humans research is in progress PCR Research is in progress for a realtime PCR method Material required for laboratory analysis Blood urine fluid or tissue sample for cytologyhistopathculture do not culture inhouse Relevant diagnostic laboratories Fungus Testing Laboratory httpstrluthscsaedufungusindexshtml MiraVista Diagnostics wwwmiravistalabscom UC Davis Coccidioidomycosis Serology Lab httpwwwucdmcucdavisedumedmicrococcihtml Treatment Fluconazole or amphotericin B is drug of choice but itra and ketoconazole are effective as well Posaconazole and voriconazole are newer and effective drugs but are expensive and little information available for veterinary medicine Bone infections may be incurable Itraconazole may be more effective for skeletal lesions Relapse is possible following treatment Treatment is recommended 16 months past resolution of clinical signs Prevention and control Avoid endemic areas Reduce animal exposure in dusty conditions such as feedlots Dust control measures might include planting grass and wetting soil People should wear facemask if dust exposure is unavoidable No vaccine is available however research is ongoing for a safeeffective vaccine for humans Suggested disinfectant for housing facilities Halogens such as iodine and chlorine in the form of bleach phenolics such as TekTrol and quaternary ammoniums Di Quat 10S and RoccalD Plus Arthroconidia are resistant to dry heat but can be inactivated by moist heat 121 C for minimum 15 minutes Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Organism is not transmitted from infected animal to another animal Conditions for restoring diseasefree status after an outbreak Outbreaks occasionally occur particularly following earthquakes or other events that disturb large amounts of soil in endemic areas More recent human outbreaks have occurred among military trainees and among archeological workers Experts who may be consulted Jane Sykes DVM UC Davis 5307523890 jesykesucdavisedu Russell Greene DVM Phoenix Vet Internal Med Services 6029539541 rtgreenecoxnet American Association of Zoo Veterinarians Infectious Disease Manual COCCIDIOIDOMYCOSIS Joe Wheat MD MiraVista Diagnostics 8666472847 jwheatmiravistalabscom References 1 BurgdorfMoisuk A IH Stalis and GW Pye 2012 Disseminated coccidioidomycosis in a koala Phascolarctos cinereus J Zoo Wildl Med 431197199 2 Burton M RJ Morton E Ramsay and EL Stair 1986 Coccidioidomycosis in a ringtailed lemur J Am Vet Med Assoc 1899120911 3 Center for Disease Control and Prevention wwwcdcgov 4 Lappin MR 2008 Polysystemic mycotic infections coccidioidomycosis In Nelson RW and C Couto eds Small Animal Internal Medicine 4th ed Mosby Elsevier St Louis Missouri Pp 1353 1354 5 Fowler ME 1988 Infectious disease of llamas and alpacas in North America In 1988 Proceedings AAZV Conference 172 6 Greene CE 2006 Coccidioidomycosis and Paracccidioidomycosis In Green CE Ed Infectious Diseases of the Dog and Cat 3rd ed Saunders Elsevier St Louis Missouri Pp 598608 7 Harwell G 1985 Coccidioidomycosis in a river otter Lutra canadensis In 1985 Proceedings AAZV Conference 50 8 Hector RF GW Rutherford CA Tsang LM Erhart O McCotter SM Anderson K Komatsu F Tabnak DJ Vugia Y Yang and JN Galgiani 2011 The public health impact of coccidioidomycosis in Arizona and California Int J Environ Res Public Health 8411501173 9 Helmick KE P Koplos and J Raymond 2006 Disseminated coccidioidomycosis in a captive Indochinese tiger Panthera tigris corbetti with chronic renal disease J Zoo Wildl Med 374542 4 10 Ingram K 1975 Coccidioidomycosis in a colony of chimpanzees In 1975 Proceedings AAZV Conference 127132 11 Iowa State Center for Food Safety and Public Health Coccidioidomycosis Fact Sheet httpwwwcfsphiastateeduFactsheetspdfscoccidioidomycosispdf Accessed 2 July 2013 12 Janssen DL BA Rideout and ME Edwards 1996 Medical management of captive tapirs In 1996 Proceedings AAZV Conference 111 13 Jessup DA ND Kock and M Berbach 1989 Coccidiomycosis in a desert bighorn sheep Ovis Canadensis nelson from California J Zoo Wildl Med 204 4713 14 Reed RE G Migaki and JA Cummings 1976 Coccidioidomycosis in a California sea lion Zalophus californianus J Wildl Dis 1233725 15 Reidarson TH LA Griner LA D Pappagianis and J McBain 1998 Coccidioidomycosis in a bottlenose dolphin J Wildl Dis 343 62931 16 Terio KA IH Stalis JL Allen JL Stott and MB Worley 2003 Coccidioidomycosis in Przewalskis horses Equus przewalskii J Zoo Wildl Med 344 33945 17 Timm KL RJ Sonn and BD Hultgren 1988 Coccidioidomycosis in a Sonoran gopher snake Pituophis melanoleucus affinis J Med Vet Mycol 262 1014 18 Wallace RJ VL Clyde VL and H Steinberg 2009 Coccidioidomycosis in a black rhinoceros Diceros bicornis J Zoo Wildl Med 402 3658 19 Wheat LJ 2010 Coccidioidomycosis in animals MiraVista Diagnostics httpwwwmiravistalabscomwpcontentuploads201207CoccidioidomycosisinanimalsJanuary 19th2012pdf Accessed 2 July 2013 American Association of Zoo Veterinarians Infectious Disease Manual CONTAGIOUS BOVINE PLEUROPNEUMONIA Fact Sheet compiled by Amanda Guthrie Sheet completed on 16 March 2011 updated on 5 April 2013 updated on 13 Feb 2018 Fact Sheet Reviewed by Mark Drew Nancy Carpenter Susceptible animal groups Domesticated bovids Bos spp cattle bison yak and water buffalo have been infected Wild bovids and camels are resistant Primarily young animals are affected Sheep and goats may be infected but do not experience pathology Causative organism Mycoplasma mycoides mycoides small colony type MmmSC Mycoplasma is a self replicating pleomorphic and prokaryotic organism resistant to betalactam antibiotics Zoonotic potential No Distribution Endemic in most of Africa Not in United States since 1892 considered to be eradicated from Western Hemisphere Occasional outbreaks in the Middle East Asia India and China and parts of Europe Spain Portugal and Italy Incubation period 1 3 months typically but can range from 5 207 days Clinical signs Similar to other pneumonias in cattle and difficult to differentiate based on clinical signs It can cause polyarthritis or joint disease in young animals Acute Severe respiratory signs such as coughing labored breathing outstretched neck and wide stance loss of appetite and weight loss and decreased milk production Chronic mild cough recurrent lowgrade fever Carriers few or no signs of illness Post mortem gross or histologic findings Thickening and inflammation of lung tissues typical of pleuropneumonia Large amounts of strawcolored fluid in the thoracic cavity Marbled appearance of lungs in both acute and chronic cases Fluid accumulation in the lungs fibrosis of lung tissue and pleura fibrin deposits throughout the thorax Diagnosis Confirmed with a blood serological screening test organism can be culturedisolated and identified with several tests Available tests include complement fixation latex agglutination and competitive ELISA Material required for laboratory analysis Live animal blood nasal secretions bronchoalveolar washes pleural fluid Dead animal lung fluids lymph nodes joint fluid and purulent discharge from lung tissue Relevant diagnostic laboratories IDEXX CBPP Ab Test available outside the US Treatment Not recommended but tylosin is reported to be effective Streptomycin oxytetracycline fluoroquinolones and chloramphenicol may slow progression of disease and predispose to formation of sequestra Treatment should only be attempted in endemic areas treatment is unlikely to eliminate organisms and will likely result in a carrier state Prevention and control Quarantine of exposed and infected animals testing and slaughter of infected animals Organism is transmitted via saliva urine fetal membranes and uterine discharges Vaccine is available in endemic areas only effective if herd coverage is high Suggested disinfectant for housing facilities Inactivated by common disinfectants such as bleach may survive in the environment for a few days Formaldehyde solution 05 30 seconds can be applied Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Cattle Bos spp bison yak water buffalo reindeer sheep and goats Direct Aerosol Transplacental Fever lethargy severe respiratory signs weight loss Occasionally causes joint disease Variable can be severe causes death rates of up to 80 of affected animals in Africa Not recommended Quarantine testing and removal of infected animals No American Association of Zoo Veterinarians Infectious Disease Manual CONTAGIOUS BOVINE PLEUROPNEUMONIA Notification Foreign animal disease contact appropriate state and federal authorities immediately Reportable disease in many countries Measures required under the Animal Disease Surveillance Plan Reportable as a foreign animal disease Measures required for introducing animals to infected animal Not recommended culling recommended Conditions for restoring diseasefree status after an outbreak all animals negative 12 months after last positive animal or last vaccinated animal slaughtered Experts who may be consulted Idexx Laboratories 18005489997 httpwwwidexxcom References 1 Amanfu W Contagious bovine pleuropneumonia lung sickness in Africa Onderstepoort J Vet Res 2009761137 2 Campbell J Contagious Bovine Pleuropneumonia cited 2018 February 13 Available from httpwwwmsdvetmanualcomrespiratorysystemrespiratorydiseasesofcattlecontagiousbovine pleuropneumonia 3 Contagious bovine pleuropneumonia CBPP Internet OIE 2018 cited 2018 February 13 Available from httpwwwoieintanimalhealthintheworldofficialdiseasestatuscbbp 4 Contagious bovine pleuropneumonia CBPP Internet EAZWV Transmissible Disease Fact Sheet 2002 cited 2018 February 13 Available from httpcymcdncomsiteswwweazwvorgresourceresmgrFilesTransmissibleDiseasesHandbookFact Sheets014ContagiousBovinePleuropdf 5 Contagious bovine pleuropneumonia Internet The Center for Food Security Public Health c2003 2015 cited 2018 February 13 Available from httpwwwcfsphiastateeduFactsheetspdfscontagiousbovinepleuropneumoniapdf 6 Contagious bovine pleuropneumonia Internet The Center for Food Security Public Health c2004 2018 cited 2018 February 13 Available from httpwwwcfsphiastateeduDiseaseInfodiseasephpnamecontagiousbovine pleuropneumonialangen 7 Contagious Bovine Pleuropneumonia Internet OIE Scientific and Technical Department 2009 cited 2018 February 13 Available from httpwwwoieintfileadminHomeengAnimalHealthintheWorlddocspdfDiseasecardsCONTAG IOUSBOVINEPLEUROPNEUMONIApdf American Association of Zoo Veterinarians Infectious Disease Manual CONTAGIOUS ECTHYMA ORF Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Domestic sheep and goats wild artiodactylids humans rarely domestic cat and dog Direct contact with vesiculo proliferative lesions or scab material Minor to severe skin proliferative lesions generally confined to skin of lips and muzzle but can affect other skin mucocutane ous areas and digestive system Typically mild and selflimiting in domestic animals but can cause fatalities in severe cases particularly in young animals and in sensitive species like musk oxen Generally no treatment is required Supportive care and treatment of secondary infections in severe cases Treatment with cidofovir systemically or topically may be beneficial Isolate infected animals Transmitted through damaged skin dispose of scab material and contaminated bedding Wear latex gloves and other protective clothing when working with known infected animals Autogenous vaccine sometimes used Yes Fact Sheet compiled by James M Rasmussen Sheet completed on updated 6 January 2018 Fact Sheet Reviewed by Anne Burgdorf Kristin J Torbin Susceptible animal groups Ruminants ovids caprids cervids typically but experimental transmission to calves monkeys camelids and possibly dogs cats and squirrels Causative organism Highly infectious epitheliotropic doublestranded DNA enveloped virus in the family Poxvidae subfamily Chordopoxvirinae genus Parapoxvirus which includes the closely related bovine popular stomatitis virus pseudocowpox virus parapox virus of reindeer parpapoxvirus of red deer in New Zealand and parapoxvirus of seals Zoonotic potential Yes orf virus is readily transmitted to humans Infection typically occurs when abraded skin contacts infected animals or fomites Distribution Orf virus has a worldwide distribution and is a common cause of disease in domestic sheep and goats and can affect a wide range of wild artiodactylids Incubation period 23 days experimentally 68 days under natural conditions Clinical signs Humans Generally cause wartlike lesions on the hands and arms of people handling infected animals Lesions progress quickly from macule papule vesicle pustule until they become crusty lesions As with animals secondary bacterial infection may occur and can cause more severe complications in immunocompromised people In uncomplicated cases they will heal in 26 weeks without scarring Animals Similar to humans in rapid progression from macule through crusty proliferative papillomatous growths Generally start on mucocutaneous regions of the muzzle around nares and lip commissures but can affect periorbital area udder legscoronary region and oral cavity Periorbital lesions may lead to visual impairment andor mechanical trauma to cornea Lesions on the muzzle or presence in oral cavity may reduce feed intake particularly in young suckling animals Lesions rarely occur in esophagus or forestomach Secondary bacterial infections and myiasis may also occur In uncomplicated cases scabs generally fall off in 4 6 weeks but may persist for months Post mortem gross or histologic findings Histologically mature lesions demonstrate epidermal hyperplasia with ballooning degeneration of keratinocytes of the stratum spinosum ulceration and intracytoplasmic inclusion American Association of Zoo Veterinarians Infectious Disease Manual CONTAGIOUS ECTHYMA ORF bodies Oftentimes secondary bacterial infections are present Diagnosis Electron microscopy of fresh or frozen lesion biopsies will typically demonstrate morphologically distinct ovoidshaped parapoxvirus virions approximately 260nm x 160nm Scab is not a preferred sample as it generally does not contain large numbers of virus PCR and sequencing of viral DNA is required to differentiate Orf virus from other parapox viruses Real time PCR can be performed on formalin fixed paraffin embedded samples if freshfrozen tissue is unavailable Material required for laboratory analysis Biopsies of lesion freshfrozen and formalin fixed Relevant diagnostic laboratories Laboratories capable of performing electron microscopy of biopsy samples can identify to the level of parapox virus Sequencing of viral DNA is required for more specific identification Treatment Lesions are generally selflimiting but in some severe cases supportive care and antibacterial therapy for secondary infections is indicated The antiviral drug cidofovir has been used with some success in the treatment of some pox virus infections However little if any benefit was subjectively noted during a course of intravenous treatment of cidofovir in two musk ox calves as compared to an untreated herd mate An experimental trial using topical spray of cidofovir sucralfate and sodium dihydrogen phosphate has shown benefit in sheep and cidofovir cream has been useful to treat lesions in people In severe unresponsive cases euthanasia should be considered before secondary complications cause significant morbidity Prevention and control Vaccination should not be used in areas where the disease has not occurred In endemic areas sheep and goats may be vaccinated with live virus vaccine which can be obtained from Colorado Serum Company PO Box 16428 Denver Colorado 80216 8005252065 httpwwwcoloradoserumcom The vaccine is an attenuated live virus product which can cause disease in naïve animals and in susceptible species and people Trial work has been done with DNA vaccines in China Neither natural infection nor vaccination confers longterm immunity but subsequent infections are generally less severe Vaccines are more protective when developed from virus obtained from the same species infected Infected animals should be isolated as long as scab material is present Virus may persist in the environment or in wool for years in cool dry areas when encrusted in scab or organic material Suggested disinfectant for housing facilities Removal and incineration or burial of organic material Sunlight heat and humidity leads to more rapid inactivation of virus but virus may persist for months to years if frozen or present in cool dry locations Fairly resistant to disinfectants but phenolics quaternary ammonium compounds and iodophors can be effective disinfectants with proper concentration and contact time Organic debris will decrease disinfectant efficacy Steam sterilization and dry heat may also be utilized for disinfection Notification Public health officials may need to be notified if zoonotic transmission occurs depending on the state Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Maintain infected animals in a quarantine situation until lesions have healed and scabs have been lost If feasible may want to bathe infected animal in order to remove all virus from fur Do not introduce infected animal to an animal with a compromised immune system Conditions for restoring diseasefree status after an outbreak Wait for all scabs to be lost from infected animals Remove bedding and biological material to the extent possible and disinfect with phenolic or quaternary ammonia disinfectants Experts who may be consulted Andrés de la Concha DVM MSPhD Texas Veterinary Medical Diagnostic Laboratory Texas AM University System 483 Agronomy Road College Station TX 77840 Tel 9798453414 Fax 9798451794 adelaconchatvmdltamuedu American Association of Zoo Veterinarians Infectious Disease Manual CONTAGIOUS ECTHYMA ORF References 1 Centers for Disease Control and Prevention Internet Orf Virus Sore Mouth Infection 2015 cited 2018 January 6 Available from httpwwwcdcgovncidoddvrdorfvirus 2 DAlterio GL Contagious ecthyma In Kaandorp J ed Transmissible Diseases Handbook 2nd edition Van Setten Kwadraat The Netherlands European Association of Zoo and Wildlife Veterinarians Infectious Disease Working Group 2004 p 447449 3 de la ConchaBermejillo A Orfcontagious ecthyma In Blackwells Fiveminute Veterinary Consult Ruminant 2nd edition Chase CCL Lutz KA McKenzie EC Tibary A eds Ames IA Wiley Blackwell 2017 p 564565 4 Essbauer S Pfeffer M Meyer H Zoonotic poxviruses Vet Microbiol 201014034229236 5 Fairley R Whelan EM Pesavento P Mercer A Recurrent localized cutaneous parapoxvirus infection in three cats N Z Vet J 2008564196201 6 Gallina L Scagliarini A Virucidal efficacy of common disinfectants against orf virus Vet Rec 2010166725 7 Guo J Rasmussen J Wünschmann A de la ConchaBermejillo A Genetic characterization of orf viruses isolated from various ruminant species of a zoo Vet Microbiol 2004998192 8 Haig DM and AA Mercer 1998 Orf Review Article Vet Res 29 311326 9 Mercer AA Schmidt A Weber O Poxviruses Birkhäuser Advances in Infectious Diseases Basel Switzerland Birkhäuser Verlag 2007 441 pp 10 Nandi S De UK Sumit C Current status of contagious ecthyma or disease in goat and sheep a global perspective Sm Rum Res 2011967382 11 Oryan A Mosadeghhesari M Zibaee S Mohammadi A Identification and phylogenetic analysis of contagious ecthyma virus from camels Camelus dromedaries in Iran Onderstepoort J Vet Res 2017841e1e5 12 Robinson AJ Kerr PJ Poxvirus infections In Williams ES and IK Barker eds Infectious Diseases of Wild Mammals 3rd ed Ames IA Iowa State University Press 2001 p 179201 13 Sonvico F Colombo G Gallina L Bortolotti F Rossi A McInnes CJ Massimo G Colombo P Scagliarini A Therapeutic paint of cidofovirsucralfate gel combination topically administered by spraying for treatment of Orf virus infections AAPS J 200911242249 14 Sprou V Valiakos G Orf virus infections in sheep or goats Vet Microbiol 201518117882 15 Vikøren T Lillehaug A Åkerstedt J Bretten T Haugum M Tryland M A severe outbreak of contagious ecthyma orf in a freeranging musk ox Ovibos moschatus population in Norway Vet Microbiol 2008127121020 16 Williams CJ Scheftel JM Elchos BL Hopkins SG Levine JF Compendium of Veterinary Standard Precautions for Zoonotic Disease Prevention in Veterinary Personnel National Association of State Public Health Veterinarians Veterinary Infection Control Committee J Am Vet Med Assoc 201524711125277 Erratum in J Am Vet Med Assoc 20152482171 17 Zhao K He W Gau W Lu H Han T Li J Zhang X Zhang B Wang G Su G Zhao Z Song D Gao F Orf virus DNA vaccines expressing ORFV 011 and ORFV 059 chimeric protein enhances immunogenicity Virol J 20118562 American Association of Zoo Veterinarians Infectious Disease Manual CORONAVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Multiple mammalian and avian taxa Fecaloral inhalation contaminated feed or fomites Diarrhea often mucoid due to enteritis respiratory discharge dyspnea lethargy death Asymptomatic infections are possible bats However when disease occurs it is often severe Supportive antibiotics to reduce secondary infections Vaccines exist for certain species Recommended for Avian Infectious Bronchitis Virus Bovine Coronavirus Transmissible Gastroenteritis Virus SARS and MERS are known to be zoonotic Other coronaviruses may gain the ability to infect a new host including humans Fact Sheet compiled by Meredith M Clancy Sheet completed on 17 Jan 2018 Fact Sheet Reviewed by Kirsten Gilardi Susceptible animal groups Birds Avian Infectious Bronchitis Virus IBV poultry Turkey Coronaviral Enteritis TCE turkeys multiple other less pathogenic avian coronaviruses in other species Mammals Nearly ever mammal family has an endemic coronavirus In Hoofstock Bovine Coronavirus BCV domestic cattle multiple ruminant species including cervids nondomestic bovids and giraffids Equine Coronavirus ECoV equids Porcine Deltacoronavirus PDCoV Porcine Epidemic Diarrhea Virus PEDV Porcine Respiratory Coronavirus PRCoV and Transmissible Gastroenteritis TGEV suids In Carnivores Canine Enteric Coronavirus CCV emerging canine respiratory coronavirus CRCoV canids Feline Coronavirus FCoV felids including both wild and captive exotic felids Note biotype that develops into feline infectious peritonitis FIP covered separately in this manual Ferret enteric coronavirus FECV formerly Epizootic Catarrhal Enteritis or ECE and Ferret Systemic Coronavirus FRSCV ferrets Middle East Respiratory Syndrome coronavirus MERSCoV humans suspected reservoir in bats camels In other mammalsmultiple species Severe Acute Respiratory Syndromeassociated Coronavirus SARSCoV humans possibly other primates carnivoresincluding palm civets raccoon dogs ferret badgers and domestic catsand bats Causative organism Each disease caused by specific coronavirus family Coronaviridae Zoonotic potential Both SARS and MERS are confirmed zoonotic diseases Distribution Avian coronavirus distribution worldwide BCoV CCV FCoV worldwide MERSCoV Middle East SARS CoV Asia PEDV discovered in UK in 1971 spread to Europe and Asia by 2013 first case in US in 2013 TGEV worldwide though less frequently in Europe epidemic form its deletion mutant PCRV first noted in 1980s exists in endemic form American Association of Zoo Veterinarians Infectious Disease Manual CORONAVIRUS FRECV first noted in 1993 in US FRSCV first noted in Spain in 2004 also present in US PDCoV first noted in US in 2014 Incubation period generally very short ranging from 1824 hours to 34 days Clinical signs One of three disease manifestations Enteric coronaviruses BCoV CCV ECoV FCoV FECV PDCoV PEDV TGEV with tropism for GI epithelial cells cause malabsorptive maldigestive diarrhea with possible dehydration metabolic acidosis and death generally seen in young animals especially BCV TGE and PED In BCV and TGE the diarrhea is often mucoid and yellow in color with possible milk clots In FECV the diarrhea begins as green and mucoid progressing to a ricewater granular stool Respiratory coronaviruses PRCoV MERSCoV SARSCoV are adapted to enter and reproduce in the upper respiratory mucosa causing fever nasal discharge cough pneumonia and possibly death Of note BCoV has been implicated as a part of bovine respiratory disease complex although whether this is due to the same or different virus remains unclear Systemic coronaviruses infect and persist in macrophages causing lethargy weight loss anorexia abdominal masses anemia peritonitis vasculitis peritoneal effusions and death Post mortem gross or histologic findings Enteric coronaviruses gross lesions include thinwalled flaccid small intestine often with yellowish contents fluid in the colon andor cecum microscopically villous atrophy and blunting with clubshaped stumpy villi often fused hyperplastic crypt epithelium Respiratory coronaviruses specifically SARS and MERS gross lesions include pulmonary edema and consolidation microscopically diffuse alveolar damage with acute exudates with edema hyaline membranes and fibrosis with mixed cellular infiltration Systemic coronaviruses specifically FSCV gross lesions include whitish nodules through peritoneal viscera peritoneal effusion microscopically pyogranulomatous inflammation of visceral peritoneum mesenteric adipose tissue liver lungs kidneys lymph nodes spleen pancreas and other peritoneal viscera Diagnosis Avian IBV ELISA available for flock screening qPCR also available Electron microscopy EM can be used as screening test for enteric coronaviruses Molecular diagnostics eg PCR most widely used for antemortem diagnosis of coronaviruses PCR generally cross reacts among the alphacoronaviruses FCoV FECV CCV TGEV and betacoronaviruses BCV PCR confirmation in presence of clinical suspicion performed by CDC approved lab for MERS SARS Indirect fluorescent antibodies IFA are often used on affected tissue in postmortem samples but can be used on antemortem swabs of nasal discharge or feces IFA available for BCV TGE CCV Material required for laboratory analysis ELISA blood serum or eggs poultry EM feces tissue IFA intestinal or respiratory tissue nasalpharyngeal swab or tracheal washbronchoalveolar lavage IHC formalinfixed tissue PCR blood serum or EDTA mucosal oropharyngeal nasal rectal swabs peritoneal fluid feces fresh tissue Relevant diagnostic laboratories Many tests widely available in state diagnostic labs in US Specific testing IDEXX ELISA IBV Cornell Animal Health Diagnostic Laboratory IFA multiple PCR individual and generic alpha and beta coronavirus viral isolation httpsahdcvetcornelledu Iowa State University Veterinary Diagnostic Laboratory PCR BCoV CCV all porcine IHC BCoV ELISA TGE PRCoV whole genome sequencing PDCoV httpvetmediastateedudiagnosticlab American Association of Zoo Veterinarians Infectious Disease Manual CORONAVIRUS Michigan State University Diagnostic Center for Population and Animal Health PCR BCoV CCV ECoV FeCoV FECV PDCoV PEDV httpswwwanimalhealthmsuedu Texas AM Veterinary Medical Diagnostic Laboratory PCR porcine BCoV CRCoV IFA BCoV FeCV EM httptvmdltamuedu Treatment Treatment is supportive In the case of enteric coronaviruses treatment of the dehydration and electrolyte abnormalities is often accompanied by antibiotics to control secondary bacterial infections Respiratory coronaviruses are often selflimiting except in the case of the rare zoonotic SARS and MERS Treatment of systemic coronaviruses is generally not successful but rather focuses on controlling clinical signs Prevention and Control Enteric coronaviruses are best prevented in similar fashion by reducing fecal contamination of environment through routine cleaning and removal of feces disinfection of enclosures bowls and other material with bleach once weekly For respiratory coronaviruses isolation of sick individuals and quarantine of new animals is important to reduce exposure of naïve animals to shed virus In production animals the allinallout technique is used to reduce exposure and contamination Vaccinations are available in many species and recommended to prevent IBV BCoV and TGEV Vaccines often are combination rotavirus and coronavirus products and have been used in exotic hoofstock although efficacy is variable and vaccine reactions have been reported in giraffids Okapia johnstonii Coronavirus vaccination is not currently recommended in domestic carnivores Suggested disinfectant for housing facilities Coronaviruses are enveloped and labile in the environment They are generally vulnerable to sunlight and basic disinfectants like bleach iodine and quaternary ammonium compounds Notification MERS and SARS are reportable to CDC TGE reportable to USDA Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Asymptomatic carriers are considered common in ferret coronaviruses Pigs and cattle that have recovered from coronaviruses are not considered at high risk for repeat disease Conditions for restoring diseasefree status after an outbreak NA Experts who may be consulted Linda Saif MS PhD Honorary Diplomate ACVM Food Animal Health Research Program Ohio Agricultural Research and Development Center The Ohio State University 1680 Madison Avenue Wooster Ohio 44691 3302633742 Saif2osuedu Simon Anthony Assistant Professor Epidemiology Columbia University Medical Center 722 West 168th Street 17th floor New York NY 10033 7605004639 Gary Whittaker PhD Cornell University College of Veterinary Medicine Microbiology Immunology C4 127 Veterinary Medical Center 6072534019 American Association of Zoo Veterinarians Infectious Disease Manual CORONAVIRUS grw7cornelledu USDA APHIS VS Center for Epidemiology and Animal Health 2150 Centre Ave Bldg B Fort Collins CO 80526 9704947200 vsceahaphisusdagov Tracey Goldstein Associate Adjunct Professor Medicine and Epidemiology University of California Davis tgoldsteinucdavisedu 5307520412 References 1 Alekseev KP Vlasova AN Jung K Hasoksuz M Zhang X Halpin R Wang S Ghedin E Spiro D Saif LJ Bovinelike coronaviruses isolated from four species of captive wild ruminants are homologous to bovine coronaviruses based on complete genomic sequences J Virol 20088212422 12431 2 American Association of Swine Veterinarians Swine Disease Manual Neumann EJ Ramirex A Schwartz KJ eds Perry IA American Association of Swine Veterinarians 2010 Available from httpsvetmediastateeduvdpamFSVDswineindexdiseases 3 Cavanagh D Coronaviruses in poultry and other birds Avian Pathol 200534439448 4 Chu DKW Leung CYH Gilbert M Joyner LH Ng EM Tse TM Guan Y Peiris JSM Poon LLM Avian coronavirus in wild aquatic birds J Virol 201185 1281512820 5 Chung JY Kim HR Bae YC Lee OS Oem JK Detection and characterization of bovinelike coronaviruses from four species of zoo ruminants Vet Microbiol 2001148396401 6 Citino SB Rotavirus and coronavirus infections in nondomestic ruminants In Fowler ME Miller RE eds Zoo and wild animal medicine Volume 4 Current therapy Philadelphia PA WB Saunders Co 1999 p 605612 7 Garner MM Ramsell K Morera N JuanSallés C Jiménez J Ardiaca M Montesinos A Teifke JP Löhr CP Evermann JF Baszler TV Nordhausen RW Wise AG Maes RK Kiupel M Clinicopathologic features of a systemic coronavirusassociated disease resembling feline infectious peritonitis in the domestic ferret Mustela putorius Vet Pathol 200845236246 8 Gu J Korteweg C Pathology and pathogenesis of severe acute respiratory syndrome Am J Pathol 200717011361147 9 Hasoksuz M Alekseev K Vlasova A Zhang X Spiro D Halpin R Wang S Ghedin E Saif LJ Biologic antigenic and fulllength genomic characterization of a bovinelike coronavirus isolated from a giraffe J Virol 20078149814990 10 Murray J Kiupel M Maes RK Ferret coronavirusassociated diseases Vet Clin N Am Exot Anim Pract 201013543560 11 Shi Z Hu Z A review of studies on animal reservoirs of the SARS coronavirus Virus Res 20081337487 12 United States Department of Agriculture Internet Technical Note Porcine epidemic diarrhea PED cited 5 Aug 2018 Available from httpwwwaphisusdagovanimalhealthanimaldisspecswinedownloadspedtechnotepdf 13 Woolums AR Lower respiratory tract diseases In Smith BP ed Large animal internal medicine 5th edition St Louis MO Elsevier 2015 p 592593 American Association of Zoo Veterinarians Infectious Disease Manual COWPOX VIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Rodent reservoir with large affected host range including Felidae Bovidae Elephantidae Equidae Canidae Mustelidae Ailuridae Herpestidae Suidae Camelidae Tapiridae Rhinocerotidae black and white Myrmecopha gidae Soricidae Cercopithecidae Callitrichidae Humans Most likely direct contact with infected animal or scabs Poxviruses are fairly resistant to environ mental inactivation From mild skin lesions to severe skin oral esophageal and respiratory lesions Skin lesions may be absent in the pulmonary form Lymph adenopathy and conjunctivitis may occur From mild to fatal although human fatalities are rare Severity may depend on virus strain as well as species infected and individual immune status Generally selflimiting Supportive care in more severe cases with antibiotics for secondary infections Systemic or topical antiviral therapy with cidofovir may be beneficial Isolation of infected animals Protective equipment including latex gloves and face shield to prevent cutaneous and mucous membrane exposure Rodent control in endemic areas Vaccinia virus vaccines available for zoo animals in some countries Yes Fact Sheet compiled by James M Rasmussen Sheet completed on updated 20 January 2018 Fact Sheet Reviewed by Sarah A Cannizzo Susceptible animal groups Rodents voles mice rats gerbils ground squirrels beaver cavy shrew felids domestic cat cheetah lynx African lion spotted leopard ocelot jaguar puma jaguarundi Asian leopard cats cattle canids dog red fox arctic fox banded mongoose marten red panda wild boar okapi llama alpaca horse Malayan tapir black rhinoceros white rhinoceros Asian elephant African elephant anteater Barbary macaque common marmoset and human Causative organism Doublestranded DNA enveloped virus in the family Poxviridae subfamily Chordopoxvirinae genus Orthopoxvirus which includes smallpox Variola virus monkeypox buffalopox vaccinia virus ectromelia camelpox horsepox raccoonpox skunkpox volepox and Uasin Gishu disease Multiple strains of cowpox exist Zoonotic potential Yes Smallpox vaccination confers protection against cowpox as well Cats are the most common source of human infection Less common sources include cattle pet rats and an Asian elephant Distribution Endemic in various rodent reservoir hosts in Great Britain Scandinavia European mainland and adjacent western Asiatic countries Incubation period 310 days Clinical signs Skin lesions usually progress through characteristic macule papule vesicle and pustule phase before becoming scabbed Generally mild selflimiting cutaneous pox lesions in humans and most animal species but can become generalized andor cause necrotizing pneumonia in certain species or immune compromised individuals Strain route and dose of virus causing infection may influence course of disease Humans Generally localized lesions on hands face arms or other points of contact with infected animal Infection may cause lymphadenopathy and flulike symptons Lesions typically resolve in 68 weeks without secondary bacterial infections which can extend the process by several weeks Systemic infections and fatalities American Association of Zoo Veterinarians Infectious Disease Manual COWPOX VIRUS may occur in immunecompromised individuals Previous vaccinia vaccination for smallpox should confer at least partial immunity Animals Mild localized pox lesions to generalized lesions with ulcerations including the conjunctiva oral cavity and esophagus Oral lesions may cause anorexia An uncommon disease in cattle but lesions most typical on udder and teats of cows and mouths of suckling calves Infection may cause pyrexia and lymphadenopathy Pulmonary disease is rare in most species but is more common in felid species Pulmonary involvement has also been seen in giant anteaters Postmortem gross or histologic findings Epitheliotropic virus The lesions undergo the classical poxvirus cascade of macules papules and later collapse of the lesion from the center giving the lesion a targetoid appearance The lesions then scab over and are slow to heal Histologically affected epithelial cells demonstrate ballooning degeneration and may have eosinophilic homogenous intracytoplasmic inclusions The affected cells often swell and rupture leaving spaces filled with neutrophils and debris pustules These lesions with intraepithelial intracytoplasmic inclusions have also been identified in the pulmonary tract and oral cavity In an outbreak in captive banded mongooses inclusions were also present in hepatocytes enterocytes as well as in cells with histiocytic and fibroblastic morphology Diagnosis Histopathology shows characteristic large homogenous eosinophilic cytoplasmic inclusion bodies in epithelial cells undergoing ballooning degeneration Electron microscopy of fresh or frozen lesion material will typically demonstrate morphologically distinct orthopoxvirus approximately 220nm x 280nm brickshaped virions with tubular surface projections Cell culture PCR and DNA sequence analysis Serologic testing is available to determine if exposure occurred Material required for laboratory analysis Biopsies of lesions freshfrozen and formalin fixed Relevant diagnostic laboratories Laboratories capable of performing electron microscopy of biopsy samples can identify to the level of Orthopox virus Sequencing of viral DNA is required for more specific identification Treatment Lesions are generally selflimiting but in some severe cases supportive care and antibiotics for secondary infections are indicated Systemic treatment with the antiviral drug cidofovir has been used with some success in the treatment of some pox virus infections but severe side effects have been reported in humans eg nephrotoxicity A compounded topical cream preparation of cidofovir is available as well In severe unresponsive cases euthanasia should be considered before secondary complications cause significant morbidity Prevention and control Control of rodents to the extent possible in endemic areas Isolated affected animals if possible Vaccination of susceptible zoo animals with modified vaccinia virus Ankara MVA is authorized in some European countries Suggested disinfectant for housing facilities Removal and incineration or burial of organic material Sunlight heat and humidity leads to more rapid inactivation of virus but virus may persist for months or longer in scabs or crusts if frozen or present in cool dry locations Fairly resistant to disinfectants but phenolics quaternary ammonium compounds and iodophors can be effective disinfectants with proper concentration and contact time Organic debris will decrease disinfectant efficacy Steam sterilization may also be utilized for disinfection Notification May be reportable is some jurisdictions Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Maintain infected animals in a quarantine situation until lesions have healed and scabs have been lost If feasible may want to bathe infected animal in order to remove all virus from fur In endemic areas may want to vaccinate susceptible species Recovered animals should have immunity to the virus Surviving infected brown rats have demonstrated continued viral shedding in feces and urine for more than a month after recovery Conditions for restoring diseasefree status after an outbreak Wait for all scabs to be lost from an infected animal Remove bedding and biological material and incinerate or dispose of with other appropriate method Disinfect environment with phenolic or quaternary ammonia disinfectants to the extent possible Experts who may be consulted Robert B Moeller Jr DVM DACVP DABT rbmoellerucdavisedu 5596795653 American Association of Zoo Veterinarians Infectious Disease Manual COWPOX VIRUS Book Chapters 1 Campe H Zimmermann P Glos K Bayer M Bergemann H Dreweck C Graf P Weber BK Meyer H Büttner M Busch U Sing A Cowpox virus transmission from pet rats to humans Germany Emerg Inf Dis 2009155 777780 2 Cardeti G Brozzi A Eleni C Polici N DAlterio G Carletti F Scicluna MT Castilletti C Capobianchi MR Di Caro A Autorino GL Amaddeo D Cowpox virus in llama Italy Emerg Inf Dis 201117815131515 3 Essbauer S Meyer H Genus Orthopoxvirus Cowpox virus In Mercer AA Schmidt A Weber O eds Poxviruses Birkhäuser Advances in Infectious Diseases Basel Switzerland Birkhäuser Verlag 2007 p 7587 4 Essbauer S Pfeffer M Meyer H Zoonotic poxviruses Vet Microbiol 201014034229236 5 Kurth A Wibbelt G Gerber H Petschaelis A Pauli G Nitsche A Rattoelephanttohuman transmission of cowpox virus Letter Emerg Inf Dis 2008144670671 6 McInerney J Papasouliotis K Simpson K English K Cook S Milne E GunnMoore DA Pulmonary cowpox in cats five cases J Fel Med and Surg 2016186518525 7 Moeller Jr RB Cowpox In Chase CCL Lutz KA McKenzie EC and A Tibary A eds Blackwells Fiveminute Veterinary Consult Ruminant 2nd ed Ames IA WileyBlackwell 2017 p 263264 8 Ninove L Domart Y Vervel C Voinot C Salez N Raoult D Meyer H Capek I Zandotti C Charrel RN Cowpox virus transmission from pet rats to humans France Emerg Inf Dis 2009155781784 9 Robinson AJ Kerr PJ 2001 Poxvirus infections In Williams ES Barker IKeds Infectious Diseases of Wild Mammals 3rd ed Ames IA Iowa State University Press 2001 p 179201 10 Schmiedeknecht G Eickmann M Köhler K Herden CE Kolesnikova L Förster C Burkhardt EH König M Thiel M Reinacher M Fatal cowpox virus infection in captive banded mongooses Mungos mungo Vet Path 2010473 547552 11 Williams CJ Scheftel JM Elchos BL Hopkins SG Levine JF Compendium of Veterinary Standard Precautions for Zoonotic Disease Prevention in Veterinary Personnel National Association of State Public Health Veterinarians Veterinary Infection Control Committee J Am Ve Med Assoc 201524711 12521277 Erratum in J Am Vet Med Assoc 20162482 171 12 Wolters M Cowpox virus In Kaandorp J ed Transmissible Diseases Handbook 2nd ed European Association of Zoo and Wildlife Veterinarians Infectious Disease Working Group Van Setten Kwadraat The Netherlands 2004 p 435436 American Association of Zoo Veterinarians Infectious Disease Manual Q FEVER Coxiella burnetii Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Ruminants cats dogs lagomorphs birds marsupials marine mammals human Two patterns 1 wild animals and ticks 2 domes tic ruminants independent of wildlife cycles Shed in high numbers within amniotic fluid and placenta Excreted in milk urine feces It also may be spread through wind and dust Mammal infections may be sub clinical or lead to fever anorexia late term abortions infertility retained placenta metritis Highly infectious Humans acute form has moderate morbidity 50 generally low mortality 1 2 Mortality with endocarditis is up to 65 Tetracycline antibiotics if showing clinical signs Appropriate disposal of placenta aborted fetuses Yes most often an acute febrile illness but chronic manifesta tion such as endo carditits can occur Fact Sheet compiled by Diana Boon Sheet completed on 22 November 2010 updated 15 November 2012 Fact Sheet Reviewed by Betsy Stringer Jane Sykes Susceptible animal groups Periparturient ruminants goats sheep cattle pigs cats dogs and wild animals lagomorphs and birds Host range includes wild and domestic mammals arthropods ixodid and argasid ticks and birds Causative organism Coxiella burnetii obligate intracellular Gramnegative bacteria Zoonotic potential Yes with acute and chronic presentations Distribution Global Incubation period Depends on number of infective organisms but usually 23 weeks Two patterns of transmission via freeranging animals and ticks or between domestic animals with no wild animal involved Tick bites are important for spread to animals but rarely spread infections to humans Human to human transmission is rare Clinical signs Periparturient ruminants present subclinical disease infertility or anorexia retained placenta metritis or late term abortion Often sporadic abortions in herds can be seen that are followed by recovery without complications In humans acute Q fever is characterized by marked pyrexia severe headache myalgia pneumonia and similar flulike signs while the chronic form is manifested as endocarditis granulomatous hepatitis optic neuritis osteomyelitis and or prolonged fever and chronic fatigue syndrome Post mortem gross or histologic findings Necrotizing placentitis with large number of organisms in trophoblasts but otherwise it is nonspecific Immunohistochemistry for C burnetii can be performed on affected tissues mammary glands supramammary lymph nodes placenta uterus aborted fetus The organism has a predilection for macrophages and monocytes American Association of Zoo Veterinarians Infectious Disease Manual Q FEVER Coxiella burnetii Diagnosis IFA antibody tests can be used to screen for exposure or to identify recent infection using paired sera Antibodies to phase 1 antigens predominate in chronic infection whereas those to phase 2 antigens predominate in acute infection A compliment fixation test is also available but is less sensitive Antibodies to both phase 1 and phase 2 antigens can persist for several years after the initial infection Other means of diagnosis include direct isolation using cell culture which requires highly specialized facilities PCR and immunohistochemical staining of placentaaborted tissues for organisms Smears of placental cotyledon vaginal discharge and lung liver or stomach contents of aborted fetus stained with Stamp modified ZiehlNeelson Gimenex Giemsa or modified Koster stain in order to detect organisms but diagnosis using this method should be supported with serologic test results and clinical findings Material required for laboratory analysis Placenta vaginal discharges and liver lung or stomach contents of aborted fetuses and from milk colostrum and feces At risk personnel contact with reproductive organs infected carcasses and fur or wool should wear adequate protective equipment to protect against small droplet and aerosol exposure Relevant diagnostic laboratories State diagnostic laboratories or NVSL Ames Iowa but submit to CDC Atlanta GA for confirmation as needed Positive test results are automatically reported to CDC if human cases involved Treatment Tetracyclines are generally used to treat animals if showing clinical signs Other active antimicrobials include azithromycin fluoroquinolones or trimethoprimsulfa drugs In humans prolonged combination antimicrobial drug therapy is required for treatment of chronic Q fever Prevention and control Vaccination is not commercially available in US In wildlife settings precautions against tick bites should be taken Ruminants particularly those in guest contact roles or domestic animals can be screened for antibodies to C burnetii especially if in a breeding program Obtain history of recent abortions if acquiring new animals from sending facility Segregation of pregnant and periparturient animals from any new acquisitions for several weeks postpartum and appropriate quarantine of newly acquired animals and appropriate disposal of birth tissues and aborted fetuses by incineration or burying are recommended At risk personnel contact with reproductive organs infected carcasses and fur or wool should wear adequate protective equipment to protect against small droplet and aerosol exposure Pasteurization of milk products inactivates the organism Suggested disinfectant for housing facilities Susceptible to ethanol glutaraldehyde gaseous formaldehyde 10 bleach solution but bacteria are extremely hardy and resistant to heat drying and many common disinfectants Notification Notifiable within the US if associated with human infection The organism also is considered a potential bioterrorism agent due to heat resistance high infectivity and ability to aerosolize Measures required under the Animal Disease Surveillance Plan Currently reported as present and sporadic to OIE every 6 months Measures required for introducing animals to infected animal Infected animals should be kept separated until the birth process is complete or acutely affected clinical animals have completed antibiotic therapy The key is to maintain a properly cleaned facility and dispose of placental tissue aborted fetuses and feces appropriately by incineration or burying Conditions for restoring diseasefree status after an outbreak The organism is enzootic in most areas where domestic ruminants cattle sheep goat are found and because of environmental persistence eradication is difficult The highest seroprevalence appears to be in sheep 42 If eradication is desired repeated testing should be performed potentially over several years as the antibodies can persist for an extended period of time after the initial infection Approximately 20 of seronegative animals will American Association of Zoo Veterinarians Infectious Disease Manual Q FEVER Coxiella burnetii continue to shed so testing for restoring disease free status becomes problematic Experts who may be consulted Jane Sykes BVSc PhD DACVIM University of California 2108 Tupper Hall Davis CA 95616 5307521363 jesykesucdavisedu Dave Van Metre DVM DACVIM Colorado State University 1678 Campus Delivery 205 VTH Fort Collins CO 80523 9702971299 davidvanmetreColoStateedu Paul Plummer DVM DACVIM Iowa State University 2426 Lloyd Vet Med Ames IA 50011 515 2948522 pplummeriastateedu References 1 ArricauBouvery N and A Rodolakis 2005 Is Q Fever an emerging or reemerging zoonosis Vet Res 36 327349 2 Buhariwalla F B Cann and TJ Marrie 1996 A dogrelated outbreak of Q Fever Clin Infect Dis 234 753755 3 CDC Viral and Rickettsial Zoonoses Branch Q Fever wwwcdcgovqfever Accessed 19 July 2013 4 Karakousis PC M Trucksis and JS Dumler 2006 Chronic Q Fever in the United States J Clin Microbiol 446 22832287 5 Mayo Clinic Diseases and Condition Q fever basics wwwmayocliniccomhealthqfeverDS00960 Accessed 19 July 2013 6 McQuiston JH and JE Childs 2002 Q fever in humans and animals in the United States VectorBorne Zoonotic Dis 23 179191 7 Merck Veterinary Manual Q Fever httpwwwmerckmanualscomvetgeneralizedconditionsqfeveroverviewofqfeverhtml Accessed 19 July 2013 8 OToole D 2004 Wyoming State Veterinary Laboratory handout httpwwwuwyoeduwyovetdiseaseupdates2004filesqfeverpdf Accessed 19 July 2013 9 Pinsky RL DB Fishbein CR Greene and KF Gensheimer 1991 An outbreak of cat associated Q Fever in the United States J Infect Dis 1641 202204 10 Porter SR G Czaplicki J Mainil R Guatteo and CL Saegerman 2011 Q Fever current state of knowledge and perspectives of research of a neglected zoonosis Internat J Microbiol V 2011 article ID 248418 22 pages wwwhindawicomjournalsijmb2011248418 11 Riemann HP RA Thompson DE Behymer R Ruppanner and CE Franti 1978 Toxoplasmosis and Qfever antibiodies among wild carnivores in California J Wildl Mgmt 421 American Association of Zoo Veterinarians Infectious Disease Manual Q FEVER Coxiella burnetii 198202 12 Riemann HP DE Behymer CE Franti C Crabb and RG Schwab 1979 Survey of Q fever agglutinins in birds and small rodents in northern California 197576 J Wildl Dis 154 515523 13 Rousset E B Durand M Berri P Dufour M Prigent P Russo T Delcroix A Touratier A Rodolakis and M Aubert 2007 Comparative diagnostic potential of three serological tests for abortive Q fever in goat herds Vet Microbiol 6 12434 28697 14 Struble K A Lacasse KO Cleveland H Polenakovik A Ruest and CP Sinave 2012 Q Fever httpemedicinemedscapecomarticle227156overview Accessed 19 July 2013 15 World Organization for Animal Health OIE Health Standards 2010 Manual of Diagnostic Tests and Vaccines for Terrestrial Animals Q Fever Chapter 2210 httpwwwoieintfileadminHomeengMediaCenterdocspdfDiseasecardsQFEVERENpdf Accessed 19 July 2013 16 Zarnke R 1983 Serologic survey for selected microbial pathogens in Alaskan wildlife J Wildl Dis 194 324329 American Association of Zoo Veterinarians Infectious Disease Manual CRYPTOCOCCOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals birds rare in reptiles and amphibians Inhalation of airborne organisms Typically respiratory central nervous system ocular or cutaneous signs possibly in combination Moderate to severe guarded prognosis with neurologic signs Antifungal drugs in some cases surgical excision of granulomas may be helpful Avoid contact with pigeon droppings Not directly transmissible from animals to humans Common source exposure can occur Fact Sheet compiled by Cynthia Stadler Sheet completed on 4 May 2011 updated 30 May 2013 Fact Sheet Reviewed by Jane Sykes Julie Harris Susceptible animal groups Mammals birds rarely in reptiles and amphibians Causative organism Most often it is associated with Cryptococcus neoformans or C gattii Zoonotic potential Animals and people may become infected by the same environmental source Humans with HIV are at a greater risk for acquiring infection Pet bird feces have been implicated as a possible source of C neoformans infection for immunocompromised people but and no mammaltomammal transmission has been documented Distribution Worldwide but especially southeastern and western Australia British Columbia in Canada and the west coast of the US In specific C neoformans is considered global and ubiquitous while C gattii likely is present in hotspots around the world and recently associated with an outbreak in the Pacific Northwest US and British Columbia Some implication has been made with Eucalyptus trees although other hardwood tree species have been implicated Incubation period Unknown May be a few months to many years in some circumstances Clinical signs Rhinitis sneezing pulmonary granulomas cryptococcomas chorioretinitis CNS signs include ataxia circling and blindness cutaneous nodules or ulceration lymphadenopathy weight loss lethargy vomiting if disease is widely disseminated Post mortem gross or histologic findings Gross lesions may include gelatinous masses and granulomas Histopathology reveals pyogranulomatous to granulomatous inflammation in affected organs with intralesional encapsulated yeasts that are round to oval with a distinctive capsule Diagnosis Cytology fungal culture tissue biopsy antigen testing serum and cerebrospinal fluid PCR not currently widely used Distinction of C gattii from C neoformans requires specialized canavanine glycine bromothymol blue agar Hardy Diagnostics Material required for laboratory analysis Samples of the tissue affected serum cerebrospinal fluid Relevant diagnostic laboratories Many state university and commercial laboratories run specific testing for cryptococcosis although results of antigen tests may vary between laboratories Culture is not hazardous for laboratory personnel and allows antifungal susceptibility testing and molecular typing Treatment Long term treatment months to years with fluconazole itraconazole voriconazole ketoconazole andor amphotericin B Flucytosine can be used in combination with one of these antifungal agents but should never be used alone due to rapid development of resistance and it may be prohibitively expensive Surgical excision of cutaneous nodules can assist with drug penetration into poorly perfused tissues American Association of Zoo Veterinarians Infectious Disease Manual CRYPTOCOCCOSIS Prevention and control Avoid accumulations of bird droppings especially from pigeons for C neoformans Prevention difficult to achieve for C gattii due to implications of contact with contaminated soil and tree bark Suggested disinfectant for housing facilities accelerated hydrogen peroxide potassium peroxymonosulfate 1 sodium hypochlorite iodine chlorhexidine Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal NA Conditions for restoring diseasefree status after an outbreak NA Experts who may be consulted Jane Sykes BVSc PhD DACVIM University of California 2108 Tupper Hall Davis CA 95616 Phone 5307521363 jesykesucdavisedu References 1 Aiello SE and MA Moses eds Merck Veterinary Manual Online 2013 httpwwwmerckmanualscomvetgeneralizedconditionsfungalinfectionsmycosescryptococcosish tml Accessed 2 August 2013 2 Cryptococcus neoformans Material Safety Data Sheets 2010 Public Health Agency of Canada httpwwwphacaspcgccalabbiorespsdsftsscryptococcusengphp Accessed 2 August 2013 3 Jones TC RD Hunt and NW King eds 1997 Veterinary Pathology 6th edition Lippincott Williams Wilkins Baltimore MD Pp 516517 4 Lagrou K J Van Eldere S Keuleers et al 2005 Zoonotic transmission of Cryptococcus neoformans from a magpie to an immunocompetent patient J Int Med 257 385388 5 Lester SJ R Malik KH Barlett and CG Duncan 2011 Crytpococcosis update and emergence of Crytpococcus gattii Vet Clin Pathol 40 417 6 Nosanchuk JD S Shoham BC Fries et al 2000 Evidence of zoonotic transmission of Cryptococcus neoformans from a pet cockatoo to an immunocompromised patient Ann Intern Med 132205208 7 Okabayashi K M Imaji T Osumi et al 2009 Antifungal activity of itraconazole and voriconazole against clinical isolates obtained from animals with mycoses Jpn J Med Mycol 509194 8 Spickler AR Cryptococcosis 2013 httpwwwcfsphiastateeduFactsheetspdfscryptococcosispdf Accessed 2 August 2013 9 Sykes J 2012 Treatment of fungal infections the which why and how of antifungal drug therapy Proc of ACVIM Forum New Orleans Louisiana 10 Sykes JE and RM Malik 2014 Cryptococcosis In Sykes JE ed Canine and Feline Infectious Diseases Elsevier Saunders St Louis Missouri Pp 599612 American Association of Zoo Veterinarians Infectious Disease Manual CRYOPTOSPORIDIOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Avians Herptiles Fish Humans Direct fecal to oral Waterborne transmission possible paratenic host transmission possible aerosol transmission in birds Gastrointestinal Diarrhea vomiting Respiratory disease documented in birds Depending on the affected species and organ system severity can vary from a mild transient selflimiting disease to a severe and fatal disease Severe disease is typical of immune suppressed patients and reptiles Nitazoxanide Alinia is licensed and approved for use in humans Oral bovine hyper immune serum is reported to be effective in reptiles Paromomycin Humatin is effective against some stages of the disease but will not eliminate infection Strict quarantine testing of new specimens biosecurity personal and environmental hygiene Yes C parvum is known to affect both animals and humans Other species C felis C canis C melea gridis C fayeri etc are occasionally isolated from immune compromised Fact Sheet compiled by Christopher J Bonar Sheet completed on 3 August 2011 updated 9 April 2013 updated 2018 Fact Sheet Reviewed by David Lindsay Christie Hicks Susceptible animal groups Mammals avian herptiles fishes Causative organism Cryptosporidium sp of which at least 20 different species exist Cryptosporidium parvum in mammals and humans C ubiquitum in man and many species C saurophilium in lizards and C serpentis in snakes are the most commonly encountered species in zoological medicine but there are many others C meleagridis C baileyi and C galli are reported in birds Some species are being debated eg C parvum C pestis but clearly there are many and molecular techniques may define still more Zoonotic potential Yes at least for mammalian forms Distribution Common in domestic dairy calves and often transmitted to humans Virtually all dairy calves become infected if sampled repeatedly during life C andersoni and C bovis are found in weaned cattle Cryptosporidium spp are present in freeranging wildlife C serpentis apparently affects both freeranging and captive squamates The reptile form is common in zoological parks and serpentariums Avian forms are found in both exotic and domestic species A human form C hominis has been transmitted to lemur species in Madagascar from the increased exposure of humans into their wild habitats Incubation period This period is not well defined in zoological specimens Reptiles can show gradual progressive illness Inapparent carriers are suspected Humans often become acutely infected and incubation time is approximately 2 to 10 days although often the exact time between exposure and onset of disease is often unknown Clinical signs Humans Diarrhea intestinal cramping low grade fever nausea vomiting malabsorption dehydration Occasionally respiratory ocular pancreatitis choecystitis cholangitis Animals Vomiting anorexia and midbody gastric swelling in snakes Diarrhea in lizards chelonians exotic and domestic mammals and birds Respiratory disease is also reported in birds Post mortem gross or histologic findings This coccidian parasite can cause a variety of pathology in different taxonomic groups In mammals enteritis is the most common In reptiles proliferative gastritis is the most common manifestation in snakes often yielding a firm mid abdominal swelling In lizards enteritis with hyperplasia and mononuclear cell infiltrate in the small intestine is more common In both gastritis and enteritis the organism can often be seen attached to the luminal American Association of Zoo Veterinarians Infectious Disease Manual CRYOPTOSPORIDIOSIS surface or within a parasitivorous vacuole within the host cells Aural and pharyngeal cell polyps are reported in iguanas Birds are often diagnosed with either enteric or respiratory tract infections In humans infections of the bile ducts respiratory tract and conjunctiva are found in immunosuppressed patients Diagnosis Diagnosis is by histopathology ELISA test on feces Meriflour IHC of gastric washings or gastric biopsies Acidfast stain of gastric wash fecal smear or cytologic preparations Low sensitivity and specificity of acidfast stains on gastric washes fecal smears and cytologic preparations makes confirmation by more sophisticated tests of both positives and negatives important FLOTAC has been shown to detect Cryptosporidium in reptiles Sheathers flotation sedimentation staining can also be used and is 83 sensitive and 99 specific Material required for laboratory analysis Fecal sample gastric wash gastric or intestinal biopsy Relevant diagnostic laboratories Many laboratories can perform these tests although some are more experienced or have more capabilities than others Much of the pioneering work on this disease in exotic animals has been performed at the University of Florida and Johns Hopkins University Treatment Nitazoxanide Alinia is licensed and approved in the US for treatment of immunesuppressed humans with clinical disease from cryptosporidiosis It is not documented to shorten the course of disease in immunologically normal humans Its effectiveness in exotic animals is not published Oral bovine hyper immune serum has been demonstrated to be effective in reptiles Paromomycin Humatin has been used to suppress the organism but it is not effective against all stages of the organism and is unable to eliminate the infection Other drugs similar to Nitazoxanide are in preclinical testing for use in humans and may show promise for exotic animals as well Drugs such as tizoxanide tizoxanideglucuronide Deritadenine and S DHPA all have shown promise in invitro testing Prevention and control Strict quarantine and testing of reptiles for Cryptosporidium has long been considered an important part of biosecurity for serpentariums Good hygiene and disinfection are essential to prevent zoonotic transmission of mammalian Cryptosporidium to human caregivers Testing of symptomatic birds reptiles and mammals should be performed and appropriate biosecurity and hygienic practices implemented to prevent spread to other animals and caregivers when positive cases are detected Suggested disinfectant for housing facilities Cryptosporidium is notoriously resistant to most common disinfectants especially chlorinebased disinfectants Heat sterilization of implements is most reliably effective as well as having separate implements and tools to prevent spread from one enclosure or exhibit to another Notification Public health officials may need to be notified if zoonotic transmission occurs In humans it is a reportable disease Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal An infected animal should not be introduced to others of the same taxonomic group However mammalian Cryptosporidium parvum has been shown to be noninfective to some reptiles Cryptosporidium has been shown to be transmissible between squamates and chelonians and wild mammals have been shown to carry C parvum Conditions for restoring diseasefree status after an outbreak Heat disinfection is the only method known to destroy oocysts and can be used to disinfect utensils cleaning equipment and surfaces Experts who may be consulted Michael Cranfield DVM Mountain Gorilla Veterinary Project 876 Mansion House Drive Baltimore MD 21217 David Lindsay PhD Professor of Parasitology Dept of Biological Sciences and Pathobiology Virginia Tech American Association of Zoo Veterinarians Infectious Disease Manual CRYOPTOSPORIDIOSIS 1410 Prices Fork Rd Blacksburg VA 24061 lindsaydvtedu References 1 Abe N Makino I Multilocus genotypical analysis of Cryptosporidium isolates from cockatiels Japan Parasit Res 2010106614911497 2 Antunes RG Simons DC Nakamura AA Meireles MV Natural infection with Cryptosporidium galli in canaries Serinus canaria in a cockatiel Nymphicus hollandicus and in lesser seedfinches Oryzoborus angolensis from Brazil Avian Dis 2008524702705 3 Cranfield MR Graczyk TK Cryptosporidium In Mader D ed Reptile Medicine and Surgery St Louis MO Saunders Elsevier Press 2006 4 Čtrnáctá V Fritzler JM Šurinová M Hrdý I Zhu G Stejskal F Efficacy of Sadenosylhomocysteine hydrolase inhibitors Deritadenine and SDHPA against the growth of Cryptosporidium parvum in vitro Experimental parasitology 201012621136 5 Current WL Cryptosporidium species In ME Fowler and RE Miller Eds Zoo and Wild Animal Medicine 4th ed Philadelphia PA WB Saunders 1999 6 DaSilva DC Homem CG Nakamura AA Teixera WFP Perri SVH Physical epidemiological and molecular evaluation of infection by Cryptosporidium galli in passerifirmes Parasit Res 20101077271277 7 Dyachenko V Kuhnert Y Schmaeschke R Etzold M Pantchev N Daughschies A 2009 Occurrence and molecular characterization of Cryptosporidium spp genotypes in European hedgehogs Erinaceeus europaeus in Germany Parasitology 2010137220516 8 Fayer R Santin M Macarisin D Cryptosporidium ubiquitum nov sp in animals and humans Vet Parasit 2010172122332 9 Feng Y Cryptosporidium in wild placental mammals Exp Parasit 20101241128137 10 Graczyk TK Cranfield MR Cryptosporidium oocysts and microsporidian spores in feces of captive snakes J Parasit 2000862 413414 11 Graczyk TK Cranfield MR Bostwick EF Hyperimmune bovine colostrums treatment of moribund leopard geckos Eublepharis macularis infected with Cryptosporidium sp Vet Res 199930377 12 Graczyk TK Balazs GH Work T Aguirre AA Ellis DM Murakawa SK Morris R Cryptosporidium sp infections in Green Turtles Chelonia mydas as a potential source of marine waterborne oocysts in the Hawaiian islands Appl Environ Microbiol 19976329252927 13 Graczyk TK Owens R Cranfield MR Diagnosis of subclinical cryptosporidiosis in captive snakes based on stomach lavage and cloacal sampling Vet Parasit 199667143145 14 Graczyk TK Cranfield MR Assessment of the conventional detection of fecal Cryptosporidium serpentis oocysts in subclinically infected captive snakes Vet Res 19962718592 15 Graczyk TK Cranfield MR Fayer R A comparative assessment of direct fluorescence antibody modified acid fast stain and sucrose flotation techniques for detection of Cryptosporidium serpentis oocysts in snake fecal specimens J Zoo Wild Med 199526396402 16 Hijjawi N Ng J Yang R Atoum MFM Ryan U 2010 Identification of rare and novel Cryptosporidium GP60 subtypes in human isolates in Jordan Exp Parasit 1252161164 17 Jacobson ER Infectious Diseases and Pathology of Reptiles A Color Atlas and Text Boca Raton FL CRC Press 2007 p 262263 283297312313347391518620624627 18 Kahn C Line S eds The Merck Veterinary Manual 9th Edition Whitehouse Station NJ Merck Co Inc 2005 p 11931195 19 Kimbell LM Miller DL Chavez W Altman N Molecular analysis of the 8S rRNA gene of Cryptosporidium serpentis in a wildcaught corn snake Elaphe guttata guttata and a fivespecies restriction fragment length polymorphismbased assay that can additionally discern C Parvum from C American Association of Zoo Veterinarians Infectious Disease Manual CRYOPTOSPORIDIOSIS wrairi Appl Environ Micriobiol 19996553455349 20 Koudela B Modry D New species of Cryptosporidium Apicomplexa Cryptosporidiidae from lizards Folia Parasitol 19984593100 21 Maikai BV Umoti JV Lawal IA Kudi AC Egembi CL Xiao L Molecular characterization of Cryptosporidium Giardia and enterocytozoan in humans in Kaduwa state Nigeria Exp Parasitol 20121314452456 22 Merck Manual Veterinary Manual Internet Overview of Cryptosporidiosis cited 2018 August 2 Available from httpmerckvetmanualcom 23 MolinaLopez RA Ramis A MartinVazquez S GomezCouso H AresMazas E Cacci SM Leiva M Darwich L Cryptosporidium baileyi infection associated with an outbreak of ocular and respiratory disease in otus owls Otus scops in a rehabilitation centre Avian Path 2010393171176 24 Ng JSY Pingault N Gibbs R Hoehler A and Ryan U Molecular characterization of Cryptosporidium outbreaks in Western and South Australia Exp Parasitol 20101254325328 25 Nolan JJ Jex AR Haydon SR Stevens MA Gasser RB Molecular detection of C cuniculus in rabbits in Australia Infect Genet and Evol 201010811791187 26 Power ML Biology of Cryptosporidium from marsupial hosts Exp Parasitol 201012414044 27 Qi M Wang R Ning C Li X Zhang L Jian F Sun Y Xiao L Cryptosporidium in pet birds genetic diversity and potential public health significance Exp Parasitol 20111284336340 28 Radadkova M Kvac O Ditrich B Sak B Xiao L Cryptosporidium muris in a reticulate giraffe Giraffe camelopardis reticulata J Parasitol 2010961211212 29 Rasambainarivo F Goodman SM Disease Risk to Endemic Animals from Introduced Species on Madagascar In Miller RE Lamberski N Calle P eds Zoo and wild animal medicine Volume 9 1st Edition Current therapy St Louis MO Elsevier 2019 p 294 30 Rena X Shaoa J Cryptosporidium tyzzeri n sp Apicomplexa Cryptosporidiidae in domestic mice Mus musculis Exp Parasitol 20121303274281 31 Rinaldi L Mihalla AD Grillo R Maurelli MP Montesano M Capasso M Gringoli G FLOTAC can detect parasitic and pseudoparasitic elements in reptiles Exp Parasitol 20121303282284 32 Robertson LJ Gjerde BK Hansen EF The zoonotic potential of Giardia and Cryptosporidium in Norweigian sheep a longitudinal investigation of six flocks of lambs Vet Parasitol 201017112140 145 33 Shi K Jian F Lv C Ning C Zhang L Ren X Dearen TK Li N Qi M Xiao L Prevalence genetic characteristics and zoonotic potential of Cryptosporidium species causing infection in farmraised rabbits in China J Clin Microbiol 201048932633266 34 Van Zeeland YRA Schoemaker NJ Kik MJL van der Giessen JWB Upper respiratory tract infection caused by Cryptosporidium baileyi in three mixed breed falcons Falco rusticolus x Falco cherrug Avian Dis Dig 200832357363 35 Wang R Zhang X Shu H Sheng L Feng Y Jian F Ning C Qi M Zhou Y Fu K Wang Y Sun Y Wang Q Xiao L Genetic characterizations of Cryptosporidium spp and Giardia duodenalis in humans in Henan China Exp Parasitol 201312714245 36 Waldren LS ChengKwokSang C Power ML Wildlife associated Cryptosporidium fayeri in human Australia Emerg Infect Dis 2010161220062007 37 Yoder JS Beach MJ Cryptosporidium surveillance and risk factors in the US Exp Parasitol 201012413139 American Association of Zoo Veterinarians Infectious Disease Manual CYTAUXZOONOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Felids wild and domestic Tickborne Amblyomma americanum and Dermacentor variabilis Domestic cats and some exotic felids some cats develop no clinical signs while others may develop high fever lethargy dyspnea depression dehydration anorexia anemia hepatosplenomegaly andor jaundice Others die acutely Exotic felids often no clinical signs Nonclinical or mild to severe including death could depend on numerous factors such as species of felid strain or genotype of parasite or other unknown factors Mortality can be high even with treatment A combination of atovaquone and azithro mycin seems to have the highest success rates Supportive care also should be provided Avoid contact with ticks by keeping cats indoors Outside cats should have effective acaricides applied No vaccine available No Fact Sheet compiled by Michael J Yabsley Sheet completed on 1 August 2013 updated 2018 Fact Sheet Reviewed by Adam Birkenheuer Susceptible animal groups Felids Cytauxzoon felis has been reported from domestic cats bobcats Lynx rufus puma Puma concolor and captive exotic felids eg tigers Panthera tigris in the United States Cytauxzoon manul infects the Pallas cat Cytauxzoon spp some genetically similar to C felis have been reported from domestic cats and numerous freeranging andor captive exotic felids in South America Africa and Europe Related Cytauxzoon spp has been reported from meerkats Suricata suricatta from South Africa and Formosan pangolins Manis pentadactyla pentadactyla from Taiwan Causative organism Cytauxzoon spp are Apicomplexan parasites in the Order Piroplasmida which are related to important human and veterinary pathogens in the genera Babesia and Theileria spp In the US Cytauxzoon felis is the causative agent of cytauxzoonosis in domestic cats and some exotic felids Bobcats and other wild felids eg cougars are the natural reservoir but chronically infected domestic cats can serve as a source of infection for ticks Outside of the US other Cytauxzoon species or genetic variants of C felis infect wild and domestic felids however clinical cytauxzoonosis is rare Zoonotic potential None Distribution C felis has been reported from numerous states in the eastern US but is likely found throughout the range of the vectors and the main wildlife reservoir bobcats Other species of Cytauxzoon have been reported in parts of South America Africa Europe and Asia Some of the Cytauxzoon likely represent novel species or have been described as separate species eg C manul but genetic data indicates that Cytauxzoon from Brazil is closely related to C felis from the US Exotic felids kept in enclosures that allow tick exposure within the natural range of any Cytauxzoon spp are at risk of infection Incubation period C felis can typically be detected in erythrocytes of infected cats approximately 13 weeks after an infected tick bite Clinical signs typically occur 516 days after infected tick bite Clinical signs Domestic cats The majority of domestic cats develop severe clinical disease but some never develop clinical signs but remain chronic carriers Those with clinical signs may develop high fever lethargy dyspnea depression dehydration anorexia anemia hepatosplenomegaly andor jaundice Captive wildexotic felids Development of clinical signs is highly variable and may depend on felid species American Association of Zoo Veterinarians Infectious Disease Manual CYTAUXZOONOSIS strain of parasite or some other factor Fatal cases have been reported in a tiger housed in Florida and lions in Brazil however asymptomatic infections have been detected in tigers in US and ocelots Leopardus pardalis oncilla Leopardus tigrinus jaguar Panthera onca and puma in Brazil Wild felids natural reservoirs Wild reservoir species rarely develop clinical signs but very rare acute mortality has been reported among young bobcats In addition three infected cougar in the US developed a transient anemia and increased serum bilirubin concentrations and increased alanine aminotransferase and aspartate aminotransferase activities soon after infection however all recovered rapidly without treatment Clinical pathological gross and histopathological findings Parasitemias of C felis on blood smears are generally low 5 even for clinically ill felids Leukopenia or pancytopenia may be present as well as thrombocytopenia and normocytic normochromic anemia Gross lesions are typically severe as death occurs due to severe occlusions of vessels by developing parasites Felids may have pale or icteric mucous membranes petechiae and ecchymoses in the lung heart lymph nodes and on mucous membranes splenomegaly lymphadenomegaly and hydropericardium Numerous large schizonts will be noted in the cytoplasm of infected macrophages that often occlude the lumens of numerous vessels of many tissues especially the lungs Despite the large numbers and size of schizonts a lack of inflammatory reaction generally is present Diagnosis Piroplasms may be detected in stained thin blood smears if sufficiently high parasitemias are present however subclinical chronic carriers generally have very low parasitemias Although feline babesiosis has not been reported in domestic cats in the US C felis trophozoites are morphologically similar to other small piroplasms so PCR testing is necessary to definitive identify C felis If possible a fine needle aspiration of a peripheral lymph node spleen or liver should be performed to identify schizonts in macrophages These intracellular schizonts are not found in babesiosis cases so can be used to definitively identify Cytauxzoon infections Several PCR protocols have been developed for the detection of C felis If PCR assays are not specific to C felis amplicons should be sequenced to confirm identification as other piroplasms can infect felids especially wild felids Material required for laboratory analysis Thin blood smears fixed and stained for detection of piroplasms and anticoagulated whole blood for PCR testing and preparation of thin blood smears Formalin fixed needle biopsies of tissues for histologic evaluation for schizonts Relevant diagnostic laboratories Many diagnostic laboratories have PCR based assays for C felis Treatment Despite treatment mortality rates can be high The greatest success has been obtained using atovaquone 15 mgkg PO tid for 10 days and azithromycin 10 mgkg PO sid for 10 days with supportive care fluid therapy and heparin Limited success has been obtained using imidocarb and diminazene diaceturate while even less success has been obtained using parvaquone buparvaquone trimethoprimsulfadiazine and sodium thiacetarsamide Prevention and control Because Cytauxzoon is tickborne limiting exposure of felids to ticks is necessary to prevent transmission For domestic cats the best prevention is to keep cats indoors For exotic or wild felids or domestic cats that are allowed outdoors an effective acaracide or acaricidetreated collar should be used to prevent or limit tick infestation If possible tick checks can also decrease risk by finding and removing ticks prior to transmission Habitat modification can also be used around a premise to decrease local habits for ticks which should decrease tick infestation rates of animals Suggested disinfectant for housing facilities Prevent tickexposure Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal This parasite is tickborne so direct contact between animals is not a risk factor for infection However tick prevention should be implemented Conditions for restoring diseasefree status after an outbreak Not applicable Experts who may be consulted Michael J Yabsley Associate Professor American Association of Zoo Veterinarians Infectious Disease Manual CYTAUXZOONOSIS College of Veterinary Medicine University of Georgia Athens Georgia 30602 706 5421741 myabsleyugaedu Adam Birkenheuer Associate Professor College of Veterinary Medicine North Carolina State University Raleigh NC 27607 919 5138288 adambirkenheuerncsuedu Leah A Cohn Professor College of Veterinary Medicine University of Missouri Columbia MO 65211 573 8827821 CohnLmissouriedu References 1 Birkenheuer AJ Marr HS Warren C Acton AE Mucker EM Humphreys JG Tucker MD Cytauxzoon felis infections are present in bobcats Lynx rufus in a region where cytauxzoonosis is not recognized in domestic cats Vet Parasitol 200815312630 2 Birkenheuer AJ Le JA Valenzisi AM Tucker MD Levy MG Breitschwerdt EB Cytauxzoon felis infection in cats in the midAtlantic states 34 cases 19982004 J Am Vet Med Assoc 2006228568 71 3 Brown HM Lockhart JM Latimer KS Peterson DS Identification and genetic characterization of Cytauxzoon felis in asymptomatic domestic cats and bobcats Vet Parasitol 20101723116 4 Brown HM Modaresi SM Cook JL Latimer KS Peterson DS Genetic variability of archived Cytauxzoon felis histologic specimens from domestic cats in Georgia 19952007 J Vet Diagn Invest 2009214938 5 Brown HM Berghaus RD Latimer KS Britt JO Rakich PM Peterson DS Genetic variability of Cytauxzoon felis from 88 infected domestic cats in Arkansas and Georgia J Vet Diagn Invest 2009215963 6 Brown HM Latimer KS Erikson LE Cashwell ME Britt JO Peterson DS Detection of persistent Cytauxzoon felis infection by polymerase chain reaction in three asymptomatic domestic cats J Vet Diagn Invest 2008204858 7 Carli E Trotta M Chinelli R Drigo M Sinigoi L Tosolini P Furlanello T Millotti A Caldin M SolanoGallego L Cytauxzoon sp infection in the first endemic focus described in domestic cats in Europe Vet Parasitol 2012 Feb 101833434352 8 Cohn LA Birkenheuer AJ Brunker JD Ratcliff ER Craig AW Efficacy of atovaquone and azithromycin or imidocarb dipropionate in cats with acute cytauxzoonosis J Vet Intern Med 2011 Jan Feb2515560 9 Filoni C CatãoDias JL Cattori V Willi B Meli ML Corrêa SH Marques MC Adania CH Silva JC Marvulo MF Ferreira Neto JS Durigon EL de Carvalho VM Coutinho SD Lutz H Hofmann Lehmann R Surveillance using serological and molecular methods for the detection of infectious agents in captive Brazilian neotropic and exotic felids J Vet Diagn Invest 2012 Jan24116673 10 Garner MM Lung NP Citino S Greiner EC Harvey JW Homer BL Fatal cytauxzoonosis in a captive reared white tiger Panthera tigris Vet Pathol 1996 Jan331826 American Association of Zoo Veterinarians Infectious Disease Manual CYTAUXZOONOSIS 11 Hoover JP Walker DB Hedges JD Cytauxzoonosis in cats eight cases 19851992 J Am Vet Med Assoc 1994 Aug 1205345560 12 Haber MD Tucker MD Marr HS Levy JK Burgess J Lappin MR Birkenheuer AJ The detection of Cytauxzoon felis in apparently healthy freeroaming cats in the USA Vet Parasitol 2007 May 311463431620 13 Harvey JW Dunbar MR Norton TM Yabsley MJ Laboratory findings in acute Cytauxzoon felis infection in cougars Puma concolor couguar in Florida J Zoo Wildl Med 2007 Jun38228591 14 Lewis KM Cohn LA Downey ME Whitney MS Birkenheuer AJ Evaluation of Cytauxzoon felis infection status in captiveborn wild felids housed in an area endemic for the pathogen J Am Vet Med Assoc 2012 Oct 152418108892 15 Maia LM Cerqueira Ade M de Barros Macieira D de Souza AM Moreira NS da Silva AV Messick JB Ferreira RF Almosny NR Cytauxzoon felis and Candidatus Mycoplasma haemominutum coinfection in a Brazilian domestic cat Felis catus Rev Bras Parasitol Vet 20132228991 16 Leclaire S Menard S Berry A Molecular characterization of Babesia and Cytauxzoon species in wild SouthAfrican meerkats Parasitology 20151425438 17 Meinkoth J Kocan AA Whitworth L Murphy G Fox JC Woods JP Cats surviving natural infection with Cytauxzoon felis 18 cases 19971998 J Vet Intern Med 2000145215 18 Peixoto PV Soares CO Scofield A Santiago CD França TN Barros SS Fatal cytauxzoonosis in captivereared lions in Brazil Vet Parasitol 20071453837 19 Pollard DA Reichard MV Cohn LA James AM Holman PJ Genetic variability of cloned Cytauxzoon felis ribosomal RNA ITS1 and ITS2 genomic regions from domestic cats with varied clinical outcomes from five states Vet Parasitol 2017244136143 20 Reichard MV Thomas JE Arther RG Hostetler JA Raetzel KL Meinkoth JH Little SE Efficacy of an imidacloprid 10 flumethrin 45 collar Seresto Bayer for preventing the transmission of Cytauxzoon felis to domestic cats by Amblyomma americanum Parasitol Res 2013112 Suppl 11120 21 Reichard MV Meinkoth JH Edwards AC Snider TA Kocan KM Blouin EF Little SE Transmission of Cytauxzoon felis to a domestic cat by Amblyomma americanum Vet Parasitol 20091611105 22 Reichard MV Edwards AC Meinkoth JH Snider TA Meinkoth KR Heinz RE Little SE Confirmation of Amblyomma americanum Acari Ixodidae as a vector for Cytauxzoon felis Piroplasmorida Theileriidae to domestic cats J Med Entomol 2010478906 23 Reichard MV Baum KA Cadenhead SC Snider TA Temporal occurrence and environmental risk factors associated with cytauxzoonosis in domestic cats Vet Parasitol 200815231420 24 Schreeg ME Marr HS Tarigo J Cohn LA Levy MG Birkenheuer AJ Pharmacogenomics of Cytauxzoon felis cytochrome b implications for atovaquone and azithromycin therapy in domestic cats with cytauxzoonosis J Clin Microbiol 20135130669 25 Shock BC Birkenheuer AJ Patton LL Olfenbuttel C Beringer J Grove DM Peek M Butfiloski JW Hughes DW Lockhart JM Cunningham MW Brown HM Peterson DS Yabsley MJ Variation in the ITS1 and ITS2 rRNA genomic regions of Cytauxzoon felis from bobcats and pumas in the eastern United States and comparison with sequences from domestic cats Vet Parasitol 20121902935 26 Shock BC Murphy SM Patton LL Shock PM Olfenbuttel C Beringer J Prange S Grove DM Peek M Butfiloski JW Hughes DW Lockhart JM Bevins SN VandeWoude S Crooks KR Nettles VF Brown HM Peterson DS Yabsley MJ Distribution and prevalence of Cytauxzoon felis in bobcats Lynx rufus the natural reservoir and other wild felids in thirteen states Vet Parasitol 201117532530 27 Yabsley MJ Murphy SM Cunningham MW Molecular detection and characterization of Cytauxzoon felis and a Babesia species in cougars from Florida J Wildl Dis 20064236674 American Association of Zoo Veterinarians Infectious Disease Manual CYTOMEGALOVIRUS CMV Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mice rats Guinea pig Swine Cattle Horses Nonhuman primates In mice urine vertical transmission in micerats tears saliva Saliva urine vertical Ocularnasal discharges urine cervical fluids Possibly milk not well documented Probably respiratory secretions Bodily secretions None in natural infections immune reproductive and hematopoetic effects when experimentally inoculated in mice Pneumonia fetal death neonatal runting neuro logic deficits deafness Abortion neonatal piglet losses runting poor weight gain inclusion body rhinitis pneumonia Rare to absent Possible abortion respiratory genital diseases produced experimentally only Immunosuppres sion corneal ulcers pharynx gitis lymph adenopathy fever in foals SIVinfected macaques similar to HIV infected humans necro Usually subclinical Subclinical to severe Subclinical when 3 wks old Subclinical Subclinical to mod erate possible foal death Majority subclinical Depopulation and restock ing with MCMVfree animals None effective Aantibiotics for secondary bacterial invaders None Symptomatic Symptomatic Isolate wild individuals from laboratory colonies Separate infected from GpCMVfree Allin allout farrowing and weaning management None needed None Screen prior to intro duction if necessary No American Association of Zoo Veterinarians Infectious Disease Manual CYTOMEGALOVIRUS CMV Humans Australian finches Intrauterine sexual contact bodily fluids transfusions and trans plants fomites Respiratory tizing enteritis encephalitis lymphadenitis pneumonitis Congenital childhood deafness Acute acquired mononucleosis like fever malaise myalgia arthralgia Immunocompro mised retinitis esophogitis pan creatitis pneumonia Depression anorexia conjunctivitis dyspnea Majority subclinical fatalities in transplant patients High mortality rate Antivirals ganciclovir or Foscarnet Symptomatic Good hygiene hand washing limiting transfusions screening donors Isolate captive from wild birds Fact Sheet compiled by Eleanor C Manela Newcomb updated by Jan Ramer Sheet completed on 1 April 2011 updated 1 September 2013 Fact Sheet Reviewed by Meredith Clancy KyoungJin Yoon Hayley Murphy Susceptible animal groups Rodents swine cattle nonhuman and human primates some other mammals some marsupials some passerine birds Causative organism Family Herpesviridae Subfamily Betaherpesvirinae except in cattle and horses where it is Gammaherpesvirinae Zoonotic potential Although the virus has a restricted host range interspecies transmission does occur in nonhuman primates No natural transmission to humans from other species documented Distribution Rodents The virus is widespread through reservoirs in wild populations Specifically in guinea pigs the virus is common in pets and laboratory populations but its distribution in the wild is unknown Swine Worldwide with 90 herd prevalence in North America Europe and Japan Cattle Worldwide Equine Widespread Nonhuman primates Widespread Humans 85 of population worldwide and in US 5085 adults are infected by age 40 If infection is acquired by mother during pregnancy then up to 20 neonates severely affected Finches reported mostly in Europe Incubation period Unknown in most species Swine 1020 days Humans 312 weeks Lifelong latent infection occurs commonly may produce periodic episodes of reactivation viral replication and shedding American Association of Zoo Veterinarians Infectious Disease Manual CYTOMEGALOVIRUS CMV Clinical signs In rats mice and squirrels no clinical signs are presented in natural infections Guinea pigs however present weight loss ruffled coat abortion and neonatal abnormalities Swine present signs of respiratory neurologic and reproductive systems Cattle present no correlation between presence of virus and specific lesions Horses present conjunctivitis oculonasal discharge and cough In finches affected birds present respiratory disease and death Humans and nonhuman primates are usually subclinical Immunocompromised nonhuman primates can present diarrhea melena dyspnea and terminal opportunistic infection In humans severe permanent disabilities in children can occur when primary infection occurs during pregnancy or when acquired in AIDS patients organ transplant and cancer chemotherapy These clinical signs range from malaise to permanent hearing loss and include mental retardation gastrointestinal pulmonary and autoimmune disease and death Post mortem gross or histologic findings Marked enlargement 6x normal of nucleus and cytoplasm of infected cells cytomegaly is observed with large intranuclear owlseye and smaller basophilic intracytoplasmic inclusions Affected organs by rodent species include mice submandibular salivary gland rats salivarylacrimal glands European ground squirrels salivary gland guinea pigs salivary glandsrenal tubules Swine macrophages in lungs nasal mucosa turbinates and upper respiratory tract Sheep cytomegaly with virus has been detected in lung tissue of lamb with Mycoplasma pneumonia Cattle monocytesmacrophages in multiple organ sites Horses leukocytes and respiratory tract and kidneys Nonhuman primates inclusion bodies in alveolar septa and septal lining liver CNS spleen kidney testes meningoencephalitis necrotizing vasculitis neutrophilic infiltrates may be prominent in CNS and gastrointestinal tract Several other species eg hamster chimpanzee and gorilla have been diagnosed based on characteristic cytomegaly in the absence of virus isolation Diagnosis Virus isolation from bodily fluids macrophages or affected tissues can be performed Horses can have nasal swabs submitted Serologic or molecular testing options ELISA IFA PCR are available Material required for laboratory analysis Tissues and bodily fluids for virus isolation include biopsies or postmortem samples or urine cervical secretions semen saliva lung lavage or blood Relevant diagnostic laboratories Pathogen Detection Laboratory California National Primate Research Center University of California Road 98 Hutchison Davis California 95616 530 7528242 Fax 530 7524816 PDLprimateucdavisedu httppdlprimateucdavisedu VRL LaboratoriesSan Antonio PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 8776157275 Fax 2106157771 httpwwwvrlsatcom American Association of Zoo Veterinarians Infectious Disease Manual CYTOMEGALOVIRUS CMV Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 913113800 8187178880 Fax 8187178881 infozoologixcom wwwzoologixcom Treatment Most species are recommended to receive symptomatic treatment If severely debilitated from disease cull may be recommended and entire groups can be depopulated if virus will interfere with laboratory studies In humans several weeks course of intravenous antivirals eg ganciclovir or Foscarnet are administered and treatment is usually lifelong for AIDS patients Prevention and control Separate wild from captive populations to minimize transmission Test individuals prior to introduction if applicable Allinallout in production facilities used with all individuals moved out as a group and premises disinfected thoroughly between groups In humans blood and bloodproduct transfusions should be limited and CMVseronegative donors selected Hightiter CMV immunoglobulins may be prophylactic for bone marrow or renal transplant recipients Suggested disinfectant for housing facilities Disinfectants or detergents should be utilized that are effective against herpesviruses Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Do not introduce infected animal to pregnant or immunocompromised individuals or to grouphoused research animals Conditions for restoring diseasefree status after an outbreak Disinfect environment depopulate and restock with CMVfree animals Experts who may be consulted Camille Nelson Kotton MD Infectious Diseases Division Massachusetts General Hospital Harvard Medical School Boston MA 02114 6177240082 Mark R Schleiss MD Pediatric Infectious Diseases University of Minnesota Medical School Minneapolis MN 55455 6126269913 References 1 httpwwwphsourceusPHZDVDCytomegalovirus20Diseasehtm Accessed 17 September 2013 2 httpwildprotwycrosszooorgListVolsGreatApesViralListGreatApeViralDishtm Accessed 17 September 2013 3 Colitz CMH and V Kuonen 2007 Ocular infections In Sellon DC and MT Long Equine Infectious Diseases SaundersElsevier St Louis Missouri Pp 111112 4 Diseases associated with viruses and Chlamydia II 2007 In Radostits OM CC Gay KW Hinchcliff and PD Constable eds Veterinary Medicine A Textbook of the Diseases of Cattle Sheep Pigs Goats and Horses 10th ed Elsevier Limited St Louis Missouri Pp 13181319 American Association of Zoo Veterinarians Infectious Disease Manual CYTOMEGALOVIRUS CMV 5 Donofrio G C Flammini F Scatozza and S Cavirani 2000 Detection of bovine herpesvirus 4 BoHV4 DNA in the cell fraction of milk of dairy cattle with history of BoHV4 Infection J Clin Micro 3812 46684671 6 Guimaraes MB 2001 Order Passeriformes Songbirds Selected infectious diseases In Fowler ME and Z S Cubas eds Biology Medicine and Surgery of South American Wild Animals 1st ed Iowa State University Press Ames Iowa P 206 7 Hoover DM and HL Thacker 1979 Ovine pulmonary cytomegalovirus Vet Path 164 413 419 8 Jacoby RO and DJ Gaertner 2006 Rat cytomegalovirus In Suckow MA SH Weisbroth and C L Franklin eds The Laboratory Rat 2nd ed Elsevier Academic Press Burlington Massachusetts Pp 434435 9 King NW 2001 Herpesviruses of nonhuman primates In Williams ES and IK Barker eds Infectious Diseases of Wild Mammals 3rd ed Blackwell Publishing Ames Iowa Pp 147 152153 10 Leendertz FH M Deckers W Schempp F Lankester C Boesch L Mugisha A Dolan D Gatherer D J McGeoch and B Ehlers 2009 Novel cytomegaloviruses in freeranging and captive great apes phylogenetic evidence for bidirectional horizontal transmission J Gen Virol 90 2386 2394 11 Mahy BW J 2009 The Dictionary of Virology Academic PressElsevier Burlington Massachusetts 520 pp 12 Martin WJ 1996 Simian cytomegalovirusrelated stealth virus isolated from the cerebrospinal fluid of a patient with bipolar psychosis and acute encephalopathy Pathobiol 64 6466 13 Schiefer B 1974 Bovine abortion associated with cytomegalovirus infection Zentralblatt fur Veterinarmedizin Relhe B 2112 145151 14 Yoon JK and N Eddington 2006 Porcine cytomegalovirus In Straw BE J J Zimmerman S DAllaire and D J Taylor eds Diseases of Swine 9th ed Blackwell Publishing Ltd Oxford United Kingdom Pp 323329 American Association of Zoo Veterinarians Infectious Disease Manual DERMATOPHYTOSIS Animal Groups Affected Transmissio n Clinical Signs Severity Treatment Prevention and Control Zoono tic Most vertebrates including mammals reptiles and avian species Direct contact with infected hairs fomites infected animals or environment rare Contact does not always result in infection Lesions can appear different in each species but most consist is a well demarcated area of alopecia with greywhite scaling crusting and mild erythema Depending on the species and complicating factors lesions may or may not be pruritic Generalized dermatophytosis can be difficult to cure but mortality is low In healthy hosts and low burden of disease dermatophytosis can be self limiting Standard of care for treatment involves topical antifungal agents in combination with systemic therapies see below for details Holding period for newly introduced animals Isolation of affected animals until mycological cure Protective clothing and good personal hygiene after handling infected animals Decontamination of all fomites brushes blankets toys cages etc and environment Vaccines do not protect against exposure in dogs and cats though may show some efficacy in cattle and horses see below Yes Specifi c species carry higher potenti al for zoonos is than others see details below Fact Sheet compiled by Samantha Lockwood Sheet completed on 8 February 2018 Fact Sheet Reviewed by Ryan Colburn Susceptible animal groups All mammals can be affected Avian speciesrare mostly seen in domestic fowl Reptilesuncommonly affected reports in lizards snakes green anacondas Eunectes murinus chameleons and one report in an iguana Pocket Petsrabbits chinchillas ferrets guinea pigs hedgehogs less commonly rats and mice Often animals with compromised or underdeveloped immune systems will be more commonly affected Young stressed elderly or sick neoplasia underlying metabolic disease animals are more likely to develop infection after exposure Animals with compromised skin barriers such as allergic patients genetic predispositions Yorkshire terries and Persian cats or long coats may also be more likely to develop infection after exposure Causative organism Three genera Microsporum Epidermophyton and Trichophyton The three genera can be categorized into anthrophilic adapted to humans zoophilic adapted to animals and geophilic normally live in environment but occasionally are infectious Both Microsporum and Trichophyton are anthrophilic and zoophilic whereas only one species of Epidermophyton E floccosum has been known to cause disease in humans anthrophilic The most common geophilic species that can cause disease are species from the M gypsum complex Overall the most common species that affect domestic animals are Microsporum canis dogs and cats M equinum horses M nanum pigs M gypseum dogs and cats T mentagrophytes horses dogs and cats M persicolor voles and several species of T mentagrophytes complex rodents rabbits hedgehogs Microsporum canis is the most common causative agent in dogs and cats but can be routinely found in horses rabbits cattle sheep goats camelids and swine Microsporum gallinae occurs in domestic birds chickens uncommon in wild birds Microsporum nanum is the most commonly isolated species in swine though T mentagrophytes T verrucosum and M canis have also been isolated Microsporum gypseum has been found in many different species of animals but is mostly geophilic It has been reported in cats dogs ruminants camelids horses pigs birds and rodents American Association of Zoo Veterinarians Infectious Disease Manual DERMATOPHYTOSIS Trichophyton spp is most commonly isolated from reptiles Trichophyton equinum is the most common cause of dermatophytosis in horses It has also been reported in dogs cats goats and sheep Trichophyton mentagrophytes is common in many species such as cattle horses pigs dogs cats and especially rabbits rodentsincluding guinea pigs T mentagrophytes var erinacei occurs in the European and African hedgehog Trichophyton verrucosum is the most common cause of dermatophytosis in cattle goats and sheep It has been reported in horses donkeys and South American camelids Trichophyton simmii affects nonhuman primates monkeys poultry and dogs Zoonotic potential Dermatophytosis poses a risk to humans especially when working in shelters or multi animal facilities M canis dogs and cats T verrucosum cattle Arthroderma benhamiae guinea pigs and Arthroderma vanbreuseghemii cats dogs rabbits mice and chinchillas appear to have a more common frequency in humans Occasionally T equinum can be transmitted to humans T rubrum the cause of athletes foot in humans has been reported to cause reverse zoonosis in dogs and cats Distribution Most species of dermatophyte are worldwide T simii is rarely seen outside of India T erinacei geographical distribution includes Europe East Asia and New Zealand M persicolor geographical distribution includes Europe and the USA The causative agent that predominates in any one particular area can vary depending on the climate geographic locations and other factors such as concentration or livestock pets or exotic animals present Humid warm tropical and subtropical areas appear to have higher incidence Incubation period The infective form of dermatophyte is the arthrospore Infection can be established within hours after exposure though clinical signs generally occur 13 weeks after exposure in animals and 414 days in humans Clinical signs CanineFeline Variable pruritus though when complicated by secondary bacterial infection pruritus is more commonly noted Trichophyton mentagrophytes can be extremely pruritic and mistakenly diagnosed as allergic disease Focal to locally extensive areas well demarcated expanding alopecia with scale crust and follicular papules these lesions are often expansive with chronicity Facial lesions are common though any of area of the body can be affected Fungal kerions are another manifestation of disease characterized by an exudative well circumscribed nodular furunculosis seen more commonly on limbs and the face of animals these are often associated with dermatophytosis in dogs EquineOne or more circular patches of erythematous alopecia with scaling and crusting Early lesions can appear as papular urticaria Lesions are most often seen in the saddle and tack areas thorax head and shoulders Pruritus is usually minimal but occasionally severe suggestive of ectoparasitism BovineNonpruritic periocular lesions mostly in calves discrete patches of alopecia with scaling whitegrey crusts papules and nodules can be present as well Fungal kerions can be seen in cattle Lesions are most commonly seen on the head neck and pelvis For bulls the dewlap and intermaxiallary space will often be affected CaprineOvinePruritus is rare Alopecia scale erythema and yellowishgrey crusting most often seen on the face pinna neck and limbs Udders and teats can be affected PorcineLesions are often diffuse but seen mostly behind the ears and on the trunk Annular areas of red to brown discoloration with superficial orangebrown crusting are noted Alopecia and pruritus are rare Pocket PetsPruritus is common The face neck and limbs are commonly affected by areas of alopecia with scale and crust Ears are often affected in rabbits ReptilesBlisters that rupture into brownyellow crusts can be seen Other manifestations include proliferative growths or nodules that are often described as appearing necrotic AvianAlopecia loss of feathers though feathers are not infected with scale and white crusts Hyperkeratosis American Association of Zoo Veterinarians Infectious Disease Manual DERMATOPHYTOSIS or white plaque formation can be seen Occasionally feather plucking and selfmutilation occur Post mortem gross or histologic findings Postmortem and gross findings are the same as clinical signs and skin lesions present antemortem The most common histopathological findings include 1 perifolliculitis folliculitis and furunculosis more specifically infiltrative lymphocytic mural folliculitis suppurative luminal folliculitis and pyogranulomatous furunculosis 2 hyperplastic or spongiotic superficial perivascular or interstitial dermatitis with prominent parakeratotic or orthokeratotic hyperkeratosis of the epidermis and hair follicles 3 intraepidermal pustular dermatitis suppurative neutrophilic epidermitis Arthroconidia and hyphae can be detected in hair shafts with HE staining but special staining such as Periodic acidSchiff PAS and Grocott methenamine silver GMS lends for an easier detection Diagnosis There is no one gold standard diagnostic test for dermatophytosis diagnosis includes multiple complementary techniques Woods lamp examination will not provide a definitive diagnosis for dermatophytosis This technique is helpful in identification of infected hairs thus allowing a clinician to pinpoint the best area to pluck hairs or brush lesions for cytological evaluation and culture sampling Trichogram and cytological evaluation of infected hairs andor scale can reveal arthrospores and hyphae in 40 70 of cases and provides a preliminary diagnosis Dermoscopy has recently been used in cats as a noninvasive diagnostic tool On evaluation variably amounts of yellow to brown crusts are common and slightly curved or broken hairs with a homogenous thickens named comma hairs are common Fungal culture is commonly used for diagnosis of dermatophyte A Mackenzie brush technique utilizing a soft bristle toothbrush is ideal for collection of samples 20 brush strokes 23 minutes of brushing or until the brush is full of hair should be achieved when collecting samples Sabourauds dextrose agar or Dermatophyte Test Media DTM are the most reliable culture plates to confirm dermatophytosis Specific dermatophyte species can be determined by assessment of macroconidia on cytological evaluation of colony growth from culture plates It is important to note that T equinum requires nicotinic acid vitamin B3 for growth on fungal cultures Polymerase Chain Reaction PCR has become a common and expedient diagnostic tool for evaluation of dermatophytosis False positives may occur due to fomite carriage or detection of nonviable dermatophyte organisms after recent treatment False negative results may be due to poor sample collection or marker used for detection does not correlate to specific dermatophyte species ie only Microsporum and Trichophyton spp are currently available for PCR testing Skin biopsy is not often used but can be helpful when fungal kerions are present negative culture or PCR results occur It is important to note that ectoparasites bacterial pyoderma and Malassezia dermatitis should be ruled out when approaching diagnostic testing for dermatophytosis Material required for laboratory analysis Infected hairs andor scale samples for infected hairsscale can be detected using Woods lamp evaluation trichogram or cytological evaluation Test media such as Sabourauds dextrose agar DTM Mycobiotic Agar Difco Detroit MI Mycosel Agar BBL Cockeysville MD Sabduets Hardy Diagnostics Mountainview CA and Derm Duet Hardy Diagnostics Mountainview CA can all be used for culture Relevant diagnostic laboratories Most clinicsclinicians will grow and review cultures inhouse Most commercial laboratories Idexx Antech and veterinary schools will offer culture Idexx laboratories offers PCR testing for Microsporum and Trichophyton spp Treatment End point of treatment is considered with two or three negative culture or PCR results at consecutive weekly 24 weeks intervals occur this is considered a mycological cure Clipping the hair especially in long coated cats or severely infected animals should be performed This is American Association of Zoo Veterinarians Infectious Disease Manual DERMATOPHYTOSIS particularly recommended in multicat facilities In single animal households it is not necessarily needed This decreases the burden of infection and allows for easier topical application of shampoos Clipping the hair can also reduce chances of false positive results on culture and PCR Effective topical agents include lime sulfur 116 dilution 2 combined miconazolechlorhexidine 11 ratio formulations and 02 enilconazole formulations The animals entire body should be treated twice weekly with topical therapies allowing contact time for 10 minutes each treatment In large animals 05 sodium hypochlorite 110 dilution of household bleach can be used as topical therapy but can be caustic to the skin Systemic antifungal therapy includes griseofulvin itraconazole terbinafine fluconazole and ketoconazole When considering systemic antifungal treatment it is imperative to note that compounded antifungal drugs have been shown to be inconsistent in dose stability and efficacy therefore are not recommended Itraconazole and terbinafine appear to have the best efficacy in treating dermatophytosis Other systemic treatment options can be used though close monitoring for side effects such as hepatic toxicity is recommended In horses other than griseofulvin no other antifungals are approved for oral use in the United States The dose of griseofulvin for large animal species is widely variable There is high evidence of spontaneous resolution therefore often in large animal species dermatophytosis will be left untreated Itraconazole fluconazole ketoconazole and terbinafine are often used in small animals dogs and cats Itraconazole is the treatment of choice for cats There are varying dosages duration and regimens available for all the azole drugs Pulse regiments with itraconazole and terbinafine have also been shown to be effective in some species Itraconazole and terbinafine are most commonly used for pulse therapy such as one week on and one week off or 2 daysweek Overall treatment for generalized or serve dermatophytosis in all animals should include a combination of systemic and topical antifungals If lesions are minimal less than 23 lesions then considering topical therapy alone is valid or spontaneous resolution Prevention and control Arthroconidia can remain viable in the environment and be infective for months to years though studies have shown over time viability decreases With the exception in cattle and horses vaccines are not efficacious at preventing disease in other species In Europe Soviet Union and Scandinavia a modified live Trichophyton verrucosum vaccine for cattle and modified live Trichophyton equinum vaccine for horses have shown to be effective The vaccine is administered intramuscularly in calves at one and three weeks of age and in horses intramuscularly twice at 14 day intervals The vaccine for cattle can have protection against T verrucosum for up to 45 years Control of dermatophytosis includes proper hygiene routine disinfection of facilities tools housing bedding and toys reducing fomites by using proper protective gear limit handling and number of people handling infected patients and isolation of infected patients Vacuumingsweeping facilities helps to remove any dander scale or infected hairs that could be lingering in the environment This is considered a mechanical clean to remove any organic debris harboring arthroconidia After removal of debris disinfection is necessary to kill remaining arthroconidia In equine medicine tack and riding gear used in infected horses should be solely used in those individuals and properly disinfected or disposed of after use Isolation of newly acquired animals for 24 weeks is recommended Fungal culture andor fungal PCR of all newly acquired animals are recommended to reduce asymptomatic carriers Clipping the fur of infected animals and proper disposal can help reduce the amount of arthrospores introduced into the environment Suggested disinfectant for housing facilities Environmental cleaning is aimed at reducing transmission of disease to animals and humans minimizing fomite carriage and shortening the course of unnecessary treatment There are three major steps in decontaminating housing facilities 1 Mechanically remove all debris fur and fomites from facility as described above American Association of Zoo Veterinarians Infectious Disease Manual DERMATOPHYTOSIS 2 Thoroughly wash all surfaces with water and detergent 3 Disinfect with 525 sodium hypochlorite chlorine bleach at a 1100 dilution is effective and less irritating to humans and animals This should be allowed to sit for 10 minutes The diluted bleach solution does not retain efficacy over time and is recommended to be made new weekly Other topical disinfectants include accelerated hydrogen peroxide 1 Formaldehyde Solution Formalin and Enilconazole Environmental Spray concentrate diluted to 02 Household cleaners labeled to be effective against Trichophyton spp can also be effective with 10 minute contact time Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Healthy noninfected animals should never be introduced to infected animals As stated above contact alone does not always result in disease but exposing a healthy animal to an infected animal is not recommended Animals should only be allowed to interact once mycological cure has been achieved Trichophyton verrucosum and Trichophyton equinum modified live vaccines in Europe both show efficacy at preventing disease in cattle and horses respectively All other vaccines have not been shown to be efficacious in other species Conditions for restoring diseasefree status after an outbreak Treating all infected animals and achieving mycological cure Disinfecting housing facilities adequately see above Following isolation protocols for newly acquired animals Experts who may be consulted Tom Lewis DVM DACVD Dermatology for Animals 4806332277 Anthea Schick DVM DACVD Dermatology for Animals 4806332277 References 1 Bettenay S RingwormWhats New Proc World Small Anim Vet Assoc 2013 P 2008 2 Bond R Topical Therapy in the Treatment of Dermatophytosis J Small Anim Dermatol for Practitioners 20092 14 3 Boothe D Small Animal Clinical Pharmacology and Therapeutics 2nd ed St Louis MO Elsevier Saunders 2012 4 The Center for Food Security and Public Health Internet Dermatophytosis c20042013 cited 2013 September 06 Available from httpwwwcfsphiastateeduFactsheetspdfsdermatophytosispdf 5 Clubb SL Dorrestein GM Quesenberry K Mycotic Diseases In Altman RB ed Avian Medicine and Surgery Philadelphia PA WB Saunders 1997 p 323331 6 Hensel P An Update On Current Systemic Antifungal Drugs J Small Anim Dermatol for Practitioners 20092 59 7 Hnilica KA May ER Sargent S Frank LA Dermatophytosis Decontaminating Multianimal Facilities Compendium 2006 56479 8 Idexx Reference Laboratories Internet IDEXX Reference Laboratories Introduces the Ringworm Dermatophyte RealPCRTM Panel for Fast and Accurate Diagnosis of Dermatophytosis in dogs and cats 2014 cited 2019 February 18 Available from httpswwwvetmarketcoilContentImagesuploadedD791D793D799D7A7D795 D7AA20D79ED7A2D791D793D794IdexxDUrealpcrdermatophyte panelpdf American Association of Zoo Veterinarians Infectious Disease Manual DERMATOPHYTOSIS 9 Kraemer A Hein J Heusinger A Mueller RS Clinical Signs Therapy and Zoonotic Risks of Pet Guinea Pigs with Dermatophytosis Mycoses 201256216872 10 Laporte C CruzEspindola C Thungrat K Schick A Lewis TP Boothe DM Quality assessment of fluconazole capsules and oral suspensions compounded by pharmacies located in the United States Am J Vet Res 2017784421432 11 Mawby D Whittemore J Genger S Papich MG Bioequivalence of orally administered generic compounded and innovatorformulated itraconazole in healthy dogs J Vet Intern Med 201428172 77 12 Merchant SR Internet Overview of Dermatophytosis 2018 cited 2019 February 18 Available from httpswwwmerckvetmanualcomintegumentarysystemdermatophytosisoverviewofdermatophytosis 13 MettlerNet Claudia Dermatophytes Diagnosis and Therapy In Proc British Small Anim Vet Congress 2010 14 Miller WH Griffin CE Campbell KL Muller GH Scott DW Fungal and Algal Skin Diseases Muller Kirks Small Animal Dermatology 7th ed St Louis MO Elsevier Mosby 2013 22343 15 Moriello K Dermatophytosis Monitoring Treatment and Treatment Failures J Small Anim Dermatol for Practitioners 200921018 16 Moriello K Diagnostic Techniques for Dermatophytosis Clin Techniques in Small Anim Pract 20011621924 17 Moriello K Treatment of Dermatophytosis in Dogs and Cats Review of Published Studies Vet Dermatol 200415 99107 18 Moriello K Hondzo H Efficacy of disinfectants containing accelerated hydrogen peroxide against conidial arthrospores and isolated infective spores of Microsporum canis and Trichophyton spp Vet Dermatol 201425191e48 19 Moriello K Coyner K Patterson S Mignon B Diagnosis and treatment of dermatophytosis in dogs and catsclinical consensus guidelines of the world association for veterinary dermatology Vet Dermatol 201728266e68 20 The National Association of State Public Health Veterinarians Animal Contact Compendium Committee Internet Compendium of Measures to Prevent Disease Associated with Animals in Public Settings 2017 2017 cited 2019 February 18 Available from httpnasphvorgDocumentsAnimalContactCompendium2017pdf 21 Pare JA Sigler L Rosenthal KL Mader DR Microbiology Fungal and Bacterial Diseases of Reptiles In Reptile Medicine and Surgery 2nd ed St Louis MO Saunders Elsevier 2006 p 218221 22 Patterson S Skin Diseases of Exotic Pets Ames IA Blackwell Publishing Company 2006 p 195 205 223 234 251 264266 277 292293 314 23 Quesenberry KE Carpenter JW Ferrets Rabbits and Rodents Clinical Medicine and Surgery 2nd ed St Louis MO Saunders 2004 24 Scott DW Miller WH Equine Dermatology 2nd ed Philadelphia PA Saunders 2011 17283 25 Scott DW Large Animal Dermatology Philadelphia PA WB Saunders 1988 17282 26 University of Guelph Internet Worms and Germs Blog 2019 cited 2019 February 18 Available from httpswwwwormsandgermsblogcom American Association of Zoo Veterinarians Infectious Disease Manual DIROFILARIA IMMITIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Many mammal species Dogs Cats Ferrets Female mosquito vector 70 out of 3000 mosquito species world wide 16 species east of the Mississippi three on the California coast including Aedes Anopheles Culex Mansonia and Psorophora spp Dogs Tricuspid regurgitation murmur right heart failure pulmonary hypertension pulmonary thrombo embolism jugular pulses allergic pneumonitis ascites hemoglobinemia and hemoglobinuria caval syndrome Cats Pulmonary granulomas dyspnea chylothorax blindness tachycardia syncope Ferrets Anorexia cough weakness dyspnea bilirubinuria Dogs Asymptomati c or mild may progress to fatal Cats Asymptomati c to fatal possible spontaneous cure with no treatment Ferrets Potentially severe 4 worms can be fatal Dogs Melarsomine dihydro chloride Cats Symptomatic treatment or surgical extraction only Ferrets Injectable moxidectin if available Dogs Macrolytic lactones monthly oral ivermectin milbemycin oxime or moxidectin or monthly topical moxidectin or selamectin or parenteral moxidectin every 6 months Mosquito control keep animals indoors Cats Same as dogs Ferrets Liquid ivermectin topical moxidectin Yes but rare Fact Sheet compiled by Andrew Moorhead Sheet completed on Updated 14 Jan 2019 Fact Sheet Reviewed by Elizabeth ArnettChinn Susceptible animal groups Mammals Dogs 100 susceptible Cats 6190 susceptible Domestic dog and wild canids wolf coyote fox and possibly Eurasian otter are definitive hosts Raccoons wolverines coyotes deer and bears are wildlife reservoirs Documented in the rabbit ferret river otter muskrat harbor seal sea lion red panda Japanese raccoon dog wild cat blackfooted cat golden cat bobcat ocelot clouded leopard snow leopard African leopard tiger African lion American black bear polar bear horse Causative organism Dirofilaria immitis a nematode intravascular parasite that lives in bloodstream of host normally pulmonary vessels Zoonotic potential Occasionally occurs and usually causes pulmonary dirofilariasis in Florida 100 cases were documented in the last 40 years Distribution Diagnosed in 48 contiguous states plus Hawaii and US territories and worldwide Incubation period Prepatent period at least 67 months in definitive host 78 months in cat Temperature dependent maturation of organism in mosquito occurs 57F In mosquito ingested L1 microfilariae molt American Association of Zoo Veterinarians Infectious Disease Manual DIROFILARIA IMMITIS into L2 in 810 days postinfection molt to L3 in 23 days after second molt then migrate to mouth parts in 12 more days Total development time can be as short as1415days In dog L3 injected into host by mosquito molt to L4 in 312 days in skin molt to juvenile adult heartworm in subcutaneous tissue and muscle in 5070 days migrate to heart via vascular system by day 70120 L1 microfilariae discharged by mature nematodes 69 months post infection and can survive up to 23 years in the bloodstream Worm longevity 57 years in dog 23 years in cat Clinical signs may not appear for one year after infection Clinical signs Lethargy weakness fatigue exercise intolerance dyspnea cough anorexia weight loss vomiting diarrhea collapse seizures sudden death Humans aberrant hostworms do not reach adult stage no microfilaremia Post mortem gross or histologic findings Female nematodes 12 males 7 microfilariae 1800 Worms found in lobar arteries and main pulmonary artery when mild eg 10 worms right atrium and caudal vena cava and rarely the right ventricle when severe eg 40 worms Dogs 1250 worms Cats 13 worms Rabbits aberrant hostgranulomatous lung nodule reported Humans coin lesion in lungs can be confused radiographically with carcinoma Diagnosis In dogs and exotic species antigen test most sensitive nearly 100 specific detects adult female D immitis protein 57 months postinfection Cats Both antigen and antibody tests preferred Ancillary tests Modified Knott or filtration test for microfilariae to differentiate D immitis from Acanthocheilonema formerly Dipetalonema reconditum thoracic radiography ultrasonographic visualization of worms Material required for laboratory analysis Inhouse antigen blood testing simple and inexpensive for dogs Blood tubes for both antigen and antibody testing for cats Relevant diagnostic laboratories Any veterinary diagnostic laboratory that performs the diagnostic testing Treatment Dogsarsenical compound melarsomine dihydrochlorideonly effective on worms 120 days old Maximum 98 efficacy on adult worms Adjunct therapy Pretreatment with macrocyclic lactone 812 weeks to eliminate migrating larvae 60 days old and allow larvae 60120 days old to reach melarsomine susceptible age Doxycycline 10 mgkg bid for 4 weeks to reduce inflammation from filarialassociated Wolbachia Surgical extraction of adult heartworms in acute caval syndrome Cats adulticide treatment not recommended Symptomatic prednisolone bronchodilators Surgical removal via right jugular venotomy or right ventriculotomy Extreme caution must be exercised with melarsomine in exotic carnivores due to narrow margin of safety Prevention and control Dogs and cats macrocyclic lactones ivermectinpyrantel Heartgard Plus Merial dog and cat Iverhart PlusVirbac TriHeartMerck milbemycin oximelufenuron Sentinel Novartis moxidectin Advantage MultiBayer dog and cat ProHeart 6Zoetis dogs only selamectin RevolutionZoetisall against L3 early L4 microfilariaemilbemycin oxime offlabel at preventive dose Preventives have some efficacy against adult heartworms but studies have mostly been performed with ivermectinpyrantel compounds Efficacy declines in late stages of L4 As of this writingresistance to heartworm preventives has been proven however it does not appear to be a concern except in the Mississippi Delta region Suggested disinfectant for housing facilities Not applicable Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal None although presence of mosquitoes will increase risk to noninfected individuals Conditions for restoring diseasefree status after an outbreak Treat affected individuals eliminate microfilariae pretreatment Topical moxidectinimidicloprid FDA labelled for microfilariae eliminination Milbemycin oxime 500 ugkg or ivermectin at 50 ug kg will also result inclearance of microfilariae mosquito control Experts who may be consulted American Heartworm Society American Association of Zoo Veterinarians Infectious Disease Manual DIROFILARIA IMMITIS PO Box 8266 Wilmington DE 198038266 infoheartwormsocietyorg httpwwwheartwormsocietyorg References 1 American Heartworm Society Internet Heartworm Guidelines 2018 cited 2019 January 14 httpswwwheartwormsocietyorgveterinaryresourcesamericanheartwormsocietyguidelines 2 Cottrell DK Use of moxidectin ProHeart 6 as a heartworm adulticide in four ferrets Exotic DVM 20046912 3 Freda S Internet Dirofilaria immitis 2003 cited 2019 January 14 Available from httpanimaldiversityummzumichedusiteaccountsinformationDirofilariaimmitishtml 4 Gamble KC Fried JJ Rubin GJ Presumptive dirofilariasis in a paleheaded saki monkey Pithecia pithecia J Zoo Wildl Med 19981504 5 Kiku M ByeongKirl B ChaeWoong L Eurasian otter Lutra lutra a definitive host for Dirofilaria immitis J Zoo Wildl Med 2003342200201 6 Lung NP Murray S Garner MM Mortality in North American river otters Lontra canadensis following administration of melarsomine for Dirofilaria immitis infection In Proc Am Assoc Zoo Vet 2006 p 14647 7 Mazzario S Cassini RR Voltan L Aresu L Frangipane di Regalbono A Heartworm Dirofilaria immitis infection in a leopard Panthera pardus pardus housed in a zoological park in northeastern Italy Parasit Vectors 2010325 8 McCall JW Genchi C Kramer LH Guerrero J Venco L Heartworm disease in animals and humans Adv Parasitol 200866193285 9 Muro A Genchi C Cordero M Simon F Human dirofilariasis in the European Union Trends Parasitol 1999159386389 10 Nakagaki K Yoshida M Nogami S Nakagaki K Experimental infection of Dirofilaria immitis in raccoon dogs J Parasit 2007932432434 11 Nayar JK Rutledge CR Mosquitoborne dog heartworm disease University of Florida Cooperative Extension Service Institute of Food and Agricultural Sciences EDIS 1998 12 Neiffer DL Klein EC Calle PP Linn M Terrell SP Walker RL Todd D Vice CC Marks SK Mortality associated with melarsomine dihydrochloride administration in two North American river otters Lontra canadensis and a red panda Ailurus fulgens fulgens J Zoo Wildl Med 2002333242248 13 Ray J Effect of reservoir host and climactic conditions on emerging heartworm disease emerging heartworm disease part 2 Publication 2644 Extension Service of Mississippi State University 2011 14 Wang F Guo JJ Tsai Y Lin JY Dirofilaria immitis infection in a captive Eurasian otter Lutra lutra J Vet Clin Sci 2008143033 American Association of Zoo Veterinarians Infectious Disease Manual EASTERN EQUINE ENCEPHALOMYELITIS EEE Fact Sheet Compiled by Erica Lipanovich Completed on updated 10 October 2017 Fact Sheet Reviewed by Elizabeth ArnettChinn Susceptible Animal Groups Birds are the principal enzootic hosts Clinical cases occur in equids and occasionally other mammals including swine cows rodents and opossums Mammals are almost always deadend hosts Snakes turtles and fish are suspected to be an amplifier or overwintering reservoir Causative Organism Eastern equine encephalomyelitis virus Family Togaviridiae genus Alphavirus There are four lineages of EEE Group I is endemic in North American and the Caribbean and causes most of the human cases The other three groups IIA IIB III and IV cause primarily equine illness in South or Central America and are now classified as the Madariaga virus Zoonotic Potential Mosquito bites from Culiseta melanura is the important vector in the maintenance cycle in birds The majority of isolates have been found in 27 species of mosquitoes eg some Aedes Coquillettidia and Culex species Distribution Western Hemisphere North American variant is found in eastern Canada all states east of the Mississippi River Arkansas Minnesota South Dakota Texas and the Caribbean islands The South American variant is confined to central and South America Incubation Period 4 to 10 days and rarely up to 3 weeks Clinical Signs Equids frequently include altered mentation impaired vision aimless wandering head pressing circling anorexia grinding of teeth esophageal paralysis irregular or ataxic gait paresis paralysis seizures coma and death Many horses progress to recumbency within 1218 hours of onset of neurological abnormalities Most deaths occur within 23 days after onset of signs Mortality of equids with clinical signs is 5090 Most people infected have no apparent illness Two types of illness can develop in humans systemic or encephalitic Systemic infection has an abrupt onset of malaise fever chills arthralgia and myalgia lasting one to two weeks Recovery is complete if there is no CNS involvement Encephalitic illness can be abrupt or become present after a few days of systemic illness such as fever headache irritability restlessness drowsiness anorexia vomiting diarrhea cyanosis altered reflexes convulsions and coma One third of all EEE human cases usually die within 2 to 10 days after onset of symptoms Those persons who recover have irreversible neurological damage Birds Most cases are asymptomatic but fatal outbreaks have occurred in emus game birds such as pheasants whooping cranes passerines and psittacines Post mortem Gross or Histological Findings Gross lesions are rare but congestion may be present in the meninges of acutely affected animals Histologic findings are typical of encephalomyelitis which include severe gliosis with necrosis of the neuropil in the cerebrum and through the corona radiate to the thalamus and perivascular cuffing throughout the mid and hindbrain and cervical spinal cord Diagnosis Clinical presentation in an endemic area EEEVspecific IgM antibody in serum or cerebrospinal fluid samples CSF and confirmed by neutralizing antibody testing of acute and convalescent phase serum specimens Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Birds equids and occasionally other mammals Mosquito Culiseta melanura Febrile altered mentation neurologic abnormalities seizures paresis paralysis death Equine fatality rate is up to 90 survivors usually exhibit longterm neurologic signs human fatality rate is 5075 Supportive care Formalin inactivated whole viral vaccine insect control Yes however not believed to transmit from horses as viremia is too low American Association of Zoo Veterinarians Infectious Disease Manual EASTERN EQUINE ENCEPHALOMYELITIS EEE Material Required for Laboratory Analysis Serum and CSF samples are collected from live animals to detect virusspecific IgM and neutralizing antibodies Brain spinal cord and other tissues may also be collected from necropsied animals Relevant Diagnostic Laboratories Only a few state laboratories or other specialized laboratories are capable of doing the testing National Center for Emerging and Zoonotic Infectious Diseases NCEZID through the CDC httpswwwcdcgovnceziddvbdspecimensubarboviralshippinghtml Accessed 2 October 2017 The state health departments must be notified upon submission Treatment Supportive and symptomatic care Prevention and Control There is no vaccine for humans Reducing exposure to mosquitoes mosquito control and vaccination in equids Vaccination of captive at risk bird species birds in areas high virus activity is often practiced No crossimmunity obtained when vaccinated for other alphaviruses eg western equine encephalitis virus or flaviviruses eg West Nile virus or bunyaviruses eg La Crosse virus Suggested Disinfectant for Housing Facilities Clean infected environment with an approved EPA disinfectant Notification Suspected cases are reported according to individual State procedure typically by notification of the State Arboviral Coordinator or State Animal Health Official Reports of positive equine cases of arboviral disease are reported to ArboNET an internetbased arbovirus surveillance and reporting system managed by state health departments and the Centers for Disease Control and Prevention ArboNET captures laboratoryconfirmed positive cases in humans horses other mammals birds and mosquitoes across the US Equine cases vary by state but those reported to ArboNET are confirmed by State Veterinarians prior to reporting Measures Required under the Animal Disease Surveillance Plan In most states reporting is mandatory Measures Required for Introducing Animals to Infected Animal Maintain infected animal in a quarantine situation Do not introduce infected animal to an animal with a compromised immune system Conditions for Restoring DiseaseFree Status after an Outbreak Clean infected environment with diluted bleach to the extent possible Minimize contact of infected staff with animal Experts Who May Be Consulted USDA APHIS Veterinary Services Center for Disease Control and Prevention 4700 River Road Unit 41 Public Health Resources Riverdale MD 207371231 State or Territorial Health Departments Telephone 301 7348093 httpswwwcdcgovmmwrinternationalrelreshtml Fax 301 7347817 wwwaphisusdagovanimalhealthindexshtml References 1 Arrigo NC Adams AP Weaver SC Evolutionary patterns of eastern equine encephalitis virus in North versus South America suggest ecological differences and taxonomic revision J Virol 2010842 10141025 2 Centers for Disease Control and Prevention Internet Eastern Equine Encephalitis 2016 cited 2017 October 2 Available from httpwwwcdcgovEasternEquineEncephalitisindexhtml 3 Franklin RP Kinde H Jay MT Kramer LD Green EGN Chiles RE Ostlund E Husted S Smith J Parker MD Eastern equine encephalomyelitis virus infection in a horse from California Emerg Infect Dis 200283 28388 4 Graham SP Hassan HK Chapman T White G Guyer C Unnasch TR Serosurveillance of eastern equine encephalitis virus in amphibians and reptiles from Alabama USA Am J Trop Med Hyg 20128635404 5 Kahn CM Line S Equine viral encephalomyelitis In The Merck Veterinary Manual 10th ed Whitehouse Station NJ Merck Co Inc 2010 p 11831189 American Association of Zoo Veterinarians Infectious Disease Manual EASTERN EQUINE ENCEPHALOMYELITIS EEE 6 Nandalur M Urban AW Internet Eastern equine encephalitis 2018 cited 2019 February 18 Available from httpemedicinemedscapecomarticle233442overview 7 Stull JW Talbot EA MacRae S Montero JT Matyas B Cantor F Konomi R DeMaria A Hayes EB Smith TL Nasci RS Sejvar JJ OLeary DR Campbell GL Noga AJ Lanciotti RS Plotinski RN Schumacher S Farnon EC Eastern equine encephalitis New Hampshire and Massachusetts September 2005 MMWR Weekly 200655697700 8 Whitley RJ Viral encephalitis New Engl J Med 19903234242250 9 United States Department of Agriculture Internet Epidemiology and Ecology of Eastern Equine Encephalomyelitis 2004 cited 2017 October 2 Available from httpswwwaphisusdagovanimalhealthemergingissuesdownloadsEEE042004pdf American Association of Zoo Veterinarians Infectious Disease Manual RESTON EBOLAVIRUS Fact Sheet compiled by Dawn Zimmerman Sheet completed on 27 December 2017 Fact Sheet Reviewed by Tim Georoff Susceptible animal groups Cynomolgus monkeys Macaca fascicularis were identified in the index case in 1989 and subsequent outbreaks among animals imported from the Philippines in 1990 1992 and 1996 An additional outbreak has been documented at a lab facility in the Phillipines in 2015 Reston ebolavirus virus has also been isolated from swine in the Philippines and China which were coinfected with porcine reproductive and respiratory syndrome virus PRRSV It is unclear if swine are an incidental host or part of the virus transmission cycle Bats in the Philippines Bangladesh and China have tested seropositive however their epidemiological role is unknown Note African green monkeys Chlorocebus aethiops and baboons Papio hamadryas are resistant to both RESTV infection Causative organism Reston virus RESTV species Reston ebolavirus family Filoviridae Zoonotic potential Humans exposed to the disease in primates and swine have become seropositive but have no apparent or clinically mild infection It is unknown how infection would affect immunecompromised people pregnant women or children Distribution Philippines and animals recently imported from Philippines China Bangladesh Geographic distribution may be larger depending of the reservoir distribution Incubation period 714 days Clinical signs In primates Anorexia lethargy or sudden death may be the only signs Fever cough nasal exudates swollen eyelids splenomegaly and renomegaly can occur Animals may also show signs of hemorrhagic fever with diarrhea or melena with frank blood bleeding from external orifices petechial to suffusive hemorrhage Post mortem gross or histologic findings Maculopapular rash splenomegaly widespread petechial hemorrhages hemorrhage in proximal duodenum and interstitial pneumonia are observed grossly Lymphoid necrosis massive fibrin deposition in spleen hepatic necrosis necrosis of adrenal cortex and pulmonary bronchiolar and alveolar epithelium interstitial nephritis and amphophilic cytoplasmic inclusion bodies in many tissues including liver adrenal gland and spleen are observed histologically Extensive viral replication in tissue macrophages and interstitial fibroblasts Diagnosis In blood during acute phase ELISA RTPCR rapid more sensitive than antigen detection ELISA and allows identification of the virus species virus isolation requires a BSL4 lab IgGIgM immunohistochemical staining and histopathology on postmortem or collected tissues to localize viral antigen Biosafety concerns during the collection and processing of the specimens Material required for laboratory analysis Testing liver samples by ELISA antigen capture is the mandatory test for confirmation or rulingout the diagnosis in suspected dead primates during quarantine httpswwwcdcgovnceziddhcppvspbpdfprimateform508pdf Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Macaque swine Fruit bats are a possible reservoir Direct contact with infected animals secretions or droplets Possible aerosol transmission in pigs Anorexia lethargy diarrhea or melena with frank blood bleeding from external orifices petechial to suffusive hemorrhage Macaque Fatal Swine Can vary from subclinical to severe Isolation of unaffected animals No successful clinical treatment Quarantine of imported primates in country of origin and in import facilities in the US Whereas the Ebola genus viruses are known to cause disease in humans this one is not American Association of Zoo Veterinarians Infectious Disease Manual RESTON EBOLAVIRUS Relevant diagnostic laboratories Viral Special Pathogens Branch Centers for Disease Control and Prevention 1600 Clifton Rd Atlanta Georgia 30333 Phone 4703120094 Treatment Based on epidemiology from prior outbreaks it appears that virus spread through grouphoused animals is unavoidable Since asymptomatic animals may be present in groups during the incubation period strict depopulation is likely the best course of action Prevention and control Preshipment quarantine of primates to be shipped from Philippines CDC licensed primate import quarantine facility with special permit required for Cynomolgus monkeys rhesus and African green monkeys Diagnostic testing of potentially affected animals personal protective equipment to prevent exposure of personnel and close coordination with importer and CDC Strict isolation of groups of imported animals Suggested disinfectant for housing facilities Hypochlorite or phenolic disinfectants are generally recommended for disinfection Ebola virus is susceptible to 2 sodium hypochlorite 2 glutaraldehyde 5 peracetic acid 1 formalin Notification CDC Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Depopulation of affected group and premise disinfection Experts who may be consulted Centers for Disease Control and Prevention CDC Viral Special Pathogens Branch or Division of Global Migration and Quarantine DGMQ May be contacted 24 hours a day through the CDC Emergency Operations Center 7704887100 References 1 Barrette RW Metwally SA Rowland JM Xu L Zaki SR Nichol ST Rollin PE Towner JS Shieh WJ Batten B Sealy TK Carrillo C Moran KE Bracht AJ Mayr GA SiriosCruz M Catbagan DP Lautner EA Ksiazek TG White WR McIntosh MT Discovery of swine as a host for the Reston ebolavirus Sci 200932559372046 2 Cameron KW Reed PE Ebola Hemorrhagic Fever In Miller RE and ME Fowler eds Fowlers Zoo Wild Animal Medicine 7th ed St Louis MO Elsevier Saunders 2011 p 416421 3 Cantoni D Hamlet A Michaelis M Wass MN Rossman JS Risks Posed by Reston the Forgotten Ebolavirus mSphere 2016 Dec 2816 4 Demetria C Smith I Tan T Villarico D Simon EM Centeno R Tachedjian M Taniguchi S Shimojima M Miranda NLJ Miranda ME Rondina MMR Capistrano R Tandoc A 3rd Marsh G Eagles D Cruz R Fukushi S Reemergence of Reston ebolavirus in Cynomolgus Monkeys the Philippines 2015 Emerg Infect Dis 201824712851291 5 Marsh GA Haining J Robinson R Foord A Yamada M Barr JA Payne J White J Yu M Bingham J Rollin PE Nichol ST Wang LF Middleton D Ebola reston virus infection of pigs clinical significance and transmission potential J Infect Dis 2011204 Suppl 3S8049 6 Miranda ME Ksiazek TG Retuya TJ Khan AS Sanchez A Fulhorst CF Rollin PE Calaor AB Manalo DL Roces MC Dayrit MM Peters CJ Epidemiology of Ebola subtype Reston virus in the Philippines 1996 J Infect Dis 1999179 Suppl 1S1159 7 Rollin PE Williams RJ Bressler DS Pearson S Cottingham M Pucak G Sanchez A Trappier SG Peters RL Greer PW Zaki S Demarcus T Hendricks K Kelley M Simpson D Geisbert TW Jahrling PB Peters CJ Ksiazek TG Ebola subtype Reston virus among quarantined nonhuman primates recently imported from the Philippines to the United States J Infect Dis 1999179 Suppl 1S10814 American Association of Zoo Veterinarians Infectious Disease Manual RESTON EBOLAVIRUS 8 Sayama Y Demetria C Saito M Azul RR Taniguchi S Fukushi S Yoshikawa T Iizuka I Mizutani T Kurane I Malbas FF Jr Lupisan S Catbagan DP Animas SB Morales RG Lopez EL Dazo KR Cruz MS Olveda R Saijo M Oshitani H Morikawa S A seroepidemiologic study of Reston ebolavirusin swine in the Philippines BMC Vet Res 201218882 9 Weingartl HM EmburyHyatt C Nfon C Leung A Smith G Kobinger G Transmission of Ebola virus from pigs to nonhuman primates Sci Rep 20122811 American Association of Zoo Veterinarians Infectious Disease Manual ECHINOCOCCOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Intermediate IHaccidental AH hosts Fecaloral Definitive DH host predation or ingestion of infected IHAH IHAH Abdominal distention and pain lethargy inappetance cough dyspnea IHAH Initially subclinical but cyst growth can lead to hepatic and respiratory disease which may be fatal IHAH Benzimidazoles or percutaneous drainage of hepatic cysts DH Praziquantel Eggs susceptible to desiccation and extreme temperatures avoid feeding potentially infected carcasses anthelmintic bait praziquantel for DH dog population management education EG95 vaccine Yes Fact Sheet compiled by M Camille Harris Sheet completed on 19 March 2011 updated 20 March 2013 Fact Sheet reviewed by Malika Kachani Philip Craig Linda Pote Susceptible animal groups Mammals primates Old World monkeys and great apes including significant number of primate cases in the literature ungulates marsupials rodents canids Causative organism Primary transmission cycles include E granulosus complex EG wolfcervid canidlivestock molecular species include E granulosus sensu stricto sheep Tasmanian sheep and buffalo strains E equinus EE horse strain E ortleppi EOr cattle strain E canadensis EC camel pig and cervid strains E felidis EF lion strain E multilocularis EM foxcanidfelidrodent E oligarthrus EOl felidagoutipaca E vogeli EV bush dogpaca E shiquicus ES Tibetan foxpika Zoonotic potential Yes Humans are susceptible by ingesting shed Echinococcus eggs EG EC EM EOl EV EOr Distribution EG Worldwide EM Northern Hemisphere EOl and EV Central and South America ES QinghaiTibet plateau of China Incubation period IHAH incubation period Months eg rodents to years eg primates depending on hydatid cyst location and growth rate DH prepatent period EG 3280 days EM 2835 days Clinical signs Larval metacestode infections of IHAH are initially subclinical and signs may not develop during the hosts life span Clinical signs are related to cyst location which is most often the liver and lungs American Association of Zoo Veterinarians Infectious Disease Manual ECHINOCOCCOSIS As cysts develop signs may include lethargy abdominal pain abdominal enlargement due to hepatomegaly inappetance and respiratory signs Cyst rupture may lead to anaphylaxis EM is most likely to eventually cause clinical disease after a 515 year asymptomatic period No clinical signs in DH are noted Post mortem gross or histologic findings Adult cestodes body length 12 11 mm are found in the small intestine of DH with EG primarily in the upper third and EM in the middle third The formation of fluidfilled cysts is primarily in hepatic and pulmonary tissues but can occur in any organ of IHAH EG and EOl are usually associated with a single cyst Similar to a metastasizing neoplasm EM and EV form masses of small cysts Viable protoscolices may be present within cysts Diagnosis Antemortem Imaging may be used to identify and classify fluidfilled cysts in IHAH see Table 25 Eckert et al 2001 along with a cytologic exam of FNA Fecal diagnosis in DH is difficult due to the small size of gravid proglottids 12mm and inability to differentiate from eggs of Taenia species Fecal coproantigen ELISA and confirmatory Echinococcus PCRs have been developed for DH Serum antibody ELISAs have been developed but Taenia false positives may occur and species validation is limited Percutaneous drainage of cysts may reveal the presence of protoscolices Postmortem Fluidfilled cysts may be seen at necropsy primarily hepatic and pulmonary In IHAH histopathology may reveal the presence of protoscolices within broodcapsules or in hydatid sand In DH the scraping filtration and counting technique can be used to extract cestodes from the intestines Material required for laboratory analysis cyst fluid serum IHAH feces small intestine DH Treatment In humans treatment options include surgical removal of cysts and ultrasoundguided partial removal of cyst fluid and injection of anthelmintic PAIR puncture aspiration injection reaspiration Alternatively anthelmintics benzimidazoles can be used for IHAHs Degenerating cysts may not require treatment and monitoring would be an option Prevention and control Infective material can be decontaminated by extreme temperatures 70C for 12 hrs 80C for 48 hrs When handling infective material personal protective equipment should be worn to reduce the risk of human exposure Ensure the DHs diet does not include potentially infected organs and carcasses Prevent scavenging and predation by susceptible mammals Decontaminate foliage or branches used for environmental enrichment Pet and feral dog population management and deworming Education of animal care workers dog owners and other atrisk human populations Anthelmintic baiting of foxes 50mg praziquantelbait EG95 vaccine has been shown to be protective against EG in sheep goats cattle and tammar wallabies Suggested disinfectant for housing facilities Chemical disinfection is unreliable but 375 bleach NaOCl solution for 1 hr metal surface or 23 hrs concrete may be effective for EM Facilities can be decontaminated by 40 relative humidity and 30C for at least 48 hrs Notification Echinococcosis is an OIE reportable disease and USDA should be notified Experts who may be consulted Dr Philip S Craig Cestode Zoonoses Research Group School of Environment and Life Sciences University of Salford Manchester M5 4WT UK 44161 2955488 44161 2955215 pscraigsalfordacuk Dr Thomas Romig Institute of Parasitology Hohenheim University 1Schloß Hohenheim 70599 Stuttgart 0711 4590 Germany Rapporteur American Association of Zoo Veterinarians Infectious Disease Manual ECHINOCOCCOSIS 49 160 9476 7579 ThomasRomigunihohenheimde Malika Kachani PhD DVM Professor of Parasitology College of Veterinary Medicine Western University of Health Sciences 309 E Second Street Pomona California 91066 909 4695302 mkachaniwesternuedu Dr Peter DePlazes University of Zurich Vetsuisse Fac Institute Parasitol Winterthurerstr 266A CH8057 Zurich Switzerland Deplazespaccessuzhch References 1 Barnes TS AW Goldizen JM Morton and GT Coleman 2008 Cystic echinococcosis in a wild population of the brushtailed rockwallaby Petrogale penicillata a threatened macropodid Parasitol 135 715723 2 Barnes TS LA Hinds DJ Jenkins GT Coleman AL Colebrook CT Kyngdon CG Gauci and MW Lightowlers 2009 Efficacy of the EG95 hydatid vaccine in a macropodid host the tammar wallaby Parasitol 136 461468 3 Blutke A D Hamel M Huttner H Gehlen T Romig K Pfister and W Hermanns 2010 Cystic echinococcosis due to Echinococcus equinus in a horse from southern Germany J Vet Diag Invest 22 458462 4 Boufana B MF Stidworthy S Bell J Chantrey N Masters S Unwin R Wood RP Lawrence A Potter J McGarry S Redrobe R Killick AP Foster S Mitchell AG Greenwood Y Sako M Nakao A Ito K Wyatt B Lord and PS Craig 2012 Echinococcus and Taenia spp from captive mammals in the United Kingdom Vet Parasit 19095103 5 Brunetti E P Kern and DA Vuitton 2010 Expert consensus for the diagnosis and treatment of cystic and alveolar echinococcosis in humans Acta Tropica 114 116 6 Eckert J MA Gemmell FX Meslin and ZS Pawlowski eds 2001 WHOOIE Manual on Echinococcosis in Humans and Animals a Public Health Problem of Global Concern World Organisation for Animal Health Office International des Epizooties Paris France 265 pp Available online at httpwhqlibdocwhointpublications2001929044522Xpdf 7 Foreyt WJ ML Drew M Atkinson and D McCauley 2009 Echinococcus granulosus in gray wolves and ungulates in Idaho and Montana USA J Wildl Dis 45 12081212 8 Gesy K M Pawlik L Kapronczai B Wagner B Elkin H Schwantje and E Jenkins 2013 An improved method for the extraction and quantification of adult Echinococcus from wildlife definitive hosts Parasit Res 112520758 9 Hegglin D and P Deplazes 2013 Control of Echinococcus multilocularis strategies feasibility and costbenefit analyses Internat J Parasit 43 327337 10 Hegglin D PI Ward and P Deplazes 2003 Anthelmintic baiting of foxes against urban American Association of Zoo Veterinarians Infectious Disease Manual ECHINOCOCCOSIS contamination with Echinococcus multilocularis Emerg Infect Dis 9 12661272 11 Laura LP B MartinezFernandez J Gonzalez MC Ferreras MJ GarciaIglesias and JF Garcia Marin 2012 Severe hepatitis due to alveolar echinococcosis Echinococcus multilocularis in a Gorilla g gorilla J Comp Path 146 90 12 OIE 2008 EchinococcosisHydatidosis In Manual of diagnostic tests and vaccines for terrestrial animals mammals birds and bees 6th ed Office International des Épizooties Paris France Pp 175 189 13 Weiss ATA C Bauer and K Kohler 2010 Canine alveolar echinococcosis morphology and inflammatory response J Comp Path 143 233238 14 Yamano K A Kanetoshi A Goto M Kishimoto N Kobayashi S Fujimoto and K Yamada 2009 Japanese monkey Macaca fuscata with alveolar echinococcosis after treatment with albendazole for 10 years serodiagnosis and determination of albendazole metabolites Parasit Res 106 6974 15 Zimmerman DM M Douglass DR Reavill and EC Greiner 2009 Echinococcus oligarthrus cystic hydatidosis in Brazilian agouti Dasyprocta leporina J Zoo Wildl Med 40 551558 American Association of Zoo Veterinarians Infectious Disease Manual EDWARDSIELLOSIS Fact Sheet compiled by Catherine Hadfield Sheet completed on 28 November 2013 updated 6 July 2013 Fact Sheet Reviewed by Leigh Clayton Lester Khoo Susceptible animal groups Various teleost species usually those found in warm water Common in American European and Japanese eels channel catfish carp bass Japanese flounder and many tropical marine teleosts It can also cause disease in some invertebrates amphibians reptiles and mammals Causative organism Enterobacteriaceae Edwardsiella tarda and Edwardsiella piscicida These species cannot be differentiated phenotypically so earlier reports of E tarda may represent E piscicida Molecular diagnostics are required for differentiation Other strains may be identified in the future Zoonotic potential Yes Usually necrotic skin wounds or gastroenteritis but it can spread systemically Distribution Worldwide Incubation period 57 days Clinical signs Acute or chronic presentation may include lethargy inappetance ulcers hyperemia petechiation erythema pale gills coelomic distension positive buoyancy and ocular lesions such as keratitis uveitis and exophthalmia Mortalities tend to be low Post mortem gross or histologic findings Congestion andor focal necrosis of spleen liver kidney and heart are observed Malodorous abscesses in the viscera or skeletal muscle may be seen Small straight Gram negative rods which may be motile can be present Inflammation often suppurative but may be granulomatous can be observed in infected organs such as kidneys Diagnosis Bacterial culture from lesions blood or organs PCR DNA hybridization or sequencing required for differentiation of E tarda and E piscicida However bacteria may be present in the gastrointestinal tract of healthy fish Material required for laboratory analysis Blood culture can be performed Tissue swabs or preferably tissue samples for bacterial culture especially kidney Samples should be transported at 4C Relevant diagnostic laboratories Most laboratories should be able to culture Edwardsiella spp but further identification may require specialist fish laboratories Treatment Removal of stressors is important for successful treatment and good supportive care should be provided Water quality and disinfection should be improved Systemic antibiotics based on culture and sensitivity and relevant legislation eg trimethoprim sulfa florfenicol can be used However as of June 2013 no FDAapproved medications are available for use in food fish Immunostimulants eg glucans glycans alginate or ascorbic acid Prevention and control Stressors eg temperature water quality stocking density and organic load should be reduced in the environment Water can be disinfected with UV or ozone E tarda vaccines are under trial Suggested disinfectant for housing facilities Susceptible to most common disinfectants l sodium Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Several teleost species especially in warm water Unknown probably oral Septicemia enteritis skin ulcers petechiae Variable can be severe with concurrent stressors Systemic antibiotics based on culture and sensitivity and regulations Remove stressors improve disinfection Yes American Association of Zoo Veterinarians Infectious Disease Manual EDWARDSIELLOSIS hypochlorite 70 ethyl alcohol iodophors phenols Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Introduction of animals should be avoided if clinical signs are present Conditions for restoring diseasefree status after an outbreak Not known animals can carry the bacteria asymptomatically Experts who may be consulted Most fish clinicians will be familiar with Edwardsiellosis and can be consulted if an outbreak is encountered References 1 Abayneh T CJ Colquhoun and H Sorum 2013 Edwardsiella piscidia sp nov a novel species pathogenic to fish J Applied Microbiol 114 644654 2 Cheng S Y Hu M Zhang and L Sun 2010 Analysis of the vaccine potential of a natural avirulent Edwardsiella tarda isolate Vaccine 28 27162721 3 Griffin MJ SM Quiniou T Cody M Tabuchi C Ware RC Cipriano MJ Mauel and E Soto 2013 Comparative analysis of Edwardsiella isolates from fish in the eastern United States identifies two distinct genetic taxa amongst organisms phenotypically classified as E tarda Vet Microbiol 165 358372 4 Lowry T and SA Smith 2007 Aquatic zoonoses associated with food bait ornamental and tropical fish J Am Vet Med Assoc 231 876880 5 Mainous ME SA Smith and DD Kuhn 2010 Effect of common aquaculture chemicals against Edwardsiella ictaluri and E tarda J Aq Anim Health 22 224228 6 Mohanty BR and PK Sahoo 2007 Edwardsiella in fish a brief review J Biosciences 32 1331 1344 7 Ringo E RE Olsen JLG Vecino S Wadsworth and SK Song 2012 Immunostimulants and nucleotides in aquaculture a review J Marine Sci Res Dev 2 122 8 Roberts RJ 2001 The bacteriology of teleosts In Roberts RJ ed 3rd edition Fish Pathology WB Saunders Philadelphia Pennsylvania Pp 297331 9 Wang WS and DH Wang 1997 Enhancement of the resistance of tilapia and grass carp to experimental Aeromonas hydrophila and Edwardsiella tarda infections by several polysaccharides Comp Immun Microbiol Infect Dis 20 261270 American Association of Zoo Veterinarians Infectious Disease Manual Ehrlichia ruminatum HEARTWATER Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals domestic and wild ruminants Infections in other mammals mice and possibly although not definitively proven in reptiles and birds Non contagious tick borne disease via Ambylomma spp ticks including US tick species A maculatum A cajennense A dissimile A americanum Acute fever anorexia diarrhea serosa or mucosa petechiae respiratory and neurologic signs Peracute sudden death Subclinical to peracute death Dependent on strain host and environment Most common is acute clinical disease Remove ticks and antibiotics eg tetracycline Submit ticks for diagnosis using the pCS20 RT or nested PCR Tick control and test for carrier status in animals prior to translocations Vaccination see below can be used in areas with endemic heartwater present No Fact Sheet compiled by Sharon L Deem Sheet completed on updated 31 July 2018 Fact Sheet Reviewed by Beth Bicknese Susceptible animal groups Ruminant species domestic and wild and other mammals mice Sheep and goats more susceptible than cattle and European breeds more susceptible than zebu type Infections in birds and reptiles have not been confirmed Causative organism Ehrlichia ruminantium previously called Cowdria ruminantium A small intracellular Gram negative pleomorphic coccus bacteria found in endothelial cells monocytes and neutrophils Zoonotic potential Not definitively although pCS20 sequences have been amplified in humans in South Africa Distribution Endemic countries are on the African continent south of the Sahara Madagascar various small islands in the Indian and Atlantic Oceans and islands in the Caribbean A foreign animal disease for US concern of entry is high due to illegal wildlife trade with infected ticks and the potential for domestic ruminants and white tailed deer in the US to serve as host species All susceptible animals legally imported eg zoo animals and stocking of exotic animal ranches to the US from heartwater endemic regions may serve as a route of introduction of E ruminantium to the American continents Ticks on tortoises from Africa can carry infected ticks Incubation period This period varies with species infected route of infection and strain of E ruminantium In domestic cattle incubation is 12 days after intravenous injection of E ruminantium vaccine The period is shorter eg 7 days when more virulent strains are used Incubation period of tick transmitted heartwater is 1821 days Clinical signs Severity ranges from subclinical infection to peracute disease Clinical signs range from mild transient fever in subclinical cases to death without premonitory signs in peracute cases ie presenting as sudden death The acute form is characterized by rapid onset of fever 415o to 42oC tachypnea inappetence petechiation on serosal and mucosal surfaces and neurologic signs eg hyperesthesia high stepping or unsteady gait twitching eyelids head pressing chewing abnormal tongue movement individual muscle tremors In domestic cattle and goats profuse fetid hemorrhagic diarrhea commonly occurs terminally Post mortem gross or histologic findings Hydrothorax pulmonary edema ascites hydropericardium heartwater cerebral edema edema of the lymph nodes and splenomegaly are observed E ruminantium found in brain endothelial cells lining capillaries as colonies in all animals that have died of heartwater Rare to find colonies in brain smears of infection carrier animals American Association of Zoo Veterinarians Infectious Disease Manual Ehrlichia ruminatum HEARTWATER Diagnosis Clinical signs in ruminants with known Amblyomma spp tick infestations may be suggestive although a number of differential diagnoses must be considered due to the nonspecific gastrointestinal and neurologic signs In peracute cases anthrax and peracute typanosomiasis are top differentials In acute cases rabies cerebral babesiosis cerebral theileriosis tetanus cerebral listeriosis coccidiosis arsenical or plant intoxication hemorrhagic septicemia and hemonchosis can be confused with E ruminantium Differential diagnoses are host species and geographical location dependent Clinical pathologic changes are variable but may include progressive anemia marked decline in thrombocytes fluctuations in total and differential white cell counts increased total bilirubin and a decrease in total serum proteins Serologic diagnostics for antibodies eg ELISA and Western blot and pathogen detection eg DNA probes and pCS20 PCR are available It is recommended that MAP1B ELISA and the pCS20 PCR nested or reverse transcript be run on samples from animals with suspected E ruminantium infection to detect both antibodies and the pathogen NB Animals that die of heartwater will not have antibodies detected in the blood Definitive diagnosis gold standard is brain smears showing the organisms in endothelial cells that stain positive with Giemsa stain In addition to the brain organisms may be identified by light microscopy in kidney lung and heart tissue Material required for laboratory analysis Brain tissue Amblyomma spp ticks and blood or bone marrow collected in anticoagulant Relevant diagnostic laboratories Submissions from suspect cases coming from the US USDAAPHISVS National Veterinary Services Laboratory NVSL 1920 Dayton Ave for packages PO Box 844 for letters Ames IA 50010 Phone 515 3377266 Fax 515 3377397 Submissions from suspect cases coming from foreign countries Foreign Animal Disease Diagnostic Laboratory FADDL Plum Island New York 40550 Route 25 for packages Orient Point NY 11957 PO Box 848 for letters Greenport NY 119440848 Phone 6313233256 Fax 631 3233366 Treatment Limited value in clinically ill animals after the onset of neurologic or gastrointestinal signs Administration of antibiotics sulfonamides and tetracyclines at the start of a febrile response may be successful Prevention and control In regions free or heartwater US control depends on tick control Amblyomma spp and regulation of animal movements eg subclinical carriers In endemic regions control is dependent on maintenance of endemic stability through vaccination and strategic tick control Vaccination infection and treatment is possible in endemic regions with intravenous injection of live E ruminantium organisms and then intravenous administration of antibiotics started at first rise in body temperature Hazard of live vaccination is that it most likely will induce carrier status Inactivated vaccines are being developed and may soon be commercially available to minimize clinical signs but they do NOT prevent infection Suggested disinfectant for housing facilities Organism is extremely fragile outside the host losing its viability within hours Tick control is backbone of heartwater prevention Appropriate acaracides are important and proper quarantine periods when moving animals from heartwater endemic to nonendemic regions Notification OIE list B notifiable disease American Association of Zoo Veterinarians Infectious Disease Manual Ehrlichia ruminatum HEARTWATER Measures required under the Animal Disease Surveillance Plan Heartwater is a reportable foreign animal disease in the US to USDAAPHIS Measures required for introducing animals to infected animal Although a noncontagious disease all infected animals should be quarantined and treated with acaricides routinely Risk of spread from infected ticks on carrier animals when animals and their ticks are introduced to new areas or when potential Amblyomma spp vector ticks in heartwater free regions feed on carrier animals and become infectious Conditions for restoring diseasefree status after an outbreak Tick control and culling Experts who may be consulted Thomas Kasari DVM MVSc MBA DACVIM DACVPM Analytical Epidemiologist National Surveillance Unit Center for Epidemiology and Animal Health USDAAPHISVS National Resources Research Center Bldg B 2150 Centre Avenue Mailstop 2E6 Fort Collins CO 805268117 970 4947351 Fax 970 4947174 tomrkasariaphisusdagov Dr Suman Mahan Zoetis BLDG 300330P Kalamazoo Michigan 49009 Tele 269 833 2636 Fax 860 686 7114 SumanMahanzoetiscom References 1 Burridge MJ Peter TF Allan SA Mahan SM Evaluation of safety and efficacy of acaricides for control of the African tortoise tick Amblyomma marmoreum on leopard tortoises Geochelone pardalis J Zoo Wildl Med 200233 5257 2 Deem SL Heartwater Ehrlichia ruminantium In Fowler ME Miller RE eds Zoo and Wild Animal Medicine Current Therapy 6 Saint Louis MO Saunders Elsevier 2007 p 438443 3 Deem SL A review of heartwater and the threat of introduction of Cowdria ruminantium and exotic Amblyomma spp ticks to the American mainland J Zoo Wildl Med 1998 29109113 4 Karasi TR Miller RS James AM Freier JE Recognition of the threat of Ehrlichia ruminantium infection in domestic and wild ruminants in the continental United States J Am Vet Med Assoc 2010237520530 5 Kock ND Heartwater In Williams ES Baker IK eds Infectious Diseases of Wild Mammals Ames IA Iowa State University Press 2001 p 477480 6 Louw M Allsopp MT Meyer EC Ehrlichia ruminantium an emerging human pathogen a further report S Afr Med J 200595948950 7 Mahan SM 2008 Heartwater In Brown C Torres A eds Foreign Animal Diseases 7th Edition Saint Joseph MO United States Animal Health Assocation 2008 p 287296 8 Peter TF Anderson EC Burridge MJ Mahan SM Demonstration of a carrier state for Cowdria ruminantium in wild ruminants from Africa J Wildl Dis 199834567575 American Association of Zoo Veterinarians Infectious Disease Manual EHRLICHIOSIS Fact Sheet compiled by Dawn Zimmerman and Danielle R Graham Snyder Sheet completed on 22 December 2017 Fact Sheet Reviewed by Majorie Bercier Susceptible animal groups Mammals reported in humans canids felids bovids camelids cervids equids and rodents Causative organism Tickborne bacteria family Anaplasmataceae small gramnegative pleomorphic obligate intracellular cocci that infect different blood cells in various animals including humans Ehrlichia chaffeensis human monocytic ehrlichiosis known reservoirs include whitetailed deer and dogs Ehrlichia ewingii canine granulocytic ehrlichiosis CGE known reservoirs include whitetailed deer and dogs Ehrlichia canis canine monocytic ehrlichiosis CME known reservoirs include dogs Ehrlichia ruminantium heartwater known reservoirs include ruminants Ehrlichia muris known reservoirs include wild small rodents Other Ehrlichia muris eauclairensis formerly E murislike agent EMLA an emerging human pathogen in Midwestern US Note Ehrlichia risticii has been reclassified as Neorickettsia risticii and Ehrlichia platys as Anaplasma platys Ehrlichia equi Ehrlichia phagocytophila and Human Granulocytic Ehrlichial Agent are now considered to be the same species and have been reclassified as Anaplasma phagocytophilum Zoonotic potential Yes via vectors or mechanical transmission Distribution Almost every state in the US has reported a case of ehrlichiosis Most human cases occur in the southcentral and southeastern US E canis is endemic in southern eastern southcentral and in southwest US and is mainly transmitted by the brown dog tick Rhipicephalus sanguineus E ewingii is found predominantly in southern and mideastern US and is mainly transmitted by the lone star tick Amblyomma americanum E chaffeensis occurs predominantly in the southeastern US and is also transmitted by A americanum Globally Ehrlichia has been reported in South America Asia Africa and Europe Incubation period Humans 510 days after a tick bite Dogs 820 days It is estimated that the infected tick must be attached to the host for 2448 hours for transmission to occur Ehrlichia can remain alive in the developing tick for up to 5 months Acute infection develops 13 weeks after transmission and lasts 24 weeks After 69 weeks the organism is eliminated in an immunocompetent animal or a parasitemia develops with no clinical signs in the subclinical phase which can last from weeks to years or mild to severe clinical signs If the animal cannot mount an effective immune response the animal becomes chronically infected Clinical signs Generally nonspecific multisystemic fever depression lethargy thrombocytopenia anemia Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Mechanical via vectors tickborne Nonspecific fever depression lethargy thrombocytopenia anemia weight loss musclejoint pain lymphadenopathy hepatocellular enzyme abnormalities Subclinical or mild illness to severe potentially fatal disease Tetracycline antibiotics doxycycline is drug of choice Tick control screened blood donors inspect animals frequently in tickinfested areas Yes American Association of Zoo Veterinarians Infectious Disease Manual EHRLICHIOSIS anorexia weight loss lymphadenopathy hepatocellular enzyme abnormalities possibly gastrointestinal signs vomiting diarrhea polymyositis polyarthritis rash ocular signs uveitis or retinal petechiae reproductive disorders and neuropathies Clinical signs depend on the strain of Ehrlichia dose of infection species immunological status of host and concurrent infections with other tickborne parasites In dogs the acute phase is generally mild and causes immunemediated platelet destruction and manifesting in lethargy anorexia lymphadenopathy fever and is often associated with the presence of ticks In the subclinical phase dogs appear normal with a somewhat reduced platelet count and elevated globulin levels this phase can last months to years In the chronic phase clinical signs recur with up to 60 of infected dogs presenting with abnormal bleeding due to reduced platelet numbers elevated globulin levels are almost always seen uveitis neurological effects and glomerulonephritis can also result most dogs do not show full pancytopenia Infections with E ewingii which primarily causes disease in the immunocompromised tend to additionally produce arthritis Post mortem gross or histologic findings Gross splenomegaly hepatomegaly and lymphadenopathy during acute phase Histologic extensive plasma cell infiltration of parenchymal organs perivascular cuffing particularly of the lungs kidneys spleen meninges and eyes Diagnosis History of exposure and clinical signs diagnosis of subclinical disease based on anamnesis geographic location persistent antibody titers mild thrombocytopenia and hypergammaglobulinemia Morulae intracytoplasmic bacterial aggregates in monocytes on blood and buffy coat smears Romanowski stain however often only seen in a small percentage of blood smears of infected dogs and only found in the bloodstream for a few days in the acute stage EnzymeLinked Immunosorbent Assay ELISA eg IDEXX snap 4DX includes Lyme disease and heartworm tests detects E canis not E ewingii not quantitative Detection of E canis serum antibodies with indirect Immunofluorescence Antibody Test IFA antibodies can be detected as early as 7 days postinfection although animals may not be seropositive until 28 days post infection It takes 69 months after infection for titers to drop Serologic crossreactions may occur with other rickettsial agents With ELISA and IFA a positive test only indicates exposure and does not imply active infection A titer 180 is considered positive If 180 considered suspect and should retest in 23 weeks titers will increase rapidly in the acute stage look for fourfold increase between paired serum samples or test again using PCR or Western blot IFA and ELISA tests detect Ehrlichia species other than E canis Polymerase Chain Reaction PCR eg Antech FastPanel PCR Canine EhrlichiosisAnaplasmosis Profile for E canis E chafeensis and E ewingii crossreacts with Anaplasma PCR can detect E canis in dogs within 410 days of exposure before they become seropositive PCR remains positive for several weeks after infection has cleared as it does not distinguish between live and dead organisms Peptide and recombinant antigens are available for E ewingii however CGE diagnosis is usually made via visualization of morulae within neutrophils PCR ELISA or Western immunoblot Western immunoblot Demonstration of ehrlichial antigen in tissue sample by immunohistochemical methods or in situ hybridization Isolation of ehrlichial species from a clinical specimen in cell culture Material required for laboratory analysis Serology serum taken within first week of illness with second sample taken 23 weeks later Retain acute phase serum sample and submit two samples together at same time PCR 05ml whole blood EDTA or biopsy specimens from organs such as lymph nodes spleen liver or bone marrow Sample blood prior to starting antimicrobial therapy to avoid false negative test results American Association of Zoo Veterinarians Infectious Disease Manual EHRLICHIOSIS Relevant diagnostic laboratories Antech FastPanel PCR Canine EhrlichiosisAnaplasmosis Profile and Zoologix PCR two tests one is E canis specific other detects but does not differentiate most common Ehrlichia species PCR panel for tickborne diseases which includes common Ehrlichia species NCSU diagnostic PCRhttpswwwcvmncsueduvthticklabhtml OSU diagnostic PCR and serology httprikilb2vetohiostateeduehrlichia Treatment Tetracycline antibiotic for at least one month usually doxycycline which allows for a more convenient dosing schedule Dramatic initial improvement usually observed within 2448 hours Treatment success should be based on remission of clinical signs decline in E canis antibody titers and concurrent decrease in gamma globulins Rifampin and Levofloxacin may also be effective Imidocarb is sometimes used in conjunction with antibiotics usually for coinfections with Babesia and Hepatozoon With severe disease blood transfusions or intravenous fluids may be necessary Corticosteroids prednisone can be used to palliate immunemediated secondary reactions such as immunemediated arthritis or platelet loss Generally the prognosis during the acute phase is good if the animal is treated properly Animals in the chronic stage have a poorer prognosis Prevention and control Exposure to ticks should be limited and use of preventatives eg permethrin considered Animals should be examined for ticks in tickinfested areas and at peak time of year April through September Vegetation can be modified to discourage tick and wild host habitation Seronegative blood donors should be used for transfusions Vaccine development against CME shows promise Suggested disinfectant for housing facilities Areawide application of acaricides and removal of leaf litter and brush are effective Consider leasttoxic pesticide for use on targeted barriers Notification Not required Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Animals may be carriers but ticks are still needed for transmission Note that transmission can occur through a blood transfusion when the donor is infected Conditions for restoring diseasefree status after an outbreak Tick control in the environment is essential Infected ticks can transmit the disease for 155 days and after treatment an animal is still susceptible to re infection with the same or another Ehrlichia species However shortterm protection has been described with some Ehrlichia infections waning after about one year Prophylactic administration of tetracycline at a lower dose is effective in preventing E canis infection in situations where disease is endemic Treatment must be extended for many months through at least one tick season if the endemic cycle is to be successfully eliminated PCR conducted several weeks after termination of treatment can provide confidence that a treatment has been effective versus an animal entering a subclinical phase Experts who may be consulted Dr Anthony Barbet Dept Infectious Diseases Pathology University of Florida barbetufledu Yasuko Rikihisa PhD Department of Veterinary Biosciences The Ohio State University CVM rikihisa1osuedu References 1 Andre MR Adania CH Machado RZ Allegretti SM Felippe PAN Silva KF Nakaghi ACH Molecular and serologic detection of Ehrlichia spp in endangered Brazilian wild captive felids J Wildl Dis 201046310171023 2 Centers for Disease Control and Prevention Internet Ehrlichiosis 2018 cited 2018 November 15 American Association of Zoo Veterinarians Infectious Disease Manual EHRLICHIOSIS Available from httpwwwcdcgovehrlichiosis 3 Iqbal Z Chaichansiriwithaya W Rikihisa Y Comparison of PCR with other tests for early diagnosis of canine ehrlichiosis J Clin Microbiol 19943216581662 4 Lappin MJ Canine ehrlichiosis In Nelson RW Couto CG eds Small Animal Internal Medicine 4th ed Philadelphia PA Elsevier Health Sciences 2009 5 Little SE 2010 Ehrlichiosis and anaplasmosis in dogs and cats Vet Clin North Am Small Anim Pract 20104011211140 6 Missouri Department of Health and Senior Services 2008 Communicable Disease Investigation Reference Manual Section 40 Diseases and Conditions Ehrlichiosis Anaplasmosis 7 Neer TM Canine monocytic and granulocytic ehrlichiosis In Greene CE ed Infectious Diseases of the Dog and Cat 2nd ed Philadelphia PA WB Saunders Co 1998 Pp139147 8 Neer TM Breitschwerdt EB Greene RT Lappin MR Consensus statement on ehrlichial disease of small animals from the Infectious Disease Study Group of the ACVIM J Vet Intern Med 200216309 315 9 Perez M Rikihisa Y Wen B Ehrlichia canislike agent isolated from a man in Venezuela antigenic and genetic characterization J Clin Microbiol 19963421332139 10 Pritt BS Sloan LM Johnson DKH Munderloh UG Paskewitz SM McElroy KM McFadden JD Binnicker MJ Neitzel DF Liu G Nicholson WL Nelson CM Franson JJ Martin SA Cunningham SA Steward CR Bogumill K Bjorgaard ME Davis JP McQuiston JH Warshauer DM Wilhelm MP Patel R Trivedi VA Eremeeva ME Emergence of a new pathogenic Ehrlichia species Wisconsin and Minnesota 2009 N Engl J Med 20113655422429 11 Rikihisa Y Diagnosis of canine monocytic ehrlichiosis development of advanced techniques to combat a global disease Vet J 201014 250251 12 Sainz Á Roura X Miró G EstradaPeña A Kohn B Harrus S SolanoGallego L Guideline for veterinary practitioners on canine ehrlichiosis and anaplasmosis in Europe Parasit Vectors2015875 13 Waner T Harrus S Bark H Bogin E Avidar Y Keysary A Characterization of the subclinical phase of canine erhlichiosis in experimentally infected beagle dogs Vet Parasit 199769307317 14 Waner T Harrus S Jongejan F Bark H Keysary A Cornelissen A Significance of serological testing for ehrlichial diseases in dogs with special emphasis on the diagnosis of canine monocytic ehrlichiosis caused by Ehrlichia canis Vet Parasit 200195115 15 Waner T Keysary A Bark H Sharabani E Harruss S Canine monocytic ehrlichiosis an overview Israel J Vet Med 1999544103107 16 Wen B Rikihisa Y Mott JM Greene R Kim HY Zhi N Couto GC Unver A Bartsch R Comparison of nested PCR with immunofluorescentantibody assay for detection of Ehrlichia canis infection in dogs treated with doxycycline J Clin Microbiol 19973518521855 17 Zhang C Xiong Q Kikuchi T Rikihisa Y Identification of 19 polymorphic major outer membrane protein genes and their immunogenic peptides in Ehrlichia ewingii for use in a serodiagnostic assay Clin Vaccine Immunol 200815 402411 American Association of Zoo Veterinarians Infectious Disease Manual ENCEPHALITOZOONOSIS ENCEPHALITOZOON CUNICULI Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Rabbits rodents canids and sporadic cases in a variety of mammals Ingestion of environmentally resistant spores passed in urinefeces of infected host transplacental Asymptomatic neurologic nephritis to endstage renal failure uveitis Frequently asymptomatic in immunocompetent adult animals However progressive disease can be fatal Variably successful prolonged benzimidazoles Environmental sanitation to prevent spore contamination Yes Fact Sheet compiled by Karen Snowden Sheet completed on 26 September 2013 Fact Sheet Reviewed by Elizabeth Didier Susan Rohrer Meredith M Clancy Susceptible animal groups Domestic rabbits rodents mice rats muskrats guinea pigs hamsters ground shrews domestic dog sporadic cases reported in a variety of wild carnivores including farmed blue fox Alopex lagopus wild red fox Vulpes vulpes martens Martes spp and mink Mustela vison Sporadic natural infections reported in several species of nonhuman primates including squirrel monkeys Saimiri sciureus emperor tamarins Saguinus imperator Goeldis monkeys Callimico goeldii and experimental infections reported in vervet monkeys Cercopithecus pygerythrus Causative organism Encephalitozoon cuniculi phylum Microsporidia intracellular eukaryotic singlecelled organism classified by some as protozoa by others as fungi Zoonotic potential Yes immunocompromised human cases reported Direct animal to human transmission has not been reported although molecular characterization shows animal and human genotypes identical Distribution Ubiquitous worldwide from tropical to temperate to cold climates Incubation period Poorly defined in natural infections and dependent on spore dose Death in experimentally infected puppies in 28 weeks and in experimentally infected immune deficient mice 1027 days Clinical signs Most frequently the infection is asymptomatic in immunocompetent adult animals Progressive neurologic signs including ataxia head tilt circling head pressing can present in rabbits and canids Progressive glomerulonephritis to endstage renal failure can occur in dogs Uveitis sometimes with cataract development can occur in rabbits Post mortem gross or histologic findings Encephalitis with multifocal to disseminated mononuclear or granulomatous inflammatory infiltrates and perivascular cuffing in the brain glomerulonephritis uveitis with cataract formation intracellular organisms commonly seen in vascular endothelium of brain glomeruli and renal tubular epithelium of kidney Diagnosis Microscopically the Gram positive organisms can be visualized in histologic sections microscopically visualized spores in body secretions such as urine sediment or CSF using modified trichrome stain or chitinbinding Calcofluor or FungiFluor stain PCR of tissue samples detect parasitespecific antibodies using IFA or ELISA American Association of Zoo Veterinarians Infectious Disease Manual ENCEPHALITOZOONOSIS ENCEPHALITOZOON CUNICULI Material required for laboratory analysis tissue body fluids for staining and microscopy to visualize intracellular organisms or spores tissue body fluids for PCR serum for antibody detection IFA ELISA Relevant diagnostic laboratories Serologic screening is available for rodentrabbit species through major laboratory research animal vendors Molecular diagnostic testing is available only through research labs not commercially available Charles River Laboratories 18772748371 A list of locations can be found at httpwwwcrivercomaboutuslocations IDEXX Reference Laboratories One IDEXX Drive Westbrook Maine 04092 18884339987 A list of locations can be found at httpwwwidexxcom Treatment Prolonged administration of albendazole has been used in humans and anecdotally used successfully in dogs Prolonged administration of fenbendazole has been reported in rabbits Prevention and control Environmental sanitation very important to prevent contamination with environmentally resistant spores transmission of spores via fomites is probable Research rodentrabbit colonies use a serologic test and cull approach to eliminate carrier animals Suggested disinfectant for housing facilities Environmentally resistant spores can be inactivated by chlorine peroxide and other disinfectants with adequate contact time Notification Not reportable in animals or humans Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Not recommended Asymptomatic seropositive animals can shed parasite spores intermittently for monthsyears posing risk of exposure of introduced uninfected animals to environmentally resistant spores Conditions for restoring diseasefree status after an outbreak Remove seropositive animals from population rigorous environmental cleanup and disinfection Experts who may be consulted Karen Snowden Texas AM University Dept of Veterinary Pathobiology 4467 College Station TX 778434467 979 8624999 ksnowdencvmtamuedu American Association of Zoo Veterinarians Infectious Disease Manual ENCEPHALITOZOONOSIS ENCEPHALITOZOON CUNICULI References 1 Akerstedt J K Nordstoga A Mathis E Smeds and P Deplazes 2002 Fox encephalitozoonsis isolation of the agent from an outbreak in farmed blue foxes Alopex lagopus in Finland and some hitherto unreported pathologic lesions J Vet Med Series B 498 400405 2 Baneaux PJ and F Pognan 2003 In utero transmission of Encephalitozoon cuniculi strain type I in rabbits Lab Anim 37 132138 3 Cray C and Y Rivas Y 2013 Seroprevalence of Encephalitozoon cuniculi in dogs in the United States J Parasitol 991 153154 4 Dado D F Izquierdo O Vera A Montoya M Mateo S Fenoy AL Galván S García A García E Aránguez L López C del Águila and G Miró 2012 Detection of zoonotic intestinal parasites in public parks of Spain Potential epidemiological role of Microsporidia Zoonoses Pub Health 59 2328 5 Didier ES 2005 Microsporidiosis an emerging and opportunistic infection in humans and animals Acta Trop 94 6176 6 Didier ES 1995 Comparison of three staining methods for detecting microsporidia in fluids J Clin Microbiol 3312 31383145 7 Franzen C and A Muller 1999 Molecular techniques for detection species differentiation and phylogenetic analysis of microsporidia Clin Microbiol Rev 122 243285 8 Giordano C A Weigt A Vercelli M Rondena G Grilli and C Guidice 2005 Immunohistochemical identification of Encephalitozoon cuniculi in phacoclastic uveitis in four rabbits Vet Ophthal 84 271275 9 HarcourtBrown FM and HKR Holloway 2003 Encephalitozoon cuniculi in pet rabbits Vet Rec 152 427431 10 Illanes OG E TiffaniCastiglioni JF Edwards and JA Shadduck 1993 Spontaneous encephalitozoonosis in an experimental group of guinea pigs J Vet Diagn Invest 5 649651 11 Johnson CH MM Marshall LA DeMaria JM Moffet and DG Korich 2003 Chlorine inactivation of spores of Encephalitozoon spp Appl Environ Microbiol 692 13251326 12 Mathis A R Weber and P Deplazes 2005 Zoonotic potential of the microsporidia Clin Microbiol Rev 183 423445 13 MullerDoblies UU K Herzog I Tanner A Mathis and P Deplazes 2002 First isolation and characterization of Encephalitozoon cuniculi from a freeranging rat Rattus norvegicus Vet Parasitol 107 279285 14 Snowden KF BC Lewis J Hoffman and J Mansell 2009 Encephalitozoon cuniculi infections in dogs a case series J Am Anim Hosp Assoc 45 225231 15 Waller T 1979 Sensitivity of Encephalitozoon cuniculi to various temperatures disinfectants and drugs Lab Anim 13 227230 16 Wasson K and RL Peper 2000 Mammalian microsporidiosis Vet Pathol 37 113128 American Association of Zoo Veterinarians Infectious Disease Manual ENCEPHALOMYOCARDITIS VIRUS EMC Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Fecooral urine or carcass ingestion Rodents are asymptomatic carriers Range from nonclinical signs to nonspecific lethargy anorexia to cardiac failure and sudden death Many infections are asymptomatic but may manifest as sudden death Supportive care for cardiac failure if possible Rodent and rodent feces control Hygienic feeding practices vaccine Yes Fact Sheet compiled by Kay Backues Sheet completed on 9 Jan 2019 Fact Sheet Reviewed by Gretchen Cole Susceptible animal groups Mammals including humans Causative organism Encephalomyocarditis virus which belongs to genus Cardiovirus in the family Picornavirus The traditional virus should be labeled EMCV1 as a new strain isolated from a wood mouse is being called EMCV2 The new strain can be distinguished serologically and by molecular testing The host range of EMCV2 remains to be determined Zoonotic potential Yes Infection in humans is common although many are asymptomatic and unrecognized Distribution Worldwide free ranging and captive In US disease primarily seen in states bordering the Gulf of Mexico Incubation period Viremia may occur within 24 hours of infection Clinical signs Many infections are nonlethal and probably subclinical Subtle nonspecific clinical signs include lethargy anorexia listlessness or dyspnea Signs of acute heart failure may occur especially in primates and artiodactylids Typical presentation is death without any prior signs of illness Neurologic signs are not common except in smaller nonhuman primates and some rodents Post mortem gross or histologic findings Gross findings primary limited to cardiovascular system myocardium severely marked with pale streaks petechiae or ecchymosis on the epicardial surface Sequelae to heart failure such as pulmonary edema hydrothorax hydropericardium froth in trachea or bronchi and fibrin in the body cavities Pulmonary edema is often severe and dramatic lungs are wet and heavy Histologic findings include lymphocytic plasmacytic necrotizing myocarditis congested and markedly edematous lungs Encephalitis is frequently seen in rodents and may be seen in larger animals but the CNS infrequently is submitted for larger animals Diagnosis Histologic appearance of affected tissues is very suggestive of disease Further diagnostics to be considered include polymerase chain reaction PCR virus isolation from tissues fresh or frozen serologic testing via virus neutralization VN hemagglutinationinhibition or ELISA for paired titer although this route is not very helpful in acute cases If animals survive antibody testing may be helpful Material required for laboratory analysis PCR on whole blood serum plasma or tissue fresh or frozen so at necropsy liver heart and spleen should be collected in most animals Tissues for virus isolation heart muscle spleen liver and brain from wildlife species In addition take intestine from rodent species American Association of Zoo Veterinarians Infectious Disease Manual ENCEPHALOMYOCARDITIS VIRUS EMC Relevant diagnostic laboratories Zoologix Inc PCR 9811 Owensmouth Avenue Suite 4 Chatsworth CA 913113800 Phone 8187178880 Fax 8187178881 Email infozoologixcom wwwzoologixcom Texas AM Veterinary Medical Diagnostic Laboratory Virus neutralization College Station Laboratory PO Box Drawer 3040 College Station TX 778413040 Phone 979 8453414 Toll Free 888 6465623 Fax 979 8451794 httptvmdltamuedu USDAAPHISVSNVSL PO Box 844 letters 1920 Dayton Ave packages Ames IA 50010 Phone 515 3377266 Fax 515 3377397 httpwwwaphisusdagovanimalhealthlabinfoservices Treatment Generally no treatment is performed because animal are often asymptomatic for infection or found dead Supportive care for cardiac failure can be provided in less than acute cases Prevention and control Consistent and long term rodent control and prevention of rodent access to animal enclosures and food sources is critical for prevention Hygienic feeding practices are important If rodent feces are detected increase rodent control measures and change feeding practices such as not leaving food bowls available overnight Enclosure surfaces and food bowls should be cleaned with appropriate disinfectants In enclosures with heavy contamination of rodent feces removal of soil and substrate should be considered Commercial vaccines are not available in the US Vaccine research is ongoing and recent trials have shown some promise in producing antibodies in tested species However USDA allows the production and use of autogenous product from an affected institutions viral isolates at that institution only To discuss this possibility available contact is Dr Mark Titus Newport Laboratories Worthington MN 56187 800 220 2522 direct phone 5073723563 wwwnewportlabscom mtitusnewportlabscom Suggested disinfectant for housing facilities 525 sodium hypochlorite or household bleach at 3 dilution can be used by adding 3 gallons bleach to 2 gallons water and mixing thoroughly This combination can be corrosive and damage clothing Potassium peroxymonosulfate and sodium chloride VirkonS 1 dilution Follow label directions Sodium carbonate soda ash 4 dilution Add 533oz sodium carbonate to 1 gallon hot water mildly caustic Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal None Conditions for restoring diseasefree status after an outbreak Remove all evidence of rodent feces in the environment clean the affected animals living spaces with an approved disinfectant see above increase rodent control reevaluate animal feeding strategies A zoo collection animal nonrodent species that recovers from disease is not considered a carrier American Association of Zoo Veterinarians Infectious Disease Manual ENCEPHALOMYOCARDITIS VIRUS EMC Experts who may be consulted Kay Backues DVM Director of Animal Health Tulsa Zoo 5701 East 36th Street N Tulsa Oklahoma 74115 Phone 918 6696243 Fax 918 6696888 kbackuestulsazooorg References 1 Gaskin JM Internet Overview of Encephalomyocarditis Virus Infection 2018 cited 2019 January 14 Available from httpswwwmerckvetmanualcomgeneralizedconditionsencephalomyocarditis virusinfectionoverviewofencephalomyocarditisvirusinfection 2 APHIS Internet Cleaning and Disinfection of Premises 2005 cited 2013 August 14 Available from httpwwwaphisusdagovemergencyresponsetoolscleaninghtdocsimagesAnnex09Cleaningpd f 3 Backues KA Encephalomyocarditis virus infection in zoo animals In Fowler ME Miller RE eds Zoo Wild Animal Medicine 6th ed St Louis MO Saunders Elsevier 2008 p 75 78 4 Canelli E Luppi A Lavazza A Lelli D Sozzi1 E Martin AMM Gelmetti D Pascotto E Sandri C Magnone W Cordioli P Encephalomyocarditis virus infection in an Italian zoo Virol J 2010764 5 Kilburn JJ Murphy DP Titus M Payton ME KA Backues KA Vaccination of llamas Llama glama with an experimental killed encephalomyocarditis virus vaccine J Zoo Wildl Med 2011426568 6 McLelland DJ Kirkland PD Rose KA Dixon RJ Smith N Serologic responses of barbary sheep Ammotragus lervia Indian antelope Antilope cervicapra wallaroos Macropus robustus and chimpanzees Pan troglodytes to an inactivated encephalomyocarditis virus vaccine J Zoo Wildl Med 200536 6973 7 Philipps A Dauber M Growth M Schirrmeier H Platzer M Krumbholz A Wutzler P Zell R Isolation and molecular characterization of a second serotype of the encephalomyocarditis virus Vet Micro 2012161 4957 8 Thomson GR Bengis RG Brown CC Picornavirus infections In Williams ES Barker IKeds Infectious Diseases of Wild Mammals 3rd ed Ames IA Iowa State Press 2001 p 119130 American Association of Zoo Veterinarians Infectious Disease Manual EQUINE INFECTIOUS ANEMIA Fact Sheet compiled by Amanda Guthrie Sheet completed on 16 March 2011 updated 5 April 2013 updated 12 Feb 2018 Fact Sheet Reviewed by Mark Drew Nancy Carpenter Susceptible animal groups All members of Equidae although donkeys and mules are less likely to develop severe clinical signs Causative organism Lentivirus in family Retroviridae subfamily Orthoretrovirinae Zoonotic potential No Distribution It is distributed nearly worldwide except a few countries including Iceland and Japan Incubation period Although usually a week to 45 days or longer is required for infection it typically takes 45 days or more for sufficient antibody to be produced to cause positive test result Clinical signs Nonspecific equid may have fever and transient inappetence Severity of disease depends on strain and dose of virus and health of the animal Acute weakness depression inappetence jaundice tachypnea tachycardia ventral pitting edema thrombocytopenia petechiae on mucus membranes epistaxis or blood stained feces Chronic recurring clinical signs that vary from mild illness and failure to thrive to fever depression petechial hemorrhages on mucus membranes weight loss anemia and dependent edema Asymptomatic Carriers with no clinical signs Post mortem gross or histologic findings Findings during febrile illness include generalized lymph node enlargement an enlarged liver with a prominent lobular pattern an enlarged spleen mucosal and visceral hemorrhages ventral subcutaneous edema and vascular thrombosis Histopathology of these tissues reveals accumulations of lymphocytes and macrophages in liver lymph nodes adrenal glands spleen meninges and lung Extramedullary hematopoiesis and proliferation of reticuloendothelial cells is evident Pathology of infected animals with no clinical signs are generally unremarkable although some may have glomerulitis retinal depigmentation and choroiditis Diagnosis Agar Gel Immunodiffusion Coggins test is only legally recognized test but now at least three rapid ELISA tests are available a positive ELISA must be verified with a Coggins test Positive animals are infected for life Material required for laboratory analysis Blood drawn by accredited veterinarian and must be submitted to an approved lab Relevant diagnostic laboratories Labs are widely available in each state Treatment None Prevention and control As no vaccine is available uninfected animals must be maintained 200m from antibody positive animals Coggins test is used for surveillance for asymptomatic carriers and at preshipment and quarantine All horses should be tested annually interstate travel requires a negative EIA test as do most horse shows or public sales Control by decreasing risk through effective fly control and proper disinfection of equipment between animals Note EIA virus can be passed from mare to foal in utero is present in milk and semen and can be transmitted venereally may be transmitted via aerosols Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Family Equidae Hematophagus insects iatrogenic blood trans fusion needles surgical instruments teeth floating etc Variable Fever weight loss icterus anemia edema and weakness Variable No treatment No vaccine keep 200m from antibody positive animals control insects No American Association of Zoo Veterinarians Infectious Disease Manual EQUINE INFECTIOUS ANEMIA Suggested disinfectant for housing facilities None virus is only transmitted via contact with blood or other bodily secretions Notification EIA is reportable to state veterinarian and federal APHIS office check state and local laws Some jurisdictions require permanent identification of positive animals with brands or tattoos Measures required under the Animal Disease Surveillance Plan Federally reportable disease Measures required for introducing animals to infected animal While not recommended positive animals should remain 200m away from uninfected animals Conditions for restoring diseasefree status after an outbreak It is recommended that positive animals be removed from the population Experts who may be consulted National Veterinary Services Laboratory USDAAPHISVSNVSL 1920 Dayton Ave for packages PO Box 844 for letters Ames IA 50010 Phone 515 3377266 Fax 515 3377397 httpswwwaphisusdagovaphisourfocusanimalhealthlabinfo servicessadiagnostictestsctdiagnostictests Resources 1 Equine Infectious Anemia Internet The Center for Food Security Public Health c20032015 cited 2018 February 12 Available from httpwwwcfsphiastateeduFactsheetspdfsequineinfectiousanemiapdf 2 Equine Infectious Anemia Internet United States Department of Agriculture Animal and Plant Health Inspection Services 2008 cited 2018 February 12 Available from httpwwwaphisusdagovpublicationsanimalhealthcontentprintableversionfsequineinfectious anemiapdf 3 Equine Infectious Anemia EIA Internet United States Department of Agriculture Animal and Plant Health Inspection Services 2017 cited 2018 February 12 Available from httpswwwaphisusdagovaphisourfocusanimalhealthnvapNVAPReferenceGuideEquineEquine InfectiousAnemia 4 Equine Infectious Anemia The Only Protection is Prevention Internet American Association of Equine Practitioners2018 cited 2018 February 12 Available from httpsaaeporghorsehealthequine infectiousanemiaonlyprotectionprevention 5 Testing for Equine Infectious Anemia EIA in the United States 2015 Internet United States Department of Agriculture Animal and Plant Health Inspection Services 2017 cited 2018 February 12 Available from httpswwwaphisusdagovanimalhealthnahmsequinedownloadsequine15Equine15isEIApdf 6 Timoney PJ Linnep FV Overview of Equine Infectious Anemia Internet cited 2018 February 12 Available from httpwwwmsdvetmanualcomgeneralizedconditionsequineinfectious anemiaoverviewofequineinfectiousanemia American Association of Zoo Veterinarians Infectious Disease Manual ERYSIPELAS Erysipelothrix rhusiopathiae Fact Sheet compiled by Cora Singleton Sheet completed on 1 March 2011 updated 31 October 2012 Fact Sheet Reviewed by Pat Morris Alex Ramirez Susceptible animal groups Swine sheep turkeys multiple other vertebrate species Causative organism Erysipelothrix rhusiopathiae a facultative anaerobic weak grampositive bacillus Zoonotic potential E rhusiopathiae causes local skin lesions erysipeloid in humans as an occupational disease of people who handle and process meat veterinarians game handlers leather workers and laboratory workers Distribution Worldwide Incubation period Bacteremia usually develops within 24 hours of exposure Bacteria may persist in joints and lymphoid tissue for months Clinical signs Acute disease Pyrexia anorexia depression stilted gait raised rhomboid light pink to purple skin lesions diamondskin lesions abortion and sudden death Chronic disease Animals that survive acute disease may show exercise intolerance and cyanosis valvular endocarditis swollen joints and lameness arthritis Post mortem gross or histologic findings Acute disease Widespread congestion petechial and ecchymotic hemorrhages microthrombi and focal necrosis mononuclear inflammation Chronic disease Proliferative nonsuppurative arthritis vegetative endocarditis Diagnosis Clinical signs and necropsy lesions especially diamondskin lesions bacterial culture and serology A variety of serologic tests are available which are more valuable for detection of chronic infection on a herd basis than for detection of acute disease in individual animals Material required for laboratory analysis Swab or tissue sample blood organs joints for culture Relevant diagnostic laboratories Multiple laboratories available Treatment Penicillin is the antibiotic of choice for acute disease but macrolides stretogramins eg quinupristindalfopristin pristinamycin virginiamycin tetracyclines lincomycin and tylosin may also be Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Swine sheep turkeys multiple other vertebrate species Bacteria shed in urine saliva nasal secretions and feces Transmitted by direct contact with infected animals or body discharges ingestion transcutaneous Apparently healthy swine can be carriers Acute disease pyrexia anorexia depression stilted gait diamond skin lesions death Chronic exercise intolerance lameness enlarged joints Mild to severe High mortality in untreated animals Acute disease penicillin Chronic disease no treatment Vaccinate herd practice good sanitation avoid overcrowding quarantine new animals eliminate chronic carriers Yes American Association of Zoo Veterinarians Infectious Disease Manual ERYSIPELAS Erysipelothrix rhusiopathiae effective Hyperimmune serum may be useful early in the course of disease No practical treatment for chronic erysipelas is available Prevention and control Vaccinate herd practice good sanitation avoid overcrowding quarantine new animals and eliminate chronic carriers Suggested disinfectant for housing facilities Phenolic alkali hypochlorite or quaternary ammonium disinfectants are effective Notification Erysipelas is not reportable to USDAAPHIS or OIE but may be reportable to local or state agencies Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Eliminate chronic carrier animals Experts who may be consulted Veterinary Diagnostic and Production Animal Medicine Department Iowa State University College of Veterinary Medicine Phone 5152941950 Fax 5152953564 httpvetmediastateeduvdpam References 1 Cowart R P 1995 An Outline of Swine Diseases A Handbook Iowa State University Press Ames Iowa Pp 2325 2 Friend M and C J Franson 1999 Field Manual of Wildlife Diseases General Field Procedures and Diseases of Birds US Department of the Interior US Geological Survey Madison Wisconsin 3 Granier F 2001 Management of erysipelas Ann Dermatol Venereol 128 3 Pt 2 42942 4 Jackson P G G and P D Cockcroft 2007 Handbook of Pig Medicine Saunders Elsevier London England Pp 5960 194196 5 Jensen W I and Cotter SE 1976 An outbreak of erysipelas in eared grebes Podiceps nigricollis J Wildl Dis 12 583586 6 Martins C M L V and A M Mendes 1979 Erysipelas in an otter Lutra lutra Anias Suppl Med Vet Lisboa 21 8393 7 United States Department of Agriculture Animal Plant and Health Inspection Services 2012 National Animal Health Laboratories Network httpwwwaphisusdagovanimalhealthnahlndownloadsallnahlnlablistpdf Accessed 03 September 2013 8 United States Department of Agriculture Animal Plant and Health Inspection Services 2011 National Veterinary Services Laboratories Diagnostic Tests Available httpwwwaphisusdagovanimalhealthlabinfoservicesdiagnostestsshtml Accessed 03 September 2013 9 Wood R L 1999 Erysipelas In Straw B E S DAllaire W L Mengeling D J Taylor eds Diseases of Swine 8th ed Iowa State University Press Ames Iowa Pp 419430 10 Work T M D Ball and M Wolcott 1999 Erysipelas in a freeranging Hawaiian crow Corviix hawaiiensis Avian Dis 43 338341 American Association of Zoo Veterinarians Infectious Disease Manual Escherichia coli STECEPEC Fact Sheet compiled by Victor Cortese Sheet completed on 19 April 2011 updated 10 August 2013 November 2018 Fact Sheet Reviewed by Guy Loneragan Franklyn Garry Susceptible animal groups Ruminants swine also for EPEC all species to a lesser degree should be considered susceptible Serotype pathogenicity tends to be strongly related to animal species Disease is almost exclusively seen in neonates Causative organism Shigatoxigenic Escherichia coli STEC O157H7 or O157nonmotile many STEC serogroups including O26 O45 O103 O111 O121 and O145 may also infect ruminants and may cause zoonotic disease For EPEC enterotoxigenic enterohemorrhagic and attaching and effacing Further identification based on pilus types K99 predominant in cattle F4 K88 F5 K99 F41 F6 987P and F18 Ecoli Zoonotic potential STEC is zoonotic and may result in mild to severe disease which may occasionally be fatal EPEC causes mild to severe in other species but rarely causes disease in humans although occasional fatal disease in infected people has occurred Distribution Highly prevalent in ruminant herds in temperate regions throughout the year with very high prevalence in summer months uncommon in swine Variable distribution within herds is observed Incubation period In STEC the incubation period is unknowable because there is no disease The patent period of fecal shedding is summer biased variable 2 weeks one week and may be sporadic or episodic For EPEC the incubation period is very short with diarrhea often seen within 1248 hours after exposure Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Shiga toxigenic genic E coli STEC ruminants swine Fecaloral animal to animal Direct contact with contaminated surfaces contaminated feed Asymptomatic infection without clinical disease in animals Nonpathogen transient predominantly but not exclusively summer commensal of ileum and large colon Oral neomycin experimental Two commercial vaccines for cattle environmental hygiene gloves when working with known colonized animals Yes young children 5 years of age at highest risk especially from direct animal contact eg at childrens zoos although STECinduced disease can occur in people of all ages Entero pathogenic E coli EPEC various serotypes based on pili typing or entero pathogenesis ruminants swine Fecaloral direct contact with infected surfaces and pastures Severe acute diarrhea usually seen between 110 days of age Severe with death common if untreated Fluid and electrolyte replacement systemic antibiotics Good colostrum transmission birthing area management vaccination of the dam preparturiton or use of oral antibody preparation at birth Not generally American Association of Zoo Veterinarians Infectious Disease Manual Escherichia coli STECEPEC Clinical signs Asymptomatic condition is noted with STEC However for EPEC severe watery diarrhea that may be blood tinged is presented and resultant severe dehydration With some attaching and effacing E coli mucosal lining maybe be sloughed and voided in the diarrhea Toxins may cause a hypersecretory diarrhea Post mortem gross or histologic findings In STEC no visible gross lesions may observe rare attaching and effacing histopathological lesions in colonic mucosal of colonized animals For EPEC fluid filled intestinal tract and mucosal lining damage is observed with some strains Diagnosis Culture and isolation using enrichment immunoconcentration selective chromogenic agar and PCR or serologic confirmation of suspect isolates is available for STEC Similarly for EPEC culture and isolation can be used with FA EM and PCR as confirmation Material required for laboratory analysis Fresh rectal feces or freshly ground deposited feces 10gm for either STEC or EPEC or for STEC environmental samples eg hide swabs surface swabs soil and water can be cultured and for EPEC intestinal section Relevant diagnostic laboratories Various veterinary research laboratories any BSL2 bacteriological laboratory if personnel are adequately trained in STEC detection methods Treatment In STEC oral neomycin sulfate in water at label dose has been used experimentally In EPEC oral electrolytes and IV fluids in severe cases systemic antibiotics and NSAIDs may be needed Prevention and control One vaccine based on siderophore technology has been shown to decrease fecal shedding of O157 and is available for use in cattle Isolate infected animal groups and prevent contact of people with animals and animal feces Clean and disinfect animal housing areas and surfaces Animal hides oral cavity and feces may contain high numbers of viable STEC O157 Handling sanitation of workers and handlers is recommended Handwashing stations recommended for visitors Several vaccines are available for use in cattle and swine to enhance colostral transmission of antibodies against the various types of enteropathogenic E coli Oral antibody preparation can be given to the neonate have also been shown to be helpful in controlling the disease Isolate infected animal groups and change birthing area is important Suggested disinfectant for housing facilities Potassium peroxymonosulfate and sodium chloride ie Virkon S avoid bleach solutions and lime as disinfectants Notification Reportable in all 50 US states if human disease occurs for STEC Measures required under the Animal Disease Surveillance Plan None currently Measures required for introducing animals to infected animal Await negative fecal test results Consider use of vaccination of known infected animals to decrease potential shedding of the bacteria Conditions for restoring diseasefree status after an outbreak For STEC isolation from contact with other animals or public for at least two weeks followed by serial negative fecal culture of all animals in group Place in cleaned and disinfected housing may wish consider permanent withdrawal from herd or euthanasia of animal having direct contact with public especially children For EPEC isolation from contact with other animals or public for at least two weeks and separation of recovered animals form newborns Experts who may be consulted Victor Cortese DVM PhD Dipl ABVP Zoetis Inc 746 Veechdale Road Simpsonville KY 40067 6106626505 victorcortesezoetiscom American Association of Zoo Veterinarians Infectious Disease Manual Escherichia coli STECEPEC Guy Loneragan BVSc PhD STEC Franklyn Garry DVM PhD EPEC Animal and Food Sciences School of Veterinary Medicine Texas Tech University MS 2141 Colorado State University Lubbock Texas 79409 1678 Campus Delivery 8067422805x268 Fort Collins CO 805231678 guyloneraganttuedu 9702970371 franklyngarrycolostateedu References 1 Blanco M Blanco J Blanco JE Ramos J Enterotoxigenic verotoxigenic and necrotoxigenic Escherichia coli isolated from cattle in Spain Am J Vet Res 199354914461451 2 Centers for Disease Control and Prevention Outbreaks of E coli O157H7 associated with petting zoos North Carolina Florida and Arizona 20042005 Morbidity and Mortality Weekly Reports Dec 23 2005 545012771280 3 Francis DH Collins JE Libal MC Zeman DH Johnson DD Neiger RD Attaching and effacing Escherichia coli infection as a cause of diarrhea in young calves J Am Vet Med Assoc 19901966897901 4 Goode B OReilly C Dunn J Fullerton K Smith S Ghneim G Keen J Durso L Davies M Montgomery S Outbreak of Escherichia coli O157 H7 infections after petting zoo visits North Carolina State Fair OctoberNovember 2004 Arch Pediatr Adolesc Med 200916314248 5 Jankel BH Francis DH Collins JE Libal MC Zeman DH Johnson DD Attaching and effacing Escherichia coli infections in calves pigs lambs and dogs J Vet Diag Invest 198911611 6 Keen JE Wittum TE Dunn JR Bono JL Durso LM Shigatoxigenic Escherichia coli O157 in agricultural fair livestock United States Emer Infect Dis 200612780786 7 Keen JE Durso LM Meehan TP Isolation of Salmonella enterica and Shiga toxigenic Escherichia coli O157 from feces of animals in public contact areas of United States zoological parks Appl Environ Microbiol 200773362365 8 Keen JE Durso LM Bono JL Laegreid WW Oral neomycin therapy reduces shiga toxigenic E coli STEC O157 fecal shedding in naturallyinfected beef cattle In Proc 87th Conf Res Workers Anim Dis 2006 p 148 9 Lim JY Yoon J Hovde CJ A brief overview of Escherichia coli O157H7 and its plasmid O157 J Microbiol Biotechnol 2010201514 10 McMillian M Dunn JR Keen JE Brady KL Jones TF Risk behaviors for disease transmission among petting zoo attendees J Am Vet Med Assoc 200723110361038 11 Moon HW Nagy B Isaacson RE Orskov I Occurrence of K99 antigen on Escherichia coli isolated from pigs and colonization of pig ileum by K99 enterotoxigenic E coli from calves and pigs Infect Immun 1977152614620 12 National Association of State Public Health Veterinarians Inc NASPHV Compendium of measures to prevent disease associated with animals in public settings 2009 National Association of State Public Health Veterinarians Inc NASPHV Morb MortWkly Rep Recom Rep 200958RR5121 13 Nguyen TD Vo TT VuKhac H Virulence factors in Escherichia coli isolated from calves with diarrhea in Vietnam J Vet Sci 2011122159164 14 Pennington H Escherichia coli O157 Lancet 2010376142835 American Association of Zoo Veterinarians Infectious Disease Manual FELINE CALCIVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Felids domestic and exotic Direct oronasal indirect fomites Acute and chronic respiratory forms mainly upper respiratory infection arthritic form lameness virulent systemic form Variable Symptomatic Prevention of exposure to infected animals vaccination disinfection No Fact Sheet compiled by Tara M Harrison Sheet completed on 2 May 2011 7 September 2012 updated January 2018 Fact Sheet Reviewed by Dalen Agnew Annabel Wise Roger Maes Rebecca Smedley Susceptible animal groups Domestic and exotic felids Causative organism Feline calicivirus FCV Zoonotic potential None Distribution Worldwide distribution is in all members of Felidae Disease is most common in multicat environments eg shelters breeding facilities and in feral cats The latter has been implicated in spreading this virus to a zoological institution in North America Reports of this infection have been made in other zoological institutions Incubation period Variable 210 days and recovery typically in 710 days in the absence of complications Clinical signs Mild upper respiratory infection ocular and nasal discharge with potential for secondary infections oral ulceration is a common transient sign Systemic infection sloughing of oral mucosa tongue foot pads and other mucosal epithelia edema pyrexia ulcerative dermatitis anorexia jaundice and death mortality rates up to 60 adult cats are more severely affected than kittens with virulent systemic infections Lymphoplasmacytic gingivitisstomatitis and arthritis limping syndrome are also observed in domestic cats Post mortem gross or histologic findings Respiratory form oral ulceration nasal and ocular discharge conjunctivitis rarely interstitial pneumonia Virulent systemic form cutaneous edema and ulceration associated with vasculitis hepatocellular necrosis interstitial pneumonia rarely gastrointestinal ulceration intestinal crypt lesions and pancreatitis have been reproduced experimentally Lymphoplasmacytic gingivitisstomatitis proliferativeulcerative lesions Limping syndrome acute synovitis with thickening of the synovial membrane and increased joint fluid Diagnosis Virus isolation VI RTPCR virus neutralization or ELISA on paired sera FA immunohistochemistry IHC always in conjunction with compatible clinical signs Material required for laboratory analysis Oropharyngeal and conjunctival swabs of lesions for VI or RT PCR use synthetic swabs paired sera to quantitate virus neutralizing antibody titers affected tissues for VI RTPCR FA or IHC Relevant diagnostic laboratories Most diagnostic laboratories can identify Treatment Supportive prevention or treatment of secondary infections Prevention and control Prevention Vaccination using FelOVax PCT CaliciVax vaccine to minimize severity of infection particularly of virulent systemic strains only killed vaccines should be used in exotic felids There have been several cases of suspected vaccineinduced calicivirus in tigers and lions in the United States personal communication Harrison 2012 Rivas 2015 Control limit access to feral cats that can carry and spread FCV and recovered animals can shed infectious virus for months to years Proper cleaning as FCV can survive up to 14 days on inanimate objects American Association of Zoo Veterinarians Infectious Disease Manual FELINE CALCIVIRUS Suggested disinfectant for housing facilities 130 dilution of commercial bleach potassium peroxymonosulfate chlorine dioxide substituted phenolic compounds quaternary compounds formulated at appropriate concentration and pH Notification None required Measures required under the Animal Disease Surveillance Plan NA Measures required for introducing animals to infected animal Vaccination of nonexposed animal and monitoring of shedding status of both infected and incoming animal preferably introduce incoming non shedding animals to infected animal only after verification that the infected animal is no longer shedding infectious FCV Conditions for restoring diseasefree status after an outbreak Many felids can become chronic carriers so continue to monitor shedding through VI or RTPCR Once absence of shedding has been verified continue to vaccinate infected animals as immunity is waning and vaccinate susceptible animals to minimize clinical signs Experts who may be consulted Dr Roger K Maes Department of Microbiology and Molecular Genetics Virology Section Chief Michigan State University Diagnostic Center for Population and Animal Health 4125 Beaumont Rd Lansing MI 38910 5174325811 maesdcpahmsuedu Dr Tara Harrison North Carolina State University College of Veterinary Medicine 1060 William Moore Dr Raleigh NC 27606 9195137350 taraharrisonncsuedu References 1 DiMartino B Ceci C DiProfio F Marsilio F In vitro inactivation of feline calicivirus FCV by chemical disinfectants resistance variation among field strains J Feline Med Surg 2009117556 564 2 Harrison TM Sikarskie J Kruger J Wise A Mullaney TP Kiupel M Maes RK Calicivirus epidemic in captive exotic felids J Zoo Wildl Med 2007382292299 3 HarrisonTM Harrison SH Sikarskie JG Armstrong D Humoral response to calicivirus in captive tigers given a dualstrain vaccine J Zoo Wildl Med 20144512338 4 Huang C Hess J Gill M Hustead D A dualstrain feline calicivirus vaccine stimulates broader cross neutralization antibodies than a singlestrain vaccine and lessens clinical signs in vaccinated cats when challenged with a homologous feline calicivirus strain associated with virulent systemic disease J Feline Med Surg 201012129137 5 Hurley KF JE Sykes JE Update on feline calicivirus new trends Vet Clin North Am Small Anim Pract 2003334759772 6 Hurley KE Pesavento PA Pedersen NC Poland AM Wilson E Foley JE An outbreak of virulent systemic feline calicivirus disease J Am Vet Med Assoc 20042242 241249 7 Pederson NC Hawkins KF Mechanisms of persistence of acute and chronic feline calicivirus infection in the face of vaccination Vet Microbiol 199547 141156 American Association of Zoo Veterinarians Infectious Disease Manual FELINE CALCIVIRUS 8 Radford AD Coyne KP Dawson S Porter CJ Gaskell RM Feline calicivirus Vet Res 2007382319335 9 Radford AD Addie D Belák S BoucrautBaralon C Egberink H Frymus T GruffyddJones T Hartmann K Hosie MJ Lloret A Lutz H Feline calicivirus infection ABCD guidelines on prevention and management J Feline Med Surg 200911556564 10 Rivas AE Langan JN Colegrove KM Terio K Adkesson MJ Herpesvirus and calicivirus infection in a blackfooted cat Fels nigripes family group following vaccination J Zoo Wildl Med 2015461141145 11 Tian J Liu D Liu Y Wu H Jiang Y Zu S Liu C Sun X Liu J Qu L Molecular characterization of a feline calicivirus isolated from tiger and its pathogenesis in cats Vet Microbiol 2016192 110117 12 Whitehead K McCue KA Virucidal efficacy of disinfectant actives against feline calicivirus a surrogate for norovirus in a short contact time Am J Infect Control 2010381 2631 American Association of Zoo Veterinarians Infectious Disease Manual FELINE IMMUNODEFICIENCY VIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Felids most infections are species specific but some evidence for interspecific transmission in captive collections Horizontal transmission is the most prevalent route prevalence suggests exposure occurs concurrent with sexual maturity Vertical transmission can occur but is the exception Asymptomatic to severe depending on the strain of the virus and stage of the disease Most often asymptomatic in non domestic felids but may include moderate to severe oral cavity disease mild to progressive anemia skin infections weight loss vomiting diarrhea and neurologic disease Usually asymptomatic but CD4 cell depletion depending on the strain can present with increased morbidity and mortality Infection is lifelong No specific treatment but supportive care indicated with clinical signs Testing all felids prior to introduction into a collection controlling feral cat populations No Fact Sheet compiled by Kristian J Krause Sheet completed on 3 August 2011 updated 25 February 2013 Fact Sheet Reviewed by Karen A Terio Susan VandeWoude Winston Vickers Susceptible animal groups Felids Causative organism Feline Immunodeficiency Virus a Lentivirus Zoonotic potential None Distribution Worldwide In domestic cats most commonly found in intact feral males In nondomestic wild felids an increase in seroprevalence correlates with sexual maturity Incubation period 36 months Clinical signs In most nondomestic felids with naturally occurring disease FIV positive cats are asymptomatic However in domestic cats and captive nondomestic felids infected with certain strains especially older cats signs can include mild to progressive anemia moderate to severe oral disease especially stomatitis mild to significant weight loss chronic or non healing skin infections vomiting diarrhea neurologic disease and atypical lymphosarcoma Post mortem gross or histologic findings Findings correlate with associated diseases if any present Diagnosis Western blot and ELISA assays are the most commonly used method of diagnosing FIV Western blot is available for domestic cats cougars and African lions and may be more sensitive than domestic cat FIV American Association of Zoo Veterinarians Infectious Disease Manual FELINE IMMUNODEFICIENCY VIRUS based ELISA PCR is available but is not as reliable because strain genetic variation is high Material required for laboratory analysis Serum plasma or whole blood can be used for diagnosis Relevant diagnostic laboratories Any laboratory capable of running the FIV ELISA is able to diagnose FIV however this assay may be less sensitive than strain specific Western Blot Treatment Most nondomestic felids do not need any treatment Treatment is for any specific clinical signs that arise and is supportive Prevention and control Felids should be tested by ELISA prior to introduction into a new facility with other felids Special care should be taken to prevent interaction with feral cats Suggested disinfectant for housing facilities FIV is labile outside the host animals It is easily inactivated by detergents and routine disinfectants Routine cleaning procedures will prevent transmission Dental and surgical instruments anesthesia circuits endotracheal tubes and other items potentially contaminated with body fluids should be thoroughly cleaned and sterilized between uses Fluid lines multidose medication containers and food can become contaminated with body fluids especially blood or saliva and should not be shared Notification Receiving institutions should be notified of an infected animal Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal No specific measures need to be taken Whether or not to introduce infected and non infected animals should be based on a population management decision knowing that noninfected animals may become infected Knowledge of the strain and likely clinical disease can assist with these decisions Conditions for restoring diseasefree status after an outbreak Not applicable as infection is lifelong Experts who may be consulted Sue VandeWoude DVM Western blot testing Professor of Comparative Medicine Department of Microbiology Immunology Pathology Director Laboratory Animal Resources Colorado State University 1619 Campus Delivery Fort Collins CO 805231619 Phone 970 4917162 Fax 970 4910523 suevlamarcolostateedu References 1 Adams H M Van Vuuren AM Bosman D Keet J New and M Kennedy 2009 The epidemiology of lion lentivirus infection among a population of freeranging lions Panthera leo in Kruger National Park South Africa J S Afr Vet Assoc 80 151156 2 Adams H M Van Vuuren S Kania AM Bosman D Keet J New and M Kennedy 2010 Sensitivity and specificity of a nested polymerase chain reaction for detection of lentivirus infection in lions Panthera leo J Zoo Wildl Med 41 608615 3 American Association of Feline Practitioners Retrovirus Guidelines 2008 J Feline Med Surg10 300 316 4 Bevins SN S Carver EE Boydston LM Lyren M Alldredge KA Logan SP Riley RN Fisher TW Vickers W Boyce M Salman MR Lappin KR Crooks and S VandeWoude 2012 Three American Association of Zoo Veterinarians Infectious Disease Manual FELINE IMMUNODEFICIENCY VIRUS pathogens in sympatric populations of pumas bobcats and domestic cats implications for infectious disease transmission PLoS One 7e31403 5 Brennan G MD Podell R Wack S Kraft JL Troyer H BielefeldtOhmann and S VandeWoude 2006 Neurologic disease in captive lions Panthera leo with lowtiter lion lentivirus infection J Clin Microbiol 4443454352 6 Franklin SP JL Troyer JA Terwee LM Lyren WM Boyce SPD Riley ME Roelke KR Crooks and S VandeWoude 2007 Frequent transmission of immunodeficiency viruses among bobcats and pumas J Virol 811096110969 7 Franklin SP JL Troyer JA Terwee LM Lyren RW Kays SPD Riley WM Boyce KR Crooks and S VandeWoude 2007 Variability in assays used for detection of lentiviral infection in bobcats Lynx rufus pumas Puma concolor and ocelots Leopardus pardalis J Wildl Dis 43700 710 8 Munson L KA Terio MP RyserDegiorgis EP Lane and F Courchamp 2010 Wild felid diseases conservation implications and management strategies In Macdonald DW and AJ Loveridge eds Biology and Conservation of Wild Felids Oxford University Press Oxford England Pp 237259 9 OBrien SJ JL Troyer MA Brown WE Johnson A Antunes M E Roelke and J PreonSlattery 2012 Emerging viruses in the Felidae shifting paradigms Viruses 4 23657 10 Roelke ME MA Brown JL Troyer H Winterbach C Winterbach G Hemson D Smith RC Johnson J PeconSlattery AL Roca KA Alexander L Klein P Martelli K Krishnasamy and S J OBrien 2009 Pathological manifestations of feline immunodeficiency virus FIV infection in wild African lions Virol 90112 11 Roelke ME J PeconSlattery S Taylor S Citino E Brown C Packer and S Vande Woude and S J OBrien 2006 Tlymphocyte profiles in FIVinfected wild lions and pumas reveal CD4 depletion J Wildl Dis 42 234248 12 Troyer JL J PeconSlattery ME Roelke W Johnson S VandeWoude N VazquezSalat M Brown L Frank R Woodroffe C Winterbach H Winterbach G Hemson M Bush KA Alexander E Revilla and SJ OBrien 2005 Seroprevalence and genomic divergence of circulating strains of feline immunodeficiency virus among Felidae and Hyaenidae species J Virol 79 82828294 13 Troyer J L ME Roelke JM Jespersen N Baggett V BuckleyBeason D Macnulty M Craft C Packer J PeconSlattery and SJ OBrien 2011 FIV diversity FIV Ple subtype composition may influence disease outcome in African lions Vet Immunol Immunopathol 143 338346 14 VandeWoude S and C Apetrei 2006 Going wild lessons from naturally occurring T lymphotrophic lentiviruses Clin Microbiol Rev 19 728762 American Association of Zoo Veterinarians Infectious Disease Manual FELINE INFECTIOUS PERITONITIS FIP Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Felids domestic cats and some exotic cat species The disease has been documented in cheetahs Primary mode of transmission is through feces The virus is highly infective and over 90 of cats in multi cat households typically seroconvert Malaise inappetance weight loss and fluctuating fever Effusive form ascites thoracic andor pericardial effusion Ocular lesions and CNS signs more common in the dry form Some cats exposed to the virus remain healthy while those that develop the disease have a poor prognosis Clinical course is a few days to several months The course is typically rapid with the effusive form of the disease and may be longer with the dry form No treatment has yet proven effective in curing cats of FIP The disease is considered fatal Proper management can decrease the incidence of FIP in catteries There is no effective vaccine No Fact Sheet compiled by Danelle M Okeson Sheet completed on December 2017 Fact Sheet Reviewed by Kay Backues Beth Bicknese Susceptible animal groups Felids domestic cats and African lion mountain lion leopard jaguar lynx serval caracal European wild cat sand cat Pallas cat and cheetah which seem to be more susceptible than other exotic felids Most deaths in domestic cats occur in cats 316 months of age and are uncommon after 5 years Causative organism Only a portion of cats infected with the coronavirus develop FIP All feline coronavirus FCoV types may induce systemic infection While the precise mechanism by which FIP develops is unclear two main hypotheses have been proposed In both cases the ability of an FCoV to replicate in macrophages is a key pathogenic event In the first hypothesis a primarily avirulent FCoV that replicates in enterocytes undergoes a mutation that allows it to replicate in macrophages In the second hypothesis the hosts immune response and viral load determine whether a cat infected with any FCoV will develop FIP from AAFP 2013 disease fact sheet Zoonotic potential No Distribution FIP may occur wherever FCoV occurs worldwide and ubiquitous among cat populations Incubation period Under experimental conditions 214 days is required for the effusive form of the disease while several weeks longer for experimentally induced drynoneffusive form Clinical signs Early signs of the disease may be nonspecific lethargymalaise fluctuating fever loss of appetite weight loss and may cause failure to thrive in young cats The disease is categorized as two forms Effusivewet form with vasculitis and polyserositis ascites thoracic andor pericardial effusion The effusive form is the more common form of the disease Noneffusivedry form with granulomatous lesions in kidneys intestinal tract leading to chronic diarrhea lymph node enlargement Ocular and neurologic signs occur in 9 of cats with the wet form but are relatively frequent in cats with the dry form Ocular signs may include chorioretinitis and retinal perivascular cuffing keratic precipitates in the anterior eye and uveitis Neurologic signs may include nystagmus cranial nerve defects seizures ataxia hyperesthesia and behavioral changes Post mortem gross or histologic findings Effusive wet form of FIP gross findings viscous thoracic or abdominal fluid pyogranulomas that tend to follow the course of the cranial mesenteric artery leading to thickened omentum containing pyogranulomas and pyogranulomas covering the serosal surface of the abdominal viscera The pyogranulomas appear as small coalescing fibrinous plaques American Association of Zoo Veterinarians Infectious Disease Manual FELINE INFECTIOUS PERITONITIS FIP Dry form gross findings pyogranuolomas that appear as raised graywhite nodules 05 2 cm in the kidneys liver intestines and visceral lymph nodes CNS lesions and ocular lesions are more common in the dry form Eye lesions may include iridocyclitis or chorioretinitis and anterior uveitis retinitis with hemorrhage andor retinal detachment and optic neuritis Pyogranulomas may be found in the brain and spinal cord or CNS lesions may manifest as diffuse meningitis Diagnosis The disease can be difficult to diagnose Currently there is no test specific for FIP Ultimately FIP must be diagnosed by applying a workable knowledge of the disease with sensible weighing of signalment history clinical signs clinicopathologic findings serology and anteor postmortem examination of affected tissues by histopathology and immunohistochemistry Pedersen Antibody testing Serology ELISA IFA immunofluorescent antibody and virusneutralization tests detect the presence of coronavirus antibodies in a cat but these tests cannot differentiate between the various strains of feline coronavirus Antigen testing Immunohistochemistry on effusions or lesions containing infected macrophages is currently the gold standard for FIP diagnosis A PCR test is offered by a commercial laboratory and is said to differentiate between the nonpathogenic coronavirus biotype and the virulent or pathogenic biotype for use in domestic cats IDEXX Material required for laboratory analysis Effusions or lesions such as pyogranulomas containing infected macrophages for immunohistochemistry IHC IHC tests for viral antigen IHC using fluorescein staining requires fresh or frozen tissue sections IHC using horseradish peroxidase HRPO staining may be performed on formalin fixed and paraffin embedded tissues Both methods may be used on cells collected from effusions that have been acetone fixed The fluorescein staining method is 510 times more sensitive than the HRPO method Test sensitivity is dependent on having infected macrophages so random biopsies of liver or kidney biopsies not containing macrophages in cats with FIP will not yield positive results Peritoneal pleural CSF fluid or tissue biopsies may be used in the PCR test Relevant diagnostic laboratories Several veterinary college laboratories and commercial veterinary labs offer FIP testing or referral to the appropriate lab University of Tennessee wwwvetutkedudiagnosticvirologyindexphp University of California Davis httpwwwsockfipinfofipstudies114instructionstoveterinariansfor sendingfipfluidsampleshtml Treatment No treatment has yet proven effective in curing the disease Supportive care can be provided Since clinical disease is caused by the cats immune response to the virus proposed treatments have been aimed at controlling that response In one study feline interferon omega reportedly induced complete or partial remission in twothirds of cats with FIP However the treatment proved totally ineffective in a larger double blinded study A pilot study at the University of Tennessee using an immunostimulant on three cats with the dry form non effusive of FIP showed some promise Two of three cats were still receiving treatment and were still alive 2 years after diagnosis Legendre Prevention and control Given the constraints on testing it may be best to manage cheetahs as if the population is endemically infected Gaffney et al In case of a suspected outbreak or a seropositive animal clinicians should contact FIP experts andor clinicians who have dealt with similar situations in a captive wildlife setting It is beyond the scope of this fact sheet to provide recommendations for every possible scenario FIP is typically a problem in grouphoused cats such as in breeding catteries or rescue groups Since there is no readily available antemortem test cats cannot be effectively tested prior to introduction to a group Strict hygiene especially for litter boxes and keeping cats in small groups can help reduce viral contamination Although a licensed FIP vaccine available no effective vaccine is available as this vaccine has not been proven to prevent FIP and it is not generally recommended by the American Association of Feline Practitioners Feline Vaccine Advisory Panel American Association of Zoo Veterinarians Infectious Disease Manual FELINE INFECTIOUS PERITONITIS FIP Suggested disinfectant for housing facilities The virus can survive for approximately 2 months in a dry environment However the virus is readily inactivated by detergents and disinfectants Notification Not a reportable disease Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal See information under prevention and control While not all cats exposed to the coronavirus that causes FIP will develop the disease it is advisable not to mix cats with known infected cats Conditions for restoring diseasefree status after an outbreak Difficult in a multicat facility when other cats in the household or facility are likely infected While many cats will not develop FIP disease they may still shed the virus Shedding may follow one of three patterns 1 persistent for 18 months or more 2 persistent for 46 months and intermittent for months thereafter or 3 cleared within 68 months most cats Pedersen Experts who may be consulted Dr Niels C Pedersen University of California Davis College of Veterinary Medicine contact information and further information on submitting samples may be found at the wwwsockfipinfo web site under information for veterinarians References 1 Addie DD Ishida T Feline infectious peritonitis therapy and prevention In Bonagura JD Twedt DC eds Kirks Current Veterinary Therapy XIV St Louis MO SaundersElsevier 2009 p12951299 2 American Association of Feline Practitioners Feline Vaccination Advisory Panel Report J Feline Med Surg 2013159785808 3 American Association of Feline Practitioners Feline Vaccination Advisory Panel Internet Disease Information Fact Sheet Feline Infectious Peritonitis 2013 cited 2019 February 18 Available from httpswwwcatvetscompublicPDFsPracticeGuidelinesGuidelinesVaccinationFelineInfectiousPerit onitisFactSheetpdf 4 Cornell Feline Health Center Internet Feline infectious peritonitis 2002 cited 2019 February 18 Available from httpswwwvetcornelledudepartmentscentersandinstitutescornellfelinehealth centerhealthinformationfelinehealthtopicsfelineinfectiousperitonitis 5 Gaffney PM Kennedy M Terio K Gardner I Lothamer C Coleman K Munson L Detection of feline coronavirus in cheetah Acinonyx jubatus feces by reverse transcriptionnested polymerase chain reaction in cheetahs with variable frequency of viral shedding J Zoo Wildl Med 201214434776 86 6 Giori L Giordano A Giudice C Grieco V Paltrinieri S Performances of different diagnostic tests for feline infectious peritonitis in challenging clinical cases J Small Anim Pract 20115231527 7 Horzinek MC Addie D Belák S BoucrautBaralon C Egberink H Frymus T GruffyddJones T Hartmann K Hosie MJ Lloret A Lutz H ABCD Update of the 2009 guidelines on prevention and management of feline infectious diseases J Feline Med Surg 2013 Jul1575309 8 IDEXX Reference Laboratories Internet Diagnostic update 2015 cited 2019 February 18 Available from httpsidexxcomliveb02da1e51e754c9cb292133b9c56c33aldryn mediacomfilerpublicdd81dd8192c9ae9b4d1b841a06748adc75acfelineinfectiousperitonitis viruspdf 9 Legendre AM Bartges JW Effect of polyprenyl immunostimulant on the survival times of three cats with the dry form of feline infectious peritonitis J Feline Med Surg 200911624626 10 OBrien SJ Troyer JL Brown MA Johnson WE Antunes A Roelke ME PeconSlattery J Emerging viruses in the felidae shifting paradigms Viruses 20124236257 11 Pedersen N A review of feline infectious peritonitis virus infection 19632008 J Feline Med Surg 2009118225258 American Association of Zoo Veterinarians Infectious Disease Manual FELINE LEUKEMIA VIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Felids High quantities of virus shed in nasal secretions saliva also shed in urine feces and milk as well as semen and vaginal fluids from infected cats most often transmitted to exotic felids via contact with or ingestion of domestic feral cats Early cats may have no signs Anorexia enlarged lymph nodes persistent fever gingivitis stomatitis persistent diarrhea neurologic signs eye conditions abortions reproductive failures Depends on individual cats immune response typically asymptomatic and transient in exotic felids No controlled studies proving effectiveness of immune modulators and interferon against the virus The retrovirus does not survive long outside the body under normal conditions Vaccination Exclusion of feral cats No Fact Sheet compiled by Danelle M Okeson Sheet completed on updated December 2017 Fact Sheet Reviewed by Kay Backues Susceptible animal groups Felids The first confirmed case of FeLVassociated lymphoma in a non domestic felid occurred in a cheetah Recent evidence suggests that the critically endangered Iberian lynx Lynx pardinus may be particularly susceptible to FeLV The virus is otherwise not considered endemic in exotic felids although antigenpositive animals have been documented as well as seropositive asymptomatic animals FeLV has been isolated in leopard cat European wildcat and cougar Causative organism A retrovirus more specifically an oncornavirus Zoonotic potential Not a zoonosis Distribution Rare but documented antigenpositive exotic cats have been found worldwide In a study of more than 18000 domestic cats 23 of cats were FeLV antigen positive on ELISA testing Prevalence was higher 36 among cats allowed outdoors Prevalence was highest among sick feral cats 152 of tested ill feral cats were FeLV positive Incubation period Infected cats may experience a prolonged period of clinical latency Clinical signs In domestic cats a variety of disease conditions are associated with retroviral infection including anemia chronic inflammatory conditions lymphoma susceptibility to secondary and opportunistic infections cutaneous abscesses oral inflammation and reproductive problems Knowledge and understanding of the outcome of FeLV infection in domestic cats has changed In the past approximately one third of cats were believed to become persistently viremic and up to two thirds to eventually clear the infection Newer research suggests that most cats remain infected for life following exposure but may revert to an aviremic state regressive infection In the case of a regressive infection no antigen or culturable virus is present in the blood but FeLV proviral DNA can be detected in the blood by polymerase chain reaction PCR Therefore two clinically relevant outcomes of FeLV exposure can be considered 1 progressive infection domestic cats typically succumb to FeLVassociated diseases within a few years However these retrovirus positive cats may live without related illness for several years A decision about euthanasia should not be made based on a positive test alone AAFP 2 regressive infection cats have an effective immune response virus replication is contained and there is no viral shedding These cats have little risk of developing FeLV associated disease Exotic cats typically belong to this group American Association of Zoo Veterinarians Infectious Disease Manual FELINE LEUKEMIA VIRUS Post mortem gross or histologic findings Cats infected with FeLV that develop progressive infection may develop FeLVrelated diseases including lymphoid malignancies nonregenerative anemia and myeloproliferative disorders Findings may also include diseases secondary to immunosuppression such as severe bacterial infections and toxoplasmosis Diagnosis Antigen testing ELISA This screening test detects the core viral antigen p27 This antigen is produced in large quantities in most infected domestic cats and most will test positive within 30 days of exposure However when results of antigen testing are negative but recent infection cannot be ruled out testing should be repeated a minimum of 30 days after the last potential exposure Antigen testing IFA Antigen testing using immunofluorescent antibody IFA testing also detects p27 antigen within infected blood cells via bone marrow or blood smears However false negatives may occur in the following scenarios with domestic cats leukopenic cats cats with regressive infection or cats that resist bone marrow infection False positives may occur with sample preparation error when background fluorescence is high or when results are interpreted by inexperienced lab personnel Confirmatory testing Cats that test positive on screening tests should be further tested with confirmatory tests A second soluble antigen test should be performed preferably using a test from a different manufacturer Virus culture is the gold standard but not readily available in North America Practitioners should be aware that cats developing regressive infection may be only transiently antigenemic and may revert to negative status on soluble antigen tests Confirmatory testing with PCR Polymerase chain reaction PCR can detect FeLV RNA or DNA within one week of viral exposure in domestic cats even when FeLV p27 antigen is not yet detectable PCR testing detects either viral RNA or cellassociated DNA provirus in blood bone marrow and tissues Material required for laboratory analysis Whole blood for antigen testing blood bone marrow or tissues for PCR testing Relevant diagnostic laboratories Most commercial veterinary laboratories most state veterinary diagnostic labs Cornell University Treatment Immune modulators and interferon inducers are used in retrovirusinfected domestic cats including FeLVinfected cats Although reports of uncontrolled studies frequently suggest dramatic clinical improvement these effects generally have not been reproduced in controlled trials Preliminary laboratory studies have identified four drugs with antiFeLV activity that may warrant further study into their mechanisms of action and feasibility for veterinary use Prevention and control In domestic cats identification and segregation of infected cats is considered the single most effective method for preventing new infections with FeLV Feral cats should be excluded from contact with exotic cats in zoos While retroviruses are generally unstable outside their host they can remain viable in dried biological deposits for more than a week As with domestic cats zoos should determine the FeLV status of all exotic cats Cats should be tested for FeLV infection at quarantine and routine exams If exotics cats are to be vaccinated testing before initial vaccination is also recommended However since routine screening tests detect antigen not antibody vaccination does not typically interfere with FeLV testing Several injectable inactivated vaccines with adjuvants and a recombinant vaccine without adjuvants designed for transdermal administration are commercially available in the United States The vaccine is not currently recommended as a core vaccine for exotic cats in zoos but may be used in situations of highrisk such as extensive exposure to infected feral cats When FeLV vaccination is determined to be appropriate a twodose primary series is recommended with the first dose administered as early as 8 weeks of age followed by a second dose administered 34 weeks later A single booster vaccination should be administered 1 year following completion of the initial series and repeated annually in cats that remain at risk of exposure American Association of Zoo Veterinarians Infectious Disease Manual FELINE LEUKEMIA VIRUS Suggested disinfectant for housing facilities Common hospital disinfectants and detergents will inactivate the retrovirus Notification Not a reportable disease Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal The virus can be shed through casual contact such as grooming Exotic felids have not been shown to maintain the infection If a zoo felid is confirmed FeLVinfected it may infect conspecifics but the risk may be low Conditions for restoring diseasefree status after an outbreak Retroviruses are unstable outside their host and are quickly inactivated by detergents and common hospital disinfectants However retroviruses can remain viable in dried biological deposits for more than a week Experts who may be consulted American Association of Feline Practitioners guidelines on Retrovirus management are available online wwwcatvetscomguidelinespracticeguidelinesretrovirusmanagementguidelines References 1 American Association of Feline Practitioners Feline Vaccination Advisory Panel Report J Feline Med Surg 2013159785808 2 American Association of Feline Practitioners Feline Vaccination Advisory Panel Internet Disease Information Fact Sheet Feline Leukemia Virus 2013 cited 2019 February 18 Available from httpswwwcatvetscompublicPDFsPracticeGuidelinesGuidelinesVaccinationFelineLeukemiaVir usFactSheetpdf 3 Cornell Feline Health Center Internet Feline infectious peritonitis 2016 cited 2019 February 18 Available from httpswwwvetcornelledudepartmentscentersandinstitutescornellfelinehealth centerhealthinformationfelinehealthtopicsfelineleukemiavirus 4 Filoni C CatãoDias JL Cattori V Willi B Meli ML Corrêa SH Marques MC Adania CH Silva JC Marvulo MF Ferreira Neto JS Durigon EL de Carvalho VM Coutinho SD Lutz H Hofmann Lehmann R Surveillance using serological and molecular methods for the detection of infectious agents in captive Brazilian neotropic and exotic felids J Vet Diagn Invest 2012241 166173 5 Geret CP Cattori V Meli ML Riond B Martinez F López G Vargas A Simon MA LopezBao JV HofmannLehmann R Lutz H Feline leukemia virus outbreak in the critically endangered Iberian lynx Lynx pardinus highthroughput sequencing of envelope variable region A and experimental transmission Arch Virol 20111565839854 6 Goodrich JM Quigley KS Lewis JC Astafiev AA Slabi EV Miquelle DG Smirnov EN Kerley LL Armstrong DL Quigley HB Hornocker MG Serosurvey of freeranging Amur tigers in the Russian Far East J Wildl Dis 2012481186189 7 Greggs WM Clouser CL Patterson SE Mansky LM Discovery of drugs that possess activity against feline leukemia virus J Gen Virol 201293 900905 8 Harrison TM McKnight CA Sikarskie JG Kitchell BE Garner MM Raymond JT Fitzgerald SD Valli VE Agnew D Kiupel M Malignant lymphoma in African lions Panthera leo Vet Pathol 2010475 952957 9 Hartmann K Feline leukemia virus and feline immunodeficiency virus In Bonagura JD Twedt DC eds Kirks Current Veterinary Therapy XIV St Louis MO SaundersElsevier 2009 p 1278 1283 10 KennedyStoskopf S Emerging viral infections in large cats In Fowler ME and RE Miller eds Zoo and Wild Animal Medicine Current Therapy 4 Philadelphia PA WB Saunders Co 1999 p 401410 11 Lee I Levy J Gorman S Crawford P Slater M Prevalence of feline leukemia virus infection and serum antibodies against feline immunodeficiency virus in unowned freeroaming cats J Am Vet Med Assoc 200222062062 American Association of Zoo Veterinarians Infectious Disease Manual FELINE LEUKEMIA VIRUS 12 Levy J Crawford C Hartmann K HofmannLehmann R Little S Sundahl E Thayer V 2008 American Association of Feline Practitioners feline retrovirus management guidelines J Feline Med Surg 2008103300316 13 Marker L Munson L Basson PA Quackenbush S Multicentric Tcell lymphoma associated with feline leukemia virus infection in a captive Namibian cheetah Acinonyx jubatus J Wildl Dis 200339690695 14 Meli ML Cattori V Martinez F López G Vargas A Simon MA Zorrilla I Munoz A Palomares F LopezBao JV Pastor J Tandon R Willi B HofmannLehmann R Lutz H Feline leukemia virus and other pathogens as important threats to the survival of the critically endangered Iberian lynx Lynx pardinusPLoS ONE 200943e4744 Available from doi101371journalpone0004744 15 OBrien SJ Troyer JL Brown MA Johnson WE Antunes A Roelke ME PeconSlattery J Emerging viruses in the felidae shifting paradigms Viruses 20124236257 American Association of Zoo Veterinarians Infectious Disease Manual FELINE PANLEUKOPENIA Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Felidae limited other carnivores Oronasal exposure to virus transplacental Depression anorexia severe dehydration leukopenia Subclinical to fatal Fluid therapy antibiotics antiemetic analgesics Vaccination disinfection No Fact Sheet compiled by Ray Wack updated by Christine Molter Sheet completed on 1 March 2011 updated 3 November 2012 updated 2 January 2018 Fact Sheet Reviewed by James Evermann Ray Wack Susceptible animal groups Felidae mustelidae procyonidae viverridae hyaenidae Causative organism Feline Panleukopenia virus FPV parvovirus in rare cases canine parvovirus 2a 2b or 2c Zoonotic potential None known Distribution Worldwide Incubation period 27 days rarely up to 14 days Clinical signs Most cases are subclinical in cats 1yr of age or those with partial protection from maternal antibodies Most cases with illness are 1 yr of age Peracute cases may result in death Acute cases present with fever anorexia depression vomiting diarrhea hematochezia severe dehydration septic shock and DIC In transplacental infections ataxia and tremors with normal mentation are observed in kittens due to cerebellar hypoplasia Retinal lesions are also possible Post mortem gross or histologic findings Virus replicates in and destroys rapidly dividing cells especially in bone marrow lymphoid tissue and gastrointestinal tract mucosa Transplacental infection may result in cerebellar hypoplasia retinal dysplasia embryonic resorption fetal mummification abortion or stillbirth At necropsy signs of sepsis and dehydration Intestinal crypts can be dilated and contain sloughed epithelial cell debris Blunting and fusion of villi may be present Eosinophilic intranuclear inclusion bodies are rare Diagnosis Hemogram often shows panleukopenia WBC 3000 with neutropenia being more common than lymphopenia and thrombocytopenia and anemia Fecal FPV antigens may be detected through an in house immunochromatographic test kit but antigen is present for short duration of time and falsenegatives are possible Definitive diagnosis can be made with IFA staining of tissue samples and PCR amplification and identification of virus DNA or virus isolation Material required for laboratory analysis Serum titers can be used to document successful vaccination using hemoagglutination inhibition or indirect immunofluorescence testing Tissue samples can be tested for presence of virus using fluorescent antibody staining of histopathology sections Virus particles can be identified in feces using virus isolation PCR amplification and identification of virus DNA or electron microscopy Relevant diagnostic laboratories Washington Animal Disease Diagnostic Lab Bustad Hall Room 155N Pullman WA 991647034 Phone 5093359696 waddlvetmedwsuedu httpwaddlvetmedwsuedu Animal Health Diagnostic Center College of Veterinary Medicine Cornell University PO Box 5786 American Association of Zoo Veterinarians Infectious Disease Manual FELINE PANLEUKOPENIA 240 Farrier Rd Ithaca NY 148525786 Phone 6072533900 Fax 6072533943 httpsahdcvetcornelledu Treatment Aggressive fluid therapy is needed to correct dehydration antibiotics to treat or prevent sepsis antiemetic if vomiting analgesia for abdominal pain and nutritional support for hypoglycemia and anorexia Leukopenia thrombocytopenia hypoalbuminemia and hypokalemia are negative prognostic factors in domestic cats with panleukopenia Prevention and control Vaccination Most cats produce a robust long lasting immunity following illness or vaccination Vaccinated queens generally transfer protective levels of antibodies The first vaccination is usually given at 69 weeks of age with booster vaccines given every 34 weeks with the last dose being administered when the kitten is 16 weeks old to ensure that interfering maternal antibodies do not inactivate the modified live virus or block vaccine response A booster should be given 1 year later Unvaccinated adults should be given a total of 2 doses of the vaccine 34 weeks apart Vaccine titers suggest that triennial or longer booster intervals are effective after the initial series Greater than 95 of domestic cats respond to primary vaccination series with protective titers that may last more than 7 years A few nondomestic cats have been documented to be nonresponders so determination of titers is recommended Killed vaccines are often used in nondomestic cats due to rare cases of vaccine induced disease with modified live vaccines though modified live vaccines are available Pregnant immunosuppressed sick cats or kittens 4 weeks of age should not be vaccinated with a modified live product FelOVax Boehringer Ingelheim is a commonly used killed vaccine given as a 1 ml dose regardless of the size of the cat A 05 ml dose FelOVax vaccine has also become commercially available recently Control Virus sheds in all secretions in the acute phase and in feces for up to 6 weeks after recovery Susceptible animals should not be with or in close proximity to positive animals until they have been vaccinated andor protective antibody titers have been demonstrated Transmission on fomites is common thus stringent infectious disease control protocols are required All surfaces should be disinfected with products labeled and proven effective against parvoviruses It may also be necessary to bathe recovered animals especially if they are to be exposed to juveniles for whom vaccine protection cannot be assured Suggested disinfectant for housing facilities Virus is very resistant to inactivation survives for a long time in environment and is transmitted on fomites Dilute household bleach formaldehyde glutaraldehyde or peroxygen disinfectants are effective Notification None required Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Susceptible animals should not be introduced to infected animals until protective antibody titers have been demonstrated in the animals to be introduced Viral shedding may occur for at least 6 weeks in infected animals and viral particles may remain infectious in the environment for more than a year Conditions for restoring diseasefree status after an outbreak Multiple swabs for PCR amplification and identification of FPV DNA should be collected from infected and exposed animals to assure that viral shedding has stopped Experts who may be consulted James Evermann MS PhD Washington Animal Disease Diagnostic Lab Bustad Hall Room 155D Pullman WA 991647034 Phone 5093393607 jfevetmedwsuedu American Association of Zoo Veterinarians Infectious Disease Manual FELINE PANLEUKOPENIA References 1 Duarte MD Barros SC Henriques M Fernandes TL Bernardino R Monteiro M Fevereiro M 2009 Fatal infection with feline panleukopenia virus in two captive wild carnivores Panthera tigris and Panthera leo J Zoo Wildl Med 2009402354359 2 Govindasamy L Hueffer K Parrish CR AgbandjeMcKenna M Structures of host range controlling regions of the capsids of canine and feline parvoviruses and mutants J Virol 2003771221112221 3 Harrison TM Mazet JK Holekamp KE Dubovi E Engh AL Nelson K Van Horn RC Munson L Antibodies to canine and feline viruses in spotted hyenas Crocuta crocuta in the Masai Mara National Reserve J Wildl Dis 200440 110 4 Hoelzer K Shackelton LA Holmes EC and Parrish CR Withinhost genetic diversity of endemic and emerging parvoviruses of dogs and cats J Virol 2008111109611105 5 Kruse B Unterer S Horlacher K SauterLouis C Hartmann K Prognostic factors in cats with feline panleukopenia J Vet Intern Med 20102412711276 6 Mouzin DE Lorenzen MJ Haworth JD and King VL Duration of serologic response to three viral antigens in cats J Am Vet Med Assoc 20042246166 7 Risi E Agoulon A Allaire F Le DreanQuenechdu S Martin V Mahl P Antibody response to vaccines for rhinotrachetitis caliciviral disease panleukopenia feline leukemia and rabies in tigers Panthera tigris and lions Panthera leo J Zoo Wildl Med 201243248255 8 Sassa Y Yamamoto H Mochizuki M Umemura T Horiuchi M Ishiguro N Miyazawa T Successive deaths of a captive snow leopard Uncia uncia and a serval Leptailurus serval by infection with feline panleukopenia virus at Sapporo Maruyama Zoo J Vet Med Sci 201173491 494 9 Squires RA Overview of feline panleukopenia Internet Merck Veterinary Manual 2018 cited 2018 January 2 Available from httpwwwmerckvetmanualcomgeneralizedconditionsfeline panleukopeniaoverviewoffelinepanleukopenia 10 Steinel A Munson L van Vuuren M Truyen U Genetic characterization of feline parvovirus sequences from various carnivores J Gen Virol 200081345350 11 Wack RF Kramer LW Cupps W Clawson S Hustead DR The response of cheetahs Acinonyx jubatus to routine vaccination J Zoo Wildl Med 199324109117 12 Zhou P Zhang X Zeng W Zheng Q Hao X Lin X Zheng Y Wang L Zhang G Li S MicroRNA expression analysis of feline and canine parvovirus infection in vivo felis PLoS ONE 1210 e0185698 Available from httpsdoiorg101371journalpone0185698 American Association of Zoo Veterinarians Infectious Disease Manual FOOT AND MOUTH DISEASE Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Artiodactylids cloven hooved animals eg cattle pigs sheep goats cervids African buffalo also a few members of other orders eg captive Asian elephants Equids are not affected Contact with affected animals high concentrations of virus are present in FMD vesicles or their bodily fluids eg saliva milk semen mechanical vectors including people ingestion eg common source water or feed insemination aerosol respiratory or oral iatrogenic Fever 23 days vesicular lesions followed by erosionsulcers on the tongue lips oral mucosa teats andor between the hooves abundant stringy saliva decreased appetite lameness abortion myocarditis in young animals Species with minimal signs eg sheep might not have characteristic vesiculation High morbidity up to 100 low mortality except for young Depending on the phase and type of outbreak infected animals and herds may be slaughtered In a large outbreak animals may be allowed to recover with palliative care Importation bans raw hides trophies unpreserved or uncooked animal products surveillance test and slaughter or quarantine until recovered and disinfection of premises strategic vaccination Human cases seem to be very rare with mild signs and not of public health significance Virus might also be carried mechanic ally in the nares for short periods Fact Sheet compiled by S W Jack updated by James Roth and Gayle Brown Sheet completed on 31 March 2011 updated 28 April 2018 Fact Sheet Reviewed by Julie Napier Susceptible animal groups Artiodactylids clovenhoofed animals eg cattle swine cervids antelope buffalo sheep goats giraffe as well as a few members of other orders eg Asian but not African elephants Causative organism Foot and mouth disease virus FMDV Aphthovirus in family Picornaviridae Multiple serotypes O A C SAT 1 SAT 2 SAT 3 Asia 1 Some strains primarily affect certain species eg the pig O Cathay strain Immunity to one serotype does not protect from other serotypes Zoonotic potential Human infections seem to be very rare with mild clinical signs and no public health significance Many of these infections were reported in people exposed to large amounts of virus in vaccine plants although cases also occurred after drinking FMDVinfected raw milk for several days Distribution Endemic in parts of Asia Africa Middle East and South America Incubation period 214 days Clinical signs Fever 23 days vesicles followed by erosionsulcers on the tongue lips oral mucosa teats and between the hooves abundant stringy saliva if mouth is significantly affected decreased appetite lameness abortion sudden death from myocarditis in newborns rare instances of sudden death in adults especially in some severely affected wildlife species The pattern of illness varies between species and some species eg sheep can have minimal signs Shedding may occur before the onset of clinical signs Cattle may be persistently infected in the pharynx but no evidence that they transmit infection African buffalo can be long term shedders and transmit the virus Post mortem gross or histologic findings TongueOral blanched foci to vesicles to complete ulceration with fibrin Interdigital redness vesicles or ulceration and similar on coronary bands are seen Vesicles or erosions may also be found on udder occasionally other sites Myocardial pallor or streaking may be observed young animals with myocardial lesions may not have vesicles Lesions are species dependent less severe in sheep and goats than cattle or swine Location of lesions can also vary between species American Association of Zoo Veterinarians Infectious Disease Manual FOOT AND MOUTH DISEASE Diagnosis Grossly it is indistinguishable from other vesicular diseases vesicular stomatitis swine vesicular disease Seneca virus A vesicular exanthema of swine Other differential diagnoses include diseases with mouth andor foot signs such as traumatic stomatitis bovine virus diarrhea bluetongue malignant catarrhal fever contagious ecthyma and epizootic hemorrhagic disease of deer Lab detection of FMDV is based upon virus isolation antigen ELISA and rRTPCR Serology tests for detecting exposure include virus neutralization and various ELISA assays Material required for laboratory analysis Before collection of samples proper authorities should be contacted and only send appropriate samples under secure conditions to authorized laboratories Preferred sample is epithelium from unruptured or freshly ruptured vesicles esophagealpharyngeal probang samples Other samples may include myocardium from heart failure deaths milk and other secretions and excretions For suspect carriers esophagealpharyngeal fluids should be submitted Relevant diagnostic laboratories National Animal Health Laboratory Network NAHLN select FMD Laboratories for a list of the 45 labs approved for FMD diagnostics FMD is a select agent and requires BSL 3BSL3 Ag Limit access to buildinglab negative air pressure HEPA filtered incoming air Double HEPA filtered air exit all sewage treated and work in specialized cabinets within lab Treatment Depending on the phase and type of outbreak infected animals and herds may be slaughtered In a large outbreak animals may be allowed to recover with palliative care Prevention and control Avoidance of sources is most important This approach can be via importation bans raw hides trophies unpreserveduncooked animal products surveillance test and slaughter or quarantine until recovered Disinfection of premises is important as the virus could persist in environment possibly up to a few months especially under cold conditions Virus is inactivated by acidification pH 6 of muscle during rigor mortis but can persist in other tissues eg in bones lymph nodes if pH remains above 60 Vaccination has been applied in outbreaks Suggested disinfectant for housing facilities Following removal of all organic debris powerwasher most disinfectants will inactivate the FMD virus eg sodium hydroxide 2 sodium carbonate 4 citric acid 02 acetic acid 2 sodium hypochlorite 3 potassium peroxymonosulfatesodium chloride 1 and chlorine dioxide Iodophors quaternary ammonium compounds are less effective Use EPAapproved disinfectants for FMD Notification REPORTABLE DISEASE Federal and State Animal Health Officials AVIC and SAHO respectively must be notified USDAAPHIS will contact the World Organization for Animal Health OIE Measures required under the Animal Disease Surveillance Plan Surveillance in zoos during an outbreak will be determined by the Responsible Regulatory Officials Federal State or Tribal depending on the epidemiology of the outbreak Contact USDAAPHIS Center for Epidemiology and Animal Health National Surveillance Unit 2150 Centre Avenue Building B Mailstop 2E6 Fort Collins CO 805268117 nationalsurveillanceunitaphisusdagov httpnsuaphisusdagov Measures required for introducing animals to infected animal No animals should be introduced into the zoo until the disease is brought under control or it is demonstrated that the zoo is free of infection and the animal to be introduced is also free of infection Contact USDAAPHIS Veterinary Services APHIS USDA 4700 River Road Unit 41 Riverdale MD 207371231 301 8513595 American Association of Zoo Veterinarians Infectious Disease Manual FOOT AND MOUTH DISEASE Conditions for restoring diseasefree status after an outbreak Surveillance to demonstrate absence of infection and absence of virus circulation according to the OIE Terrestrial Animal Health Code Time to regain FMD free status varies with method of eradication and surveillance eg use and type of vaccination It may be possible for the zoo to be declared an FMD free compartment according to OIE Guidelines Experts who may be consulted When FMD is suspected you must contact Federal and State Animal Health Officials AVIC and SAHO respectively USDAAPHIS will contact the OIE References 1 Acha PN Szyfres B Foot and mouth disease In Zoonoses and Communicable Diseases Common to Man and Animals Volume II Chlamydioses Rickettsioses and Viroses 3rd edition Scientific and Technical Publication No 580 Pan American Health Organization Washington DC PAHO 2003 p 133145 2 Amass SF Pacheco JM Mason PW Schneider JL Alvarez RM Clark LK Ragland D Procedures for preventing the transmission of footandmouth disease virus to pigs and sheep by personnel in contact with infected pigs Vet Rec 20031535137140 3 Amass SF Mason PW Pacheco JM Miller CA Ramirez A Clark LK Ragland D Schneider JL Kenyon SJ Procedures for preventing transmission of footandmouth disease virus OTAW97 by people Vet Microbiol 200410334143149 4 Bartley LM Donnelly CA Anderson RM Review of footandmouth disease virus survival in animal excretions and on fomites Vet Rec 2002151667669 5 Bauer K Foot andmouth disease as zoonosis Arch Virol Suppl 1997139597 6 Committee on Foreign and Emerging Diseases of the United States Animal Health Association Internet Foreign Animal Diseases 7th edition c2008 cited 2018 Jan 16 Available from httpwwwaphisusdagovemergencyresponsedownloadsnahemsfadpdf 7 Foot and Mouth Disease Internet USDA APHIS Veterinary Service cited 2018 Jan 16 Available from httpwwwaphisusdagovpublicationsanimalhealth2013fsfmdgeneralpdf 8 Foot and Mouth Disease Fact Sheet Internet The Center for Food Security and Public Health Iowa State University cited 2018 Jan 16 Available from httpwwwcfsphiastateeduFactsheetspdfsfootandmouthdiseasepdf 9 Footandmouth Disease Internet The Merck Veterinary Manual cited 2018 Jan 16 Available from httpwwwmerckmanualscomvetgeneralizedconditionsfootand mouthdiseaseoverviewoffootandmouthdiseasehtml 10 Kitching RP Global epidemiology and prospects for control of footandmouth disease Curr Top Microbiol Immunol 2005288133148 11 National Animal Health Laboratories Network NAHLN Briefing July 2010 Internet USDA SPHIS cited 2018 Jan 16 Available from httpwwwaphisusdagovanimalhealthnahlndownloadsNAHLNBriefingCurrentpdf 12 Prempeh H Smith R Müller B Foot and mouth disease the human consequences the health consequences are slight the economic ones huge Brit Med J 20013227286565566 13 Schaftenaar W Use of vaccination against foot and mouth disease in zoo animals endangered species and exceptionally valuable animals Rev Sci Tech 2002213613623 14 Sellers RF Donaldson AI Herniman KA Inhalation persistence and dispersal of footand mouth disease virus by man J Hyg 1970684565573 15 Thomson GR Vosloo W Bastos AD Foot and mouth disease in wildlife Virus Res 200391145161 16 Torres A Footandmouth disease In Brown C Torres A eds Foreign Animal Diseases 7th edition Committee of Foreign and Emerging Diseases of the US Animal Health Association Boca Publications Group Inc Boca Raton FL USAHA 2008 p 261275 American Association of Zoo Veterinarians Infectious Disease Manual FOOT AND MOUTH DISEASE 17 Wright CF Gloster J Mazelet L Paton DJ Ryan ED Shortlived carriage of footandmouth disease virus in human nasal cavities after exposure to infected animals Vet Rec 201016724928 931 18 9 CFR PART 94Rinderpest FootAndMouth Disease Exotic Newcastle Disease African Swine Fever Classical Swine Fever Swine Vesicular Disease and Bovine Spongiform Encephalopathy Prohibited and Restricted Importations Internet ECFR cited 2018 Jan 16 Available from httpwwwecfrgovcgi binretrieveECFRgpSIDc1a545d13df32ce5ce464b3867ca835frPARTn9y101436 19 Foot and Mouth Disease Fact Sheet Internet The Center for Food Security and Public Health Iowa State University cited 2018 Jan 16 Available from httpwwwcfsphiastateeduFactsheetspdfsfootandmouthdiseasepdf 20 Bartley LM Donnelly CA Anderson RM Review of footandmouth disease virus survival in animal excretions and on fomites Vet Rec 2002151667669 21 Foreign Animal Disease Preparedness and Response Plan Guidelines Cleaning and Disinfection Internet USDA APHIS cited 2014 Jul Available from httpswwwaphisusdagovanimalhealthemergencymanagementdownloadsnahemsguidelinescle aningdisfectionpdf 22 Biosafety in Microbiological and Biomedical Laboratories Appendix D Agriculture Pathogen Biosafety Internet Centers for Disease Control Eradication cited 2018 April Available from httpswwwcdcgovbiosafetypublicationsbmbl5bmbl5appendixdpdf 23 Approved Disinfectants for FMD Virus Internet Center for Food Security and Public Health Iowa State University c2017 cited 2018 April Available from httpwwwcfsphiastateedupdf libraryFMDResourcesDisinfectantsForFMDViruspdf 24 Potential Pesticides to use Against the Causative Agents of Selected Foreign Animal Diseases in Farm Settings Internet USDA APHIS Animal Health c2017 cited 2018 April 16 Available from httpswwwaphisusdagovanimalhealthemergencymanagement downloadsfadepadisinfectantspdf 25 FootandMouth Disease FMD Response Internet USDA APHIS Animal Health c2015 cited 2018 April 16 Available from httpswwwaphisusdagovanimalhealthemergency managementdownloadsfmdplanrrgeepdf 26 Foot and Mouth Disease Internet OIE c2013 cited 2018 April 16 Available from httpwwwoieintfileadminHomeengAnimalHealthintheWorlddocspdfDiseasecardsFOOT ANDMOUTHDISEASEpdf American Association of Zoo Veterinarians Infectious Disease Manual GIARDIASIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Contact with or ingestion of contaminated food water soil or animals Diarrhea abdominal pain bloating dehydration lethargy anorexia Generally mild Fenbendazole metronidazole Personal and environmental hygiene Yes Fact Sheet compiled by Gwen E Myers Sheet completed on 1 February 2011 updated 15 August 2013 Fact Sheet Reviewed by Joseph Camp George D Di Giovanni Susceptible animal groups Mammals predominantly canids felids and humans Causative organism Giardia lamblia syn G intestinalis G duodenalis etc currently eight assemblages or genotype groups are identified and named AH Dogs are most commonly infected with Assemblages C and D while cats are infected with Assemblage F Humans are most commonly infected with Assemblages A and B with a few cases of E and F reported Zoonotic potential Yes although the taxonomic issues are under review to verify this conjecture as very few welldocumented cases of zoonotic transmission have been published in the peerreviewed literature Distribution Worldwide Incubation period Time from exposure to clinical signs is generally 714 days although some infected animsl some show clinical signs as early as 5 days Clinical signs Abdominal pain diarrhea gas or bloating lethargy dehydration weight loss anorexia and vomiting are typical depending on severity of infection Post mortem gross or histologic findings Histopathologic changes in the intestines vary from villous atrophy of the intestinal wall to hyperplasia of goblet cells and vacuolated epithelial cells Diagnosis Two morphologic forms of Giardia exist trophozoites and cysts The trophozoite a motile form is binucleated pear shaped and flagellated Diagnosis of Giardia infection can be difficult in that cysts are shed intermittently and are delicate and artifacts grass pollen yeast etc mimic to varying degrees the morphology of Giardia cysts Microscopy of fresh feces may identify motile trophozoites that appear as a face with the two nuclei forming the eyes and median bodies forming the mouth Mix a drop of fresh liquid feces with a drop of normal saline Trophozoites are not often found in semiformed or firm feces Trophozoites have a concave ventral surface and a rapid falling leaf motion which may be the only motion visible may be the flagella Duodenal fluid aspiration and examination of the sediment for motile trophozoites requires either endoscopy or exploratory laparotomy to obtain duodenal fluid making this an impractical means of diagnosing Giardia Zinc sulfate fecal by centrifugation is better than zinc sulfate fecal flotation but due to intermittent shedding of cysts the sensitivity is approximately 70 Fecal ELISA tests identify Giardia specific antigens from trophozoites avoiding the problem of intermittent cyst excretion in the feces False negative ELISA results are not common but a negative fecal ELISA does not eliminate the possibility of Giardia infection in an animal with appropriate clinical signs Positive test results can occur in asymptomatic dogs and cats since some animals may harbor the organisms without having clinical signs IDEXX Laboratories has an inhouse quick SNAP Giardia test that is ELISAbased Immunofluorescence American Association of Zoo Veterinarians Infectious Disease Manual GIARDIASIS IFA test identifies cysts In one study this test was the best single test for detecting subclinical giardiasis Material required for laboratory analysis Feces Relevant diagnostic laboratories Any laboratory capable of diagnosing protozoal fecal parasites Treatment Fenbendazole and metronidazole have been used although high doses have been associated with neurological dysfunction Furazolidone Furoxone Suspension SmithKline Beecham 4 mgkg BID for 7 days is available as a suspension and is convenient to administer to cats and small dogs and has been shown to be effective in cats Quinacrine 66 mgkg BID For 5 days has been shown to be 100 effective in dogs Approximately half of the dogs treated developed minor and reversible anorexia fever or lethargy Quinacrine has been shown to improve clinical signs in cats but not to eliminate infection however quinacrine is not currently available in the US Prevention and control Giardia vaccine Pfizer is on the market but it is not intended to prevent infection in the vaccinated animal Instead the vaccine is licensed as an adjunct to treatment and is used to reduce the shedding of cysts by the vaccinated patient Cysts are very resistant and can survive several months outside the host in wet cold conditions even water but they are susceptible to desiccation in dry and hot conditions Proper hygiene especially to prevent human infectionzoonosisis important Suggested disinfectant for housing facilities Removal of organic matter prior to disinfection with bleach diluted to a 132 solution Notification None required Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Recommended to keep infected or shedding animals isolated until clear of parasite Conditions for restoring diseasefree status after an outbreak Decontamination and disinfection of environment and when possible bathing animal prior to placing in cleaned environment Experts who may be consulted Centers for Disease Control and Prevention Division of Foodborne Waterborne and Environmental Diseases Waterborne Disease Prevention Branch 1600 Clifton Rd Atlanta GA 30333 800CDCINFO httpwwwcdcgovnceziddfwedindexhtml References 1 Ballweber LR L Xiao DD Bowman G Kahn and VA Cama 2010 Giardiasis in dogs and cats update on epidemiology and public health significance Trends Parasit 264 180189 2 Feng Y and L Xiao 2011 Zoonotic potential and molecular epidemiology of Giardia species and giardiasis Microbiol Rev 241 110140 3 Lebbad M I Petersson L Karlsson S BoteroKleiven J O Andersson B Svenungsson and SG Svärd 2011 Multilocus genotyping of human Giardia isolates suggests limited zoonotic transmission and association between assemblage B and flatulence in children PLoS Negl Trop Dis 58 e1262doi101371journalpntd0001262 4 Leib MS and AM Zajac 1999 Giardiasis in dogs and cats Vet Med 949 793802 5 Leib MS 2010 Giardia and Tritrichomonas foetus an update SA136 Proc Western Vet Conf Las Vegas Nevada 6 Meyer EA and S Radulescu 1979 Giardia and giardiasis Adv Parasitol 17 147 7 Nazer H 2013 Giardiasis EMedicine httpemedicinemedscapecomarticle176718overview Accessed 28 August 2013 American Association of Zoo Veterinarians Infectious Disease Manual GIARDIASIS 8 Rishniw M J Liotta M Bellosa D Bowman and KW Simpson 2010 Comparison of 4 Giardia diagnostic tests in diagnosis of naturally acquired canine chronic subclinical giardiasis J Vet Int Med 242 293297 9 Zajac AM J Johnson and SE King 2002 Evaluation of the importance of centrifugation as a component of zinc sulfate fecal flotation examinations J Am Anim Hosp Assoc 38 221224 American Association of Zoo Veterinarians Infectious Disease Manual GLANDERS Fact Sheet compiled by Annette Gendron Sheet completed on Updated 4 Sep 2018 Fact Sheet Reviewed by Sarah Churgin Susceptible animal groups Equids are primarily affected with the chronic progressive form seen more often in horses while the acute form is more common in donkeys and mules Other animals such as dogs cats including zoo wild felids sheep goats camels wild cats bears wolves hamsters mice and guinea pigs are at risk Cattle and pigs are resistant Causative organism Burkholderia mallei also previously designated Pseudomonas mallei Bacillus mallei Pfeifferella mallei Mycobacterium mallei Loefferella mallei Malleomyces mallei and Actinobacillus mallei has been Animal group s affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primarily equids also a risk to exotic felids humans dogs cats sheep goats camels hamsters mice and guinea pigs Injection Ingestion and inhalation of particles or direct contact between open skin or mucous membrane and infected tissue or secretions Nonequid species often by ingestion of infected horse meat Chronically infected asymptomatic horses are still highly infectious Loss of stamina dyspnea acute coughing high fever nasal discharge and ulcers epistaxis fulminant septicemia Chronic cutaneous or generalized lymphadenopathy and ulcerated skin nodules Horses more commonly see chronic progressive form while acute sepsis is more common in donkeys and mules Felids develop localized nodules on nasal mucosa and bloody nasal discharge within 814 days after consuming infected meat The course of infection is dependent on the route of exposure Acute aerosolsepsis leads to death typically in 4 7 days to 34 weeks after onset of illness Chronic form can last for years in horses with periodic relapses Antibiotics may be used in endemic areas though will us Need at least two given concurrently Euthanasia required in nonendemic areas Strict entry requirements from endemic areas to non endemic areas CFT test and PCR used for diagnosis Mallein13 tests used commonly in endemic regions Reportable in nonendemic areas to OIE and USDA as well as local veterinary authorities Yes Potential bio terrorism weapon7 Tier 1 Select Agent American Association of Zoo Veterinarians Infectious Disease Manual GLANDERS identified as the causative agent It is a gramnegative nonmotile nonspore forming aerobic and facultative anaerobic bacillus as well as a facultative intracellular and hostadapted pathogen Zoonotic potential Zoonotic transmission occurs through ingestion of contaminated meat and injection ingestion and inhalation of infectious particles or direct contact between open skin or mucous membranes and infected tissue or secretions Distribution Reemerging transboundary disease endemic with increasing outbreaks in parts of the Middle East Asia as well as Central and South America also seen Africa It has been eradicated from North America Australia Japan and Western Europe through surveillance and destruction of affected animals and strict import restrictions Incubation period In natural infections 47 days to several monthsyears Clinical signs The organism is zoonotic with four basic forms in both horses and humans cutaneous farcy upper respiratory pulmonary and septicemic In equids the acute cutaneous form is more common in mules and donkeys with death typically occurring in 47 days to 3 4 weeks after onset of illness The chronic cutaneous form of the disease is more common in horses and causes regional lymphadenopathy and skin nodules that ulcerate and drain with induration enlargement and nodularity of regional lymphatics on the extremities and in other areas The chronic form is characterized by flares and remissions over years The acute respiratory form results in the highest mortality and may begin with ulceration of the nasal mucosa and nodules that secrete bloody discharge often leading to sepsis The stellate scars in the nasal mucosa from healed ulcers are considered characteristic of the disease Nasal infections may spread to the lower respiratory system The pulmonary form occurs in most clinical cases often in combination with other forms of glanders and is characterized by nodular abscesses The septic form of glanders results in coughing a high fever and release of an infectious nasal discharge often followed by fulminant septicemia and death within days Multiorgan abscesses develop predominantly in the lung liver and spleen and often lead to septic shock Other lesions that can be seen are osteomyelitis meningitis orchitis or brain abscesses Death may occur within 12 weeks or several months Apparent survivors act as carriers and maintain the spread of the disease Zoo and wild felids consuming infected meat will develop localized nodules on nasal mucosa and conjunctiva with bloody nasal discharge within 814 days after consuming contaminated meat Post mortem gross or histologic findings Nodules granulomas and ulcer formation seen in various tissues Histopathologic lesions within the respiratory tract include vasculitis and thrombosis of vessels of the nasal mucosa with ulceration suppuration and spread to the submucosa In addition glanders induces a neutrophilic leukocytosis and anemia caused by depressed erythropoietic activity in the bone marrow Gram or Giemsa stains of lesion exudates may reveal the organisms Diagnosis Clinical and bacteriological diagnosis of glanders is difficult in the early stages of the disease Nearly 90 of infections exist as nonclinical or latent Complement Fixation CF is the official test recommended by the OIE for international movement of equids Unfortunately in addition to false negative and false positive reactions the test cannot differentiate B mallei from B pseudomallei or an infected from a maleinized previously tested animal The Mallein test is the most commonly used test for glanders and uses a protein fraction of the glanders organism to test for a cellmediated hypersensitivity response It is injected intradermally ie intrapalpebral or is given topically by ocular drop Palpebrae will swell markedly in 12 days in a positive reaction The test is used more frequently in domesticated animals in endemic regions but the sensitivity and specificity of the test depend largely on what protein fraction is used The Mallein test may give a false positive by cross reaction with Streptococcus equi B pseudomallei or other Burkhlderia ssp and may also leave the horse with a transient or permanent CF test for glanders and interfere with future serological testing Culture of the organism is the gold standard Due to its highly infectious nature however suspected isolates American Association of Zoo Veterinarians Infectious Disease Manual GLANDERS should only be sent to an accredited reference laboratory Automated bacterial identification systems do not always correctly identify this organism which can be a particular problem when the index of suspicion for B mallei infection is low Final differentiation of cultures of B mallei from B pseudomallei mellioidosis can be done with rapid low risk DNA testing at a designated laboratory with 16S rRNA sequencing and the use of a variety of molecular typing methods fliC PCR flip RTPCR et A Western Blot test has been developed and an ELISA test using another immunoreactive protein is in development Material required for laboratory analysis Serum andor infected tissue Relevant diagnostic laboratories NVSLUSA Complement Fixation 515 3377200 httpwwwaphisusdagovanimalhealthlabinfoservicesaboutnvslshtml OIE httpswwwflideeninstitutesinstituteofbacterialinfectionsandzoonosesibiz Germany and httpwwwcvrlaecontactsphp Dubai Treatment No vaccine is available for animal or human use though several promising avenues are currently being pursued in rodent and onhuman primate models Information on antibiotic treatment is sparse and while gentamycin azithromycin doxycycline ciprofloxacin and sulfonamides are thought to be effective for treatment in man and some laboratory animals mortality would likely still be high and multiple antibiotics must be used concurrently As a rule authorities forbid the treatment of glanders horses outside endemic areas Animals diagnosed with glanders in nonendemic regions must be euthanized Prevention and control Any equids entering the US or other nonendemic countries must have a negative CF test for glanders Suggested disinfectant for housing facilities Decontamination can be achieved with common disinfectants solutions of benzalkonium chloride 1 sodium hypochlorite 70 ethanol 2 glutaraldehyde iodine mercuric chloride in alcohol and potassium permanganate heat treatment to 72C 130F Notification In suspected cases of glanders USDAAVIC and state and local Veterinarians should be alerted Internationally cases should be reported to the Office International des Epizooties OIE the World Health Organization WHO and the state and local veterinary authority in each country Measures required under the Animal Disease Surveillance Plan Reportable disease Measures required for introducing animals to infected animal Infected animals would be isolated in endemic countries or euthanized in nonendemic countries Conditions for restoring diseasefree status after an outbreak Disinfection and euthanasia recommended Isolation and testing of exposed animals if permitted Experts who may be consulted NVSL and OIE personnel see websites above References 1 Alibasoglu M Yesildere T Calislar T Inal T Calsikan U Glanders outbreak in lions in the Istanbul zoological garden Berl Munch Tierarztl Wochenschr 19869925763 2 AlAni FK Roberson J Glanders in horses a review of the literature Veterinarski Arhiv 200716203 3 Alkafaw AA AlAni FK Albassam LS Hematological changes in Arabian horses infected with Glanders Vet Rec 197710121427 4 Aschenbroich SA Lafontaine ER Hogan RJ Melioidosis and glanders modulation of the innate immune system barriers to current and future vaccine approaches Expert Rev Vaccines 2016159116381 5 Centers for Disease Control and Prevention Internet Glanders 2018 cited 2019 February 21 Available from httpswwwcdcgovglandersindexhtml American Association of Zoo Veterinarians Infectious Disease Manual GLANDERS 6 Dohre SK Kamthan A Singh S Alam SI Kumar S Identification of a new diagnostic antigen for Glanders using immunoproteome analysis Comp Immunology Microbiology and Infectious Disease 2017532632 7 Dvorak GD Glenda D and Spickler AR Glanders J Am Vet Med Assoc 200823345705778 8 Elschner MC Scholz HC Melzer F Saqib M Marten P Rassbach A Dietzsch M Schmoock G de Assis Santana VL de Souza MM Wernery R Use of a Western Blot technique for the serodiagnosis of Glanders BMC Vet Res 201174 9 Gee JE Sacchi CT Glass MB De BK Weyant RS Levett PN Whitney AM Hoffmaster AR Popovic T Use of 16S rRNA gene sequencing for rapid identification and differentiation of Burkholderia mallei and B pseudomallei J Clin Microbiol 20034146474654 10 Khan I Wieler LH Melzer F Elschner MC Muhammad G Ali S Sprague LD Neubauer H Saqib M Glanders in Animals A Review on Epidemiology Clinical Presentation Diagnosis and Countermeasures Transbound Emerg Dis 201260204221 11 Missouri Department of Health Senior Services InternetGlanders and Melioidosis 2016 cited 2019 February 21 Available from httpshealthmogovemergenciesertmedglandersphp 12 Naureen A Saqib M Muhammad G Hussain MH Asi MNComparative evaluation of Rose Bengal plate agglutination test mallein test and some conventional serological tests for diagnosis of equine Glanders J Vet Diag Invest 2007164362367 13 Paar M Glanders and farcy a remerging disease Eq Vet Ed 200921151152 14 Peacock SJ Schweizer HP Dance DA Smith TL Gee JE Wuthiekanun V DeShazer D Steinmetz I Tan P Currie BJ Management of Accidental Laboratory Exposure to Burkholderia pseudomallei and B mallei Emerg Infect Dis 200814111 15 Russell P Eley SM Ellis J Green M Bell DL Kenny DJ Titball RWComparison of efficacy of ciprofloxacin and doxycycline against experimental melioidosis and Glanders J Antimicrob Chemother 2000458138 16 Torres AG Steinmetz I Recent Progress in melioidosis and glanders Front Microbiol 2012312 17 URen JM Van Ert MN Schupp JM Easterday WR Simonson TS Okinaka RT Pearson T Keim P Use of a RealTime PCR TaqMan Assay for Rapid Identification and Differentiation of Burkholderia pseudomallei and Burkholderia mallei J Clin Microbiol 2005431157715774 18 Whitlock GC Estes DM Torres AG Glanders off to the races with Burkholderia mallei FEMS Microbiol Letter 200727711522 American Association of Zoo Veterinarians Infectious Disease Manual HANTAVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Humans Rodentia Chiroptera Didelphimorphia Soricomorpha Infection in rodents occurs horizontally often associated with fighting Humans are infected via inhalation of the virus in aerosolized urine feces or saliva by direct contact with these materials or by the bite of an infected rodent Early signs include fatigue fever myalgia nausea vomiting and abdominal pain Later signs include coughing shortness of breath and tachycardia Illness can progress rapidly to severe cardiorespiratory failure and shock In humans Sin Nombre Hantavirus has a 50 mortality rate No cure exists Avoid contact with wild and peridomestic rats and mice rodent control use appropriate personal protective equipment especially respiratory when infestations are severe Yes Fact Sheet compiled by Gerardo Suzán and A Alonso Aguirre Sheet completed on February 21 2018 Fact Sheet Reviewed by Peter Black Susceptible animal groups Humans Other mammal species may be infected through contact with rodents but they are not known to have clinical signs or to transmit the virus to humans Carrier rodents include cotton rat Sigmondon hispidus deer mouse Peromyscus maniculatus Rice rat Oryzomys palustris and whitefooted mouse Peromyscus leucopus Causative organism Hantavirus Sin Nombre in the Americas causes a pulmonary syndrome while Old World hantaviruses in Eastern Asia cause hemorrhagic fever with renal syndrome and epidemic nephropathy in Europe Zoonotic potential Yes directly from rodents or their contaminated products Distribution Hantavirus pulmonary syndrome is distributed in the Americas in rural areas in peridomestic settings barns outbuildings and sheds Old World hantaviruses that produce hemorrhagic fever with renal syndrome and epidemic nephropathy are reported in both rural and urban areas Incubation period 1 to 5 weeks Clinical signs In humans early signs include fatigue fever myalgia thighs hips back and shoulders nausea vomiting and abdominal pain Later up to 10 days postinfection signs include coughing and shortness of breath and tachycardia Illness can progress rapidly to severe cardiorespiratory failure and shock Post mortem gross or histologic findings Hantavirus pulmonary syndrome is characterized by a unique constellation of pulmonary hematological and reticuloendothelial pathological findings Findings may include pleural effusions alveolar edema and fibrin and an interstitial mononuclear cell infiltrate Immunoblast type cells in the lungs blood bone marrow lymph nodes liver and spleen Hematological findings include leftshifted neutrophilic leukocytosis thrombocytopenia hemoconcentration in severe cases and circulating immunoblasts American Association of Zoo Veterinarians Infectious Disease Manual HANTAVIRUS Diagnosis Detection of hantavirusspecific IgM antibodies or a 4fold or greater increase in hantavirus specific IgG antibody titer and detection of hantavirus antigen by immunohistochemistry in serum Other tissues including lung spleen kidney liver and heart can be used for Immunohistochemistry IHC and reverse transcriptasePCR RTPCR as postmortem options Material required for laboratory analysis Nobuto blood filter strips Advantec Nobuto Blood Filter Strip ColePalmer is used with whole blood Relevant diagnostic laboratories Centers for Disease Control and Prevention Viral Special Pathogens Branch 1600 Clifton Rd Atlanta GA 30333 Hotline 877 2323322 404 6391510 Treatment While no primary cure for hantavirus pulmonary syndrome supportive treatment should include respiratory intensive care management and oxygen therapy Ribavirin in treating hantavirus pulmonary syndrome has little effect Prevention and control Avoid contact with wild and peridomestic rats and mice Rodent control in and around houses specially if heavy rodent infestation is present Ventilation helps to remove aerosolized virus inside structures prior to cleanup While cleaning infested structures use rubber boots or disposable shoe covers rubber or latex gloves protective goggles Use appropriate respiratory protection when infestations are severe Suggested disinfectant for housing facilities Two types of disinfecting solutions are recommended to clean up rodent materials 1 GeneralPurpose Household Disinfectant Prepare according to the label if not prediluted Almost any agent commercially available in USA is sufficient as long as the label states that it is a disinfectant Effective agents include those based on phenols quaternary ammonium compounds and hypochlorite 2 Hypochlorite Solution 110 bleach solution can be used in place of a commercial disinfectant When using chlorine solution avoid spilling the mixture on clothing or other items that might be damaged by bleach Wear rubber latex vinyl or nitrile gloves when preparing and using chlorine solutions Chlorine solutions should be prepared fresh daily Notification Request immediate notification of test results from the laboratory to the regional public health authority Measures required under the Animal Disease Surveillance Plan Field researchers directly involved in disease ecology studies should follow the CDC guidelines for sampling small mammals for virologic testing Mills et al 1995 Measures required for introducing animals to infected animal Do not introduce infected animals to other places Conditions for restoring diseasefree status after an outbreak Thorough cleanup and disinfection and rodent control should be performed Minimize contact of humans with rodents Antibody and molecular surveillance in rodents and disease surveillance in humans Experts who may be consulted Centers for Disease Control and Prevention Viral Special Pathogens Branch 1600 Clifton Rd Atlanta GA 30333 877 2323322 404 6391510 American Association of Zoo Veterinarians Infectious Disease Manual HANTAVIRUS References 1 Aberle SW Lehner P Ecker M Aberle JH Arneitz K Khanakah G Radda A Radda I Popow Kraupp T Kunz C Heinz FX Nephropatia epidemica and Puumala virus in Austria Euro J Clin Microbiol Infect Dis 199918467472 2 Arai S Bennett SN Sumibcay L Cook J Song JW Hope A Parmenter C Nerurkar VR Yates TL Yanagihara R Phylogenetically distinct hantaviruses in the masked shrew Sorex cinereus and dusky shrew Sorex monticolus in the United States Am J Trop Med Hyg 2008782348351 3 Arai S Gu SH Baek LJ Tabara K Bennett SN Oh HS Takada N Kang HJ TanakaTaya K Morikawa S Okabe N Yanagihara R Song JW Divergent lineages of newfound hantaviruses harbored by phylogenetically related crocidurine shrew species in Korea Virol 2012424299 105 4 Arai S Nguyen ST Boldgiv B Fukui D Araki K Dang CN Ohdachi SD Pham TD Boldbaatar B Satoh H Yoshikawa Y Morikawa S TanakaTaya K Yanagihara R Oishi K 2013 Novel bat borne hantavirus Vietnam Emerg Infect Dis 1971159116 5 Glass GE Livingstone W Mills JN Hlady WG Fine JB Biggler W Coke T Frazier D Atherley S Rollin PE Ksiazek TG Peters CJ Childs JE 1998 Black Creek Canal virus infection in Sigmodon hispidus in southern Florida Am J Trop Med Hyg 59 699703 6 Guo WP Lin XD Wang W Tian JH Cong ML Zhang HL Wang MR Zhou RH Wang JB Li MH Xu J Holmes EC Zhang YZ Phylogeny and origins of hantaviruses harbored by bats insectivores and rodents PLoS Pathol 201392e1003159 7 Hutchinson KL Rollin PE Peters CJ Pathogenesis of a North American hantavirus Black Creek Canal virus in experimentally infected Sigmodon hispidus Am J Trop Med Hyg1998595865 8 Mills JN Corneli A Young JC Garrison LE Khan AS Ksiazek TG CDC 2002 Hantavirus pulmonary syndrome United States updated recommendations for risk reduction MMWR Morb Mortal Wkly Rep 2002 51RR9 112 9 Mills JN Yates TL Childs JE Parmenter RP Ksiazek TG Rollin PE Peters CJ Guidelines for working with rodents potentially infected with hantavirus J Mamm 199576 716722 10 Nolte KB Federsen RM Foucar K Zaki SR Koster FT Madar D Merlin TL McFeeley PJ Umland ET Zumwalt RE Hantavirus pulmomary syndrome in the United States a pathological description of a disease caused by a new agent Human Path 199526 110120 11 Nuzum EO Rossi CA Stephenson EH LeDuc JW Aerosol transmission of Hantaan and related viruses to laboratory rats Am J Trop Med Hyg 198838 636640 12 Plyusnin A Hörling J Kanerva M Mustonen J Cheng Y Partanen J Vapalahti O Kukkonen SK Niemimaa J Henttonen H Niklasson B Lundkvist A Vaheri A Puumala hantavirus genome in patients with nephropathia epidemica correlation of PCR positivity with HLA haplotype and link to viral sequences in local rodents J Clin Microbiol 19973510901096 13 Pratt HD Brown RZ Biological factors in domestic rodent control Atlanta GA US Department of Health Education and Welfare Public Health Service Centers for Disease Control and Prevention 1979 publication no 798144 32 pp 14 Scott HG Borom MR 1977 Rodentborne disease control through rodent stoppage Washington DC US Department of Health Education and Welfare Public Health Service Centers for Disease Control and Prevention 1977publication no 778343 34 pp American Association of Zoo Veterinarians Infectious Disease Manual HELICOBACTER Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Multiple taxa primates felids primarily cheetahs but lions tigers and domestic cats and other small felids have been reported canids rodents ferret sea otters Disease is described best in humans but induced and natural disease has been reported in multiple species Not well understood but probably through conspecific grooming and fecal oral transmission Gastro intestinal signs primarily gastritis but hepatic and intestinal disease occurs in some species signs range from asymptomatic to anorexia vomiting regurgitation stomach ulceration diarrhea with undigested food in feces and weight loss Nonclinical or mild to severe depending on immune status of animal and cofactors that are not well understood Multimodal symptomatic treatment to reduce Helicobacter spp load can reduce gastric irritation and clinical signs but reinfection recrudescence is likely Difficult but iatrogenic exposure can be prevented through appropriate cleaning of endoscopy equipment Possibly Fact Sheet compiled by Copper AitkenPalmer Sheet completed on 20 February 2018 Fact Sheet Reviewed by Lily Parkinson Susceptible animal groups Humans are the most broadly susceptible group Within the veterinary field felids in particular cheetah ferrets nonhuman primates and rodents are susceptible Gastritis associated with Helicobacterlike organisms is a profound cause of morbidity and mortality in the cheetah S African cheetah 40 of the mortalities Cheetah Research Council indicated that 86 of cheetah study population is affected A few reports of Helicobacterlike organisms have been reported in association with gastritis in other species including felids bobcat Felis rufus Pallas cat F manul Canada lynx F lynx canadensis fishing cats F viverrina margays F wiedii sand cats F margarita African lion Panthera leo snow leopards P uncia Siberian tiger P tigris altaica jaguar P onca domestic dogs southern sea otter Enhydra lutris nereis and nonhuman primates cynomolgus monkeys Laboratory induced infections to study Helicobacter spp primarily have involved domestic ferrets macaques pigs guinea pigs hamsters and mice Causative organism The genus Helicobacter was created in 1989 with approximately 20 species currently described across all taxa The essential property of almost all Helicobacter spp is the presence of sheathed flagella and in most species possession of strong ureolytic urease producing ability particularly those associated with gastric mucosa Considerable diversity in cell morphology is present with respect to cell length number and location of flagella and presence of periplasmic fibrils H pylori has a global distribution and infects human gastric mucosa predominately the gastric cardia with evidence for infection in cats The most commonly described pathogenic species of Helicobacter include H pylori human H heilmannii cat dog H felis mouse model Helicobacter acinonychis formerly H acinonyx persists in the gastric fundus in cheetah H mustelae domestic ferrets and H enhydrae southern sea otter H acinonychis lacks the cag American Association of Zoo Veterinarians Infectious Disease Manual HELICOBACTER pathogenicity island PAI but is otherwise the most closely related Helicobacter to H pylori The PAI is the characteristic component causing the human neutrophilic inflammatory response but has not been associated with Helicobacter spp infecting cheetah Multiple strains of H acinonychis have been reported but the demographic of these strains within North America and other populations of felids is poorly understood The urease produced by Helicobacter and the flagella allow the organism to survive in the gastric environment over a wide spectrum of pH penetrate into gastric mucous layer and reach the gastric epithelium where it can then attach to cells Both cellular immune response and humoral response to H pylori are believed to contribute to disease pathogenesis In cheetah gastritis is associated with single species or multispecies infections of Helicobacter spp H pylori like H heilmannii H felis or H acinonychis formerly H acinonyx Helicobacterassociated gastritis causes morbidity and mortality in captive cheetah but this reaction to Helicobacter spp is not seen in free ranging cheetahs when infected with the same Helicobacter spp It has been hypothesized that immunomodulation caused by chronic stress elevated glucocorticoids or other factors may play a role in the pathogenesis of cheetah gastritis Pet cats are frequently colonized by H heilmannii without substantial correlation between infection and degree of gastritis Differences in the pathogenicity of Helicobacter spp across taxa are apparent making understanding the pathogenesis epidemiology and treatment difficult An occurrence of natural infection with H pylori in a group of cynomolgus monkeys was associated with chronic active gastritis and gastric erosions H pylori were isolated from these monkeys in different countries within Asia with multiple strains isolated Zoonotic potential The exact route of transmission of H pylori among people is unknown Several routes of transmission of H pylori have been proposed including fecaloral oraloral gastrooral and via respiratory droplets In humans familial associated spread from persontoperson is suspected Under controlled laboratory conditions human sourced H pylori has been shown to infect nonhuman primates However H pylori occurring naturally in monkeys or other species are unlikely to represent a major route of transmission to humans since close contact between nonhuman primates and humans is typically limited H pylori has been cultured from feline salivary and gastric sections and H pylori DNA has been found in in feline feces and dental plaque raising the possibility that H pylori could be transmitted from cats to humans via saliva vomit or feces H pylori in humans can be excreted through several routes with concentrations highest in vomitus In developing countries it is suspected that H pylori may have an environmental reservoir eg untreated water or contaminated food Transmission of Helicobacter and subsequent clinical disease between humans and animals is poorly studied but veterinarians should be careful and take personal protective precautions for potential exposure In humans H pylori is associated with gastric cancer and is a known carcinogen of the stomach Human medical endoscopists and endoscopy nurses have significantly higher rates of H pylori than other medical professionals Because of this appropriate precautions using proper personal protective equipment gloves masks should be used by veterinary staff conducting endoscopy performing dental procedures handling saliva or fecal material Distribution H pylori is the most common bacterial infection in the world affecting people with estimates that it infects half of the people worldwide but causes clinical disease in only a small percentage of those infected The discrepancy between infection and clinical disease is a problem for physicians it is difficult to discern when to treat patients To help with this challenge standardized human medical guidelines recommend only treating people suffering from peptic ulcer disease or mucosally associated lymphoma American Association of Zoo Veterinarians Infectious Disease Manual HELICOBACTER The distribution of Helicobacter spp in animals is poorly understood and under studied Hand raised cheetah have been found to be Helicobacter negative until introduced to other cheetah personal comm S Citino But it can be assumed that most cheetah freeranging and captive have been exposed to various Helicobacter spp of varying strains Incubation period Unknown Clinical signs Clinical signs range across taxa but most are consistent with gastrointestinal signs Cheetah with Helicobacterassociated gastritis display partial or full anorexia as the most common clinical sign leading to vomiting regurgitation diarrhea with undigested meat in feces gastroesophageal reflux disease GERD acquired lower esophageal sphincter dysfunction acquired hiatal hernia and weight loss Clinical pathological gross and histopathological findings Helicobacterassociated gastritis cannot be identified by gross evaluation of the stomach by endoscopy Gastric ulcers can be identified via antemortem endoscopy evaluation or postmortem gross evaluation but further testing is needed to identify Helicobacter As a spiral shaped bacterium cytology can be helpful when diagnosing Helicobacterassociated gastritis Histopathologic and immunological findings in cheetah with Helicobacterassociated gastritis are described as florid lymphocyte and plasma cell infiltrates within the gastric lamina propria and glandular epithelium parietal cell apoptosis leading to gland hyperplasia goblet cell metaplasia fibrosis and atrophy of the glandular fundus Cheetahs with severe gastritis have larger numbers of active B cells and plasma cells Diagnosis Rapid urease test C13urea breath test UBT serology gastric biopsy with histopathology rec minimum 5 biopsies for submission for gastritis helicobacter evaluation and touch cytology are all highly accurate invasive diagnostic tests for gastric Helicobacter organisms whereas culture and polymerase chain reaction are the only means to identify Helicobacter to the species level Material required for laboratory analysis Stomach multiple fundic biopsies recommended for cheetah ferret dogs and cats biopsies full thickness with mucosa for histopathology once initial diagnosis and grading of gastritis has been performed noninvasive C13urea breath test UBT can offer an alternative to repeated biopsies for therapeutic monitoring Relevant diagnostic laboratories Karen Terio DVM PhD DACVP cheetahhistopathology diagnosis and grading Zoological Pathology Program University of Illinois LUMC Bldg 101 Rm 0745 2160 S First St Maywood IL 60153 Phone 7082166183 Fax 7082165934 kterioillinoisedu Treatment Triple therapy with a proton pump inhibitor PPI in combination with amoxicillin and clarithromycin is the established treatment for H pylori Metronidazole is used in the place of amoxicillin as part of the triple therapy for penicillin hypersensitive patients Metronidazole is an important treatment for Helicobacter but resistance among strains of H acinonychis and H pylori have been reported For human cases of H pylori resistance to metronidazole has been reported in up to 80 and resistance to clarithromycin in 210 of strains cultured Resistance to one antibiotic when triple therapy is attempted reduces the efficacy of therapy up to 50 For H pylori quadruple therapy incorporating a bismuth compound with a PPI tetracycline and metronidazole has been a choice for rescue therapy if triple medication course is not successful Ranitidinebismuth citrate has been shown to overcome metronidazole and clarithromycin resistance and can be used in place of a PPI for rescue therapy as studied in humans PPI triple therapy has been shown to provide American Association of Zoo Veterinarians Infectious Disease Manual HELICOBACTER the most consistent and durable therapy in humans The exact mechanism by which PPI exert their effect on H pylori eradication is not clear but it is suspected that the potent acid suppression creates an optimal pH for bacterial growth and cell division allowing the key antibiotics amoxicillin and clarithromycin to act more effectively on the bacterium H pylori resistance to amoxicillin is not often reported but amoxicillin is less effective when used alone on H pylori than clarithromycin or metronidazole Because treatment of Helicobacter requires the use of several medications compliance is a significant challenge to success Resistance of H pylori toward levofloxacin is rising worldwide due to a point mutation reducing quinolone susceptibility Because the quinolones are used for second line therapy when triple or quadruple courses are ineffective a major concern for human medicine exists Resistance to amoxicillin and tetracycline is low due to the need for multiple simultaneous mutations in genes The comparison of drug resistance across different Helicobacter species is poorly studied but H acinonychis is used to model Helicobacter drug resistance In cheetah optimal treatments are described as lansoprazoleclarithromycinamoxicillin treatment group which produced a shortterm decrease in inflammation when compared to controls Lansoprazole has been shown to have direct bacteriocidal activity against Helicobacter spp Prednisone should not be used because it has no effect on gastric inflammation and does not reduce Helicobacter load Further treatment protocols recommend omeprazoleclarithromycinamoxicillin or tetracyclinemetronidazolePeptoBismol for 28 days to achieve shortterm Helicobacter eradication in cheetahs Alternative treatments for delayed gastric emptying in cheetah associated with bacterial gastritis have been described using both YU pyloroplasty and incisional gastropexy This procedure was combined with Helicobacter multitherapy for tetracycline metronidazole and bismuth subsalicylate for one week Prevention and control Personal protective equipment such as wearing barrier gloves and hand washing is recommended to prevent exposure Proper cleaning of endoscopy equipment requires use of a detergent enzymatic cleaner and brush mechanical cleaning over manual cleaning preferred to remove blood mucus and tissue from the endoscope channels prior to disinfection The World Congresses of Gastroenterology recommends that endoscopes be soaked in 2 activated glutaraldehyde for at least 10 minutes after cleaning to prevent transfer of Helicobacter between patients Sterilization of biopsy forceps or the use of disposable biopsy forceps is preferred to prevent transfer of Helicobacter Typically as biopsy forceps penetrate the gastric mucosa they are difficult to clean and pose a significant risk for cross transfer among patients Suggested disinfectant for housing facilities None Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal None Conditions for restoring diseasefree status after an outbreak Because transmission is poorly understood it is suspected there cannot be a diseasefree status for susceptible species Helicobacterassociated disease does not present as an outbreak It is believed that secondary factors are necessary to result in clinical disease ie gastritis associated with Helicobacter across all taxa Experts who may be consulted Karen Terio DVM PhD DACVP Zoological Pathology Program University of Illinois LUMC Bldg 101 Rm 0745 2160 S First St American Association of Zoo Veterinarians Infectious Disease Manual HELICOBACTER Maywood IL 60153 Phone 7082166183 Fax 7082165934 kterioillinoisedu Scott B Citino DVM DACZM White Oak Conservation Center 581705 White Oak Road Yulee Florida 32097 9042253387 scottcwogilmancom References 1 Batchelder M Fox JG Hayward A Yan L Shames B Murphy JC Palley L Natural and experimental Helicobacter mustelae reinfection following successful antimicrobial eradication in ferrets Helicobacter 199613442 2 Brown LM Helicobacter pylori Epidemiology and routes of transmission Epi Rev 200022283297 3 Chatfield J Citino S Munson L Konopka S Validation of the C13urea breath test for use in cheetahs Acinonyx jubatus with Helicobacter J Zoo Wildl Med 200435137141 4 Citino SB Munson L Efficacy and longterm outcome of gastritis therapy in cheetahs Acinonyx jubatus J Zoo Wildl Med 200536401416 5 Dailidiene D Dailide G Ogura K Zhang M Mukhopadhyay AK Eaton KA Cattoli G Kusters JG Berg DE Helicobacter acinonychis Genetics and rodent infection studies of a Helicobacter pylorilike gastric pathogen of cheetahs and other big cats J Bacteriol 2004186356365 6 De Francesco V Ierardi E Hassan C Zullo A Helicobacter pylori therapy present and future World J Gastrointest Pharmacol Ther 201236873 7 Devaux L Huynh M Hernandez J Nicolier A Upper gastrointestinal endoscopy in ferret and the histological assessment of the endoscopic biopsies Vet Record 2015178496 8 Doi SQ Kimbason T Reindel J Dubois A Molecular characterization of Helicobacter pylori strains isolated from cynomolgus monkeys M fascicularis Vet Microbiol 2005108133139 9 Eaton KA Dewhirst FE Radin MJ Fox JG Paster BJ Krakowka S Morgan DR Helicobacter Acinonyx SpNov Isolated from Cheetahs with Gastritis Int J of Syst Bacteriol 19934399106 10 Ford AC Axon ATR Epidemiology of Helicobacter pylori infection and public health implications Helicobacter 20101516 11 Goh KL Update on the management of Helicobacter pylori infection including drugresistant organisms J Gastroen Hepatol 200217482487 12 Kinsel MJ Kovarik P Murnane RD Gastric spiral bacteria in small felids J Zoo Wildl Med 199829214220 13 Kodama M Murakami K Sato R Okimoto T Nishizono A Fujioka T Helicobacter pyloriinfected animal models are extremely suitable for the investigation of gastric carcinogenesis World J Gastroenterol 20051170637071 14 Lane E Lobetti R Burroughs R Treatment with omeprazole metronidazole and amoxicillin in captive South african cheetahs Acinonyx jubatus with spiral bacteria infection and gastritis J Zoo Wildl Med 2004351519 15 Lane EP Miller S Lobetti R Caldwell P Bertschinger HJ Burroughs R Kotze A van Dyk A Effect of diet on the incidence of and mortality owing to gastritis and renal disease in captive cheetahs Acinonyx jubatus in South Africa Zoo Biol 201231669682 American Association of Zoo Veterinarians Infectious Disease Manual HELICOBACTER 16 Munson L Diseases of Captive Cheetahs AcinonyxJubatus Results of the Cheetah Research Council Pathology Survey 19891992 Zoo Biol 199312105124 17 Munson L Nesbit JW Meltzer DGA Colly LP Bolton L Kriek NPJ Diseases of captive cheetahs Acinonyx jubatus jubatus in South Africa A 20year retrospective survey J Zoo Wildl Med 199930342347 18 Munson L Terio KA Worley M Jago M BagotSmith A Marker L Extrinsic factors significantly affect patterns of disease in freeranging and captive cheetah Acinonyx jubatus populations J Wildl Dis 200541542548 19 Neiffer DL Pardo AD Klein EC Use of pyloroplasty YU to treat presumed delayed gastric emptying in a cheetah Acinonyx jubatus J Zoo Wildl Med 200031552557 20 Neiger R Dieterich C Burnens A Waldvogel A CorthesyTheulaz I Halter F Lauterburg B Schmassmann A Detection and prevalence of Helicobacter infection in pet cats J Clin Microbiol 199836634637 21 Neiger R Simpson KW Helicobacter infection in dogs and cats Facts and fiction J Vet Int Med 200014125133 22 Shen Z Batac F Mannion A Miller MA Bakthavatchalu V Ho C Manning S Paster BJ Fox JG Novel ureasenegative Helicobacter sp H enhydrae sp nov isolated from inflamed gastric tissues of southern sea otters Dis Aq Org 2017123111 23 Terio KA Munson L Marker L Aldridge BM Solnick JV Comparison of Helicobacter spp in cheetahs Acinonyx jubatus with and without gastritis J Clin Microbiol 200543229234 24 Terio KA Munson L Moore PF Characterization of the gastric immune response in cheetahs Acinonyx jubatus with Helicobacterassociated gastritis Vet Pathol 201249824833 25 Wack RF Eaton KA Kramer LW Treatment of gastritis in cheetahs Acinonyx jubatus J Zoo Wildl Med 199728260266 American Association of Zoo Veterinarians Infectious Disease Manual HELMINTHS OF UNGULATES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals mostly ungulates Fecaloral mainly from grazing on contaminated pastures Weight loss progressive weakness anemia diarrhea failure to thrive ventral edema Large range with some cases mild but infection can be fatal in animals with concurrent debilitating conditions Anthelminthic treatment based on parasite susceptibility pasture rotation use of mixed species exhibits Routine fecal examination and deworming based on these findings promote good general health of the animals Yes but with proper precautions risk is low Fact Sheet compiled by Rebecca Bloch Sheet completed on 9 June 2011 updated 30 October 2012 Fact Sheet Reviewed by Thomas Craig Holly Haefele Susceptible animal groups Ungulates other mammals Causative organism Trematodes cestodes nematodes acanthocephalans Zoonotic potential A risk of contracting Trichinella spp Spirometra spp or Taenia spp is present from consumption of undercooked pork or beef or eating watercress with Fasciola species attached The public health significance is low and can be avoided with proper food safety Distribution Worldwide though the particular parasite of concern in a given area will vary by location temperature and moisture conditions Incubation period Varies by parasite and environmental conditions and often larvae become dormant during unfavorable conditions both in the host and environment Clinical signs These presentations depend on the type of infection and the age previous experience with the parasite and health status of the animal and may be absent in an otherwise healthy animal In more severely affected animals clinical signs may include weight loss progressive weakness anemia diarrhea and hypoproteinemia with development of subcutaneous edema especially in the intermandibular space and ventral abdomen Post mortem gross or histologic findings Thin body condition with depletion of internal fat stores Adult parasite presence in the organ it inhabits with possible associated inflammation of this tissue Anemia and fluid in body cavities may also be seen Diagnosis Sample 510 of animals in a herd situation and more may be necessary based on housing and predisposition to being affected Fecal egg counts can be performed quantitatively with tests like the McMasters test for animals housed in larger groups or can be performed qualitatively with a simple float test for small numbers of animals Quantitative fecal exams performed before and after deworming for a comparative fecal egg count reduction fecal larval cultures larval culture sensitivities and pasture larval counts are recommended in areas facing large amounts of parasite resistance to anthelminthic medications Material required for laboratory analysis Fresh fecal samples are optimal if they can be analyzed within 1 2 hours but otherwise refrigerate at 4oC Samples kept in anoxic conditions do not develop and are useful for prolonged periods of time if cool Refrigerated samples can be shipped over a 2448h period to an outside lab packed with ice or other coolant but do not freeze samples Relevant diagnostic laboratories Most parasitology laboratories are capable of running larval cultures to speciate the parasite American Association of Zoo Veterinarians Infectious Disease Manual HELMINTHS OF UNGULATES Treatment Supportive care for animals that are debilitated by this infection Anthelminthic administration based on parasite level and susceptibility is recommended Anthelminthic resistance is a problem in some areas an example being Haemonchus contortus in Texas Drug alternatives such as copper oxide wire particles and bioactive condensed tannins can be used The best time to make use of routine deworming ie not clinically affected animals is during the offseason when the parasites are in the host and not on the ground Off season timing is determined by the specific parasites being targeted Prevention and control Options for prevention include pasture rotation housing dead end hosts with definitive hosts ie equids housed with ruminants timely removal of feces to prevent eggs from developing into infective third stage larvae use of elevated feeding stations or feed troughs to remove food sources from the ground and reduction of numbers or elimination of intermediate hosts Routine monitoring of fecal parasite levels through fecal exams during peak larval parasite times of spring and summer comparative fecal egg count reduction fecal larval cultures larval culture sensitivities and pasture larval counts are recommended in problem situations Characterization of the abundance and type of parasites present at postmortem examination should be performed Additional monitoring and treatment for neonates lactating females and other animals under higher stress conditions should be considered More recent avenues of control include the following Creation of refugia by allowing for survival of some parasites through treatment of only the most affected animals to create a pool of parasites that are not resistant to the commonly used anthelminthics These parasites can dilute the genetics from anthelminthic resistant parasites Use of a nematodetrapping fungus Duddingtonia flagrans administered orally to reduce developing larvae numbers once they are deposited in feces Work is being undertaken to create vaccines for specific parasites to reduce the impact of infection but these are not commercially available Suggested disinfectant for housing facilities Remove fecal material promptly from enclosures Appropriate sanitation and disinfection should be performed Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal To prevent introduction of a novel or resistant parasite to the resident population quarantine with repeat fecal examinations is recommended If possible the new animal should be housed on a dry lot or other surface that can be completely cleaned to prevent reinfection following anthelminthic treatment Repeat fecal examination is recommended 7 days following treatment with at least two negative samples before the animal is introduced to pasture Conditions for restoring diseasefree status after an outbreak Reestablish a parasite control plan based on culture and parasite load Remove as much fecal material from the environment as possible Experts who may be consulted Thomas M Craig DVM PhD Department of Veterinary Pathobiology Texas AM University College Station Texas 778434467 phone 979 8459191 tcraigcvmtamuedu References 1 Ballwebber LR 2006 Diagnostic methods for parasitic infection in livestock Vet Clin Food Anim 22 695705 2 Craig TM 2000 General considerations for determining the epidemiology and control of gastrointestinal nematodes in wild and exotic ruminants In Proceedings AAZV and IAAAM joint conference New Orleans Louisiana Pp 435437 3 Fleming SA T Craig RM Kaplan JE Miller C Navarre and M Rings 2006 Anthelminthic American Association of Zoo Veterinarians Infectious Disease Manual HELMINTHS OF UNGULATES resistance of gastrointestinal parasites of small ruminants J Vet Intern Med 20 435444 4 Fontenot D K A KinneyMoscona RM Kaplan and J Miller 2008 Effects of copper oxide wire particle bolus therapy on trichostrongyle fecal egg counts in exotic artiodactylids J Zoo Wild Med 39 642645 5 Fontenot D K and JE Miller 2012 Alternatives for gastrointestinal parasite control in exotic ruminants In Miller RE and ME Fowler eds Zoo and Wild Animal Medicine Current Therapy Volume 7 WB Saunders Co St Louis Missouri Pp 581588 6 Goossens E J Vercruysse F Vercammen and P Dorny 2006 Evaluation of three strategic parasite control programs in captive wild ruminants J Zoo Wild Med 37 2026 7 Helminths 2008 In Bowman D D ed Georgis Parasitology for Veterinarians 9th ed WB Saunders Company Philadelphia Pennsylvania Pp 115239 8 Kenyon F AW Greer GC Coles G Cringoli E Papadopoulos J Cabaret B Berrag M 9 Pybus MJ Liver flukes 2001 In Samuel WM and MJ Pybus eds 2001 Parasitic diseases of wild mammals 2nd ed Iowa State University Press Ames Iowa Pp 121396 10 Varady JA VanWyk E Thomas J Vercruysse and F Jackson 2009 The role of targeted selective treatments in the development of refugiabased approaches to the control of gastrointestinal nematodes of small ruminants Vet Parasitol 164 311 11 Various authors Rhinoceridae Miller RE Tapiridae Janssen DL Equidae Walzer C Suidae and Tayassuidae Morris PJ and AL Shima Hippopotamidae Miller MA Camelidae Fowler ME Giraffidae Bush M Cervidae and Tragulidae Flach E Bovidae and Antilocapridae Citino SB Sheep Goats and Goatlike Animals Fowler ME In Fowler ME and RE Miller eds 2003 Zoo and Wild Animal Medicine 5th edition Saunders St Louis Missouri Pp 5645 5734 582 85 59699 607609 620622 632 639 6467 67172 682 American Association of Zoo Veterinarians Infectious Disease Manual HEMOTROPIC MYCOPLASMA HEMOBARTONELLOSIS FELINE INFECTIOUS ANEMIA OR HEMOTROPHIC MYCOPLASMOSIS Fact Sheet compiled by Gretchen A Cole Sheet completed on 21 June 2011 updated 5 March 2013 updated 9 January 2018 Fact Sheet Reviewed by Sathya Chinnadurai Susceptible animal groups Felids canids ursids Causative organism Specialized mycoplasma bacteria that lack a cell wall and are small diameter 01 10µm They can be circular or bar shape which aggregate and form pinion teeth on the surface of red blood cells Mycoplasma haemofelis formerly Hemobartonella felis and Eperythrozoon felis M haemocanis M haemomuris M wenyonii M haemosuis Zoonotic potential Yes one report in an immunodeficiency virusinfected human coinfected with Mycoplasma haemofelis and Bartonella henselae in Brazil Distribution Worldwide Incubation period In the domestic cat it takes 217 days from infection until parasites are seen in blood Peak parasitemia occurs over 15 days Clinical signs generally begin 1 month after infection Clinical signs Commonly fever anorexia and weight loss are observed Additionally tachycardia anemia decreased hemoglobin slight to moderate icterus vomiting and splenomegaly may be seen Post mortem gross or histologic finding No pathognomonic postmortem findings are associated with this disease Emaciation splenomegaly 25 x normal size friable spleen icterus and bone marrow hyperplasia may be observed Diagnosis Mycoplasmas cannot grow in culture media PCR is the most reliable diagnostic test Blood smear should be examined by direct microscopy before starting treatment Organisms may be found in fresh uncoagulated blood smear These smears should be examined daily for 57 days since parasitemia is cyclic Parasites are found on the surface of the erythrocyte extracellular or free in the smear It is recommended to use Giemsa WrightGiemsa MayGruenwaldGiemsa or WrightLeishman stains to be able to differentiate this organism from stain precipitate refractile artifacts and Cytauxzoon the latter is intracellular normally found in the center and occurring singly Direct Coombs test may be positive in some species during the acute phase Material required for laboratory analysis Microscope blood smear slide and stain Blood in EDTA and standard blood shipment supplies to submit for PCR Relevant diagnostic laboratories Most commercial veterinary laboratories can examine blood smears and submit a sample for PCR testing Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Felids Canids Ursids Mice Cattle Swine Blood sucking arthropods fleas and ticks Vertical in utero during parturition or lactation Horizontal bite wounds Iatrogenic blood transfusion or infected needles Fever Anorexia Weight loss Anemia Tachycardia Splenomegaly Vomiting Can vary from mild to severe and can lead to death in some animals Antibiotics blood transfusion steroids if an immune mediated component is suspected Eliminate and prevent arthropods Yes American Association of Zoo Veterinarians Infectious Disease Manual HEMOTROPIC MYCOPLASMA HEMOBARTONELLOSIS FELINE INFECTIOUS ANEMIA OR HEMOTROPHIC MYCOPLASMOSIS Treatment Common treatments in domestic cat include tetracycline doxycycline or enrofloxacin If severe anemia is present consider glucocorticoid treatment such as prednisolone Prevention and control Prevent and eliminate arthropod vectors flea and tick control Blood for transfusion should be PCR tested Suggested disinfectant for housing facilities Standard cleaning and disinfection of areas to remove blood and control of ectoparasites should eliminate the organism from housing facilities Notification Currently none Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Eliminate fleas and ticks In nondomestic cats negative animals have been housed with positive animals without evidence of horizontal transfer However since carrier state may occur the possibility of transmission in animals with direct contact or close enough to share ectoparasites should be considered Conditions for restoring diseasefree status after an outbreak Treat affected animals eliminate ectoparasites and prevent exposure to new ectoparasites Due to carrier state may not be able to consider a population diseasefree Experts who may be consulted Joanne Messick DVM DACVP Associate Professor Comparative Pathobiology Purdue University 625 Harrison Street West Lafayette IN 47907 7654961748 jmessicpurdueedu References 1 André MR Adania CH Allegretti SM Machado RZ Hemoplasmas in wild canids and felids in Brazil J Zoo Wildl Med 201142342347 2 Dos Santos AP dos Santos RP Biondo AW Dora JM Goldani LZ de Oliveira ST Guimarães AMS Timenetsky J de Morais HA González FHD Messick JB Hemoplasma infection in HIV positive patient Brazil Emerg Infect Dis 20081419221924 3 Haefner M Burke TJ Kitchell BE Lamont LA Schaeffer DJ Behr M Messick JB Identification of Haemobartonella felis Mycoplasma Haemofelis in captive nondomestic cats J Zoo Wildl Med 200334139143 4 Harvey JW Hemotrophic mycoplasmosis Hemobartonellosis In Greene CE ed Infectious diseases of the dog and cat 3rd ed St Louis MO Saunders Elsevier 2006 p 252260 5 Harvey JW Hemotrophic Mycoplasmosis Haemobartonellosis In Tilley LP and Smith FWK eds Blackwells Five Minute Veterinary Consult Canine and Feline 4th ed Ames IA Blackwell Publishing 2007 p 591 6 Iso T Suzuki J Sasaoka F Sashida H Watanabe Y Fujihara M Nagai K Harasawa R Hemotropic mycoplasma infection in wild black bears Ursus thibetanus japonicas Vet Microbiol 201316184189 7 Fard RMN Vahedi S Mohammadkhan F Haemotropic mycoplasmas haemoplasmas a review Int J Adv Biol Biom Res 20142514841503 8 Messick JB Hemotropic Mycoplasmas Hemoplasmas MerckVetManualcom cited 2018 Jan 9 Available from httpwwwmerckvetmanualcomcirculatorysystembloodparasiteshemotropic mycoplasmas American Association of Zoo Veterinarians Infectious Disease Manual HEMOGREGARINES OF REPTILES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Reptiles including tuatara Vectorborne vector varies by species or genera of parasite eg leeches for Haemogregarina of aquatic turtles ticks for Hemolivia and a wide range of invertebrates for Hepatozoon in terrestrial reptiles Usually none Usually non clinical Mild disease may be observed in unnatural hosts No effective treatment known for reptiles A decrease in parasitemias but not clearance has been noted with atovaquone proguanil in one study Avoid contact with potential vectors Captive animals should have effective and safe acaricides applied No Fact Sheet compiled by Michael J Yabsley Sheet completed on 7 August 2013 updated 2018 Fact Sheet Reviewed by Ellis C Greiner Guilherme G Verocai Susceptible animal groups Reptiles Certain genera are generally detected in certain groups but recent genetic data suggests that many of these parasite species have broad host ranges For example the genus Haemogregarina is most commonly reported from aquatic turtles whereas Hepatozoon has a wide range of reptilian hosts including snakes lizards tuatara and tortoises Causative organism There are currently four genera of haemogregarines Apicomplexa Adeleiorina reported from reptiles Haemogregarina are intraerythrocytic parasites that are most commonly reported from aquatic turtles Leeches are the only known vectors for aquatic turtle parasites Numerous other hosts such as alligators snakes and tortoises have reported Haemogregarina spp infections However these reports are based on morphologic data from only intraerythocyte stages which is insufficient to distinguish the genera The absence of morphologic data for other life stages and vectors is a common problem among all genera and species of hemogregarines of reptiles that has hindered appropriate classification Hepatozoon are intraleukocytic parasites that infect a wide range of reptiles as well as mammals and birds Many species infecting terrestrial reptiles previously classified within Haemogregarina were transferred to Hepatozoon and so this change should be considered for a correct and uptodate diagnosis Karyolysus are intraerythrocytic parasites of lizards in the genera Lacerta and Podarcis These parasites are transmitted by mites Hemolivia are intraerythrocytic parasites of tortoises and lizards and a few amphibians Parasites with known life cycles utilize ticks in the genera Amblyomma or Hyalomma as vectors Zoonotic potential None Distribution Worldwide depending on range of appropriate hosts and vectors Incubation period Highly variable It is also unknown for most species as most species have only been detected in naturally infected hosts that have unknown histories Generally in experimental trials parasites are not observed in the blood for several weeks Clinical signs Generally no clinical signs are noted in natural hosts although the parasites are often observed in blood smears during routine examination Unnatural hosts eg experimental studies or captive exotic animals may exhibit lethargy and anorexia Clinical pathological gross and histopathological findings Animals with very high parasitemias may develop mild anemia Unnatural hosts may develop leukocytosis and elevated AST Lesions are generally mild and microscopic Intracellular stages can be observed in liver lung or spleen of vertebrate hosts Granulomas are sometimes observed surrounding haemogregarine stages Histopathologic lesions eg necrosis and severe American Association of Zoo Veterinarians Infectious Disease Manual HEMOGREGARINES OF REPTILES inflammatory infiltrates surrounding parasite stages in liver and lungs may be more severe in unnatural hosts Diagnosis Examination of stained thin blood smears Meronts can be observed by histologic examination of liver and other organs from tissues collected at post mortem examinations Material required for laboratory analysis Thin blood smears fixed and stained for detection of intracellular parasite stages Formalin fixed tissues for histologic evaluation for meronts Relevant diagnostic laboratories Many diagnostic laboratories can examine blood smears and tissue sections for parasites Treatment No effective treatment known for reptiles A decrease in parasitemias but not clearance has been noted with atovaquoneproguanil in one study Prevention and control Because the haemogregarines are vectorborne limiting exposure of reptiles to ectoparasites is necessary to prevent transmission Four acaricides chlorpyrifos cyfluthrin lindane and permethrin proved efficacy against tick infestation in leopard tortoises Suggested disinfectant for housing facilities It is not a matter of disinfection but rather prevention of exposure to ectoparasites and limiting environmental contamination with tick lifestages Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal These parasites are vectorborne so direct contact between animals is not a risk factor for infection However ectoparasite prevention should be implemented Conditions for restoring diseasefree status after an outbreak na Experts who may be consulted Michael J Yabsley Associate Professor College of Veterinary Medicine University of Georgia Athens Georgia 30602 706 5421741 myabsleyugaedu References 1 Burridge MJTrevor F Allan SA Mahan SM Evaluation of safety and efficacy of acaricides for control of the African tortoise tick Amblyomma marmoreum on leopard tortoises Geochelone pardalis J Zoo Wildl Med 2002335257 2 Foronda P SantanaMorales MA Orós J AbreuAcosta N OrtegaRivas A LorenzoMorales J Valladares B Clinical efficacy of antiparasite treatments against intestinal helminths and haematic protozoa in Gallotia caesaris lizards Exp Parasitol 2007116 361365 3 Krampitz HE Haberkorn A Experimental treatment of Hepatozoon infections with the anticoccidial agent toltrazuril Zentralbl Veterinarmed B 198835131137 4 Siddall ME Phylogeny of adeleid blood parasites with partial systematic revision of the haemogregarine complex J Euk Microbiol 199542116125 5 Telford SR Jr Hemoparasites of the Reptilia Color Atlas and Text Boca Raton FL CRC Press 2008 376 p 6 Wozniak EJ Kazacos KR Telford Jr SR McLaughlin GL Characterization of the clinical and anatomical pathological changes associated with Hepatozoon mocassini infections in unnatural reptilian hosts Int J Parasitol 199626141146 7 Wozniak EJ Telford Jr SR DeNardo DF McLaughlin GL Butler JF Granulomatous hepatitis associated with Hepatozoon sp meronts in a southern water snake Nerodia fasciata pictiventris J Zoo Wildl Med 1998296871 American Association of Zoo Veterinarians Infectious Disease Manual HEPATITIS A Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Humans nonhuman primates Fecaloral route Occasionally mild illness anorexia lethargy vomiting fever and diarrhea liver enzyme elevation jaundice common in humans Rarely fatal most recover acute infections without permanent liver damage Rarely indicated supportive care Vaccination or immune globulin potentially Yes Fact Sheet compiled by Zoltan S Gyimesi Sheet completed on 4 February 2011 21 August 2013 updated 30 January 2018 Fact Sheet Reviewed by Ed Ramsay Susceptible animal groups Humans nonhuman primates chimpanzees Old World monkeys New World monkeys Causative organism Hepatitis A virus HAV Hepatovirus genus Picornaviridae family Both human and simian strains Zoonotic potential Yes Distribution Worldwide Incubation period 1550 days fecaloral transmission Following exposure and infection virus can be shed in feces prior to seroconversion or clinical signs Clinical signs Virus rarely causes clinical disease in nonhuman primates Infected individuals can be viremic for up to 30 days prior to the onset of clinical signs Seroconversion may be associated with transient liver enzyme elevation AST ALT total bilirubin Nonspecific illness anorexia lethargy fever or gastrointestinal disease is possible Duration of viremia and fecal shedding can be 2 months or more Post mortem gross or histologic findings Hepatocellular degeneration and necrosis Kupffer cell proliferation and lymphocytic periportal hepatitis can be observed Histologic changes that may be present are similar to liver lesions caused by infection with this virus in humans Diagnosis Blood testing for antibodyantigen Liver biopsyhistopathology Fecal PCR Material required for laboratory analysis Whole blood serumplasma Feces or liver potentially Relevant diagnostic laboratories VRL Laboratories 7540 Louis Pasteur Road Suite 200 San Antonio Texas 78229 8776157275 fax 2106157771 AnthonyCookevrlnet Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 91311 8187178880 8187178881 fax infozoologixcom Treatment This is not typically indicated Supportive care can be provided Prevention and control In humans immune globulin containing sufficient antiHAV concentrations to be protective or inactivated vaccine typically for people at higher risk can be administered Vaccines can be given postexposure during outbreaks per WHO Suggested disinfectant for housing facilities Sodium hypochlorite or 2 glutaraldehyde American Association of Zoo Veterinarians Infectious Disease Manual HEPATITIS A Notification Public health officials may need to be notified if zoonotic primate to human transmission occurs Measures required under the Animal Disease Surveillance Plan None currently Measures required for introducing animals to infected animal HAV can remain infective in stored feces for at least 30 days If concerned about introduction of animals to a known infected animal animals that are seronegative ie not immune the seronegative animal could be immunized with the human HAV vaccine prior to introduction Similarly a seropositive animal with negative stool samples by PCR is probably recovered and no longer infectious to others Conditions for restoring diseasefree status after an outbreak Clinically significant outbreaks are uncommon Diseasefree status should be obtainable via appropriate environmental disinfection and making sure primates are either seronegative or seropositive but no longer shedding HAV Experts who may be consulted Linda J Lowenstine DVM PhD DACVP Professor Emeritus University of California Davis Vet Med Pathology Microbiology and Immunology Davis CA 95616 Phone 5307521182 Fax 5307523349 ljlowenstineucdavisedu References 1 Bower WA Nainan OV Han X Margolis H Duration of viremia in hepatitis A virus infection J Infect Dis 20001821217 2 Brack M Virus hepatitis A In Heijink I RyserDegiorgis MP eds EAZWV Transmissible Diseases Handbook 2nd ed Houten Netherlands Van Setten Kwadraat 2004 p 427429 3 CDC Internet Centers for Disease Control and Prevention cited 30 January 2018 Available from httpswwwcdcgovhepatitishavindexhtm 4 Dienstag JL Isselbacher KJ Acute viral hepatitis In Braunwald E Fauci AS Kasper DL Hauser SL DL Longo Jameson JL eds Harrisons Principles of Internal Medicine 15th ed New York NY McGrawHill 2001 p 17211737 5 Lerche NW Emerging viral diseases of nonhuman primates In Fowler ME ed Zoo and Wild Animal Medicine Current therapy 3 Philadelphia PA WB Saunders Company 1993 p 340344 6 Mbithi JN Springthorpe VS Sattar SA Chemical disinfection of hepatitis A virus on environmental surfaces Appl Environ Microbiol 1990561136013604 7 McCaustland KA Bond WW Bradley DW Ebert JW Maynard JE Survival of hepatitis A virus in feces after drying and storage for 1 month J Clin Microbiol 1982165957958 8 Ramsay E Montali RJ Viral hepatitis in New World primates In Fowler ME ed Zoo and Wild Animal Medicine Current therapy 3 Philadelphia PA WB Saunders Company 1993 p 355358 9 Robertson BH Viral hepatitis and primates historical and molecular analysis of human and nonhuman primate hepatitis A B and the GBrelated viruses J Viral Hepat 200184233242 10 WHO Internet World Health Organization cited 30 January 2018 Available from httpwwwwhointmediacentrefactsheetsfs328en American Association of Zoo Veterinarians Infectious Disease Manual HEPATITIS B VIRUS HBV Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primates esp gibbons wooly monkeys apes humans also rodents birds bats Transmitted vertically perinatal or horizontal percutaneous or mucosal exposure to infected body fluids ie blood saliva sexual fluids wound exudate Weight loss lethargy anorexia icterus abdominal discomfort nausea vomiting pyrexia joint pain Often asymptomatic in nonhuman primates but can cause severe disease in gibbons and wooly monkeys increased prevalence of hepatocellular carcinoma in chronic infections in woodchucks humans Supportive care antivirals or αinterferon can be attempted but to date unsuccessful in animal cases Human recombinant vaccine should be considered for non exposed primates Assumed but unproven Fact Sheet compiled by Ellen Bronson med vet DACZM Sheet completed on 31 January 2011 updated 12 March 2013 and 14 January 2018 Fact Sheet Reviewed by Sam Sander Susceptible animal groups Hepadnaviruses are divided into two genera Orthohepadnavirus in mammals Avihepadnavirus in birds Orthohepadnavirus infect humans apes and rodents Human Hepatitis B virus consists of at least 10 genotypes A through J with several subgenotypes Nonhuman primate hepatitis B viruses are speciesspecific and infect chimpanzees orangutans gorillas gibbons and woolly monkeys Rarely reported or experimental in other primates macaques baboons spider monkey vervet monkey and ruffed lemurs Speciesspecific rodent hepadnaviruses also infect woodchucks ground squirrels and arctic squirrels Most recently hepadnaviruses have been identified in multiple species of bats Avihepadnaviruses infect birds including ducks geese herons storks cranes Other hepadnaviruses have recently been identified in fish African cichlid white sucker bluegill and amphibians Tibetan frog Woodchucks and ducks are used as experimental models for hepatitis B in humans Chimpanzees were historically used as a surrogate model for human HBV but federal regulation in US no longer permits their use for invasive research Causative organism Orthohepadnaviruses Mammals Human hepatitis B virus at least 10 genotypes most with several subgenotypes Chimpanzee hepatitis B virus ChHBV Orangutan hepatitis B virus OuHBV Gorilla hepatitis B virus GoHBV Gibbon hepatitis B virus GiHBV Woolly monkey hepatitis B virus WMHBV Woodchuck hepatitis virus WHV Ground squirrel hepatitis virus GSHV Arctic ground squirrel hepatitis virus ASHV Bat hepatitis virus Avihepadnaviruses Birds Duck hepatitis B virus Heron hepatitis B virus Stork hepatitis B virus Crane hepatitis B virus Ross goose hepatitis B virus American Association of Zoo Veterinarians Infectious Disease Manual HEPATITIS B VIRUS HBV Snow goose hepatitis B virus Parrot hepatitis B virus Zoonotic potential Transmission of nonhuman primate hepatitis B viruses to humans is in theory possible although yet unproven transmission of human HBV infection to nonhuman primates is well documented Risk analysis should be performed for primate and veterinary staff in zoos and rehabilitation centers to assess need for vaccination against HBV Distribution Multiple species and subspeciesspecific and regional variants exist but many are thought to crossinfect other species although further epidemiologic and molecular studies are ongoing and needed Recombination between ape variants has been proven Infection has been shown in freeranging chimpanzee gorilla orangutan and gibbon populations Incubation period 30 180 days average 75 90 days Clinical signs Infection can result in 1 Acute transient or fulminant hepatitis with fever anorexia lethargy nausea vomiting icterus abdominal discomfort ascites Increases in alanine transferase ALT and aspartate aminotransferase AST documented in several species 2 Asymptomatic infection or mild disease and clearance of the virus with lifelong immunity 3 Chronic hepatitis leading to liver failure or hepatocellular carcinoma Increases in ALT and AST possible Post mortem gross or histologic findings Hepatitis hepatic necrosis hepatic fibrosis is seen in humans gibbons and wooly monkeys but rarely in other primates Chronic infections can lead to hepatic cirrhosis and hepatocellular carcinoma in humans as well as in woodchucks to a lesser degree in ground squirrels and ducks but has not been reported in nonhuman primates More cases with histologic and clinical disease may become evident as nonhuman primates diagnosed only in the past few decades age and develop chronic disease Diagnosis Increased ALT and AST on biochemical analysis Since the genome of human and nonhuman primate hepatitis B viruses are similar human Hepatitis B testing is applicable in nonhuman primates as follows HBsAg and HBsAB indicates active acute or chronic infection HBsAg and HBsAB indicates exposure but clearance of virus and natural immunity or vaccination HBcAg indicates acute infection 6 mo HBcAB indicates acute or chronic infection indicates previous exposure or chronic infected carrier status HBeAg indicates active virus production and infectivity HBeAg and HBeAB indicates active virus production and high infectivity HBeAg and HBeAB indicates low or no viral shedding and typically a predictor of longterm clearance of virus but still potentially infectious PCR testing also available and indicates infectivity if positive Material required for laboratory analysis Serum for liver enzyme analysis and serology testing serum or whole blood EDTA or ACD for PCR testing Relevant diagnostic laboratories 1 VRL Labs PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 Tel 877615 7275 wwwvrlnet HBsAg HBsAB HBcAB 0510 ml serum for each test required Hepatitis B PCR 2 ml fresh EDTA whole blood 2 Zoologix Inc 9811 Owensmouth Ave Suite 4 Chatsworth CA 91311 Tel 8187178880 httpwwwzoologixcomprimateDatasheetsHepatitisBhtm Hepatitis B total antibody testing ELISA 05 ml EDTA whole blood or spun serumplasma Qualitative real time PCR 02 ml EDTA or ACD whole blood 02 ml plasma or serum 02 ml freshfrozenfixed liver tissue American Association of Zoo Veterinarians Infectious Disease Manual HEPATITIS B VIRUS HBV Treatment Supportive care no specific treatment proven in nonhuman primates In humans tenofovir or entecavir and other nucleoside analog antivirals or αinterferon are given if high HBeAg and DNA and increased ALT chronic active hepatitis In humans antivirals suppress the virus but do not provide a cure while αinterferon cures a low percent of those treated for 1 year Lamivudine and αinterferon have been attempted in limited cases in chimpanzees and woodchucks respectively without signs of improvement Prevention and control Screen colony once and new animals at preshipment or quarantine examination with HBsAg or PCR Avoid adding positive breeding animals to negative and unvaccinated groups Vaccination can be used to protect negative HBsAB or PCR animals if exposed to positive animals Two single antigen recombinant vaccines are currently available in the US in humans Engerix B and Recombivax HB and given at 0 1 and 6 months with lifelong immunity in humans Suggested disinfectant for housing facilities 110 bleach The virus can survive up to 7 days even on surfaces contaminated by dried bloodbodily fluids Notification None Measures required under the Animal Disease Surveillance Plan NA Measures required for introducing animals to infected animal Animal to be introduced should be tested if HBsAg or PCR and HBsAB animal should be vaccinated before introduced to positive HBsAg or PCR animal Conditions for restoring diseasefree status after an outbreak Area should be completely cleaned and disinfected All animals should be tested with HBsAg or PCR and HBsAB to determine status Animals that are HBsAg or PCR and HBsAB should be immunized Experts who may be consulted Robert E Lanford PhD Southwest National Primate Research Center Department of Virology and Immunology Texas Biomedical Research Institute 7620 NW Loop 410 San Antonio TX 78227 210 258 9445 rlanfordtxbiomedorg References 1 Bonvicino CR Moreira MA Soares MA Hepatitis B virus lineages in mammalian hosts Potential for bidirectional crossspecies transmission World J Gastroenterol 20142076657674 2 Centers for Disease Control and Prevention CDC Internet Hepatitis B Questions and Answers for Health Professionals 2018 cited 2018 December 29 Available from httpswwwcdcgovhepatitishbvhbvfaqhtm 3 Gerlich WH Medical virology of hepatitis B how it began and where we are now Virol J 201310239 4 Heckel JO Rietschel W Hufert FT Prevalence of hepatitis B virus infections in nonhuman primates J Med Primatol 2001301419 5 Lanford RE Chavez D Brasky KM Burns RB RicoHesse R Isolation of a hepadnavirus from the woolly monkey a New World primate Proc Natl Acad Sci 19989557575761 6 SaNguanmoo P Rianthavorn P Amornsawadwattana S Poovorawan Y Review Hepatitis B virus infection in nonhuman primates Acta Virol 2009537382 7 Thornton SM Walker S Zuckerman JN Management of hepatitis B virus infections in two gibbons and a western lowland gorilla in a zoological collection Vet Rec 2001149113115 8 World Health Organization Internet Hepatitis B 2018 cited 2018 December 29 Available from httpswwwwhointennewsroomfactsheetsdetailhepatitisb American Association of Zoo Veterinarians Infectious Disease Manual DUCK VIRAL ENTERITIS DUCK PLAGUE Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Ducks geese swan of all ages Bird to bird contact or via environment water is important for transmission Spontaneous viral shedding by duck plague carriers particularly during spring Diarrhea blood stained vent cyanotic bill inability to fly convulsions polydipsia hypersensitivity to light Moderate to severe No effective treatment Minimize exposure vaccine for commercial flocks No Fact Sheet compiled by Gwen E Myers Sheet completed on 21 February 2011 updated 15 August 2013 Fact Sheet Reviewed by Simone Stoute Gary Riggs Susceptible animal groups Ducks geese swan susceptibility varies greatly among waterfowl species blue winged teal Canada goose mallard Muscovy pintail other aquatic birds do not become infected with exception of two coots in Spain during an epizootic All ages are susceptible Juveniles may be more susceptible than adults but in commercial waterfowl adult breeders mortality may be higher than young ducks Sometimes higher mortality reported in females than in males Carriers can produce infected offspring which also may shed virus Causative organism Herpesvirus Anatid herpesvirus 1 Zoonotic potential No Distribution North America Europe Asia Africa Incubation period Bird to bird contact or via environment Water appears important for transmission Incubation period exposure to death is 37 days in domestic ducks as long as 14 days in wild populations Clinical signs Hypersensitivity to light with birds seeking cover and darkened areas extreme thirst droopiness decreased egg production bloody discharge from vent or bill inappetence ataxia inability to fly convulsions and phallus prolapse Birds can also have a characteristic cold sore lesion under tongue especially during the carrier state Shedding oral cloacal fecal egg from tissues and body fluids of carcasses Spontaneous virus shedding by duck plague carriers particularly during spring may be related to physiological stresses of daylight duration change and onset of breeding Post mortem gross or histologic findings Gross Buccal cavity whitish plaques in pharynx occasionally Esophagus petechial to ecchymotic hemorrhages necroticdiphtheriticcheesy membranous lesions along longitudinal folds on mucosal surface if slightly longer course particularly caudal esophagus and common in swans Proventriculus focal mucosal hemorrhage andor necrosis Intestines Hemorrhagic enteritis Variable extent from petechiation and small ulcers eg in jejunum to hemorrhagicnecrotic annular rings ducks or discs button ulcers geese swans in intestines related to lymphoid tissue distribution in ileum Cloaca mucosal hemorrhages later necroticdiphtheriticcaseous membranous lesions as in esophagus Cardiovascular system petechiae to paintbrush hemorrhages on surface particularly at base and in coronary grooves common or in myocardium May be particularly visible on pericardial fat American Association of Zoo Veterinarians Infectious Disease Committee Manual 2013 DUCK VIRAL ENTERITIS DUCK PLAGUE Liver Pinpoint hemorrhages petechiae andor focal necrosis May be swollen friable pale copper colored Thymus and bursa of Fabricius young birds hemorrhages surrounding tissues edematous Histologic Focal hemorrhages in most organs Liver Necrosis of hepatocytes with hemorrhage and limited heterophil infiltration Occasional areas of caseous necrosis with surrounding coagulation necrosis are observed Gastrointestinal tract Necrosis of epithelial cells sloughed into lumenthat have been raised from surface by hemorrhage Large eosinophilic intranuclear inclusion bodies may be found in hepatocytes bile duct epithelial cells epithelial cells of esophagus intestine bursa of Fabricius pancreatic cells and Hassalls corpuscles Diagnosis Generally a postmortem diagnosis Viral isolation mortality and lesions following animal sub inoculation serum neutralization ID of a herpesvirus using EM microscopic confirmation of viral intranuclear inclusion bodies in tissue cells and PCR Material required for laboratory analysis Tissue samples liver lung spleen kidney cloacal swabs Relevant diagnostic laboratories State Animal Disease Diagnostic laboratories Texas Veterinary Medical Diagnostic Lab College Station Laboratory PO Box Drawer 3040 College Station Texas 778413040 979 8453414 Treatment No successful treatment Prevention and control Prevention aimed at minimizing exposure of the populationatrisk depopulation removal of birds from the infected environment sanitation and disinfection Avirulent livevirus vaccine developed for domestic white Pekin ducks but it is not reliable in protecting other species Suggested disinfectant for housing facilities Virus is hardy survives for weeks in ideal environmental conditions Phenolic based disinfectants Chlorine bleach water may be decontaminated by chlorination 3ppm Scrub concrete ponds with hypochlorite 525 solution Notification Reportable to State Veterinarian and USDAAPHISVS involvement Measures required under the Animal Disease Surveillance Plan No known requirements as this is reportable for trackingsurveillance Measures required for introducing animals to infected animal Not recommended infected animals should be isolated or culled Conditions for restoring diseasefree status after an outbreak Quarantine depopulate clean and disinfect environment for captive flocks Experts who may be consulted Simone Stoute DVM PhD DACPV Director Cornell University Duck Research Laboratory Department of Population Medicine and Diagnostic Sciences College of Veterinary Medicine Cornell University PO Box 217 Eastport NY 11941 6313250600 sts66cornelledu American Association of Zoo Veterinarians Infectious Disease Committee Manual 2013 DUCK VIRAL ENTERITIS DUCK PLAGUE References 1 Brand CJ and DE Docherty 1984 A survey of North American migratory waterfowl for duck plague duck virus enteritis virus J Wildl Dis 20 261266 2 Hansen WR SE Brown SW Nashold and DL Knudson 1999 Identification of duck plague virus by polymerase chain reaction Avian Dis 43 106115 3 Hess JC and JA Pare 2004 Viruses of waterfowl Sem Av Exot Pet Med 13 176183 4 Leibovitz L 1971 Duck plague In Davis J W and others eds Infectious and Parasitic Diseases of Wild Birds Iowa State University Press Ames Iowa Pp 2233 5 Wobeser GA 1997 Duck plague In Diseases of Wild Waterfowl 2nd ed Plenum Press New York New York Pp 1527 American Association of Zoo Veterinarians Infectious Disease Manual ENDOTHELIOTROPHIC ELEPHANT HERPESVIRUS EEHV Fact Sheet compiled by Lauren Howard Sheet completed on 25 January 2011 updated 3 January 2013 January 3 2018 Fact Sheet Reviewed by Gretchen Cole Susceptible animal groups Infant and juvenile Asian and very occasionally African elephants are more likely to die from EEHV Hemorrhagic disease than older animals although there are reported cases of fatalities in elephants up to 40 years old Adult elephants of both species may be subclinical carriers or may display a milder form of the disease with intermittent oral and vaginalvestibular lesions Causative organism Elephant Endotheliotropic Herpesviruses EEHV Novel genus names Probosciviruses Several types and multiple strains have been isolated and identified from fatal cases and clinically ill elephants Zoonotic potential None known Distribution Seven related speciestypes of EEHV have been identified in captive Asian or African elephants throughout the world Multiple cases of the same hemorrhagic disease have been identified in wild Asian calves in Asia Most captive and all wild elephants likely carry several EEHV types in a latent state EEHV 1 34 test used does not distinguish between 3 and 4 and 5 detected in trunk washes of clinically normal camp elephants in India Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Asian elephants especially ages 18 years Rarely African elephants Direct transmission between animals via trunk secretions and saliva or other body fluids Signs may be very mild Edema of head neck trunk legs Cyanotic swollen tongue Lethargy anorexia mild colic diarrhea or constipation Lameness Alterations in sleep patterns Monocytopenia thrombocytopen ia Can be fatal in young elephants if not and even when promptly treated It may cause ulcers or vesicles in mouth and on vaginal mucosa Milder clinical or subclinical forms exist In African elephants carrier state also exists in lymphoid lung nodules and possibly reactivated in skin nodules Antiviral medications Famciclovir orally or rectally Ganciclovir intravenously acyclovir orally rectally or intravenously Supportive care intravenous fluid support plasma transfusions see eehvinfoorg for more It is recommended to run PCR on whole blood of Asian elephants 18 years of age weekly to detect early viremia before clinical signs No American Association of Zoo Veterinarians Infectious Disease Manual ENDOTHELIOTROPHIC ELEPHANT HERPESVIRUS EEHV EEHV Strain Species Clinical Picture 1A Asian Hemorrhagic disease 1B Asian Hemorrhagic disease 2 African Hemorrhagic disease lung nodules skin nodules 3 AsianAfrican Hemorrhagic disease lung nodules skin nodules 4 Asian Hemorrhagic disease 5 Asian Hemorrhagic disease 6 African Lung nodules 7 African Lung nodules skin nodules Incubation period In retrospective analysis of clinical cases EEHV viremia has been detectable on quantitative PCR of whole blood 1 to 2 weeks prior to clinical signs It is suspected that EEHV infections usually remain latent with sporadic subclinical reactivation ie shedding in trunk washes or other secretions throughout the lifetime of an infected elephant Clinical signs Changes in hemogram monocytopenia thrombocytopenia may occur before clinical signs of illness Initial signs may be mild or vague lethargy decreased food or water intake mild colic diarrhea lameness or stiffness oral mucosal lesions ocular lesions and alterations in sleep patterns may occur More severe signs include edema of the head neck trunk and thoracic limbs and lingual cyanosis Post mortem gross or histologic findings Gross necropsy findings may include pericardial effusion with diffuse petechial hemorrhages throughout the heart tongue and visceral surfaces Lingual cyanosis and hepatomegaly may also be seen Ulcerations of the oral cavity larynx and large intestine have been seen Histologic findings may include extensive microhemorrhages and edema in the heart and tongue with lymphocytic monocytic and neutrophilic infiltration of the myocardium Capillary endothelial cells of the myocardium tongue and hepatic sinusoids may contain amphophilic to basophilic viral inclusion bodies These herpesviral particles are usually intranuclear and occasionally intracytoplasmic but have not been seen outside of cells Diagnosis PCR on whole blood detects viremia Viremia may be low and remain lowsubclinical or may increase and lead to EEHV Hemorrhagic Disease serial testing is recommended in any viremic elephant Close evaluation of the hemogram can identify early monocytopenia and thrombocytopenia Virus can also be detected in serum of severely affected animals Postmortem PCR analysis can be done on heart liver tongue intestines and any other hemorrhagic tissues PCR on lung nodules can be performed it is important to note that several EEHV types have been found by PCR in lung nodules of asymptomatic carrier Africans but not known yet in asymptomatic Asians Trunk wash or saliva swab PCR may demonstrate EEHV shedding which occurs sporadically in most elephants at one point or another Material required for laboratory analysis Whole blood in EDTA tube frozen PCR Frozen serum PCR future antibody testing no test available as of 2018 Transfer all liquid samples to plastic tubes before shipping Heart liver spleen lymph nodes intestines skin or mucosal nodules lung nodules frozen PCR Cell pellet from centrifuged trunk wash realtime PCR or saliva swab in DNA preservative Fresh unfrozen samples of serum positive trunk washes and lesions needed for attempts at cell culture American Association of Zoo Veterinarians Infectious Disease Manual ENDOTHELIOTROPHIC ELEPHANT HERPESVIRUS EEHV Relevant diagnostic laboratories Smithsonian National Zoological Park Department of Pathology Attn Erin LatimerLaura Richman 3001 Connecticut Ave NW Washington DC 20008 202 6334252 703 8559611 latimeresiedu Please call oremail before sending samples Baylor College of Medicine Department of Virology and Microbiology Performs quantitative real time PCR on whole blood or trunk wash samples For details contact Dr Paul Ling plingbcmedu Lab phone 713 798 8475 Cell phone 281 460 1696 Treatment Famciclovir 815 mgkg orally or rectally TID for Asian elephants has been reported Brock et al 2012 Ganciclovir has also been used but must be given intravenously Acyclovir has been used in several Asian countries Prevention and control Weekly blood collection for whole blood PCR is recommended for Asian elephants 1 to 8 years of age to detect viremia early on in disease process and allow for early treatment Weekly CBCs may also help detect early viremia Bank frozen whole blood serum and trunk wash on all clinical elephants and herdmates for potential future study Once prevalence is known from ongoing investigations informed decisions can be made in regards to movement of individual elephants between populations Suggested disinfectant for housing facilities Bleach diluted to 110 solution in water is often used to disinfect surfaces contaminated with most herpesviruses although it has not been proven to inactivate EEHV Notification No special notification process required Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Calves should not be isolated from their dams unless necessary to facilitate treatment Conditions for restoring diseasefree status after an outbreak No cure is available for latent herpesviral infection It is assumed to be endemic in both Asians and Africans Experts who may be consulted Website with information on detection treatment etc wwweehvinfoorg Erin LatimerLaura Richman Smithsonians National Zoological Department of Pathology 3001 Connecticut Ave NW Washington DC 20008 2026334252 703 8559611 latimeresiedu Dennis Schmitt DVM treatment advice 203 Karls Hall Missouri State University American Association of Zoo Veterinarians Infectious Disease Manual ENDOTHELIOTROPHIC ELEPHANT HERPESVIRUS EEHV 901 South National Ave Springfield MO 65897 Phone 4178365091 dennisschmittmissouristateedu Lauren Howard DVM Dipl ACZM Associate Director of Veterinary Services San Diego Zoo Safari Park 15500 San Pasqual Valley Road Escondido CA 920277017 Phone 760 291 5407 lhowardsandiegozooorg Paul Ling PhD Department of Biology and Microbiology Baylor College of Medicine plingbcmedu Lab phone 713 798 8475 Cell phone 281 460 1696 References 1 Atkins L Zong JC Tan J Mejjia A Heaggans SY Nofs SA Stanton JJ Flanagan JP Howard L Latimer E Stevens MR Hoffman DS Hayward GS Ling PD Elephant endotheliotropic herpesvirus 5 a newly recognized elephant herpesvirus associated with clinical and subclinical infections in captive Asian elephants Elephas maximus J Zoo Wildl Med 2013441136143 2 Association of Zoos Aquariums Internet Elephant TABSSP Research and Necropsy Protocol Elephas maximus and Loxodonta africana 2017 cited 2018 29 December Available from httpelephantcareorgwpcontentuploadsElephResearchandNecropsyProtocolJune2017pdf 3 Brock AP Isaza R Hunter RP Richman LK Montali RJ Schmitt DL Koch DE Lindsay WA Estimates of the pharmacokinetics of famciclovir and its active metabolite penciclovir in young Asian elephants Elephas maximus Am J Vet Res 20127312 19961999 4 Bronson E McClure M Sohl J Wiedner E Cox S Latimer EM Pearson VR Hayward GS Fuery A Ling PD Epidemiologic evaluation of EEHV 3B infection in an African elephant Loxodonta africana J Zoo Wildl Med 201748335343 5 Denk D Redrobe S Latimer E Hayward GS Cracknel J Classens A Steinbach F McGowan S Dastjerdi A Fatal elephant endotheliotropic herpesvirus type 5 infection in a captive Asian elephant Vet Rec 2012171153801 6 Fowler ME Elephant endotheliotropic herpesvirus EEHV infection In Fowler ME Mikota SK eds Biology Medicine and Surgery of Elephants Ames IA Blackwell Publishing 2006 p 132 133 7 Fuery A Tan J Peng R Flanagan JP Tocidlowski ME Howard LL Ling PD Clinical infection of two captive Asian elephants Elephas maximus with EEHV 1B J Zoo Wildl Med 201647319324 8 Fuery A Browning GR Tan J Long S Hayward GS Cox SK Flanagan JP Tocidlowski ME Howard LL Ling PD Clinical infection of captive Asian elephants Elephas maximus with EEHV 4 J Zoo Wildl Med 201647311318 9 Hardman K Dastjerdi A Gurrala R Routh A Banks M Steinbach F Bouts T Detection of elephant endotheliotropic herpesvirus type 1 in asymptomatic elephants using TaqMan realtime PCR Vet Rec 20121708205 10 Hayward GS Conservation clarifying the risk from herpesvirus to captive Asian elephants Vet Rec 2012170 202203 American Association of Zoo Veterinarians Infectious Disease Manual ENDOTHELIOTROPHIC ELEPHANT HERPESVIRUS EEHV 11 Isaza R Hunter RP Richman LK Montali RJ Schmitt DL Koch DE Lindsay WA Famciclovir pharmacokinetics in young Asian elephants Elephas maximus In Proc Am Assoc Zoo Vet 2003 p 8283 12 Kendall R Howard L Masters N Grant R The impact of EEHV on the captive Asian elephant Elephas maximus population of the United Kingdom and Ireland 19952013 J Zoo Wildl Med 201647405418 13 Latimer E Zong JC Heaggans SY Richman LK Hayward GS Detection and evaluation of novel herpesviruses in routine and pathological samples from Asian and African elephants identification of two new probosciviruses EEHV5 and EEHV6 and two new gammaherpesviruses EGHV3B and EGHV5 Vet Microbiol 20111472841 14 Reid CE Hildebrandt TB Marx N Hunt M Thy N Reynes JM Schaftenaar W Fickel J Endotheliotropic elephant herpes virus EEHV infection the first PCRconfirmed fatal case in Asia Vet Q 2006282 6164 15 Richman LK Elephant herpesviruses In Fowler ME Miller RE eds Zoo and Wild Animal Medicine Current Therapy 6 St Louis MO Saunders Elsevier 2008 p 349354 16 Richman LK Montali RJ Cambre RC Schmitt D Hardy D Hildbrandt T Bengis RG Hamzeh FM Shahkolahi A Hayward GS Clinical and pathological findings of a newly recognized disease of elephants caused by endotheliotropic herpesviruses J Zoo Wildl Med 2000361112 17 Richman LK Hayward GS Elephant herpesviruses In Fowler ME Miller RE eds Zoo and Wild Animal Medicine 7th ed St Louis MO Elsevier 2012 p 496502 18 Schaftenaar W Reid C Martina B Fickel J Osterhaus ADME Nonfatal clinical presentation of elephant endotheliotropic herpes virus discovered in a group of captive Asian elephants Elephas maximus J Zoo Wildl Med 2010414626632 19 Schmitt D Hardy D Montali RJ Richman LK Lindsay WA Isaza R West G Use of famciclovir for the treatment of endotheliotropic herpesvirus infections in Asian elephants Elephas maximus J Zoo Wildl Med 2000314518522 20 Stanton JJ Zong JC Eng C Howard L Flanagan J Stevens M Schmitt D Wiedner E Graham D Junge RE Weber MA Fischer MA Mejia A Tan J Latimer E Herron A Hayward GS Ling PD Kinetics of viral loads and genotypic analysis of elephant endotheliotropic herpesvirus1 infection in captive Asian elephants Elephas maximus J Zoo Wildl Med 20134414254 21 Stanton JJ Nofs SA Peng R Ling PD Development and validation of quantitative realtime polymerase chain reaction assays to detect elephant endotheliotropic herpesviruses2 3 4 5 and 6 J Virol Meth 20121867377 22 Stanton JJ Zong JC Latimer E Tan J Herron A Hayward GS Ling PD Detection of pathogenic elephant endotheliotropic herpesvirus in routine trunk washes from healthy adult Asian elephants Elephas maximus by use of a realtime quantitative polymerase chain reaction assay Am J Vet Res 2010718925933 23 Wiedner E Howard L Isaza R Treatment of elephant endotheliotrophic herpesvirus EEHV In Fowler ME Miller RE eds Zoo and Wild Animal Medicine 7th ed St Louis MO Elsevier 2012 p 537543 24 Zachariah A Zong JC Long SY Latimer EM Heaggans SY Richman LK Hayward GS Fatal herpesvirus EEHV hemorrhagic disease in wild and orphan Asian elephants in Southern India J Wildl Dis 201349238193 American Association of Zoo Veterinarians Infectious Disease Manual EPSTEINBARR VIRUS HUMAN HERPESVIRUS 4 EBVRELATED LYMPHOCRYPTOVIRUSES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic EBV affects primarily humans EBVrelated viruses affect a wide range of NHP Old World monkeys apes some New World species Lymphocrypto virus has been associated with carcinomas of sea lions Direct contact through saliva EBV in man mostly asymptomatic but can manifest as Infectious Mononucleosis Burkitts lymphoma nasopharyngeal carcinoma hairy leukoplakia immunodeficiency associated lympho proliferative disease In other primates lympho proliferative disorders are presented EBVrelated viruses usually asymptomatic may cause lympho proliferative disorders Fatal in cases of malignant tumors or lymphomas None reported Ubiquitous Yes possible zooanthro ponotic disease Fact Sheet compiled by Sam Rivera updated by Jan Ramer Sheet completed on 1 June 2011 updated 23 July 2013 Fact Sheet Reviewed by Sam Rivera Kevin Brunner Susceptible animal groups EBV Pongidae EBVrelated simian viruses Old and New World NHP Causative organism EpsteinBarr virus Human herpesvirus 4 EBVrelated lymphocryptoviruses LCV Papiine herpesvirus 1 Cercopithecine herpesvirus 14 Macacine herpesvirus 4 Panine herpesvirus 1 Pongine herpesvirus 2 Gorilline herpesvirus 1 Callitrichine herpesvirus 3 Zoonotic potential Yes Distribution EBV in man Worldwide EBVrelated LCV found in most old world NHP and some new world NHP American Association of Zoo Veterinarians Infectious Disease Manual EPSTEINBARR VIRUS HUMAN HERPESVIRUS 4 EBVRELATED LYMPHOCRYPTOVIRUSES Incubation period Variable Clinical signs These diseases are presented mainly as asymptomatic infections EBV in man can cause infectious mononucleosis nasopharyngeal carcinomas Burkitts lymphoma nonHodgkins lymphoma in great apes can possibly cause malignant lymphomas in macaques axillaryinguinal lymphadenopathy similar to EBV induced infectious mononucleosis in humans without pharyngitis and splenomegaly Bcell lymphoma epithelial hyperkeratotic lesions on oral cavity esophagus chest hands and genitalia in baboons malignant lymphoma in orangutan leukemia in gorilla Bcell lymphoma in common marmoset Bcell lymphoma Post mortem gross or histologic findings Lymphoproliferative disorders Diagnosis Virus isolation serology PCR Histopathology Immunohistochemistry Material required for laboratory analysis Serum whole blood lymph nodes spleen bone marrow Relevant diagnostic laboratories Pathogen Detection Laboratory California National Primate Research Center Road 98 Hutchison University of California Davis California 95616 530 7528242 Fax 530 7524816 PDLprimateucdavisedu httppdlprimateucdavisedu BioReliance SerologyPCR Laboratories 14920 Broschart Rd Rockville Maryland 20850 301 6102227 310 6102587 ahsbioreliancecom Virus Reference Laboratories Inc 7540 Louis Pasteur Road San Antonio Texas 78229 887 6157275 Fax 210 6157771 Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 913113800 8187178880 Fax 8187178881 infozoologixcom Treatment None reported Prevention and control Ubiquitous in captive collections Suggested disinfectant for housing facilities Lipid solvents soap UVlight heat Notification None at this time Measures required under the Animal Disease Surveillance Plan None at this time Measures required for introducing animals to infected animal Ubiquitous in captive collections American Association of Zoo Veterinarians Infectious Disease Manual EPSTEINBARR VIRUS HUMAN HERPESVIRUS 4 EBVRELATED LYMPHOCRYPTOVIRUSES Conditions for restoring diseasefree status after an outbreak Latent infections preclude establishment precludes a diseasefree status after an outbreak Experts who may be consulted ChihLing Zao PhD Chief Scientific Officer VRL Laboratories PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 Phone 8776157275 Fax 2106157771 chihlingzaovrlnet References 1 httpwwwprimateportalorg Accessed 6 August 2013 2 Bennett T C Abee and R Henrickson eds 1998 Nonhuman Primates in Biomedical Research Diseases Academic Press San Diego California 512 pp 3 Ehlers B A Ochs F Leendertz M Goltz C Boesch and K MätzRensing 2003 Novel simian homologues of EpsteinBarr Virus J Virol 7719 1069510699 4 Lerche N W 2005 Common viral infections of laboratory primates In WolfeCoote S ed The Handbook of Experimental Animals The Laboratory Primate Elsevier Academic Press San Diego California Pp 7589 5 Lipscomb T P D P Scott R L Garber A E Krafft M M Tsai J Hl Lichy J K Taubenberger F Y Schulman F M D Gulland 2000 Common metastatic carcinoma of California sea lions Zalophus californianus evidence of genital origin and association with novel gammaherpesvirus Vet Path 376 609617 6 Voevodin AF and PA Marx eds 2009 Lymphocryptoviruses In Simian Virology Willey Blackwell Ames Iowa Pp 323346 American Association of Zoo Veterinarians Infectious Disease Manual EQUINE HERPESVIRUS Fact Sheet compiled by John Flanders Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals equids primarily recombinant EHV19 strains have been shown to infect ursids artiodactylids camelids rhinoceros and rodents EHV1 aerosol droplets contact fomite Infected foals etal membranes and aborted fetuses are highly contagious EHV3 sexually transmitted flies feeding on vaginal discharge of infected mares fomites EHV4 aerosol droplets contact fomite EHV9 unknown fomite transmission suspected EHV1 abortion in mares and mild respiratory disease in horses 2 years neurologic form more common in older animals signs range from ataxia to paralysis and death EHV3 ulcers along cutaneous mucous membranes especially genital tract EHV4 respiratory disease in horses 2 years old Depression nasal discharge fever Rarely causes abortion in pregnant mares EHV9 neurologic signs in affected aberrant hosts including ataxia seizures and progressive disease EHV1 mild to severe possible outbreaks if uncontrolled EHV3 generally mild with lesions resolving within two weeks EHV4 mild infections secondary bacterial infections can increase severity EHV9 ranges from mild illness to severe disease with progression in a short time period EHV1 supportive care for encephalo myelitis EHV3 topical antiseptics to prevent infection and reduce discomfort EHV4 supportive care EHV9 supportive care seizure control EHV1 vaccination all pregnant mares isolation of known cases EHV3 no vaccine available isolation of cases EHV4 vaccination of horses 5 years old EHV9 no vaccine available Not reported American Association of Zoo Veterinarians Infectious Disease Manual EQUINE HERPESVIRUS Sheet completed on 1 August 2013 Fact Sheet Reviewed by Ray Wack John Vacek Susceptible animal groups Equids EHV 1 3 4 exoticzoo cases of infection with a recombinant EHV1EHV9 virus have been published in onager Equus hemionus polar bear Ursus maritimus Grevys zebra E grevyi plains zebra E quagga blackbuck Antilope cervicapra Thomsons gazelle Eudorcas thomsonii reticulated giraffe Giraffa camelopardalis reticulata llama Lama glama alpaca Vicugna pacos black bear Ursus americanus guinea pig Cavia porcellus and Bactrian camel Camelus bactrianus Experimental infection has been demonstrated in Syrian hamsters Mesocricetus auratus domestic dogs Canis lupus familiaris and domestic pigs Sus scrofa Causative organism Equine viral abortion Equine Herpesvirus 1 EHV1 Equine herpes myeloencephalopathy EHV1 Equine coital exanthema EHV3 Equine rhinopneumonitis EHV4 Gazelle herpesvirus 1 EHV9 Zoonotic potential No evidence for potential zoonosis is associated with any EHV strain Distribution EHV strains are endemic worldwide with no specific distribution pattern EHV19 can be carried by exotic equids with no clinical signs Incubation period EHV1 Abortion in pregnant mares 24 weeks following exposure Lifelong infection with potential for recrudescence during stress or treatment with steroids Neurologic form incubation averages 38 days but up to 14 days EHV3 As short as 2 days EHV4 210 days following exposure EHV19 recombinant unknown Clinical signs EHV1 abortion Sporadic or abortion storm can be observed Spontaneous abortion of fetus within amniotic membranes in pregnant mares with no premonitory signs in the last trimester of gestation Foals that are born alive are extremely weak and die within days EHV1 encephalomyelopathy Encephalomyelitis varies in severity Mild cases are noted with slight ataxia urinary incontinence flaccid tail decreased anal tone limb edema and pyrexia Severe cases result in paralysis seizures blindness and ultimately death Paresis and paralysis are often noted with an ascending pattern from the hindlimbs Colic ocular lesions anorexia and pyrexia are also reported Mild cases may resolve uneventfully EHV3 Vesicular and ulcerative lesions are noted on the superficial mucosa of the external reproductive organs Lesions are transient and heal in several weeks leaving spots of depigmented skin Stallions may be reluctant to breed Affected horses may become lifelong carriers with flareups possible EHV14 respiratory disease Most common in foals older than 2 months when maternal immunity is waning Increased rectal temperature serous to mucopurulent nasal discharge anorexia and depression with recovery by 3 weeks Clinical signs are uncommon in horses over 2 years of age Abortion in pregnant mares may occur rarely EHV19 recombinant Range of clinical signs usually results in neurological disease in affected animals Polar bears and black bears have been reported with tremors excessive blinking ptyalism opisthotonos seizures and progressive neurologic disease A giraffe was euthanized due to ataxia incoordination abdominal pain and a progressively deteriorating condition Thomsons gazelles have been reported with recumbency seizures and progressive neurologic disease EHV related abortion has been reported in a Asian rhino Guinea pigs housed in the same building as affected Thomsons gazelles were reported with abortion hindlimb paralysis and ataxia American Association of Zoo Veterinarians Infectious Disease Manual EQUINE HERPESVIRUS Post mortem gross or histologic findings EHV1 abortion splenomegaly grey necrotic foci in liver and pleuralperitoneal edema in aborted fetuses Herpesviral intranuclear inclusion bodies in affected tissue EHV1 encephalomyelopathy Cases are noted with areas of hemorrhage throughout the CNS and vasculitis and thrombosis of neural endothelial cells with ischemic necrosis histologically EHV3 ulcers and vesicles on the vaginal vestibular vulvar preputial or penial mucosa of affected horses Similar lesions may also be noted on oral mucosa or teats EHV14 respiratory disease Focal areas of necrosis in liver spleen and lungs with intranuclear inclusion bodies Bronchointerstitial pneumonia may be noted when infected with secondary bacterial infections EHV19 recombinant Nonsuppurative encephalitis with or without lymphohistocytic cuffing multifocal gliosis and vasculitis have been reported in a variety of affected species Intranuclear inclusion bodies are sporadically reported Diagnosis EHV1 abortionencephalomyelopathy Pathology Based on gross and histologic pathology in aborted foals increased likelihood if intranuclear inclusion bodies are noted Vasculitis in CNS tissue of encephalomyelitis cases IHC demonstrates viral presence in affected tissues CSF analysis positive EHM horses typically have xanthochromia with increased protein A monocytic pleocytosis is variably present CSF samples are not accurate for PCR or ELISA testing Viral isolation gold standard Growth in horse and rabbit cell cultures allows differentiation from EHV4 which only grows on equine cell cultures Isolation from nasal swabs or blood samples of neurological horses best results when taken during initial pyrexia High viral burdens are more likely to have rapid turnaround time PCR can detect viral presence in collected tissues including nasal swabs or uncoagulated EDTA blood at low levels Nonquantitative is run more routinely but quantitative realtime is available Paired serology fourfold or greater increase in virus neutralizing antibody titers or a single titer of 1256 or higher are consistent with positive diagnosis However this approach cannot distinguish between EHV1 and EHV4 ELISA test pregnant mare serum when fetal tissues are not available to diagnose EHV3 Clinical based on physical exam findings Paired serology comparison of acute and convalescent serum samples for a rise in antibody titers Electron microscopy investigation of clinical samples including scrapings from the affected mucosa Virus isolation growth in equine cell cultures EHV4 Clinical signs Virus isolation growth only on equine origin cell lines ELISA can distinguish EHV4 from EHV1 Paired serology comparison of acute and convalescent serum samples for a rise in antibody titrers EHV19 recombinant PCR analysis of collected tissue samples Western Blot detection of viral proteins in neurologic tissue Material required for laboratory analysis EHV1 Serum for ELISA testing fetal tissue lung thymus spleen for histologic diagnosis nasal swabs or blood EDTA for virus isolation or PCR analysis American Association of Zoo Veterinarians Infectious Disease Manual EQUINE HERPESVIRUS EHV3 serum scrapings of mucosa from affected areas EHV4 nasal swabs whole blood serum for various testing modalities EHV19 recombinant nasal swabs serum CNS tissue Relevant diagnostic laboratories Realtime PCR analysis offered by httpwwwaphisusdagovvsnahssequineehvehvehmrecommendations051611pdf httpwwwvetmeducdaviseducehehv1diagnosticcfm Treatment EHV1 encephalomyelopathy Strict isolation supportive care for encephalomyelitis Urinary bladder decompression and rectal evacuation for incontinent patients and sling support if recumbent Corticosteroids given IV once to twice daily for 35 days followed by a tapered regimen to decrease CNS inflammation Treatment with antiviral medications has not been investigated although good in vitro efficacy has been demonstrated EHV3 Antiseptic lotions and ointments to prevent secondary infection or discomfort Discontinue breeding until all lesions are healed EHV14 respiratory disease Supportive care EHV19 recombinant Supportive care Prevention and control EHV1 abortion Inactivated vaccines have been used to prevent abortion with dosing at 5 7 and 9 months of pregnancy Literature does not currently indicate a protective effect of vaccination but vaccines are successful at producing a high antibody response and limit nasal shedding In cases of outbreaks prophylactic vaccination of all horses is controversial Isolation of pregnant mares and maintenance of closed groups is recommended to prevent further outbreaks in cases of infection Any horse with respiratory signs also should be isolated Horses will become infected lifelong with possible recrudescence during times of stress EHV1 myeloencephalopathy quarantine exposed horses No vaccine has been shown to be protective however it is recommended to vaccinate with inactivated vaccines to increase antibody titers and decrease shedding Concerns have been noted that horses that have been vaccinated frequently are more likely to develop myeloencephalopathy EHV3 No vaccines are available Isolation of affected horses Horses will become infected lifelong with possible recrudescence during times of stress EHV14 respiratory disease Immunity after natural infection is short lived Modifiedlive vaccines available for pneumonia inactivated vaccines are also capable of inducing a high antibody response Vaccine will decrease severityincidence but still not prevent the disease Horses 5 years old should have the first vaccination at 34 months of age with boosters every 6 months or as determined by the product Horses will become infected lifelong with possible recrudescence during times of stress EHV19 recombinant No vaccine available maintain separation of potential host species from aberrant hosts that have demonstrated susceptibility Suggested disinfectant for housing facilities Being an enveloped virus EHV is susceptible to most disinfectants and detergents Notification No special notification requirements for any viral strain Measures required under the Animal Disease Surveillance Plan None currently for any viral strain Measures required for introducing animals to infected animal It is recommended that an isolation period of 2128 days be placed on any animal that has tested positive or exhibited clinical signs of any form of the disease Affected animals will remain latently infected following the quarantine period and may continue to shed virus during times of stress Conditions for restoring diseasefree status after an outbreak EHV infected animals will remain latently infected for the duration of their lives They should remain isolated from healthy individuals American Association of Zoo Veterinarians Infectious Disease Manual EQUINE HERPESVIRUS Experts who may be consulted Nicola Pusterla DVM PhD DACVIM UC Davis School of Veterinary Medicine 3109 Tupper Hall Davis CA 95616 5307527991 npusterlaucdavisedu References 1 Anonymous Recommendations for horses exposed to equine herpes virus EHV1 or equine herpes virus myeloencephalopathy EHM 2011 httpwwwaphisusdagovvsnahssequineehvehvehm recommendations051611pdf accessed 31 July 2013 2 Anonymous American Association of Equine Practitioners Guidelines on Vaccination 2012 httpwwwaaeporgehvhtm accessed 31 July 2013 3 Anonymous Equine herpesvirus 1 4 related diseases 2013 httpwwwaaeporgimagesfiles Equine Herpesvirus Final030513pdf accessed 31 July 2013 4 Bildfell R C Yason D Haines and M McGowan 1996 Herpesvirus encephalitis in a camel Camelus bactrianus J Zoo WildlMed 273 409415 5 Borchers K D Böttner D Lieckfeldt A Ludwig K Frölich B Klingeborn F Widèn G Allen and H Ludwig 2006 Characterization of equid herpesvirus 1 EHV1 related viruses from captive Grevys zebra and blackbuck J Vet Med SciJap Soc Vet Sci 687 757760 6 Carter G and D Wise 2006 Herpesviridae a concise review of veterinary virology wwwivisorgadvancestocadvancesasp accessed July 29 2013 7 Donovan TA MD Schrenzel T Tucker AP Pessier B Bicknese MDM Busch AG Wise R Maes M Kiupel C McKnight and RW Nordhausen 2009 Meningoencephalitis in a polar bear caused by equine herpesvirus 9 EHV9 Vet Path Online 466 11381143 8 Fukushi H T Tomita A Taniguchi Y Ochiai R Kirisawa T Matsumura T Yanai T Masegi T Yamaguchi and K Hirai 1997 Gazelle herpesvirus 1 a new neurotropic herpesvirus immunologically related to equine herpesvirus 1 Virol 2271 3444 9 Fukushi H A Taniguchi K Yasuda T Yanai T Masegi T Yamaguchi and K Hirai 2000 A hamster model of equine herpesvirus 9 induced encephalitis J Neurovirol 64 314319 10 Greenwood Alex D K Tsangaras Simon YW Ho Claudia A Szentiks Veljko M Nikolin G Ma A Damiani Marion L East A Lawrenz H Hofer and N Osterrieder 2012 A potentially fatal mix of herpes in zoos Curr Biol 2218 17271731 11 Hoenerhoff MJ EB Janovitz LK Richman DA Murphy TC Butler and M Kiupel 2006 Fatal herpesvirus encephalitis in a reticulated giraffe Giraffa camelopardalis reticulata Vet Path Online 435 769772 12 House JA DA Gregg J Lubroth EJ Dubovi and A Torres1991 Experimental equine herpesvirusl infection in llamas Lama glama J Vet Diagn Invest 32 137143 13 Kasem S S Yamada M Kiupel M Woodruff K Ohya and H Fukushi 2008 Equine herpesvirus type 9 in giraffe with encephalitis EmergInfect Dis 1412 1948 14 Kennedy MA E Ramsay V Diderrich L Richman G Allen and LN Potgieter 1996 Encephalitis associated with a variant of equine herpesvirus 1 in a Thomsons gazelle Gazella thomsoni J Zoo Wildl Med 274 533538 15 Knowles DP 2011 Members of the Family Herpesviridae Subfamily Alphaherpesvirinae In MacLachlan NJ and EJ Dubovi eds Fenners Veterinary Virology 4 ed Elsevier Inc London UK Pp 184195 American Association of Zoo Veterinarians Infectious Disease Manual EQUINE HERPESVIRUS 16 Lunn DP N DavisPoynter MJBF Flaminio DW Horohov K Osterrieder N Pusterla and HGG Townsend 2009 Equine herpesvirus1 consensus statement J Vet Int Med 233 450461 17 Montali RJ GP Allen JT Bryans LG Phillips and M Bush 1985 Equine herpesvirus type 1 abortion in an onager and suspected herpesvirus myelitis in a zebra J Am Vet Med Assoc 18711 12481249 18 Narita M A Uchimura K Kimura N Tanimura T Yanai T Masegi H Fukushi and K Hirai 2000 Brain lesions and transmission of experimental equine herpesvirus type 9 in pigs Vet Path Online 375 476479 19 Rebhun WC DH Jenkins RC Riis SG Dill EJ Dubovi and A Torres 1988 An epizootic of blindness and encephalitis associated with a herpesvirus indistinguishable from equine herpesvirus I in a herd of alpacas and llamas J Amer Vet Med Assoc 1927 953956 20 Schlipf JW and MO Smith 2009 Equine herpes myeloencephalopathy In Smith BP ed Large Animal Internal Medicine Elsevier Inc St Louis Missouri Pp 982984 21 Schrenzel MD TA Tucker TA Donovan MD Busch AG Wise RK Maes and M Kiupel 2008 New hosts for equine herpesvirus 9 Emerg Infect Dis 1410 1616 22 Wilkins PA and AR Woolums 2009 Equine herpes viruses In Smith BP ed Large Animal Internal Medicine Elsevier Inc St Louis Missouri Pp 545547 23 Wohlsein P A Lehmbecker I Spitzbarth D Algermissen W Baumgärtner M Böer M Kummrow L Haas and B Grummer 2011 Fatal epizootic equine herpesvirus 1 infections in new and unnatural hosts Vet Microbiol 14934 456460 American Association of Zoo Veterinarians Infectious Disease Manual FELINE RHINOTRACHEITIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Felidae Droplets fomites Ocular nasal discharge anorexia depression High morbidity low mortality Famciclovir lysine supportive care Vaccination No Fact Sheet compiled by Ray Wack updated by Christine Molter Sheet completed on 1 March 2011 updated 3 November 2012 updated 2 January 2018 Fact Sheet Reviewed by James Evermann Lynelle Johnson Ray Wack Susceptible animal groups Felidae Causative organism Feline herpesvirus type1 Zoonotic potential None Distribution Worldwide Incubation period 2 6 days recrudescence 7 days after stressful event Clinical signs Fever sneezing keratoconjunctivitis ulcerative keratitis salivation facial dermatitis Initially serous then mucopurulent ocular and nasal discharge anorexia and depression are observed typically Chronic cases may develop ulcerative keratitis Disease generally has high morbidity and low mortality except in kittens immunocompromised or geriatric cats Coinfection with other respiratory viruses especially calicivirus and secondary bacterial infections are common In cheetah proliferative skin lesions at mucocutaneous interfaces have been observed Clinical signs may persist up to 6 weeks Postmortem gross or histologic findings Erythematous swollen nasal mucus membranes and conjunctiva hyperemic larynx and trachea serous or purulent discharge in nares or eyes early in the disease acidophilic intranuclear inclusions may be seen in affected epithelial cells Diagnosis Clinical signs tend to be more upper respiratory and ocular than with calicivirus infections but generally are challenging to differentiate PCR and viral isolation performed on oronasal swabs can indicate presence of the infectious organism but do not confirm FHV1 as the causative agent of disease PCR performed on facial dermatitis lesions and some ocular lesions including corneal sequestra is highly correlated with FHV1 as the causative agent of disease Cytology identification of acidophilic intranuclear inclusions affected epithelium is diagnostic In latently infected cats PCR and virus isolation is usually negative due to sequestered viral DNA in neurons Material required for laboratory analysis Oronasal swabs conjunctival scraping respiratory epithelium Relevant diagnostic laboratories Washington Animal Disease Diagnostic Lab Bustad Hall Room 155N Pullman WA 991647034 Phone 5093359696 waddlvetmedwsuedu httpwaddlvetmedwsuedu Animal Health Diagnostic Center College of Veterinary Medicine Cornell University PO Box 5786 240 Farrier Rd Ithaca NY 148525786 Phone 6072533900 Fax 6072533943 httpsahdcvetcornelledu American Association of Zoo Veterinarians Infectious Disease Manual FELINE RHINOTRACHEITIS Treatment General supportive treatment including broad spectrum antibiotics for secondary bacterial infections famciclovir can inhibit viral replication and lessen clinical signs Lysine supplementation may be used Oxygen or nebulization can be required in severe cases with respiratory distress or hard secretions Nutritional support and fluid therapy are often required due to anorexia Proliferative skin lesions may require wide excision or cryosurgery in cheetahs Prevention and control Inactive and modified live vaccines either injectable or intranasal formulations usually in combination with other felid viruses are available Vaccination does not prevent infection or shedding but can reduce severity of signs and decrease the amount of shedding Generally only inactivated vaccines are used in nondomestic felids Primary vaccination consists of 1 ml of vaccine FelOVax Boehringer Ingelheim given every 2 3 weeks from 6 weeks through 18 weeks of age or a minimum of 3 vaccines in an unvaccinated adult cat Response to vaccination should be documented with serum neutralization SN titer 2 3 weeks after the last vaccine A SN titer of or equal to 116 is considered protective Antibody titers frequently decline rapidly in exotics and may not accurately reflect susceptibility Cellular and mucosal immunity are important in moderating or preventing disease Triennial booster vaccinations are recommended but more frequent vaccination may be required if there is high exposure risk due to the rapid antibody decline is some species In cheetahs predictors of FHV infection included a dam receiving a preparturition modified live vaccine being from a small litter being born to a primiparous dam and male sex Suggested disinfectant for housing facilities Virus susceptible to most disinfectants including dilute household bleach quaternary ammonium disinfectants peroxygen disinfectants Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Felids should be vaccinated with response to vaccine documented prior to exposure to known positive cats Conditions for restoring diseasefree status after an outbreak Virus is shed intermittently potentially for remaining life of infected animal but does not survive long in dry environments Experts who may be consulted James Evermann MS PhD Washington Animal Disease Diagnostic Lab Bustad Hall 155D Pullman WA 991647034 Phone 5093393607 jfevetmedwsuedu References 1 Hussein ITM Menashy RV Field H Penciclovir is a potent inhibitor of feline herpesvirus1 with susceptibility determined at the level of virusencoded thymidine kinase Antivir Res 200878268 274 2 Kuehn NF Dyer NW Hauptman J Taylor SM Feline respiratory disease complex Feline herpesviral rhinotracheitis feline calicivirus Internet Merck Veterinary Manual 2018 cited 2018 January 2 Available from httpswwwmerckvetmanualcomcatownerslungandairway disordersofcatsfelinerespiratorydiseasecomplexfelineherpesviralrhinotracheitisfeline calicivirus 3 Junge RE Miller RE Boever WJ Scherba G Sundberg J Persistent cutaneous ulcers associated with feline herpesvirus type 1 infection in a cheetah J Am Vet Med Assoc 199119810571058 4 Mouzin DE Lorenzen MJ HaworthJD King VL 2004 Duration of serologic response to three viral antigens in cats J Am Vet Med Assoc 20042246166 5 Munson L Wack R Duncan M Montali RJ Boon D Stalis I Crawshaw GJ Cameron KN Mortenson J Citino S Zuba J Junge RE Chronic eosinophilic dermatitis associated with persistent feline herpes virus infection in cheetahs Acinonyx jubatus Vet Pathol 200441170176 American Association of Zoo Veterinarians Infectious Disease Manual FELINE RHINOTRACHEITIS 6 Risi E Agoulon A Allaire F Le DreanQuenechdu S Martin V Mahl P Antibody response to vaccines for rhinotrachetitis caliciviral disease panleukopenia feline leukemia and rabies in tigers Panthera tigris and lions Panthera leo J Zoo Wildl Med 201243248255 7 Rivas AE Langan JN Colegrove KM Terio K Adkesson MJ Herpesvirus and calicivirus infection in a blackfooted cat Felis nigripes J Zoo Wildl Med 20154611415 8 Schultz RD Duration of immunity for canine and feline vaccines a review Vet Microbiol 2006117 7579 9 Stiles J Townsend WM Rogers QR Krohne SG Effect of oral administration of Llysine on conjunctivitis caused by feline herpesvirus in cats Am J Vet Res 20026399103 10 Thomasy SM Lim CC Reilly CM Kass PH Lappin MR Maggs DJ Evaluation of orally administered famciclovir in cats experimentally infected with feline herpesvirus type1 Am J Vet Res 2011728595 11 Thomasy SM Schull O Outerbridge CA Lim CC Freeman KS Strom AR Kass PH Maggs DJ Oral administration of famiciclovir for treatment of spontaneous ocular respiratory or dermatologic disease attributed to feline herpesvirus type 1 59 cases 20062014 J Am Vet Med Assoc 2016249552638 12 Thomasy SM Whittem T Bales JL Ferrone M Stanley SD Maggs DJ Pharmacokinetics of penciclovir in healthy cats following oral administration of famciclovir or intravenous infusion of penciclovir Am J Vet Res 20127310921099 13 Summers SC RuchGallie R Hawley JR Lappin MR Effect of modified live or inactivated feline herpesvirus1 parenteral vaccines on clinical and laboratory findings following viral challenge J Feline Med Surg 2017198824830 14 Wack RF Kramer LW Cupps W Clawson S Hustead DR The response of cheetahs Acinonyx jubatus to routine vaccination J Zoo Wildl Med 199324109117 15 Witte CL Lamberski N Rideout BA Fields V Teare CS Barrie M Haefele H Junge R Murray S Hungerford LL Development of a case definition for clinical feline herpesvirus infection in cheetahs Acinonyx jubatus housed in zoos J Zoo Wildl Med 201344363444 16 Witte CL Lamberski N Rideout BA Vaida F Citino SB Barrie MT Haefele HJ Junge RE Murray S and Hungerford LL Epidemiology of clinical feline herpesvirus infection in zoohoused cheetahs Acinonyx jubauts J Am Vet Med Assoc 20172518 946956 American Association of Zoo Veterinarians Infectious Disease Manual FIBROPAPILLOMATOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Sea turtles especially green sea turtles Unknown viral etiology water bourne direct contact and Ozobranchus leech are suspected Horizontal transmission experimentally proven Masses on the skin and viscera Depends on location of nodules and immune function Morbidity can reach 92 Mortalities can reach 88 Supportive care surgical debridement debulking euthanasia None in captivity quarantine affected individuals No Fact Sheet compiled by Catherine Hadfield Sheet completed on 8 April 2011 updated 5 July 2013 Fact Sheet Reviewed by Leigh Ann Clayton Lawrence Herbst Craig Harms Susceptible animal groups Predominantly green turtles Chelonia mydas are affected However Kemps and olive Ridley Lepidochelys kempii and L olivacea and loggerhead sea turtles Caretta caretta also may be Rarely hawksbill turtles Eretmochelys imbricata have been affected The problem has not been reported in leatherback sea turtles Dermochelys coriacea Causative organism An alphaherpesvirus chelonid fibropapillomaassociated herpesvirus CFPHV consistently is detected and lesions can be transmitted using cellfree tumor extracts but the virus has not been isolated in culture Virus types appear to cluster based on geographic origin rather than host species western Atlantic Florida Barbados recently reported from Texas Atlantic Puerto Rico recently reported from Gulf of Guinea midwestPacific Hawaii Australia Indonesia and eastern Pacific Costa Rica California It is possible that other viruses such as tornovirus retroviruses and reoviruses are involved Changes in the environment coinfections or ecological factors affecting disease expression or virus transmission are likely causes for the recent emergence of FP epizootics at multiple locations around the world Zoonotic potential None Distribution Worldwide but primarily circumtropical Prevalence of disease varies with location 0 92 It may be associated with eutrophic coastal ecosystems with high human population densities and agricultural runoff The issue was first documented in the 1930s Reported increase in prevalence in the late 1950s especially in specific areas such as the Florida Keys and Indian River Lagoon Florida and Hawaii Prevalence seems to be decreasing in Hawaii while increasing in other regions Incubation period Clinically apparent FP developed 15 43 weeks after experimental inoculation Initiation of tumor growth was positively correlated with water temperature Inoculated turtles developed antibodies to CFPHV in 1 year if they developed tumors Turtles that did not develop tumors did not seroconvert Clinical signs Whitegreyblack nodules 01 to 30 cm diameter focal or multifocal often involving the head neck and limbs develop as fibropapillomas Internal nodules fibromas are less common Many fibropapillomatous lesions will resolve spontaneously Number and severity may increase with curved carapace length CCL then decrease as CCL increases further When tumors are numerous or large in size they may impinge on function of affected structures which leads to progressive debilitation and death Larger or ulcerated masses often have secondary infections Postmortem gross or histologic findings Fibropapillomas are raised sessile or polypoid masses with American Association of Zoo Veterinarians Infectious Disease Manual FIBROPAPILLOMATOSIS verrucous or smooth surfaces Internal tumors can be found on the heart lungs liver gall bladder kidneys skeletal muscle and gastrointestinal tract and are generally described as fibromas myxofibromas and fibrosarcomas of lowgrade malignancy Common histologic descriptions include vacuolation of the cytoplasm balloon degeneration of epidermal cells and benign papillary epidermal hyperplasia especially in the stratum spinosum occurring on thick stalks of proliferating fibrovascular stroma characterized by disorganized collagen fibers Perivascular mononuclear cell inflammation is often observed in the deeper layers of the dermis Diagnosis Clinical diagnosis is usually based on presence of skin or oral masses consistent in appearance with fibropapillomas Endoscopy laparoscopy radiography ultrasonography MRI and coeliotomy can be useful diagnostic modalities for identifying visceral tumors Definitive diagnosis requires compatible histopathology findings Further support of a diagnosis occurs if intralesional DNA of CFPHV are detected by polymerase chain reaction PCR from tissue obtained from tumors In situ hybridization ISH can be used to detect CFPHV in nuclei of infected epithelial cells Material required for laboratory analysis Formalinfixed tissue for histology and frozen tissue for PCR Relevant diagnostic laboratories All histopathology laboratories can assess tissues for compatible lesions Herpesviral PCR and sequencing is available at the University of Florida and HubbsSeaWorld Research Institute Treatment Supportive care appropriate temperature good water quality low stocking density fluid therapy adequate nutrition and as needed systemic antibiotics The lesions may be excised surgically laser surgery followed by second intention healing is usually recommended Controlled studies on improved outcomes are lacking Acyclovir has been found anecdotally to be useful Tumors on and around the eyes are most important to remove Turtles with internal tumors may require euthanasia Prevention and control Currently no prevention and control measures for wild populations are available In captivity fibropapillomatous turtles should be quarantined from unaffected turtles including by a separate water system Some turtle rehabilitation centers will not accept turtles affected by fibropapillomas Suggested disinfectant for housing facilities Standard disinfectants effective for herpesviruses should be effective against CFPHV Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Unaffected individuals should not be introduced to affected turtles Conditions for restoring diseasefree status after an outbreak None known It is probable that affected turtles are CFPHV carriers for life Experienced marine turtle rehabilitation facilities consider release of animals if they remain tumorfree for one year after surgical removal although sufficient longterm housing is rarely available in large stranding events to accommodate this approach Experts who may be consulted Alonso Aguirre DVM MS PhD Executive Director SmithsonianMason School of Conservation VA 540 6350461 aaguirr3gmuedu Larry Herbst DVM PhD Professor Department of Pathology and Department Of Microbiology Immunology Institute for Animal Studies Albert Einstein College of Medicine NY American Association of Zoo Veterinarians Infectious Disease Manual FIBROPAPILLOMATOSIS 718 8397135 lawrenceherbsteinsteinyuedu Thierry Work MS DVM USGS NWHCHFS Honolulu HI 808 792 9520 Thierryworkusgsgov UF Diagnostic Lab Tissue PCR for herpesvirus notify laboratory before shipping for submission forms and parameters use ice packs or dry ice via FedEx UPS or DHL Costs July 2013 10000testsample Turnaround time is 23 weeks httplabsvetmedufledusamplerequirementsmicrobiologyparasitologyserologyzoomedinfections April Childress University of Florida College of Veterinary Medicine 2015 SW 16th Ave Building 1017 Room V2238 Gainesville FL 32608 352 294 4420 ChildressAufledu References 1 Aguirre AA and PL Lutz 2004 Marine turtles as sentinels of ecosystem health is fibropapillomatosis an indicator Ecohealth 1 275283 2 Balazs GH and SG Pooley eds 1991 Research plan for marine turtle fibropapilloma NOAA US Dept Commerce Honolulu HI 110 pp 3 Chaloupka M GH Balazs and TM Work 2009 Rise and fall over 26 years of a marine epizootic in Hawaiian green sea turtles J Wildl Dis 45 11381142 4 Croft LA JP Graham SA Schaf and ER Jacobson 2004 Evaluation of magnetic resonance imaging for detection of internal tumors in green turtles with cutaneous fibropapillomatosis J Am Vet Med Assoc 9 14281435 5 Duarte A P Faisca NS Loureiro R Rosado S Gil N Pereira and L Tavares 2012 First histological and virological report of fibropapilloma associated with herpesvirus in Chelonia mydas at Principe Island West Africa Arch Virol 157 11551159 6 Ene A M Su S Lemaire C Rose S Schaff R Moretti J Lenz and LH Herbst 2005 Distribution of chelonid fibropapillomatosis associated herpesvirus variants in Florida molecular genetic evidence for infection of turtles following recruitment to neritic developmental habitats J Wildl Dis 41 489 497 7 Fei Fan Ng T C Manire K Borrowman T Langer L Ehrhart and M Breitbart 2009 Discovery of a novel singlestranded DNA virus from a sea turtle fibropapilloma by using viral metagenomics J Virol Mar 25002509 8 Foley AM BA Schroeder AE Redlow KJ FickChild and WG Teas 2005 Fibropapillomatosis in stranded green turtles Chelonia mydas from the eastern United States 198098 trends and associations with environmental factors J Wildl Dis 41 2941 9 Guimaraes dos Santos R AS Margins E Torezani C Baptistotte J Farias PA Horta TM Work GH Balazs 2010 Relationship between fibropapillomatosis and environmental quality a case study American Association of Zoo Veterinarians Infectious Disease Manual FIBROPAPILLOMATOSIS with Chelonia mydas off Brazil Dis Aquat Org 89 8795 10 Guimaraes SM HM Gitirana AV Wanderley C MonteiroNeto and GL Hajdu 2013 Evidence of regression of fibropapillomas in juvenile green turtles Chelonia mydas caught in Niteroi southeast Brazil Dis Aquat Org 102 243247 11 Herbst LH EC Greiner LM Ehrhart DA Bagley and PA Klein 1998 Serological association between spirorchidiasis herpesvirus infection and fibropapillomatosis in green turtles from Florida J Wildl Dis 34 496507 12 Herbst LH ER Jacobson R Moretti T Brown JP Sundberg and PA Klein 1995 Experimental transmission of green turtles fibropapillomatosis using cellfree tumor extracts Dis Aquat Org 22 1 12 13 Kang KI FJ TorresVelez J Zhang PA Moore DP Moore S Riverax and CC Brown 2008 Localization of fibropapillomaassociated turtle herpesvirus in green turtles Chelonia mydas by in situ hybridization J Comp Path 139 218225 14 Murakawa SKK and GH Balazs eds 2009 Bibliography of fibropapillomas in marine turtles NOAA US Dept Commerce Honolulu HI 47 pp httpwwwturtlesorgFIBROBIBLIO20091108pdf Accessed 2 August 2013 15 Patricio AR LH Herbst A Duarte X VeleezZuazo N Loureiro N Pereira L Tavares and GA Toranzos 2012 Global phylogeography and evolution of chelonid fibropapillomaassociated herpesvirus J Gen Virol 93 10351045 16 Tristan T DJ Shaver J Kimbro T deMaar T Metz J George and A Amos 2010 Identification of fibropapillomatosis in green sea turtles Chelonia mydas on the Texas coast J Herp Med Surg 20 109112 American Association of Zoo Veterinarians Infectious Disease Manual HERPESVIRUS B Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Macaques other non human primates humans Bites scratches fomites saliva or bodily fluids mucosal absorption possible laboratory transmission ie needle puncture Macaques generally intermittent mucosal pustules Non macaque species Sometimes are herpeslike mucosal lesions are associated with the point of infection Most cases present with fever and encephalitis manifesting neurologic signs including dsyphagia ataxia confusion paresthesia and paralysis Non macaque species Without treatment it is very fatal 70 80 Some patients continue to have neurologic sequelae after recovery Antivirals such as ganciclovir valacyclovir and famciclovir Many patients opt to remain on drugs for years after initial infection Personal protective equipment including gowns or coveralls gloves goggles and a mask or respirator Yes Fact Sheet compiled by Melinda Rostal Sheet updated on 3 May 2011 updated 30 October 2012 Fact Sheet Reviewed by Richard Eberle Jan Ramer Susceptible animal groups The disease occurs naturally in all macaques Humans and other nonhuman primates are susceptible Causative organism Macacine herpesvirus 1 also called herpes B virus or B virus Zoonotic potential Yes Distribution All reported cases in humans have been people that work with captive macaques or have been exposed in the field Macaques are usually asymptomatic and may have been seronegative at the last screening or even at the time of the exposure prior to seroconversion One report of human infection from Vietnam has been documented otherwise no cases from individuals has been reported in Asia in areas that macaques inhabit Incubation period 2 days to 23 weeks usually 58 days Two cases were reported where the patient had no previous exposure to macaques or exposure had occurred over 10 years previously Clinical signs Macaques 80100 of sexually mature macaques especially if they have contact with other macaques are seropositive for B virus They rarely have clinical signs indicating infection or recrudescence however they will occasionally have herpeslike skin mucosal pustules Research on shedding frequency is inconclusive although it increases during periods of stress including the breeding season Humans Sometimes there are herpeslike skinmucosal lesions associated with the point of infection accompanied by pain and itching and erythema Most cases present with fever and encephalitis manifesting in neurologic signs including dsyphagia ataxia confusion paresthesia and paralysis Latency is established American Association of Zoo Veterinarians Infectious Disease Manual HERPESVIRUS B and reactivation can occur Post mortem gross or histologic findings Macaques Most often histological evidence of acute infection is present without gross pathology The virus often remains latent in the trigeminal or sacral nerve ganglia from which culture or PCR may be used to detect the virus If oral or genital lesions are present there may be vesicle formation with leukocytic invasion of the area when keratinized cells overlying the vesicle slough a plaque of necrotic fibrinous material remains overlying the base of the ulcer Intranuclear inclusions can be seen in tissues showing recent signs of degeneration Humans Few reports of histological findings have been documented Inclusion bodies are not typically found Reported findings include severe inflammatory and degenerative changes in the spinal cord particularly in the cervical cord and brainstem the thalamus and hypothalamus may also be infected Diagnosis B virus antibody ELISA or B virus recombinant ELISA assays are used A negative antibody titer does not indicate the animal is not infected only that it is not currently producing antibioties Rising titers may be associated with viral shedding period Diagnosis is often based on Western blot or virus neutralizing antibodies as well as virus isolation PCR has been developed as well Material required for laboratory analysis For serology 0520 ml serum in plastic tube Store and ship at 20ºC or with dry ice For virology Swabs of vesicle or other lesions Place swab in 12 ml viral transport media store at 80ºC CSF autopsy samples of brainstem biopsies from the site of inoculation place in plastic storageshipment tubes Ship samples on dry ice according to US Department of Transportation regulations Relevant diagnostic laboratories B virus is a BSL 4 agent B Virus Research and Resource Laboratory Dr Julia Hilliard Georgia State University Viral Immunology Center 161 Jesse Hill Jr Dr Atlanta GA 303024118 jhilliardgsuedu For emergency 404 3588168 Enteric Respiratory and Neurological Virus Laboratory Dr David Brown Central Public Health Laboratory 61 ColindaleA ve London NW9 5HT England dbrownphlsorguk Virus Reference Laboratory nonhuman primates only VRL San Antonio 7540 Louis Pasteur Dr Ste 200 San Antonio Texas 78229 210 6147350 AnthonyCookevrlnet Treatment Non macaques Antivirals are used to attempt to control or prevent encephalitis Recommended medications include ganciclovir valacyclovir and famciclovir Many patients must remain on antivirals for years after exposure FEAU 2fluoro5ethylAraU is a new antiviral that appears effective in cell culture but has not been used in a human case Prevention and control All macaques need to be treated as B virusinfected Due to the severity of American Association of Zoo Veterinarians Infectious Disease Manual HERPESVIRUS B infection with B virus in humans the US Centers for Disease Control and Prevention CDC developed guidelines to prevent B virus in workers handling macaques httpwwwcdcgovmmwrpreview mmwrhtml00015936htm The most recently updated version of these recommendations was given in 2002 by the B Virus Working Group The recommendations are briefly outlined below Personnel must wear appropriate personal protective equipment including glasses and faceshields masks long sleeve protecting clothing and nitrile or latex gloves If the animal is not sedated leather gloves extending to the shoulder should be used Personnel must be trained in the associated risks of infection and appropriate response protocols Upon possible exposure the person should immediately wash the wound or lavage the mucous membrane exposed for 15 minutes Collect baseline serum and culture samples from the person and the macaque Starting prophylaxis with an antiviral within 24 hours is recommended if the case meets one of the following criteria o Exposure of mucosa or injured skin to an ill or immunocompromised or shedding macaque o Exposure of mucosa or injured skin that is not adequately cleaned o Laceration is of the head neck or torso o Deep puncture bite or a needle puncture associated with macaque CSF fluid herpeslike lesions eyelids or mucosa o A postcleaning culture of wound is positive for B virus o A laceration is caused by an object contaminated by macaque mucosal genital or saliva secretions Prophylaxis with an antiviral should be considered if the case meets one of the following criteria o Exposure of mucosa or injured skin that has been adequately cleaned o A needles puncture was associated with blood from an ill or immunocompromised macaque o Skin that was recently exposed to contaminated macaque body fluid or cell culture has been lacerated Suggested disinfectant for housing facilities Macaque housing should be cleaned with hot water and detergent by staff utilizing appropriate PPE such as masks and face protection while cleaning Currently efforts are underway to create specific pathogen free SPF colonies of macaques and some groups has successfully maintained populations of macaques that are 993 free of B virus for longer than 7 years This process involves initially keeping the macaques isolated and culling seropositive animals No current recommendations for disinfecting housing facilities are available since in seropositive populations the virus tends to be ubiquitous and in SPF populations positive animals should be culled All macaques should be treated as if positive for B virus Research is also underway to create a B virus vaccine for macaques Notification B virus has been a CDC Select Agent however as of 4 December 2012 it is no longer a select agent B virus infections are not reportable on a national level although states may vary in their reporting requirements Measures required under the Animal Disease Surveillance Plan This virus is not listed under Annex A or B Measures required for introducing animals to an infected animals If a seronegative animal is introduced to a seropositive animal it should be expected that the animal will seroconvert eventually especially after the onset of sexual maturity SPF colonies must cull seropositive animals and closely monitor cagemates to prevent the virus from becoming established in the colony Conditions for restoring diseasefree status after an outbreak No specific standards exist at this time however it is recommended to test the animals for antibodies one month apart and again following a time American Association of Zoo Veterinarians Infectious Disease Manual HERPESVIRUS B period of greater than 6 months but less than 12 months Experts who may be consulted Dr Julia Hilliard Georgia State University PO Box 4118 Atlanta GA 303024118 jhilliardgsuedu For emergency 404 3588168 References 1 CDC 1987 Guidelines for prevention of herpesvirus simiae B virus infection in monkey handlers MMWR 36 680682 687689 2 Cohen J D Davenport J Stewart S Deitchman H JK and Chapman 2002 Recommendations for prevention of and therapy for exposure to B virus cercopithecine herpesvirus 1 Clin Infect Dis 35 11911203 3 Elmore D and R Eberle 2008 Monkey B virus Cercopithecine herpesvirus 1 Comp Med 58 11 22 4 Hilliard JK and JA Ward 1999 B virus specific pathogenfree breeding colonies of macaques Macaca mulatta retrospective study of seven years of testing Lab Anim Sci 49 144148 American Association of Zoo Veterinarians Infectious Disease Manual HERPESVIRUS HOMINIS TYPES 1 AND 2 Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Predominantly affects humans but can cause disease in NHP Aotidae Callitrichidae Cebidae Hylobatidae Lemuridae Pongidae Scandentia Direct contact or airborne Mostly asymptomatic but can result in recurrent rhinitis labial herpes lingual plaquesulcers rhinitis nasal discharge conjuctivitis salivation ataxia ulcerative dermatitis death Fatal disease in Cebidae Callitrichidae and tree shrews Rarely fatal in Pongidae Acyclovir valacyclovir Avoid contact with humans with active herpes lesions Zooanthro ponotic disease Fact Sheet compiled by Sam Rivera updated by Jan Ramer Sheet completed on 1 June 2011 updated 23 July 2013 Fact Sheet Reviewed by Sam Rivera Kevin Brunner Susceptible animal groups Aotidae Callitrichidae Cebidae Hylobatidae Lemuridae Pongidae Scandentia Causative organism Herpesvirus hominis types 1 and 2 Zoonotic potential Zooanthroponotic disease Distribution Worldwide Incubation period In NHP 214 days after experimental infection Clinical signs In great apes oral and pharyngeal vesicles and ulcers vesicles on the lips and nose conjunctival lesions pustules vesicles andor ulcerated lesions of the genitalia listlessness anorexia Infant great apes diarrhea vomiting dyspnea vesicles death Other NHP conjunctival oral and cutaneous lesions vesicles to ulcers rhinitis keratitis weakness depression anorexia excessive salivation nasal discharge myoclonus ataxia seizures Peracute death has been seen in callitrichids Post mortem gross or histologic findings Multifocal vesicular and necrotizing dermatitis face arms chest legs gingivitis and stomatitis hepatomegaly with mottling congestion or necrotic foci splenomegaly with congestion pulmonary edema lymphadenopathy ocular lesions conjunctivitis blepharitis ulcers adrenal enlargement necrosis or hemorrhage CNS lesions edema hemorrhage focal softening and necrosis congested meninges multifocal meningoencephalitis in gibbons with multifocal nonsuppurative perivascular cuffing necrosis and gliosis and Cowdry type A intranuclear inclusions in spleen and liver Diagnosis Serology virus isolation PCR insitu hybridization histopatology Material required for laboratory analysis Material from vesicles or other lesion serum or whole blood Relevant diagnostic laboratories Pathogen Detection Laboratory California National Primate Research Center Road 98 Hutchison University of California Davis California 95616 American Association of Zoo Veterinarians Infectious Disease Manual HERPESVIRUS HOMINIS TYPES 1 AND 2 530 7528242 Fax 530 7524816 PDLprimateucdavisedu httppdlprimateucdavisedu BioReliance SerologyPCR Laboratories 14920 Broschart Rd Rockville Maryland 20850 301 6102227 310 6102587 ahsbioreliancecom Virus Reference Laboratories Inc 7540 Louis Pasteur Road San Antonio Texas 78229 877 6157275 Fax 210 6157771 Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 913113800 8187178880 8187178881 infozoologixcom Treatment Acyclovir valacyclovir Prevention and control Avoid contact with humans with active herpes lesions In owl monkeys a modified live vaccine has been shown to be protective Suggested disinfectant for housing facilities Lipid solvents soap UVlight heat Notification None at this time Measures required under the Animal Disease Surveillance Plan None at this time Measures required for introducing animals to infected animal Keep susceptible species away from known positive NHP Conditions for restoring diseasefree status after an outbreak Many NHP antibodypositive latent infections possible so exposure and disease free status is difficult Experts who may be consulted ChihLing Zao PhD Chief Scientific Officer VRL Laboratories PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 Phone 8776157275 Fax 2106157771 chihlingzaovrlnet American Association of Zoo Veterinarians Infectious Disease Manual HERPESVIRUS HOMINIS TYPES 1 AND 2 References 1 httpwwwprimateportalorg Accessed 6 August 2013 2 httpwildprotwycrosszooorgListVolsGreatApesViralHerpesSimplexHerpesSimplexInfHerpes SimplexInfhtm Accessed 6 August 2013 3 Bennett T C Abee and R Henrickson eds 1998 Nonhuman Primates in Biomedical Research Diseases Academic Press San Diego California 512 pp 4 Maria J L J H Bos J Groen and G M Dorrestein 2005 Herpes simplex infection in a juvenile orangutan Pongo pygmaeus pygmaeus J Zoo Wildl Med 36 1 131134 5 OttJoslin JE 1993 Zoonotic diseases of nonhuman primates In Fowler ME ed Zoo Wild Animal Medicine Current Therapy 3 WB Saunders Co Philadelphia Pennsylvania Pp 358373 6 Voevodin AF and PA Marx eds 2009 Simplexviruses In Simian Virology WilleyBlackwell Ames Iowa Pp 267293 American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN VARICELLA VIRUS CEROPITHECINE HERPESVIRUS 6 7 9 AND VARICELLAZOSTER VIRUS HUMAN HERPESVIRUS 3 Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Varicella zoster virus VZV affects man and Pongidea Simian Varicella Virus SVV affects African and Asian NHP Direct contact inhalation of aerosolized virus VZV chickenpox or zoster in NHP SVV generalized vesicular eruptions hyperthermia Rarely a fatal disease Severity depends on age and immune competency Acyclovir Vidarabine mono phosphate Foscarnet and other antivirals Avoid contact between humans with chickenpox Zoster and nonhuman primates Isolate affected NHP Not reported as a zoonotic disease Fact Sheet compiled by Sam Rivera updated by Jan Ramer Sheet completed on 1 June 2011 updated 23 July 2013 Fact Sheet Reviewed by Sam Rivera Kevin Brunner Susceptible animal groups VZV Pongidae SVV Old world NHP apes and humans Causative organism Simian varicella virus Ceropithecine herpesvirus 6 7 and 9 Varicellazoster virus Human herpesvirus 3 Zoonotic potential Not reported Distribution Simian Varicella Viruses occur naturally in Africa and Asia and are found worldwide in captive populations Human VaricellaZoster Virus is found worldwide Incubation period VZV 714 days SVV 1015 days Clinical signs VZV In Pongidae pruritic pustulovesicular rash conjunctivitis fever anorexia lethargy lymphadenopathy coughing and sneezing can be observed Zoster with severe axillary and thoracic cutaneous ulceration was reported in an elderly gorilla with concurrent immunosuppressive disease SVV generalized vesicular rash mild fever anorexia lethargy vesiculoulcerative dermatitis is observed Although rarely a fatal disease high fatality within 48 hours has been reported in natural outbreaks Post mortem gross or histologic findings VZV in Pongidae occasionally chickenpoxlike disease or oralperioral vesicles SVV vesiculoulcerative lesions of the skin and oral mucous membranes hemorrhages and necrosis in internal organs Diagnosis Serology virus isolation PCR EM Material required for laboratory analysis Vesicular material whole blood or serum Relevant diagnostic laboratories Pathogen Detection Laboratory California National Primate Research Center Road 98 Hutchison University of California Davis California 95616 530 7528242 Fax 530 7524816 PDLprimateucdavisedu American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN VARICELLA VIRUS CEROPITHECINE HERPESVIRUS 6 7 9 AND VARICELLAZOSTER VIRUS HUMAN HERPESVIRUS 3 httppdlprimateucdavisedu BioReliance SerologyPCR Laboratories 14920 Broschart Rd Rockville Maryland 20850 301 6102227 310 6102587 ahsbioreliancecom Virus Reference Laboratories Inc 7540 Louis Pasteur Road San Antonio Texas 78229 877 6157275 Fax 210 6157771 Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 913113800 8187178880 8187178881 infozoologixcom Treatment VaricellaZoster immunoglobulins acyclovir famcyclovir valacyclovir trifluridine vidarabine monphosphate foscarnet Prevention and control Avoid contact between humans with chickenpox or zoster and NHP Suggested disinfectant for housing facilities Organic solvents detergents proteases UVlight heat Notification None at this time Measures required under the Animal Disease Surveillance Plan None at this time Measures required for introducing animals to infected animal Selflimiting disease animals can be introduced once skin lesions heal Conditions for restoring diseasefree status after an outbreak Selflimiting disease Experts who may be consulted ChihLing Zao PhD Chief Scientific Officer VRL Laboratories PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 Phone 8776157275 Fax 2106157771 chihlingzaovrlnet References 1 httpwwwprimateportalorg Accessed 6 August 2013 2 httpwildprotwycrosszooorgListVolsGreatApesViralVaricella American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN VARICELLA VIRUS CEROPITHECINE HERPESVIRUS 6 7 9 AND VARICELLAZOSTER VIRUS HUMAN HERPESVIRUS 3 ZosterChickenpoxVaricellaChickenpoxVaricellahtmControl Accessed 6 August 2013 3 Bennett T C Abee and R Henrickson eds 1998 Nonhuman Primates in Biomedical Research Diseases Academic Press San Diego California 512 pp 4 Lerche N W 2005 Common viral infections of laboratory primates In WolfeCoote S ed The Handbook of Experimental Animals The Laboratory Primate Elsevier Academic Press San Diego California Pp 7589 5 Masters N H Niphuis E Verschoor J Breuer M Quinlivan T Wawrzynczyk and M Stidworthy 2010 Debilitating clinical disease in a wildborn captive western lowland gorilla Gorilla gorilla gorilla coinfected with varicella zoster Virus VZV and Simian Tlymphotropic virus STLV J Zoo Wildl Med 41713716 6 Myers MG and BL Connelly 1992 Animal models of varicella J Infect Dis 166Suppl 1S48 S50 7 OttJoslin JE 1993 Zoonotic diseases of nonhuman primates In Fowler ME ed Zoo Wild Animal Medicine Current Therapy 3 WB Saunders Co Philadelphia Pennsylvania Pp 358373 8 Voevodin AF and PA Marx eds 2009 Varicelloviruses In Simian Virology WilleyBlackwell Ames Iowa Pp 295307 American Association of Zoo Veterinarians Infectious Disease Manual INFECTIOUS BOVINE RHINOTRACHEITIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Ruminants cattle goats sheep swine red deer American and Malaysian buffalo and Brazilian tapirs Direct contact or aerosolization of viral particles from an infected animal It also is transmitted sexually and via artificial insemination Infection may become latent and can reoccur with stress resulting in viral shedding Decreased milk production Upper respiratory disease conjunctivitis corneal disease and panophthalmitis and reproductive neurologic and gastrointestinal signs Encephalitis in calves Mild to severe depending on secondary bacterial invasion No treatment for the virus itself but supportive care should be provided Antibiotics in the feed and water are used to treat the secondary bacterial infections Vaccination isolation or removal of affected individuals and young until fully vaccinated decrease stress Use of a marker vaccine is helpful for screening IBR is eradicated in 6 countries is possible in others No Fact Sheet compiled by Christie Hicks Sheet completed on updated 5 February 2018 Fact Sheet Reviewed by AJ Marlar Susceptible animal groups Ruminants especially cattle goats swine red deer Malaysian buffalo and Brazilian tapirs Young animals at weaning age and those in crowded conditions are especially susceptible However the disease does occur in adult animals especially nonvaccinated pregnant ruminants Causative organism Bovine Herpesvirus 1 an alphaherpesvirus Zoonotic potential None Distribution Worldwide distribution is considered present Eradication is being attempted in several western European countries Incubation period 2 to 6 days Outbreaks reach a maximum intensity by the 2nd to 3rd week with mostly all recovered by the 4th to 6th week Uncomplicated BHV1 IBR can resolve in 4 to 5 days if no secondary infections are present Clinical signs An early sign is a decrease in milk production Respiratory signs include coughing serous to mucopurulent nasal discharge Ophthalmic signs include conjunctivitis with an ocular discharge and corneal opacity or panophthalmitis Red Nose muzzle hyperemia respiratory distress due to discharges salivation anorexia and pyrexia may also be seen Secondary infections are possible and can lead to a bronchopneumonia Neonates may present with generalized infection similar to a septicemia enteritis andor encephalitis IBR has been associated with a high mortality rate in calves 1 month of age with no preceding signs Mid to lateterm abortions can occur up to 100 days post exposure with infection of the dam and genital tract infections occurring Infertility and birth defects have also been seen Subclinical infections can occur Post mortem gross or histologic findings Within the upper respiratory tract and trachea petechial to ecchymotic hemorrhages are observed in the mucous membranes of the nasal cavity and paranasal sinuses Focal areas of necrosis are present in the nose pharynx larynx and trachea which may join together to form plaques The sinuses can be filled with a serous to a serofibrinous exudate that may extend into the pharynx The pharyngeal and pulmonary lymph nodes may become swollen and hemorrhagic If the tracheitis extends into the bronchi and bronchioles the epithelium can be sloughed into the airways Nasal lesions consist of clusters of gray necrotic foci on the mucous membranes of the septal mucosa andor with pseudodiphtheritic American Association of Zoo Veterinarians Infectious Disease Manual INFECTIOUS BOVINE RHINOTRACHEITIS yellow plaques Aborted fetuses have multifocal nonraised white lesions throughout the liver Placentitis is occasionally seen Diagnosis For acute cases PCR may be performed A serum neutralization test can be used with paired serum antibody titers at least 2 weeks apart except in abortion cases as the titer is already at its highest level ELISA for an antibody titer with a concurrent rise is available but also indirect hemagglutination and complement fixation serology as well Virus isolation via nasal fluids at the early onset of disease is possible Gross lesions at necropsy and histopathology Immunoperoxidase virus isolation and fluorescent antibody staining on fetal tissues can also be performed in abortion cases Patients with corneal lesions would require ruling out malignant catarrhal fever infectious bovine keratoconjunctivitis Moraxella bovis and squamous cell carcinoma Material required for laboratory analysis Nasal fluids serum plasma milk placenta andor tissues for example the liver Relevant diagnostic laboratories Any state laboratory can perform the testing Treatment While no treatment for the virus itself exists one may treat for secondary bacterial infections with antibiotics and supportive care Most cases recover in 4 to 5 days if secondary infections are not present Prevention and control Vaccination with a modified live vaccine MLV given parenterally SC or IM or IN is possible MLV given IM during pregnancy may cause abortions especially in the third to eighth months of gestation therefore a MLV is best administered twice before breeding with the second administration occurring 30 days prior to prebreeding and the next vaccination within 12 months afterwards The MLV is also not safe for nursing calves unless the dam has been vaccinated within the last year and at prebreeding with the same vaccine Vaccinating with an inactivated multivalent vaccine given SC or IM will protect against abortions if given prior to breeding The use of the IN vaccine may be helpful for a local rapid immune response in those that are already pregnant and may prevent new cases in an outbreak as long as the individuals vaccinated are not showing any clinical symptoms at the time of IN vaccination For control it is important to vaccinate at 6 to 8 months of age or 2 to 3 weeks before weaning before introduction into the herd prior to breeding and annually thereafter Quarantine all new individuals 4 weeks after arriving with testing for IBR before arrival and before entrance into the herd Eradication can be attempted by screening all individuals that are at least 1 year of age and removing any seropositive reactors this process should continue annually The best way to differentiate between the natural virus versus a vaccine titer is to use ELISA to test for Glycoprotein E gE gE is present in natural infections however newer marker vaccines have deleted gE from their makeup Caution must be used as conventional vaccines still contain gE and can cause a false seropositive result Currently IBR is eradicated in Austria Denmark Finland Sweden Switzerland and Norway Suggested disinfectant for housing facilities As an enveloped virus it can be managed by lipid solvents bleach and hydrogen peroxides This virus is also inactivated by UV light and heat Notification No Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal A period of 23 weeks after the illness starts should be waited before introducing any new individuals into the herd Viral particles can still be seen in nasal secretions throughout this time All new arrivals into the herd must be vaccinated prior to entry and then revaccinated in 3 months and again at 6 months Conditions for restoring diseasefree status after an outbreak Serologic testing to detect any seropositive individuals Removal of these individuals andor creating 2 separate herds The animals that fully recover from this disease will have longterm immunity to future outbreaks Experts who may be consulted Any state veterinarian References American Association of Zoo Veterinarians Infectious Disease Manual INFECTIOUS BOVINE RHINOTRACHEITIS 1 Andrews AH Respiratory Diseases In Andrews AH Blowey RW Boyd H Eddy RG eds Bovine Medicine Diseases and Husbandry of Cattle 2nd Edition Oxford UK Blackwell Science Ltd 2004 p 289293 2 Ardans A Herpesviridae In Hirsh DC MacLachlan NJ Walker RL eds Veterinary Microbiology 2nd Edition Ames IA Blackwell Publishing Professional 2004 p 323325 3 Furtado MM Jácomo AT Kashivakura CK Tôrres NM Marvulo MF Ragozo AM Pereira de Souza SL Neto JS Vasconcellos SA Morais ZM Cortez A Richtzenhain LJ Silva JC Silveira L Serologic survey for selected infectious diseases in freeranging Brazilian tapirs Tapirus terrestris in the Cerrado of Central Brazil J Zoo Wild Med 201041133136 4 Kahn C Line S eds Infectious Bovine Rhinotracheitis In The Merck Veterinary Manual 9th Edition Whitehouse Station NJ Merck Co Inc 2005 p 11931195 5 Kahn C Line S eds Infectious Bovine RhinotracheitisBovine Herpesvirus In The Merck Veterinary Manual 10th Edition Whitehouse Station NJ Merck Co Inc 2010 p 1226 1321 1322 6 Pasquini C Pasquini S eds Guide to Bovine Clinics 3rd Edition Pilot Point TX Sudz Publishing 1996 p 62 and 252 7 The Cattle Site Internet Cattle Disease Guide Infectious Bovine Rhinotracheitis c20002014 cited 2018 February 5 Available from httpwwwthecattlesitecomdiseaseinfo174infectiousbovine rhinotracheitisibr 8 Troedsson MHT Christensen BW Diseases of the reproductive system In Smith BP ed Large Animal Internal Medicine 4th Edition St Louis MO Mosby Elsevier 2009 p 14571459 9 Wolfe BA Bovidae Except Sheep and Goats and Antilocapridae In Miller RE Fowler ME eds Zoo and wild animal medicine Volume 8 Current therapy St Louis MO Elsevier 2015 p 638 10 Zimmerman AD Buterbaugh RE Herbert JM Hass JM Frank NE Luempert III LG Chase C Efficacy of bovine herpesvirus1 inactivated vaccine against abortion and stillbirth in pregnant heifers J Am Vet Med Assoc 2007 23113861389 11 Zoetis Internet Zoetis United States c2019 cited 2018 February 5 Available from httpwwwzoetisuscom American Association of Zoo Veterinarians Infectious Disease Manual KOI HERPESVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Fishes specifi ally members of the genus Cyprinus Horizontal and via fomites and possibly arthropod vectors Signs may be nonspecific but can include enophthalmia branchitis hemorrhagic gills branchial necrosis areas of skin depig mentation and blisters Mortality may reach 100 and frequently is over 80 None Strict biosecurity and quaran tine protocols should be followed based on information available through the OIE and USDA No Fact Sheet compiled by Gregory A Lewbart Sheet completed on 4 September 2013 Fact Sheet Reviewed by Denise Petty Thomas Waltzek Ruth FrancisFloyd Susceptible animal groups Carp and koi Cyprinus carpio with evidence that goldfish Carassius auratus and other cyprinids can be nonclinical carriers of the virus Causative organism Cyprinid herpesvirus3 Koi Herpesvirus or KHV Zoonotic potential None Distribution Global especially in temperate geographical areas except for Australia The disease was first identified in England 1996 Incubation period Incubation period varies depending on water temperature most cases are detected at 22o255oC Latent infections can likely persist for months or even years Arthropods such as the fish louse Argulus sp are likely vectors Clinical signs Clinical signs include but are not limited to lethargy enophthalmia depigmented areas and blisters of the body surface branchitis branchial hemorrhage branchial necrosis and high mortality Post mortem gross or histologic findings At necropsy affected fish may have generalized possibly sanguineous edema organ hemorrhage intestinal inflammation branchial hemorrhage branchial necrosis mottled organs and excessive abdominal adhesions Diagnosis Diagnosis can be made directly with viral isolation from spleen or caudal kidney on a susceptible cell line such as Koi Fin KF this technique usually requires sacrificial euthanasia Nonlethal direct methods utilizing polymerase chain reaction PCR that can be performed on blood gill tissue biopsies and feces Nonlethal indirect methods include enzymelinked immunosorbent assay ELISA and virus neutralization VN on blood but currently test is not available Positive indirect method samples only indicate that a fish has produced antibodies to the virus and may not or ever have been infected with KHV although this can vary by testing specificity Material required for laboratory analysis Live moribund fish are the best specimens for an accurate diagnosis Virus isolation from appropriate tissues is superior to PCR and the indirect methods abovementioned Relevant diagnostic laboratories Testing is available at various approved state and federal laboratories httpwwwaphisusdagovanimalhealthlabinfoservicesdownloadsApprovedLabsAquaculturepdf including PCR at httpwwwvetdnacomarchivekoiherpes Treatment None are effective or recommended American Association of Zoo Veterinarians Infectious Disease Manual KOI HERPESVIRUS Prevention and control Facilities holding and importing high risk cyprinid fishes should be diligent in following standard quarantine protocols and adhere to appropriate and periodic testingscreening as prescribed by the OIE and USDA A modified live vaccine called Cavoy Novartis Inc was approved for use on koi by the FDA in 2012 but the company is no longer distributing the vaccine Suggested disinfectant for housing facilities Disinfection protocol depends on the size type and nature of the materials and sites to be disinfected When an active outbreak of KHV is confirmed the infected stocks should be depopulated and all areas that held the infected fish must be disinfected The virus can survive in the environment for about 3 days but can be inactivated by sodium hypochlorite 200 ppm for 1 hour quaternary ammonium 500 ppm for 1 hour formalin ozone organic iodophors gamma and ultraviolet radiation pH extremes of 40 or 1000 and heating at 600 C for 15 minutes All equipment and tanks raceways and ponds should be disinfected USDA APHIS also recommends that incoming water to the farms be treated with sand filtration and UV Notification All suspect cases should be necropsied and USDA contacted for proper routing of diagnostic samples Confirmed cases must be reported to the USDA Measures required under the Animal Disease Surveillance Plan Once an infection is reported a facility has to follow the recommendations described in the International Aquatic Animal Health Code and the Diagnostic Manual for Aquatic Animal Diseases by OIE to be declared free of KHV In the US USDA recommendations must be followed Measures required for introducing animals to infected animal Not applicable Conditions for restoring diseasefree status after an outbreak See the OIE and USDA web sites for current information Periodic testing with negative results may be required A complete summary of the disease and diagnostic procedures may be found on the Office International des Epizooties OIE web site Experts who may be consulted References 1 Bergmann SM H Schutze U Fischer D Fichtner M Riechardt K Meyer D Schrudde and J Kempter 2009 Detection of koi herpes virus KHV genome in apparently healthy fish Bull Euro Assoc Fish Pathol 29 145152 2 Costes B V Stalin Raj B Michel G Fournier M Thirion L Gillet J Mast F Lieffrig M Bremont and A Vanderplasschen 2009 The major portal of entry of koi herpesvirus in Cyprinus carpio is the skin J Virol 83 28192830 3 Eide K T MillerMorgan J Heidel R Bildfell and L Jin 2011 Results of total DNA measurement in koi by tissue koi herpesvirus realtime PCR J Virol Meth 172 8184 4 ElMatbouli M M Saleh and H Soliman 2007 Detection of cyprinid herpesvirus type 3 in goldfish cohabiting with CyHV3infected koi carp Cyprinus carpio koi Vet Rec 161 792793 5 Gilad O S Yun KB Andree MA Adkison A Zlotkin H Bercovier A Eldar and RP Hedrick 2002 Initial characteristics of koi herpesvirus and development of a polymerase chain reaction assay to detect the virus in koi Cyprinus carpio koi Dis Aquat Organ 482 101108 6 Goodwin A 2012 Herpesviruses in fish Southern Regional Aquaculture Center SRAC publication No 4710 May 2012 7 pp 7 Gray WL L Mullis SE LaPatra JM Groff and A Goodwin 2002 Detection of koi herpesvirus DNA in tissues of infected fish J Fish Dis 25 171178 8 Hartman KH RPE Yanong DB Pouder BD Petty R FrancisFloyd AC Riggs and TB Waltzek 2013 Koi herpesvirus disease KHVD University of Florida Extension Fact Sheet VM 149 httpedisifasufleduvm113 Accessed 9 September 2013 9 Hedrick RP O Gilad S Yun JV Spangenberg GD Marty RW Nordhausen MJ Kebus H Bercovier and A Eldar 2000 A herpesvirus associated with mass mortality of juvenile and adult American Association of Zoo Veterinarians Infectious Disease Manual KOI HERPESVIRUS koi a strain of common carp J Aquat Anim Health 12 4457 10 Hedrick RP TB Waltzek and TS McDowell 2006 Susceptibility of koi carp common carp goldfish and goldfish x common carp hybrids to Cyprinid herpesvirus 2 and Cyprinid herpesvirus 3 J Aquat Anim Health 18 2634 11 Noga EJ 2010 Fish disease diagnosis and treatment WileyBlackwell Ames Iowa 536 pp 12 Office International des Epizooties 2013 Diseases listed by the OIE Aquatic Animal Health Code 15th Edition OIE Aquatic Animal Health Standards Commission Aquatic Animals Commission Office International des Epizooties Available wwwoieintengnormesfcodeensommairehtm Accessed 9 September 2013 13 Perelberg A M Smirnov M Hutoran A Diamant Y Bejerano and M Kotler 2003 Epidemiological description of a new viral disease afflicting cultured Cyprinus carpio in Israel Isr J Aquac Bamidgeh 55 512 14 Perelberg A M Ilouze M Kotler and M Steinitz 2008 Antibody response and resistance of Cyprinus carpio immunized with cyprinid herpes virus 3 CyHV3 Vaccine 26 37503756 15 Ronen A A Perelberg J Abramowitz M Hutoran S Tinman I Bejerano MSteinitz and M Kotler 2003 Efficient vaccine against the virus causing a lethal disease in cultured Cyprinus carpio Vaccine 2132 46774684 16 Shimizu T N Yoshida H Kasai and M Yoshimizu 2006 Survival of koi herpesvirus KHV in environmental water Fish Path 41 153157 17 StHilaire S N Beevers K Way RM Le Deuff P Martin and C Joiner 2005 Reactivation of koi herpesvirus infections in common carp Cyprinus carpio Dis Aquat Org 67 1523 18 StHilaire S N Beevers C Joiner RP Hedrick and K Way 2009 Antibody response of two populations of common carp Cyprinus carpio L exposed to koi herpesvirus J Fish Dis 32 311 320 19 Waltzek TB and RP Hedrick 2003 Koi Herpesvirus update 2004 Calif Vet JulyAugust P 14 20 Waltzek TB G O Kelley DM Stone K Way L Hanson H Fukuda I Hirono T Aoki AJ Davison and RP Hedrick 2005 Koiherpesvirus represents a third cyprinid herpesvirus CyHV3 in the family Herpesviridae J Gen Virol 86 16591667 21 Waltzek TB GO Kelley ME Alfaro T Kurobe AJ Davison and RP Hedrick 2009 Phylogenetic relationships in the family Alloherpesviridae Dis Aquat Org 84 179194 American Association of Zoo Veterinarians Infectious Disease Manual MACROPOD HERPESVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Macropods potoroids possibly other marsupials Direct contact MaHV1 death pyrexia respiratory signs conjunctivitis anogenital vesicles MaHV2 death conjunctivitis oral and anogenital lesions MaHV3 possibly anogenital ulcerations Severe fatal clinical disease reported with MaHV1 and 2 Mild lesions in immune compromised individuals with MaHV 3 None known Supportive care Efficacy of antiviral drugs unknown Isolate positive individuals from negative individuals Not reported unlikely Fact Sheet compiled by Joseph A Smith Sheet completed on 1 February 2011 updated 15 July 2013 Fact Sheet Reviewed by James Wellehan Roman Pogranichniy Susceptible animal groups This disease generally affects macropods and potoroids MaHV1 was first described in parma wallabies Macropus parma MaHV2 was first described in grey dorcopsis Dorcopsis muelleri luctuosa and quokkas Setonix brachyurus MaHV3 was first described in eastern grey kangaroos M giganteus Nonspecified herpesvirus infections have also been reported in tammar wallabies M eugenii western grey kangaroos M fuliginosus brushtailed rat kangaroos Bettongia penicillata and rufous rat kangaroos Aepyprymnus rufescens MaHV1 has been experimentally induced in brushtailed possums Trichosurus vulpecula Causative organism Alphaherpesviruses Macropodid herpesvirus 1 MaHV1 and Macropodid herpesvirus 2 MaHV2 Gammaherpesvirus Macropodid herpesvirus 3 MaHV3 Zoonotic potential Not reported unlikely Distribution Clinical disease has only been reported in captive animals One study reported seropositive rates of 23 of wild marsupials and 41 of captive marsupials in Australia although specificity of the serologic testing is unknown MaHV1 and MaHV2 have only been reported in animals in Australia MaHV3 has been reported in captive eastern grey kangaroos in the US as well as in wild eastern grey kangaroos Incubation period Not known Clinical signs MaHV1 Fatal systemic infections resulting in severe clinical signs including pyrexia respiratory signs conjunctivitis and anogenital vesicles MaHV2 Fatal systemic disease characterized by conjunctivitis and lesions on the oral and anogenital mucous membranes MaHV3 Typically a subclinical systemic disease Mild to moderate ulcerative cloacitis found in immunocompromised individuals may be associated with this virus Post mortem gross or histologic findings American Association of Zoo Veterinarians Infectious Disease Manual MACROPOD HERPESVIRUS MaHV1 GrossVesicles and ulcers of skin lips eyelids and anogenital mucosa rhinitis mild to severe keratitis Histologicnecrotic epithelium and inflammatory debris numerous large basophilic or eosinophilic intranuclear inclusions MaHV2 Grosspurulent conjunctivitis red edematous lung lesions pinpoint 1mm yellow foci in the liver erythematous mucosal lesions in the gastrointestinal tract mesenteric lymphadenopathy erythematous mucous membranes yellow plaques on reproductive tract Histologicdisseminated focal necrosis intranuclear acidophilic or basophilic inclusions MaHV3 GrossUlcerative cloacitis was found in MaHV3 positive individuals A definitive association with the virus has not been proven HistologicNo inclusions were identified in PCRpositive tissues Diagnosis Virus isolation PCR or serology Serology is not available in North America Material required for laboratory analysis Swab or tissue sample of affected tissue Relevant diagnostic laboratories Herpesvirus consensus PCR University of Florida Zoological Medicine Laboratory httplabsvetmedufledusamplerequirementsmicrobiologyparasitologyserologyzoomedinfections Serologic tests are not commercially available in North America Treatment No successful treatment is reported Clinical signs should be treated with supportive care The use of antiviral drugs with these viruses has not been reported Prevention and control Specific guidelines have not been reported or investigated Generally positive individuals should be kept physically separated from negative individuals to prevent direct transmission Care should also be taken to prevent indirect transmission through fomites The role of vectors in the transmission of these viruses is unknown Suggested disinfectant for housing facilities No studies of disinfectant efficacy have been reported to date However as enveloped viruses macropod herpesviruses are presumed to be unstable in the environment and should be susceptible to the most common disinfectant strategies Notification Not a reportable disease Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Animals should be assumed to be infected for life with the possibility of transmitting virus to noninfected animals Conditions for restoring diseasefree status after an outbreak Due to lifelong infections removal of positive animals from the group is the only known method for obtaining a diseasefree status Experts who may be consulted Joseph A Smith DVM Fort Wayne Childrens Zoo 3411 Sherman Blvd Fort Wayne IN 46808 2604276815 Email vetkidszooorg Jim Wellehan DVM PhD DACZM DACVM Zoological Medicine Service University of Florida Gainesville FL 32160 Email wellehanjufledu References 1 Acland HM 1981 Parma wallaby herpesvirus infection J Wildl Dis 17 471477 American Association of Zoo Veterinarians Infectious Disease Manual MACROPOD HERPESVIRUS 2 Callinan RB and B Kefford 1981 Mortalities associated with herpesvirus infection in captive macropods J Wildl Dis 17 311317 3 Dickson J WI Hopkinson and W Coackley 1980 Herpesvirus hepatitis in rat kangaroos Aust Vet J 56 463464 4 Finnie EP IR Littlejohns and HM Acland 1976 Mortalities in parma wallabies Macropus parma associated with probable herpesvirus Aust Vet J 52 294 5 Guliani S GA Smith PL Young JS Mattick and TJ Mahony 1999 Reactivation of a macropodid herpesvirus from the eastern grey kangaroo Macropus giganteus following corticosteroid treatment Vet Microbiol 68 5969 6 Smith JA JFX Wellehan RM Pogranichniy AL Childress JA Landolfi and KA Terio 2008 Identification and isolation of a novel herpesvirus in a captive mob of eastern grey kangaroos Macropus giganteus Vet Microbiol 129 236245 7 Webber CE and JM Whalley 1978 Widespread occurrence in Australian marsupials of neutralizing antibodies to a herpesvirus from a parma wallaby Aust J Exp Biol Med Sci 56 351357 8 Wilcox R P Vaz N Ficorilli P Whiteley C Wilks and J Devlin 2011 Gammaherpesvirus infection in a freeranging eastern grey kangaroo Macropus giganteus Aust Vet J 89 5557 9 Wilks CR B Kefford and RB Callinan 1981 Herpesvirus as a cause of fatal disease in Australian wallabies J Comp Path 91 461465 10 Zheng T A M Napier JS OKeefe and B M Buddle 2004 Experimental infection of possums with macropodid herpesvirus 1 New Zeal Vet J 52 2025 American Association of Zoo Veterinarians Infectious Disease Manual MALIGNANT CATARRHAL FEVER MCF Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Many species of Artiodactyla including bovids cervids giraffids suids Blue and black wildebeest are common maintenance hosts Direct contact with infected individuals and bodily fluids nasal and ocular secretions Fomites Water Rangeland Feed Aerosol transmission also important for some of the viruses Transmitted only between carriers and clinically susceptible animals Affected animals do not transmit MCF to their conspecifics Mucous membrane ulceration and inflammation high fever oral and nasal exudates corneal opacities and lymph adenopathy Additional signs may include neurologic signs diarrhea arthritis and skin lesions Typically fatal in susceptible species Up to 25 of cattle may develop chronic disease with a waxing and waning course Up to 5 may clinically recover but most eventually die None usually ineffective Separate clinically susceptible species from known carrier species such as sheep goats and wildebeest in known infected areas to prevent direct transmission Prevent fomite transmission Use precautions to prevent aerosol transmission No Fact Sheet compiled by Danelle M Okeson and Enrique Yarto Sheet completed on updated December 2017 Fact Sheet Reviewed by Gretchen Cole Susceptible animal groups Cervidae Bovidae Giraffidae Suidae Causative organism Herpesviruses classified in the genus Macavirus At least 10 viruses have been identified that are categorized within the MCF virus group Some have been associated with MCF in clinically susceptible species Alcelaphine herpesvirus 1 AlHV1 classic African MCFwildebeestassociated carried by wildebeest susceptible species Cervidae and Bovidae Ovine herpesvirus 2 OvHV2 sheepassociated carried by domestic and wild bighorn sheep considered endemic in domestic sheep susceptible species ruminant species and swine Most MCF cases in domestic cattle and bison in the US are due to OvHV2 European breeds of cattle Bos taurus are relatively resistant but Bali cattle bison and some cervid species such as Pere Davids deer are highly susceptible Caprine herpesvirus 2 CpHV2 carried by domestic and exotic goats considered endemic in domestic goats clinically susceptible species whitetailed deer Sika deer moose and pudu A herpesvirus referred to as malignant catarrhal fever viruswhite tailed deer MCFVWTD carrier unknown susceptible species whitetailed deer IbexMCFV carried by Nubian ibex Capra nubiana prior to a case in a captive bongo Tragelaphus euryceros the virus was not considered pathogenic Alcelaphine herpesvirus 2 AlHV2 identified in but nonpathogenic in Jacksons hartebeest clinically American Association of Zoo Veterinarians Infectious Disease Manual MALIGNANT CATARRHAL FEVER MCF susceptible species Barbary red deer Cervus elaphus barbarus Other herpesviruses categorized in the same group as the pathogenic MCF viruses have been identified in aoudad roan antelope musk ox gemsbok but do not yet appear to cause disease under natural conditions Zoonotic potential No Distribution Disease may occur worldwide in situations in which clinically susceptible species are in contact with carrier species Incubation period It varies depending on several factors such as amount of virus transmitted and host In field outbreaks the incubation period for bison is about 40 to 70 days Cattle have become ill in as few as 9 days while other evidence suggests that some cattle may be subclinically infected for 20 months or more before developing the disease The latter case could be due to a long period of subclinical infection followed by viral reactivation leading to clinical disease Cattle have become infected 1173 days after the administration of blood from OvHV2 infected sick cattle Clinical signs These vary with susceptibility of affected species Highly susceptible species may have a peracute course with few to no clinical signs or sudden death after nonspecific signs such as depression weakness and diarrhea Acute disease may involve high fever and a loss of appetite Clinical signs may include mucous membrane ulceration and inflammation high fever oral and nasal exudates corneal opacities common in domestic cattle and lymphadenopathy Additional signs may include neurologic signs diarrhea arthritis and skin lesions may also develop Domestic sheep Systemic necrotizing vasculitis or polyarteritis nodosa has been found to be associated with OvHV2 Freeranging bighorn sheep muscle atrophy marked weight loss and bilaterally symmetric alopecia with hyperpigmentation and crusting over the face medial surfaces of the pinnae dorsal trunk distal limbs perineal area and tail was found in a freeranging bighorn sheep affected by OvHV2 Moose lymphocytic vasculitis in the brain and panuveitis were seen in a captive moose which died of CPHV2 Carrier species wildebeest do not typically develop clinical signs Post mortem gross or histologic findings These may vary with disease severity and course but often include inflammation and epithelial necrosis in the gastrointestinal respiratory and urinary tracts with lymphoproliferation infiltration of nonlymphoid tissues particularly the renal cortex and periportal areas of the liver by lymphoid cells and vasculitis Diagnosis PCR polymerase chain reaction is the method of choice for viral detection Serological tests for antibodies include competitive inhibition ELISA cELISA immunoperoxidase test IPT neutralization test NT and others Detection of antibodies indicates infection not necessarily disease In susceptible species such as cattle bison and deer detection of MCF antibodies indicates infection but is not diagnostic of disease lack of antibodies when performing cELISA usually is an indicative of a lack of infection with the exception of very early stages of infection 1 week before antibodies can be produced Material required for laboratory analysis Antibody testing by cELISA serum or plasma Antemortem detection of viral DNA by PCR whole blood in EDTA Postmortem detection of viral DNA by PCR preferred fixed tissue samples lymph node or spleen but lung brain kidney and intestine among others are also acceptable Relevant diagnostic laboratories Washington Animal Disease Diagnostic Laboratory WADDL Pullman Washington httpwwwvetmedwsuedumcf National Veterinary Services Laboratories NVSL in Ames Iowa NSW GovernmentDepartment of Primary Industries Treatment No treatment is available or usually ineffective Supportive care may be administered but American Association of Zoo Veterinarians Infectious Disease Manual MALIGNANT CATARRHAL FEVER MCF disease is often acute and fatal in highly susceptible species Some animals may die without clinical signs Occasional reports of recovery in treated cattle exist but some cattle may also recover without treatment Prevention and control Separate clinically susceptible species from carrier species such as wildebeest domestic and exotic sheep and domestic and exotic goat species Bovids particularly bison and water buffalo are highly susceptible to MCF Exotic members of the bovidae family such as bongo antelope have died from MCF traced back to an exotic goat species Wildebeestassociated MCF has occurred in domestic cattle in the US when the two species were housed together Cervids should not be mixed with sheep goats or wildebeest Prevent direct contact and fomite transmission Transmission of the wildebeestassociated form AlHV1 and the sheepassociated form OvHV2 is believed to occur primarily from either direct contact with infected body fluids or secretions or via fomites such as water sources feeders caretakers and birds Calving is considered a high risk period for transmission Use precautions to prevent aerosol transmission Transmission of the disease over relatively short distances has occurred indicating that direct contact is not absolutely necessary Aerosol transmission is a significant mode of transmission of OvHV2 in domestic sheep Suggested disinfectant for housing facilities Herpesviruses causing MCF are typically fragile and quickly inactivated in harsh environments so common disinfectants are likely effective However if heavy organic debris is present the OIE recommends 3 sodium hypochlorite Notification The wildebeestassociated and sheepassociated forms are reportable diseases under USDA APHISVS National Animal Health Reporting System MCF clinical signs may appear similar to foreign animal diseases such as rinderpest and foot and mouth disease Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Clinically susceptible species should not be introduced to carrier species Clinically susceptible species should be physically separated from carrier species In addition separate keeper staff and equipment should be used to prevent fomite transmission Conditions for restoring diseasefree status after an outbreak See prevention and control measures Experts who may be consulted Hong Li DVM PhD Animal Disease Research Unit USDAARS Washington State University Phone 509 3356002 Fax 509 3358328 3019 ADBV WSU Pullman WA 991646630 hlivetmedwsuedu or HongLiARSUSDAGOV References 1 Barnard BJH Van de Pypekamp HE Wildebeestderived malignant catarrhal fever unusual epidemiology in South Africa Onderstepoort J Vet Res 1988556971 2 Bengis RG Kock RA Fischer J Infectious animal diseases the wildlifelivestock interface Rev sci tech Off Int Epiz 20022125365 3 Center for Food Security Public Health Iowa State University Internet Malignant Catarrhal Fever c20122016 cited 2019 March 5 Available from httpwwwcfsphiastateeduFactsheetspdfsmalignantcatarrhalfeverpdf 4 Crawford TB Li H Rosenburg SR Nordhausen RW Garner MM Mural folliculitis and alopecia caused by infection with goatassociated malignant catarrhal fever virus in two sika deer J Am Vet Med Assoc 2002221843847 American Association of Zoo Veterinarians Infectious Disease Manual MALIGNANT CATARRHAL FEVER MCF 5 Gasper D Barr B Li H Taus N Peterson R Benjamin G Hunt T Pesavento PA Ibexassociated malignant catarrhal feverlike disease in a group of bongo antelope Tragelaphus euryceros Vet Pathol 2012493492497 6 Heuschele WP Malignant catarrhal fever In Fowler ME ed Zoo and Wild Animal Medicine Current Therapy 3rd Ed Philadelphia PA WB Saunders Company 1993 p 504506 7 Heuschele WP Reid HW Malignant catarrhal fever In Williams ES Barker IK eds Infectious Diseases of Wild Mammals 3rd ed Ames IA Iowa State University Press 2001 p 157164 8 Li H Cunha CW Taus NS Knowles DP Malignant catarrhal fever inching toward understanding Annu Rev Anim Biosci 20142209233 9 Li H Kunha CW Taus NS Malignant catarrhal fever understanding molecular diagnostics in context of epidemiology Int J Mol Sci 20111268816893 10 Li H Gailbreath K Bender LC West K Keller J Crawford TB Evidence of three new members of malignant catarrhal fever virus group in muskox Ovibos moschatus Nubian ibex Capra nubiana and gemsbok Oryx gazella J Wildl Dis 200339875880 11 Li H Keller J Knowles DP Crawford TB Recognition of another member of the malignant catarrhal fever virus group an endemic gammaherpesvirus in domestic goats J Gen Virol 200182227232 12 Loken T Aleksandersen M Reid H Pow L Malignant catarrhal fever caused by ovine herpesvirus2 in pigs in Norway Vet Rec 1998143464467 13 Modesto P Grattarola C Biolatti C Varello K Casalone C Mandola ML Caruso C Dondo A Goria M Rocca F Decaro N First report of malignant catarrhal fever in a captive pudu Pudu pudua Res Vet Sci 201599212214 14 Okeson DM Garner MM Taus NS Li H Coke RL Ibexassociated malignant catarrhal fever in a bongo antelope Tragelaphus euryceros J Zoo Wildl Med 200738460464 15 OToole D Li H Sourk C Montgomery DL Crawford TB Malignant catarrhal fever in a bison Bison bison feedlot 19932000 J Vet Diagn Invest 200214183193 16 Pesavento PA Dange RB Ferreras MC Dasjerdi A Pérez V LaRoca A Silváin JB Diab S Jackson K Phillips IL Li H Cunha CW Wessels M 2018 Systemic Necrotizing Vasculitis in Sheep Is Associated With Ovine Herpesvirus 2 Vet Pathol Sep 10 17 Pesavento PA Cunha CW Li H Jackson K OToole D In Situ Hybridization for Localization of Ovine Herpesvirus 2 the Agent of SheepAssociated Malignant Catarrhal Fever in FormalinFixed Tissues Vet Pathol 20185618792 18 Seeley KE Junge RE Jennings RN Cunha CW Li H Moose Alces alces mortality associated with caprine herpesvirus 2 cphv2 in a zoological collection J Zoo Wildl Med 2018493774778 19 Slater OM Peters Kennedy J Lejeune M Gummer D Macbeth B Warren A Joseph T Li H Cinha CW Duignan PJ Sheepassociated Malignant Catarrhal Fever like skin disease in a freeranging bighorn sheep Ovis canadensis Alberta Canada J Wildl Dis 2017531153158 20 Wambua L Wambua PN Ramogo AM Mijele D Otiende MY Wildebeestassociated malignant catarrhal fever perspectives for integrated control of a lymphoproliferative disease of cattle in sub Saharan Africa Arch Virol 20161611110 21 Washington State University Internet Veterinary Microbiology and Pathology Research Malignant Catarrhal Fever MCF cited 2017 December 18 Available from httpvmpvetmedwsueduresearchmalignantcatarrhalfeveroverview 22 Washington State University Veterinary Medicine Extension Internet Malignant Catarrhal Fever in cattle cited 2019 March 5 Available from httpss3wpwsueduuploadssites2050201603MCF factsheetpdf American Association of Zoo Veterinarians Infectious Disease Manual PSITTACID HERPESVIRUS 1PACHECOS DISEASE Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Psittacines rarely passerines Ingestion of contaminated material from oral secretions or feces Aerosol route is possible but not proven Death with few premonitory signs Rarely nonspecific signs including lethargy and the presence of bile pigments in urine Three of four PcHV1 genotypes have been associated with oral and cloacal mucosal papillomas Dependent on viral genotype and species of birds death can range from single birds to flock majority Virtually all birds showing signs of the acute form will die unless treated Mucosal papillomas cause considerable morbidity but are rarely fatal Acyclovir is very effective at stopping outbreaks when the entire flock is treated Closed flocks isolating or culling subclinical carriers and testing new arrivals at quarantine may assist in disease prevention No Fact Sheet compiled by Nadia Stegeman Sheet completed on 3 August 2011 updated 20 March 2013 Fact Sheet Reviewed by David N Phalen Lauren V Powers Susceptible animal groups Psittacines and less commonly passerines although it has been reported in birds such as finches canaries and barbets family Lybiidae Causative organism Psittacid herpesvirus 1 PsHV1 formerly Pachecos disease PD virus has 4 genotypes corresponding to 3 serotypes and is an alphaherpesvirus The pathogenicity of genotype varies significantly although all four genotypes have been shown to cause PD Recently in African grey parrots psittacid herpesvirus 2 PsHV2 was identified from cloacal mucosa Zoonotic potential None reported Distribution Presumably worldwide due to bird trade but it is most prevalent in densely populated captive psittacine collections Case reports have documented confirmed disease in North America Europe Africa AustraliaNew Zealand the Middle East and Asia A recent study suggests a 7 prevalence of PsHV1 infection in the general US population of parrots It is suspected that these viruses have evolved with Central and South American parrots Incubation period Experimentally 510 days to establish infection Papillomas develop within a year of infection Clinical signs Acute Death with no premonitory signs aside from possible depression anorexia diarrhea and yellow urates biliverdinuria In antemortem clinical chemistries marked AST elevation can be found Chronic Oralcloacal papillomas that produce tenesmus and can be associated with frank blood from the American Association of Zoo Veterinarians Infectious Disease Manual PSITTACID HERPESVIRUS 1PACHECOS DISEASE cloaca In extreme cases and when bile duct and pancreatic duct carcinomas develop chronic wasting can occur Post mortem gross or histologic findings Due to rapid death acutely affected birds may show no gross lesions However when abnormalities are present they may be in the liver spleen kidneys and intestines Histopathological findings include multi organ eg spleen intestines pancreas trachea air sacs necrotizing lesions hemorrhage and congestion of the liver spleen and kidneys and hepatomegaly or splenomegaly may be seen Intranuclear inclusion bodies Cowdry Type A are most common in the liver but have been demonstrated in the kidneys spleen pancreas and small intestines In the chronic form of the disease mucosal papillomas may be seen most commonly in the oral and cloacal mucosa or upper gastrointestinal tract These lesions are found in the disease complex termed internal papillomatosis of parrots IPP A high prevalence of carcinomas in the bile duct and pancreatic duct has been observed in aviaries where IPP had been noted in birds infected with PcHV1 genotype 3 These tumors can be but not always detected with coelomic ultrasound and are associated with a rise in serum GGT Many ventricular and cloacal carcinomas appear to be caused by PsHVs Cloacal carcinomas have a grave prognosis due to the reportedly high metastatic rate One case report discusses chronic active pancreatitis with diabetes mellitus weight loss PUPD glucosuria and hyperglycemia associated with PsHV1 infection in a cockatiel Nymphicus hollandicus Diagnosis Inapparently infected birds Gross identification of mucosal papillomas PCR or realtime PCR on cloacal oral mucosal swabs and whole blood It is important to note that the virus is shed intermittently leading to the possibility of false negative results by PCR However the majority of birds remain PCR positive at all time the sensitivity of mucosal swabs is higher than that of whole blood Serology has practical merit Birds that are serologically positive are likely latently infected Postmortem specimens Characteristic histologic findings electron microscopy cell culture immunofluorescent antibody staining and PCR Material required for laboratory analysis It is important to note that the virus is shed intermittently leading to the possibility of false negatives However the majority of birds remain PCR positive at all times The sensitivity of mucosal swabs is higher than that of whole blood Pachecos Disease Whole blood tissues frozen liverspleen or swabs frozen liverspleen for culture choanalcloacal swabs histopathology of liver spleen pancreas intestine crop Subclinically infected birds Choanalcloaca swabs serum whole blood Relevant diagnostic laboratories Veterinary Molecular Diagnostics 5989 Meijer Dr Suite 5 Milford Ohio 45150 5135761808 PCR based DNA probe can detect all PsHV1 variants Treatment Acyclovir 80100mgkg three times a day for 10 days Zovivax GlaxoSmithKline has been shown to reduce the sickness and death of PsHV1 affected birds and generally after a few days of treatment all deaths cease Acylovir has been associated with kidney damage in some species but this problem is uncommon or rare Mucosal papillomas typically wax and wane and only require surgical intervention in extreme cases Surgical resection of papillomas is a palliative treatment Prevention and control Screening and isolation of infected individuals is critical PCR positive birds American Association of Zoo Veterinarians Infectious Disease Manual PSITTACID HERPESVIRUS 1PACHECOS DISEASE should be housed separately from other parrots Macaws conures and Amazon parrots and should be carefully examined prior to acquisition That being said not all PcHV1 genotypes are serologically cross reactive meaning that infection with one variant of the virus does not protect from infection from another Control methods in the midst of an outbreak are debated While some support catching and moving individual birds others advocate minimal disturbances until the outbreak is over Immediate treatment of exposed birds with acyclovir at 1mgml drinking water and 400mgkg of soft mash is indicated Gavage feeding at 70100mgkg BID has also been suggested Commercial monovalent vaccine killed virus for PsHV1 is derived from a single unreported serotype It is not known how much protection this vaccination provides against variants other than genotype 1 Complications from vaccine include injection granulomas and acute death Cockatoos appear to be overrepresented in populations experiencing complications Additionally the product Psittimmune PDV Biomune in Lenexa Kansas no longer appears available One case report suggests autogenous formalin inactivated vaccine with aluminum hydroxide gel adjuvant may stop virus spread decreasing morbidity and mortality Individuals with this disease can continue to be used as breeders However all eggs must be artificially incubated and handraised until vertical transmission impacts are better established Suggested disinfectant for housing facilities As PsHV1 is an enveloped virus it is readily inactivated by commonly used disinfectants EPA approved disinfectant virucidal fungicidal bacteriocidal or sodium hypochlorite bleach solution 800ppm is effective for most herpesviruses It can also be inactivated by heating to 56oC for 10 minutes or by exposing it to pH 5 Notification None required although notification to institutions that received birds previously exposed to chronic shedders is recommended Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Isolating infected and exposed individuals testing exposed individuals after clinical signs in the aviary subside Experts who may be consulted David N Phalen DVM PhD DABVP Avian Director Wildlife Health and Conservation Center University of Sydney Sydney NSW davidphalensydneyeduau References 1 Herpesviridae 1995 In Ritchie BW Avian Viruses Function and Control Wingers Publishing Lake Worth Florida Pp 171222 2 Katoh H H Ogawa K Ohya and H Fukushi 2010 A review of DNA viral infections in psittacine birds J Vet Med Sci 729 10991106 3 Phalen D M Falcon and E Tomaszewski 2007 Endocrine pancreatic insufficiency secondary to chronic herpesvirus pancreatitis in a cockatiel Nymphicus hollandicus J Av Med Surg 212 140145 4 Phalen D E Tomaszewski and D Styles 2009 Epizootiology diversity and pathogenicity of Psittacid Herpesviruses Proc Annu Conf Assoc Av Vet Milwaukee Wisconsin 4751 5 Phalen D and R Woods 2009 Psittacid Herpesviruses and mucosal papillomas of psittacine birds in Australia Fact Sheet Australian Wildlife Health Network httpwwwwildlifehealthorgauPortals0DocumentsFactSheetsHerpesviruses20Psittacine2 0Aug2020092022pdf Accessed 13 August 2013 6 Phalen DN 2006 Psittacid herpesviruses In Harrison GJ and T Lightfoot eds Clinical American Association of Zoo Veterinarians Infectious Disease Manual PSITTACID HERPESVIRUS 1PACHECOS DISEASE Avian Medicine Vol II Spix Publishing Inc Palm Beach Florida Pp 732734 7 Styles D K EK Tomaszewski and DN Phalen 2005 A novel psittacid herpesvirus found in African grey parrots Psittacus erithacus erithacus Avian Pathol 34 150154 8 Tomaszewski EK W Wigle and DN Phalen 2006 Tissue distribution of psittacid herpesviruses in latently infected parrots repeated sampling of latently infected parrots and prevalence of latency in parrots submitted for necropsy J Vet Diagn Invest 18 536544 9 Tomaszewski EK M Gravendyck EF Kaleta and DN Phalen 2004 Genetic characterization of a herpesvirus isolate from a superb starling Lamprotornis superbus as a psittacid herpesvirus genotype 1 Avian Dis 481 212214 10 Tomaszewski EK EF Kaleta and DN Phalen 2003 Molecular phylogeny of the psittacid herpesvirus causing Pachecos disease correlation of genotype with phenotypic expression JVirol 77 1126011267 American Association of Zoo Veterinarians Infectious Disease Manual PSEUDORABIES AUJESZKYS DISEASE Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Swine are the only natural hosts of the virus However it affects a wide range of mammalian hosts excluding humans and some non human primates Primarily through venereal route or horizontal transmission via oral nasal digestive or reproductive mucosa Other potential methods of transmission include mechanical via fomites or vehicles and viral aerosol ization Pyrexia depression anorexia tremors incoordination vomiting ptyalism foaming blindness convusions coma and death High and low virulence strains are known Disease is highly virulent and often 100 fatal in susceptible nonsuids No treatment is available Surviving animals are infected for life Vaccination is available with regulatory permission and is effective at reducing clinical signs Infected operations are quarantined and infected animals removed Feral swine may be monitored to identify high risk areas No Fact Sheet compiled by Kerri Pedersen and Yvonne Nadler Sheet completed on 9 September 2013 Fact Sheet Reviewed by Tom Deliberto Troy Bigelow Evan Sorley Lowell Anderson Mark Schoenbaum Susceptible animal groups Domestic and feral swine are the primary hosts but disease can be transmitted to other mammalian species The virus is known to infect deer foxes raccoons skunks bears rats coyotes mink and panthers Cattle goats dogs and cats also are susceptible to the disease Experimental infection has been seen in rhesus monkeys marmosets and several bird species Causative organism Pseudorabies also referred to as Aujeszkys disease is caused by Suid herpesvirus 1 Varicellovirus in family Herpesviridae Zoonotic potential None Distribution Pseudorabies occurs worldwide but has virtually disappeared from domestic pigs in several parts of Europe Great Britain and New Zealand US implemented an eradication program and as of 2004 all commercial swine were considered pseudorabiesfree However pseudorabies is considered endemic in US feral swine Incubation period Typically 26 days and suckling pigs have shorter incubation period of 48 hours Clinical signs Clinical signs are variable and morbidity and mortality decreases with increasing age in swine Pregnant sows may abort or have stillborn young whereas newborn piglets may present with neurologic disease or high mortality rates especially in piglets from herds with no prior exposure Weaned pigs present respiratory illness with fever anorexia and weight loss Sneezing rubbing of the nose and coughing may occur with or without trembling and incoordination Adult swine can exhibit mild respiratory distress fever during acute American Association of Zoo Veterinarians Infectious Disease Manual PSEUDORABIES AUJESZKYS DISEASE infection Surviving individuals become lifelong carriers of the virus while exhibiting minimal to no further clinical signs In swine the virus may become latent in cranial nerve ganglia may recrudesce and shed live virus months later Pseudorabies is virulent in susceptible animal species which often experience intense pruritus or mad itch which causes them to scratch and bite themselves Other clinical signs include respiratory problems general neurologic signs weakness convulsions and fever Clinical pathological gross and histopathological findings Gross lesions are minimal or absent and none are pathognomonic Serous or fibrinonecrotic rhinitis may be found Tonsilar inflammation may be observed as fibrinous exudate or an erosive fibrinonecrotic lesion Small 1 mm pale foci in liver andor spleen appear as slightly irregular or with vague edges and not a crisp welldemarcated appearance in young piglets liver lesions are more common than in adults but occur only occasionally Reddened foci may be scattered on the pleura of the lungs and with or without pulmonary edema congestion or consolidation Nonsuppurative meningoencephalitis is noted upon examination of white and gray matter mononuclear perivascular cuffing neuronal necrosis thickened meninges In nonsuid species edema congestion and hemorrhage in the spinal cord have been noted These lesions are usually found in the portion of the spinal cord that innervates the area of pruritus Microscopically cellular infiltration and neuronal degeneration is seen CNS lesions are similar to those found in pigs but milder in severity Diagnosis Serologic tests for virus or antibody detection are available and include serum neutralization SN latex agglutination LA and enzymelinked immunosorbent assay ELISA A fluorescent antibody test on tissue sections immunohistochemistry on formalinfixed tissues or virus isolation may be used to identify virus in the brain tonsils and spleen A polymerase chain reaction PCR test has been described but is not in common use Material required for laboratory analysis Serum or tissue with brain spleen and lung are preferred tissues for diagnosis in suids Diagnostic samples should be kept cold for virus isolation submission Nasal swabs or samples of oropharyngeal fluid or tonsil tissue from suspected porcine can be used for virus isolation The virus may also be found in the lung spleen liver kidney or lymph nodes In other species the virus may be isolated from the pruritic area of the skin and from the spinal cord area innervating the pruritic area Relevant diagnostic laboratories Most diagnostic laboratories can test for pseudorabies Treatment No treatment is available Prevention and control Vaccination can be effective at preventing and controlling outbreaks in domestic swine permission must be obtained from state animal health official for vaccine usage State and Federal regulations prevent movement of infected pigs and monitoring to identify newly infected animals Since feral swine are a known reservoir measures are taken to prevent contact between feral and domestic swine Infected domestic herds are placed under quarantine Infected animals movements are controlled and regulated In severe cases depopulation is a method of control The risk to zoological animals exists from biosecurity breaches allowing infected feral swine reservoirs or other wildlife from coming into contact with zoological animals Sound biosecurity measures are highly effective in preventing introduction into zoological facilities Suggested disinfectant for housing facilities PRV is susceptible to inactivation by sodium hydroxide bleach iodinebased products phenolic disinfectants quaternary ammonium compounds formaldehyde and chlorhexadine These disinfectants are not effective unless contaminated objects have been thoroughly cleaned before the disinfectants are applied PRV is also susceptible to thermal inactivation Notification Pseudorabies is a notifiable disease only when found in commercial production swine American Association of Zoo Veterinarians Infectious Disease Manual PSEUDORABIES AUJESZKYS DISEASE Measures required under the Animal Disease Surveillance Plan httpwwwaphisusdagovvsnahss swineprvprvsurveillanceplanfinaldraft041608pdf for current National Surveillance Plan Proposed changes Veterinary Services National Surveillance Plan under review in 2013 httpwwwaphisusdagov animalhealthanimaldisspecswinedownloadsmanageswinebrucnpseuvirus100861conceptpdf Measures required for introducing animals to infected animal Do not introduce noninfected animals to infected animals animals should be tested prior to moving them and prior to introducing to known diseasefree animals Conditions for restoring diseasefree status after an outbreak In commercial swine herds quarantine animal testing and removal from herd will be under the direction of an Accredited veterinarian Premises should be disinfected and left vacated for at least 30 days following removal of infected animal Experts who may be consulted Federal and state veterinary authority AVIC and state veterinarian respectively References 1 httpwwwaphisusdagovpublicationsanimalhealthcontentprintableversionpseudorabiesreport pdf Accessed 26 August 2013 2 Aujeszkys disease Pseudorabies virus AD and PRV httpwwwthepigsitecom pighealtharticle135aujeszkysdiseasepseudorabiesvirusadorprv Accessed 26 August 2013 3 Davidson WR 2006 Wild Swine In Field Manual of Wildlife Diseases in the Southeastern United States Southeastern Cooperative Wildlife Disease Study 3rd edition University of Georgia Athens Georgia Pp 105134 4 Kluge J P G W Beran H T Hill and K B Platt 1999 Pseudorabies Aujeszkys disease In Straw BE S DAllaire WL Mengeling and DJ Taylor eds Diseases of Swine 8th ed Iowa State University Press Ames Iowa pp 233246 5 Merck Manual Overview of Pseudorabies httpwwwmerckmanualscom vetnervoussystempseudorabiesaujeszkysdiseasemaditchoverviewofpseudorabieshtmlqts calt Accessed 26 August 2013 6 Muller T E C Hahn F Tottewitz M Kramer B G Klupp T C Mettenleiter and C Freuling 2011 Pseudorabies virus in wild swine a global perspective Arch Virol 156 16911705 7 Pedersen K S N Bevins J A Baroch J C Cumbee Jr S C Chandler B S Woodruff T T Bigelow and T J DeLiberto 2013 Pseudorabies in feral swine in the United States 20092012 J Wildl Dis 49370913 8 Pork Industry Handbook Psuedorabies Aujeszkys Disease Purdue University Cooperative Extension Service httpwwwuwexeducesanimalscienceswinedocumentsPIH38pseudopdf Accessed 26 August 2013 9 Spickler AR Aujeszkys Disease httpwwwcfsphiastateeduDiseaseInfofactsheetsphp Accessed 26 August 2013 10 USDA APHIS Technical Bulletin No 1923 2008 Pseudorabies Aujeszkys Disease and its eradication a review of the US experience httpwwwaphisusdagovpublicationsanimalhealthcontentprintableversionpseudorabiesreport pdf Accessed 9 September 2013 11 Veterinary Services Frequently Asked Questions Pseudorabies httpwwwaphisusdagov animalhealthanimaldisspecswinefaqshtml Accessed 26 August 2013 American Association of Zoo Veterinarians Infectious Disease Manual Saimariine Herpesvirus 1 SaHV1 Fact Sheet compiled by Elizabeth E Hammond Sheet completed on 14 September 2018 Fact Sheet Reviewed by Genny Dumonceaux Susceptible animal groups Natural hosts squirrel monkeys Saimiri sciureus spider monkeys Ateles sp capuchins Cebus sp possibly woolly monkeys Lagothrix sp Aberrant hosts Owl monkeys Aotus sp marmosets Callithrix sp tamarins Saguinus sp titi monkeys Callicebus sp Causative organism Saimiriine herpesvirus Alphaherpesvirus aka Herpesevirus tamarinus Herpesvirus T Herpesvirus platyrrhinae Zoonotic potential slight one case report of a lab worker with nonfatal encephalitis secondary to a squirrel monkey bite Distribution South and Central America worldwide in captivity for natural hosts Incubation period 710 days Clinical symptoms Squirrel monkeys spider monkeys capuchins oral lesions rare or asymptomatic owl monkeys titi monkeys marmosets tamarins anorexia oral lesions pruritus sneezing nasal discharge diarrhea swollen eyelids 76100 mortality 23d after onset of clinical signs once infected always a carrier latent infections with intermittent shedding resembles herpes simplex infection Post mortem gross or histologic findings Gross ulcerative dermatitis mucosal ulceration Histopathology hepatic necrosis with multinucleated syncytial cells and intranuclear inclusion bodies Also necrosis in spleen kidney lung intestines and adrenal gland necrosis of the epidermis with multinucleated Animal groups affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Natural host species squirrel monkeys spider monkeys capuchins and possibly woolly monkeys Susceptible species owl monkeys titi monkeys spider monkeys all marmosets and tamarins Fecaloral route aerosols fomites sexual transmission Natural hosts oral lesions rare or asymptomatic owl monkeys titi monkeys marmosets and tamarins anorexia oral lesions pruritis sneezing nasal discharge diarrhea swollen eyelids 76100 mortality 23d after onset of clinical signs Natural hosts asymptomatic to oral lesions owl monkeys titi monkeys marmosets and tamarins have a 76 100 mortality rate None May try herpes antiviral therapy famcyclovir gamcyclovir although no data is available on efficacy Do not mix squirrel monkeys spider monkeys and capuchins with owl monkeys titi monkeys marmosets or tamarins Do not share cleaning utensils enrichment or perching materials etc due to risk of fomite transmission Serological screening of natural hosts Possible but only one report of non fatal encephalit is in a human secondary to a squirrel monkey bite American Association of Zoo Veterinarians Infectious Disease Manual Saimariine Herpesvirus 1 SaHV1 giant cells with intranuclear viral inclusions Inflammatory response may be minimal in acute disease Lesions may be minimal if encephalitis is present Diagnosis virus isolation molecular techniques serology histopathology clinical signs and history of contact with natural host Material required for laboratory analysis serum whole blood skin oral mucosa liver Relevant diagnostic laboratories VRL Laboratories PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio TX 78229 USA 18776157275 wwwvrlnet Zoologix 9811 Owensmouth Ave Ste 4 Chatsworth CA 913113800 USA 8187178880 wwwzoologixcom Treatment none supportive care Prevention and control Prevent contact between squirrel monkeys spider monkeys and capuchins with owl monkeys titi monkeys marmosets or tamarins Prevent cross contamination by excluding the use of shared equipment and enrichment devices A live vaccine has been effective in owl monkeys however vaccineinduced disease has been observed Suggested disinfectant for housing facilities most common disinfectants will kill the herpesvirus including chlorine bleach and quaternary ammonium Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Do not introduce natural host species to susceptible species once infected animals will remain carriers and sporadically shed virus Conditions for restoring diseasefree status after an outbreak Disinfect environment cleaning tools furniture etc Avoid mixing natural hosts with susceptible species Experts who may be consulted References 1 Calle PP Joslin JO New World and Old World Monkeys In Miller RE and Fowler ME eds Zoo and wild animal medicine Current therapy 8th ed St Louis MO Saunders 2015 p 301335 2 Joslin JO Other primates excluding great apes In Miller RE and Fowler ME eds Zoo and wild animal medicine Current therapy 5th ed St Louis MO Saunders 2003 p 346381 3 King NW Herpesvirus Infections In Williams ES and Barker IK eds Infectious disease of wild mammals Ames IA Iowa State University Press 2001 p147178 4 Lewis AD Internet Gross morbid anatomy of nonhuman primates cited 2018 August 3 Available from wwwcldavisorgcgibindownloadcgipid87 5 Lowenstine LJ Health problems in mixed species exhibits In Miller RE and Fowler ME eds Zoo and wild animal medicine Current therapy 4th ed Philadelphia PA WB Saunders 1999 p 2629 6 OttJoslin JE Viral diseases in nonhuman primates In Miller RE and Fowler ME eds Zoo and wild animal medicine Current therapy 2nd ed Philadelphia PA WB Saunders 1986 p 674697 American Association of Zoo Veterinarians Infectious Disease Manual SA8 CERCOPITHECINE HERPESVIRUS 2 Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Cercopithecidae predominantly African green monkey and baboon Direct contact Mostly asymptomatic transient vesicular stomatitis in young animals Small vesicles and pustules can be found on genital and oral mucous membranes Mild Oral and genital lesions Experimental infection has resulted in pneumonia No treatment needed due to nature of infection Symptom atic treat ment for severe lesions would be indicated Disease rare despite high virus prevalence Not reported Fact Sheet compiled by Sam Rivera updated by Jan Ramer Sheet completed on 1 June 2011 updated 23 July 2013 Fact Sheet Reviewed by Sam Rivera Kevin Brunner Susceptible animal groups Cercopithecidae Causative organism SA8 Cercopithecine herpesvirus 2 Zoonotic potential None Distribution African green monkey natural host but is found in captivity worldwide Common asymptomatic infection of baboons Incubation period Unknown Clinical signs Most infections are clinically silent transient vesicular stomatitis in young animals Oral and genital vesicles and pustules are possible Occasional severe genital lesions have been noted with inguinal lymphadenopathy Post mortem gross or histologic findings Vesicular stomatitis Diagnosis Serology virus isolation Material required for laboratory analysis Material from the lesions whole blood or serum Relevant diagnostic laboratories Pathogen Detection Laboratory California National Primate Research Center Road 98 Hutchison University of California Davis California 95616 530 7528242 Fax 530 7524816 PDLprimateucdavisedu httppdlprimateucdavisedu BioReliance SerologyPCR Laboratories 14920 Broschart Rd American Association of Zoo Veterinarians Infectious Disease Manual SA8 CERCOPITHECINE HERPESVIRUS 2 Rockville Maryland 20850 Phone 301 6102227 Fax 310 6102587 ahsbioreliancecom Virus Reference Laboratories Inc 7540 Louis Pasteur Road San Antonio Texas 78229 877 6157275 Fax 210 6157771 Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 913113800 8187178880 Fax 8187178881 infozoologixcom Treatment Symptomatic treatment for severe lesions would be indicated Prevention and control Disease rare despite high virus prevalence Suggested disinfectant for housing facilities Lipid solvents soap UVlight heat Notification None at this time Measures required under the Animal Disease Surveillance Plan None at this time Measures required for introducing animals to infected animal None at this time Conditions for restoring diseasefree status after an outbreak Latent infection possible lifelong infection Experts who may be consulted ChihLing Zao PhD Chief Scientific Officer VRL Laboratories PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 Phone 8776157275 Fax 2106157771 chihlingzaovrlnet References 1 httpwwwprimateportalorg Accessed 6 August 2013 2 Bennett T C Abee and R Henrickson eds 1998 Nonhuman Primates in Biomedical Research Diseases Academic Press San Diego California 512 pp 3 Lerche N W 2005 Common viral infections of laboratory primates In WolfeCoote S ed The Handbook of Experimental Animals The Laboratory Primate Elsevier Academic Press San Diego California Pp 7589 4 Voevodin AF and PA Marx eds 2009 Simplexviruses In Simian Virology WilleyBlackwell Ames Iowa Pp 267293 American Association of Zoo Veterinarians Infectious Disease Manual TESTUDINID HERPESVIRUSES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All tortoises are considered susceptible Experimental work has shown that intranasal and intramuscular inoculation is followed by development of the disease Close contact is considered one of the most relevant events for natural transmission to occur It is not clear if aerosolization plays a significant role Classic but not necessarily always occurring clinical signs include diphtheronecrot ic stomatitis and glossitis nasal ocular and oral discharge conjunctivitis lethargy anorexia respiratory and neurological signs Depends of the species affected and on the viral genotype involved TeHV1 2 and 3 have been associated with clinical disease More recently also TeHV4 was detected in a clinically ill tortoise coinfected with Mycoplasma sp Close to 100 morbidity and mortality have been reported for naïve Hermanns tortoises while Greek tortoises are considered more resistant Antivirals eg acyclovir and gan cyclovir have been shown to be effective in vitro Separation of the diseased individuals from those clinically healthy animals serologic and molecular testing of the exposed individuals six months quarantine and serological testing avoiding species mixing and crowding disinfection of the enclosures with virucidal agents No Fact Sheet compiled by Francesco C Origgi Sheet updated on 30 August 2013 updated 2018 Fact Sheet Reviewed by Douglas R Mader Susceptible animal groups All tortoises are considered susceptible Causative organism Testudinid herpesviruses TeHVs previously known as tortoise herpesviruses have four currently known genotypes TeHV1 2 3 and 4 In diseased individuals TeHV1 2 and 3 have been detected or isolated The TeHV3 genotype includes at least two genogroups A B that might be characterized by distinct virulence but both lethal Genogroup A is the most common genogroup B is putatively the most virulent More recently TeHV4 has been detected in a clinically ill leopard tortoise Stigmochelys pardalis Zoonotic potential No Distribution TeHV1 and 3 have been detected worldwide TeHV2 has been detected only in the US until now TeHV4 has been detected in the US in a clinically healthy imported Bowsprit tortoise and in in a captivebred leopard tortoise coinfected with Mycoplasma sp in Europe Both Bowsprit and leopard tortoises are African tortoises TeHV1 and 3 have been detected more commonly in the genus Testudo but also in several other tortoise species not autochthonous of the Eurasian area TeHV2 has been detected only in desert tortoises Gopherus agassizii up to date It is likely that at least for some of the genotypes the current area of distribution might only partially overlaps with their original ones because of the extensive movements that the species have undergone especially because of the pet trade According to multiple studies conducted on wild tortoises the following geographical classification of the genotypes has been proposed TeHV1 and 3 Eurasian TeHV2 American TeHV4 African Incubation period Following experimental infection in Greek tortoises the first clinical signs were recorded 7 to 12 days post inoculation The overall course of the disease lasted 25 weeks American Association of Zoo Veterinarians Infectious Disease Manual TESTUDINID HERPESVIRUSES Clinical signs The disease originally was called stomatitis and rhinitis disease or running nose and it was named after its most common clinical signs that include a diphtheronecrotic stomatitis and a glossitis with nasal oral and eye discharge The discharges are generally clear intermittent and recurrent Monolateral or bilateral recurrent conjunctivitis is also common Cervical edema and epistaxis in severe cases has been reported The oral plaques have been shown to develop and eventually fully regress in the survival animals within a 25 weeks period of time during an experimental transmission study in Greek tortoises Following the loss of the crusts covering the healing plaques no scar can be detected after the resolution of the oral lesions A band of chalky white material can be observed along the rim of the external aspect of the mandible after the oral discharge has resolved Respiratory and neurological signs might follow along more general signs such as lethargy and anorexia Not all the clinical signs described above can be detected in the same diseased individuals and some infected tortoise might not develop obvious clinical signs at all Similar clinical signs were observed also in a recent transmission study carried out with TeHV3 in Hermans tortoises It is important to consider that none of the clinical signs described above are specific for TeHVs since similar oral plaques have also been described in tortoises infected with less common iridovirus and virus X topivirustortoise picornavirus Additionally nasal discharge and conjunctivitis in absence of stomatitis are commonly described in tortoises infected with Mycoplasma agassizii an etiologic agent of the upper respiratory tract diseaseURTD Post mortem gross or histologic findings Classic gross lesions include diphtheronecrotic plaques over the mucosa of the oral cavity and the tongue occasionally extending over the mucosa of the esophagus and of the trachea up to the lung Hepatomegaly and enteritis have also been described The histologic hallmark of the disease is the presence of eosinophilic to amphophilic intranuclear inclusions in most of the epithelial tissues Inclusions can also be observed within the central nervous system either associated or not with inflammation Inclusions are likely to be detectable for a limited time during the initial phase of the disease Diagnosis The clinical diagnosis relies on the detection of the clinical signs described above The clinical diagnosis requires the confirmation by laboratory testing Multiple molecular and serological tests are available for the diagnosis of Testudinid herpesvirus infection Serology The available serological tests comprise an ELISA and a serum neutralization test SNT while the molecular diagnostic tests comprise multiple PCR protocols for the partial amplification of different herpesvirus genes The ELISA test has been developed to detect TeHV3 exposure and it has been validated for Greek and Hermanns tortoises The test detects the large majority of the antibody developed by the host against the virus after seroconversion Although the test can detect the exposure to TeHV3 relatively early following the infection for a reliable diagnosis it is recommended to test a suspected individual two times no less than 8 weeks a part A modified version of the same test has been shown to be able to detect TeHV2 exposure in desert tortoises although in this format the test has not been fully validated SNT similarly to the ELISA allows the detection of the exposure of an individual to a Testudinid herpesvirus due to the presence of circulating antiTeHVs antibody serum neutralizing in this case following seroconversion This test can be applied to any species of tortoise and it requires live virus to be carried out SNT can detect seroconversion to TeHVs 25 weeks after the ELISA test For this reason it is suggested to test the suspected animals two times 1012 weeks apart for a reliable detection of the occurred seroconversion when using the SNT Both ELISA and SNT show comparable specificity and sensitivity Molecular diagnosis Several PCR protocols have been developed for the diagnosis of TeHVs infection A PCR test targeting the partial sequence of the viral DNA polymerase gene is available for the specific detection of TeHV1 Another protocol has been developed for the detection of the partial sequence of the helicase gene of TeHV3 The same protocol allows also the detection of the homologous gene of the TeHV1 genotype following a specific modification of the test conditions A PCR test directed to the amplification of the partial sequence of the ribonucleotide reductase RR large subunit of TeHV3 has also been developed This test can also amplify the homologous gene portion of TeHV2 although a specific PCR protocol is also American Association of Zoo Veterinarians Infectious Disease Manual TESTUDINID HERPESVIRUSES available for the partial amplification of TeHV2 RR Finally a PCR protocol not specifically developed for TeHVs but more in general for the detection of the members of the family Herpesviridae is also available and allows the detection of all the 4 genotypes of TeHVs known up to date partial amplification of the DNA polymerase gene the target is a different region from that used for TeHV1 amplification Recently a PCR protocol has been developed to differentiate viral strains belonging to distinct genogroups A B within the TeHV3 genotype which might be associated with distinct virulence Histopathology routine histopathologic diagnosis of TeHVs infection is more often considered a post mortem diagnostic method It is based on the detection of the classic intranuclear inclusions An immunohistochemistry and an in situ hybridization method are also available for the detection of TeHVs antigen and DNA in tissue respectively and can be used to enhance the sensitivity of the histopathological diagnosis Electron microscopy is also commonly used to detect the presence of the virus in tissues Viral isolation Viral isolation of TeHV1 and 3 can be performed on reptilian cell cultures TH1 cells subline B1 ATCC CCL50 Classic cytopathic effects include cell rounding with cell detachment and lysis plaque formation Material required for laboratory analysis Serology 0205 ml serum in plastic tube Store at 4ºC and ship refrigerated Virology Pharyngeal swabs are collected for live animals For dead animals it is helpful to send the entire carcass if available or 1 g portions of each organ ideally If this approach is not possible the head including the tongue of the suspected individual can be submitted Place samples in viral transport media with antibiotic 12 ml for swabs and 3 ml per each tissue sample Store the samples at 4ºC for very shortterm storage and 80ºC for longterm storage Ship samples refrigerated or on dry ice accordingly Preserve the entire carcass and the head at 4ºC and ship refrigerated immediately Molecular diagnostic Same samples described for virology but in this case viral transport media is not required Samples can be stored and shipped also as described for the virology samples with the exception that for molecular diagnostic the samples can be stored also at 20ºC if 80ºC freezers are not available If only formalinfixed paraffinembedded tissues are available whole tissue blocks can be used If not possible please send 3 sections 20μthick each per tissue block in a plastic tube DNAse and RNAsefree The samples do not need to be refrigerated but should protected from light Histopathology The entire carcass is preferred if the carcass can be stored at 4ºC and shipped immediately refrigerated If the necropsy is performed in situ please collect routine samples of all the organs including the brain Samples need to be placed into a container with 10 buffered formalin Relevant diagnostic laboratories From US permits may be required for shipment to international labs Wildlife Diagnostic Laboratory at the Centre for Fish and Wildlife Health FIWI University of Bern Vetsuisse Faculty Länggassstrasse 122 3012 Bern Switzerland 41 31 631 2443 Fax 41 31 631 2635 Francescooriggivetsuisseunibech Institut Für Umwelt und Tierhygiene Universität Hohenheim Garbenstrasse 30 70599 Stuttgart Germany 49 711 459 22468 Fax 49 711 459 22431 Rachelmarschanggooglemailcom American Association of Zoo Veterinarians Infectious Disease Manual TESTUDINID HERPESVIRUSES Staatliches Veterinäruntersuchungamt Westernfeldtrasse 1 32758 Detmold Germany 49 05231 911640 Contact person Silvia Blahak Veterinary Laboratory Agency Weybridge Woodham Lane New Haw Addlestone Surrey KT15 3NB United Kingdom Contact person Sally Drury College of Veterinary Medicine University of Florida 2015 SW 16Ave 32610 Gainesville Fl USA 352 294 4420 childressaufledu Treatment Acyclovir and gancyclovir have been shown to be effective against TeHV3 in vitro Acyclovir also has been used to treat infected animals at 80mgkg PO SID or TID An in vivo study in marginated tortoises Testudo marginata showed that a single administration of this dose acyclovir results in a serum concentration of the drug which is lower than that reported to be effective against the virus in vitro Broad spectrum antibiotics and supportive rehydration therapy have also been described as part as the therapeutic protocol proposed for TeHVs infected tortoises The duration of the treatment may vary but it should be no less than two to three weeks unless otherwise suggested by the clinical evaluation and laboratory testing Prevention and control Tortoises showing clinical signs consistent with TeHVs infection should be isolated from clinically healthy individuals and tested for the presence of TeHVs PCR virus isolation and for the exposure to the virus by ELISA or SNT All clinical animals should also be treated with antiviral drugs and supportive therapy as appropriate Serological tests needs to be repeated after 8 ELISA or 1012 weeks SNT for all the tortoises showing clinical signs that tested negative at the first sampling Clinically healthy exposed animals should be closely monitored and tested for viral exposure similarly to what described above Serologically andor PCR positive animals that have recovered from the disease and clinically healthy animals that have seroconverted andor have tested positive by PCR following viral exposure should be considered carrier for life Currently no evidence exists that supports vertical transmission of the virus Preventive measures include 1 All the tortoises entering into established collections should be tested for the presence and exposure to the virus ideally both by molecular and serological tests Viral isolation is also recommended Animals should be tested during the quarantine period which ideally should last no less than 6 months Molecular diagnostic tests and viral isolation are relevant in the acute stage of the disease and during viral recrudescence when the virus is actively replicating Serological tests are relevant especially after the acute stage of the disease during the latency of the virus when seroconversion has occurred and no active viral replication can be detected Testing an animal during the acute stage of the disease with serological tests only is likely to provide a false negative result since seroconversion has not occurred yet However this is still recommended since some diseased animals might not be showing a primary infection but differently a recrudescence of the infection and so they might have already seroconverted Additionally for naïve negative animals this would be considered the preimmune serum Clinically healthy infected animals that have survived the acute stage of the disease are likely to shed the virus only sporadically and this can determine a high rate of false American Association of Zoo Veterinarians Infectious Disease Manual TESTUDINID HERPESVIRUSES negative animals if tested solely by PCR andor virus isolation at that time It is recommended to repeat two serological tests no less than 8 or 1012 weeks apart when running the ELISA test or the SNT respectively Occasional non reactors do exist 2 It is very important to avoid mixing of different tortoise species due to evidence of different species specific resistancessensitivity to TeHVs Mixing of different species might be fatal for the less resistant species 3 It is important to avoid overcrowding since close contact between tortoises is considered to enhance the transmission of TeHVs 4 Contaminated soil might contain viable virus for 24 up to 924 weeks according to the season of the year Exposure to full sunlight of the contaminated soil might reduce the viability of the virus present 5 Disposable gloves and shoe cover should be changed when moving from pen to pen and when touching different tortoises An appropriate hands disinfectant is also recommended 6 A veterinary health check should be performed ideally every 6 months For tortoises from temperate climates a health check performed before and after brumation is critical Suggested disinfectant for housing facilities Any proven virucidal compound may be used to disinfect contaminated instrument andor pen furniture Notification TeHVs associated diseases are not reportable at the moment Measures required under the Animal Disease Surveillance Plan NA Measures required for introducing animals to an infected animals If a seronegative animal is introduced to a seropositive animal it should be expected that the seronegative animal will seroconvert eventually Conditions for restoring diseasefree status after an outbreak NA Experts who may be consulted Francesco C Origgi DVM PhD DACVM DACVP DECZM Herpethology Centre for Fish and Wildlife Health FIWI Vetsuisse Faculty University of Bern Länggassstrasse 122 BernCH 41 31 631 2443 Fax 41 31 631 2635 Francescooriggvetsuisseunibech References 1 Bicknese EJ Childress AL Wellehan JF A novel herpesvirus of the proposed genus Chelonivirus from an asymptomatic bowsprit tortoise Chersina angulata J Zoo Wildl Med 201041353358 2 Gandar F Wilkie GS Gatherer D Kerr K Marlier D Diez M Marschang RE Mast J Dewals BG Davison AJ Vanderplasschen AF The genome of a tortoise herpesvirus Testudinid Herpesvirus 3 has a novel structure and contains a large region that is not required for replication in vitro or virulence in vivo J Virol 201589221143811456 3 Jacobson ER Berry KH Wellehan JFX Origgi FC Childress AL Braun J Schrenzel M Yee J Rideout B Serologic and molecular evidence for testudinid herpesvirus 2 infection in wild Agassizs desert tortoises Gopherus agassizii J Wildl Dis 201248747757 4 Marschang RE Gravendyck M Kaleta EF 1997 Herpesviruses in tortoises investigations into virus isolation and the treatment of viral stomatitis in Testudo hermanni and T graeca Zentralbl Veterinarmed B 199744385394 5 Marschang RE Schneider RM Antibodies to viruses in wildcaught spurthighed tortoises Testudo graeca in Turkey Vet Rec 2007161102103 American Association of Zoo Veterinarians Infectious Disease Manual TESTUDINID HERPESVIRUSES 6 Marschang RE Frost JW Gravendyck M Kaleta EF Comparison of 16 chelonid herpesviruses by virus neutralization tests and restriction endonuclease digestion of viral DNA J Vet Med B Infect Dis Vet Pub Health 200148393399 7 Marschang RE Gleiser CB Papp T Pfitzner AJ Böhm R Roth BN Comparison of 11 herpesvirus isolates from tortoises using partial sequences from three conserved genes Vet Microbiol 2006117258266 8 Origgi FC Tortoise Herpesvirus In Mader DR ed Reptile Medicine and Surgery St Louis MO WB Saunders Co 2006 p 814821 9 Origgi FC Testudinid herpesviruses a review J Herpetologic Med Surg 2012224254 10 Origgi FC Klein PA Mathes K Blahak S Marschang RE Tucker SJ Jacobson ER Enzymelinked immunosorbent assay for detecting herpesvirus exposure in Mediterranean tortoises spurthighed tortoise Testudo graeca and Hermanns tortoise Testudo hermanni J Clin Microbiol 20013931563163 11 Origgi FC Romero CH Bloom DC Klein PA Gaskin JM Tucker SJ Jacobson ER Experimental transmission of a herpesvirus in Greek tortoises Testudo graeca Vet Pathol 2004415061 12 VanDevanter DR Warrener P Bennett L Schultz ER Coulter S Garber RL Rose TM Detection and analysis of diverse herpesviral species by consensus primer PCR J Clin Microbiol 19963416661671 American Association of Zoo Veterinarians Infectious Disease Manual HISTOPLASMOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Inhalation ingestion of micro conidia from environment Nonspecific reflecting organ involvement Asymptomatic infection is most common but can progress to rapidly fatal illness Itraconazole or fluconazole amphotericin B Avoid contaminated soil especially areas where bird feces accumulate in endemic areas Not directly but humans are infected from environment Fact Sheet compiled by Maria Spriggs Sheet completed on 3 August 2011 updated 17 Feb 2018 Fact Sheet reviewed by Tiffany Wolf Susceptible animal groups Mammals including humans birds because of higher body temperature are not typically susceptible to natural infection although a single case report exists in an Eclectus parrot Published zoowildlife cases include dorcas gazelle snow leopard Patagonian cavy skunk spiny rat twotoed sloth ninebanded armadillo common opossum paca African pygmy hedgehog Bengal tiger European hedgehog sea mammals Causative organism Histoplasma capsulatum Zoonotic potential No although commonsource infection of people and animals is possible Distribution Worldwide except Antarctica In the US most common in region of Ohio Missouri and Mississippi Rivers The organism is found commonly in soil that contains bird and bat manure as nitrogenrich soil supports fungal growth Bats may play role in spreading disease as they can develop chronic intestinal dissemination and shed yeast in feces The organism may be inhaled or ingested and may remain within the lungs or disseminate systemically Incubation period 1216 days Clinical signs Subclinical infection is most common When signs are present they may be chronic and nonspecific Pulmonary form pneumonia wheezes fever weight loss cough depression Mediastinal lymphadenitis form hilar lymphadenopathy cough respiratory distress Progressive disseminated form Any tissue can be involved In domestic cats fever weight loss anemia interstitial lung disease hepatomegaly splenomegaly and rarely oral and lingual ulcerations In domestic dogs fever large bowel diarrhea intestinal blood loss anemia depression Any species bone lesions ocular lesions CNS skin nodules Equine abortion mare appears healthy but placenta involved Post mortem gross or histologic findings Pulmonary form miliary or larger gray granulomas may be calcified Disseminated form visceral organs are generally thickened gastrointestinal mucosa hemorrhagic enlarged liver with variegated pale pattern lymphadenopathy Histoplasma organisms are usually numerous in granulomas and infected tissue Diagnosis Cytologyhistopathology gold standard Diagnosis can be made by FNAcytology especially rectal scrapings blood film or abnormal fluids and tissues With tissue biopsy organisms are difficult to detect with routine HE stain but stain well with PAS Gomoris methenamine silver and Gridleys fungal stains Yeast forms in macrophages and giant cells are round to ovoid structures with thin cell wall and a thin clear zone between the cell wall and cellular cytoplasm Clinical pathology Nonregenerative anemia thrombocytopenia might visualize organism in cells on buffy coat smear American Association of Zoo Veterinarians Infectious Disease Manual HISTOPLASMOSIS Radiography diffuse interstitial miliary or nodular infiltrates hilar lymphadenopathy dogscats rarely osseous lesions are present and when present they are more typical in distal limbs Culture lung skin lesions or bone marrow give highest yield in disseminated cases Antigen detection greatest sensitivity when test both urine and serum and CSF in CNS cases Urine Histoplasma EIA is highly specific and sensitive in dogs Serology variably reliable but may be useful in mild cases with negative antigen results Molecular PCR not well established high rate of false negatives in published studies Material required for laboratory analysis Serum urine tissue or fluid sample for cytologyhistopathculture Relevant diagnostic laboratories MiraVista Diagnostics for antigen testing wwwmiravistalabscom also does azole levels Many state and university labs run serology including Cornell Kansas State Treatment Infection can be selflimiting and resolve without treatment but treatment is recommended Itraconazole or amphotericin B traditionally is drug of choice However fluconazole may be better for ocular or CNS involvement Wilson et al 2018 found fluconazole to be an effective treatment in dogs with no difference in survival remission or disease relapse rates as compared to itraconazole Posaconazole and voriconazole are newer and effective drugs but are expensive and have little information in vet medicine literature Treatment interval is 46 months and at least 1 month after resolution of clinical signs and after antigen concentrations are negative or below 2 ngmL Prognosis is fair to excellent for pulmonary histoplasmosis and guarded to good for disseminated disease Prevention and control Avoid contaminated soil Suggested disinfectant for housing facilities The only proven disinfectant is 3 formalin If an accumulation of bird or bat manure is discovered in a building removing the material by handbroomshovel is NOT always the best Leaving the material alone with signs to warn of health risk may be best course of action Truckmounted or trailermounted vacuum systems are recommended for buildings with large accumulations to reduce risk of dust exposure It is recommended to use a vendor experienced in removal of infectious materials See httpwwwcdcgovnioshdocs2005109 Notification None required Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Direct transmission from infected animal to human or other animal is unlikely because yeast phase is not as infectious as mycelial phase Conditions for restoring diseasefree status after an outbreak NA Experts who may be consulted Joe Wheat MD MiraVista Labs jwheatmiravistalabscom 8666472847 Lynn Guptill DVM PhD Dipl ACVIM Purdue University College of Veterinary Medicine 625 Harrison Street West Lafayette IN 47907 7654941107 guptillcpurdueedu References 1 Aulakh HK Aulakh KS Troy GC Feline histoplasmosis a retrospective study of 22 cases 19862009 J Amer Anim Hosp Assoc 201248182187 American Association of Zoo Veterinarians Infectious Disease Manual HISTOPLASMOSIS 2 Cook AK Cunningham LY Cowell AK Wheat LJ Clinical evaluation of urine Histoplasma capsulatum antigen measurement in cats with suspected disseminated histoplasmosis J Feline Med Surg 201214 512515 3 Lappin MR Polysystemic mycotic infections histoplasmosis In Nelson RW Couto C eds Small Animal Internal Medicine 4th ed St Louis MO Mosby Elsevier 2008 p 1356 4 EspinosaAviles D Taylor ML del Rocio ReyesMontes M PerezTorres A Molecular findings of disseminated histoplasmosis in two captive snow leopards Uncia uncia J Zoo Wildl Med 200839450 454 5 Taboada J Grooters AM Histoplasmosis blastomycosis sporotrichosis candidiasis pythiosis and lagenidiosis In Ettinger SJ Feldman EC eds Textbook of Veterinary Internal Medicine 7th ed Philadelphia PA Saunders Elsevier 2010 p 971983 6 Farinas F Flores L Rodriguez P Sabalete T Quevedo MA Disseminated histoplasmosis in a dorcas gazelle Gazella dorcas neglecta kept in captivity conditions in Spain Rev Iberoam Micol 200926 152154 7 Duncan M Fungal diseases in all taxa In Fowler ME Miller RE eds Zoo and Wildlife Medicine 5th Ed St Louis MO Saunders Elsevier 2003 p 727732 8 Greene CE Histoplasmosis In Greene CE ed Infectious Diseases of the Dog and Cat 3rd ed St Louis MO Saunders Elsevier 2006 p 577584 9 Jacobsen B Baumgartner W Bialek R Disseminated histoplasmosis in a European hedgehog Erinaceus europaeus in Northern Germany Mycoses 201154538541 10 Cahn CM Line S Histoplasmosis In The Merck Veterinary Manual 10th Ed Whitehouse Station NJ Merck Co Inc 2010 p 584585 11 Keller DL Steinberg H Sladky KK Disseminated histoplasmosis in a Bengal tiger Panthera tigris J Zoo Wildl Med 201142727731 12 Lainson R Shaw JJ Pneumocystis and Histoplasma infections in wild animals from the Amazon region of Brazil Trans Royal Soc Trop Med Hyg 197569 5058 13 Histoplasmosis fact sheet Internet Louisiana Office of Public Health 2017 cited 2018 November 15 Available from httpwwwdhhlouisianagovofficesmiscdocsdocs249ManualHistoplasmosisManualpdf 14 Naiff RD Mok WY Naiff MF Distribution of Histoplasma capsulatum in Amazonian wildlife Mycopathologia 198589165168 15 Quist EM Belcher C Levine G Johnson M Heatley JJ Kiupel M Giri D Disseminated histoplasmosis with concurrent oral candidiasis in an Eclectus parrot Eclectus roratus Avian Path 201140207211 16 RosasRosas A JuanSalles C Garner MM Pathological findings in a captive colony of maras Dolichotis patagonum Vet Rec 200615872731 17 Wheat J 2010 Histoplasmosis in Veterinary Medicine MiraVista Diagnostics wwwmiravistalabscom 18 Wilson AG KuKanich KS Hanzlicek AS Payton ME Clinical signs treatment and prognostic factors for dogs with histoplasmosis J Am Vet Med Assoc 2017252201214 19 Woolf A GremillionSmith C Pathologic findings in rabiessuspect randomsource and accidentally killed skunks J Am Vet Med Assoc 198618910891091 American Association of Zoo Veterinarians Infectious Disease Manual HUMAN METAPNEUMOVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals all primates should be considered susceptible particularly great apes In vivo virus replication in small rodents Aerosols fomites direct contact with nasal and respiratory secretions Transmission via feces also possible None to severe lethargy lack of appetite upper and lower less common respiratory signs eg nasal discharge sore throat fever cough Mild prior exposure to fatal naïve animals Supportive care and treatment for secondary bacterial infections Streptococcus pneumoniae documented in chimpanzees Proper and strict enforcement of biosecurity measures early detection isolation of infected animals if feasible Yes Fact Sheet compiled by Owen M Slater Sheet completed on 24 January 2018 Fact Sheet Reviewed by James G Johnson III Susceptible animal groups Disease documented in chimpanzees mountain gorilla Sulawesi crested macaques and brownheaded spider monkeys However all primates should be considered susceptible Fatalities reported in wild and captive great apes Causative organism Human metapneumovirus Paramyxoviridae Pneumovirus Zoonotic potential Yes Distribution Worldwide with highest occurrence between winter early summer in North America Incubation period Approximately 57 days Clinical signs Animals None to severe including lethargy decreased appetite cough dry or productive nasal discharge and sneezing Clinical signs indistinguishable from respiratory syncytial virus RSV or other respiratory viral infections Humans Signs usually consistent with upper respiratory tract infection and sometimes lower respiratory tract infection eg bronchitis bronchiolitis pneumonia such as fever wheezing cough nasal congestion and less so dyspnea diarrhea and vomiting particularly in children Immunocompetent adults typically have mild clinical signs Almost all children have been exposed to the virus by 5 years of age and 100 by 10 years Reinfection common Post mortem gross or histologic findings Gross findings Nasal discharge dehydration Histologic findings Among those cases with evidence of pneumonia marked subacute to acute necrotizing bronchointerstitial pneumonia characterized by bronchial epithelial hyperplasia and necrosis diffuse alveolar damage with hyaline membranes and type II pneumocyte hyperplasia Secondary purulent bronchopneumonia not uncommon Diagnosis Ante mortem PCR on respiratory specimens and feces immunofluorescence or enzyme immunoassay on respiratory secretions Serology on acute and convalescent sera Post mortem PCR VI Material required for laboratory analysis Nasopharyngeal swab oropharyngeal swab nasal wash tracheal aspirate or BAL feces serum Pathologic specimens eg lung tissue also acceptable Relevant diagnostic laboratories Labs capable of performing PCR testing on human respiratory viruses Treatment Supportive care especially for treatment of dehydration and secondary bacterial infections Several fatal cases of hMPV in chimpanzees often have underlying Streptococcus pneumoniae infections Prevention and control It is recommended that all employees working in close contact with non human primates wear gloves and face masks always Personnel with symptoms consistent with a respiratory infection should stay home andor not visit freeranging primate troops Isolate infected and cohortinfected animals if practical and review andor enhance biosecurity protocols American Association of Zoo Veterinarians Infectious Disease Manual HUMAN METAPNEUMOVIRUS Suggested disinfectant for housing facilities Routine disinfection protocols 01 sodium hypochlorite Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal No required measures However it is recommended that no introductions occur during active disease Serology can be performed prior to any new introductions to determine if any animals are naïve and therefore more likely to develop severe disease Conditions for restoring diseasefree status after an outbreak Virus is cleared by infected animals Disease free status restored after each outbreak Experts who may be consulted Dr Fabian Leendertz Dr Eileen Schneider Robert Koch Institute Centers for Disease Control and Prevention Nordufer 20 1600 Clifton Rd Berlin 13353 Atlanta GA 30333 Germany USA References 1 Hamelin ME Abed Y Boivin G Human metapneumovirus a new player among respiratory viruses Clin Infect Dis 200438 983990 2 Kaur T Singh J Tong S Humphrey C Clevenger D Tan W Szekely B Wang Y Li Y Alex Muse E Kiyono M Descriptive epidemiology of fatal respiratory outbreaks and detection of a humanrelated metapneumovirus in wild chimpanzees Pan troglodytes at Mahale Mountains National Park Western Tanzania Am J Primatol 20087075565 3 Köndgen S CalvignacSpencer S Grützmacher K Keil V MätzRensing K Nowak K Metzger S Kiyang J Becker AL Deschner T Wittig RM Evidence for Human Streptococcus pneumoniae in wild and captive chimpanzees A potential threat to wild populations Sci Rep 201771 14581 4 Köndgen S Kühl H NGoran PK Walsh PD Schenk S Ernst N Biek R Formenty P MätzRensing K Schweiger B Junglen S Pandemic human viruses cause decline of endangered great apes Curr Biol 200818260264 5 Palacios G Lowenstine LJ Cranfield MR Gilardi KV Spelman L LukasikBraum M Kinani JF Mudakikwa A Nyirakaragire E Bussetti AV Savji N Human metapneumovirus infection in wild mountain gorillas Rwanda Emerg Infect Dis 201117711713 6 Panda S Mohakud NK Pena L Kumar S Human metapneumovirus review of an important respiratory pathogen Int J Infect Dis 2014254552 7 Slater OM Terio KA Zhang Y Erdman DD Schneider E Kuypers JM Wolinsky SM Kunstman KJ Kunstman J Kinsel MJ Gamble KC Human Metapneumovirus Infection in Chimpanzees United States Emerg Infect Dis 2014201221152118 American Association of Zoo Veterinarians Infectious Disease Manual INCLUSION BODY DISEASE Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Snakes especially members of Boidae and Pythonidae usually in human care Undetermined likely through direct contact vertical transmission Ophionyssus natricis mites may be vector Variable asymptomatic to severe disease NonCNS anorexia regurgitation stomatitis pneumonia and lymphoproliferati ve disorders CNS disorientation ataxia head tremors and opisthotonos Usually fatal None Supportive therapy may be elected in individual cases Maintenance of a closed group or strict quarantine of new arrivals and testing with the intent to cull infected snakes mite control No Fact Sheet Compiled by Erica Wilson Lipanovich and Rich Sim Completed on updated 11 January 2019 Fact Sheet Reviewed by Rachel Marschang Tara Harrison Susceptible Animal Groups Almost exclusively snakes of the Boidae and Pythonidae families Similar inclusions have also been reported in palm vipers Bothriechis marchi Eastern kingsnakes Lampropeltis getulus and corn snakes Elaphe guttata Causative Organism Family Arenaviridae genus Reptarenavirus this etiological agent has only recently been identified It seems that pathogenic and nonpathogenic reptarenaviruses exist and pathogenic ones can affect species differently Arenaviral coinfections may be common in snakes clinical for IBD Older literature suspected a retrovirus was causative Zoonotic Potential No Distribution Worldwide Incubation Period weeks to years Clinical Signs Highly variable infected animals can be asymptomatic or develop severe disease which can include anorexia regurgitation neurological signs disorientation ataxia head tremors opisthotonus inability to right itself and flaccid paralysis or secondary bacterial infections stomatitis and pneumonia Pythons are reported to have a more acute severe and CNSinvolved disease progression without regurgitation or other gastrointestinal signs Boas especially boa constrictors commonly have regurgitation anorexia and CNS signs Boas can maintain high levels of viremia and accumulated widespread intracytoplasmic inclusions without clinical signs and may have more chronic disease course Lymphoproliferative disorders have recently been associated with IBD in boa constrictors Post mortem Gross or Histological Findings Eosinophilic to amphophilic intracytoplasmic IC inclusions in HEstained tissue sections composed of 68 kDa reptarenaviral nucleoprotein NP Cells with inclusions can frequently be observed in the absence of associated inflammation Tissue tropism can be diverse Within the CNS inclusions may be observed in neurons and glial cells With acute neurologic disease eg pythons inclusions are often limited to the CNS With American Association of Zoo Veterinarians Infectious Disease Manual INCLUSION BODY DISEASE chronic disease eg boa constrictors inclusions can be seen in epithelial cells enteric respiratory and renal hepatocytes pancreatic acinar cells and mononuclear cells Diagnosis As detailed above finding IC inclusions or virus by PCR in a live python can be challenging less so for a boa Antemortem diagnostic options include o Light microscopy exam of a peripheral blood smear for IC inclusions in WBCs with HE or Wright Giemsa stain o Arenavirus RTPCR at University of Florida of an esophageal swab or whole blood sample o Tissue biopsies esophageal tonsils liver kidney obtained via endoscopy with IC inclusions seen on HE stain Arenavirus RTPCR at University of Florida For postmortem histopathology andor PCR on brain kidney liver pancreas are recommended Of note immunohistochemical testing of blood and tissues for NP used to be available at University of Florida but has been discontinued Material Required for Laboratory Analysis Blood esophageal swabs serum or biopsies from the liver tonsils or gastric mucosa Contact laboratory for handling and shipping instructions Relevant Diagnostic Laboratories University of Florida Veterinary Diagnostic Lab April Childress University of Florida 2015 SW 16th Ave Building 1017 Room V2186 Gainesville FL 32608 Phone 3522944420 Please contact April Childress childressaufledu prior to sample submission Sample Submission Form for PCR and sequencing Treatment There is no effective treatment Supportive measures include antimicrobial and fluid therapy Appropriate environmental conditions including temperature and humidity are essential Diazepam may be useful for treatment of seizures Prevention and Control Quarantine of all incoming snakes for a minimum of 90 days Good hygiene prevention of exposure to infected animals pest control and removal of infected animals See below for disinfection recommendations Snakes suspected of IBD should be isolated Diagnostic samples mentioned above should be collected and submitted for evaluation Infected snakes should be euthanized and necropsied Suggested Disinfectant for Housing Facilities Arenaviruses are an enveloped RNA virus they can be inactivated by most detergents and disinfectants including 1 sodium hypochlorite phenolic compounds 3 acetic acid lipid solvents and detergents eg sodium dodecyl sulfate SDS formaldehyde and glutaraldehyde 2 Arenaviruses in general are inactivated with heating to 5660C 122140F exposure to gamma or UV irradiation exposure to pH less than 55 or greater than 852 autoclaving incineration and boiling Notification No Measures Required under the Animal Disease Surveillance Plan None Measure Required for Introducing Animals to Infected Animal Not recommended Conditions for Restoring DiseaseFree Status after an Outbreak Sick snakes should never be introduced into an established collection It is unknown what percentage of snakes with reptarenavirus infection will develop clinical signs and how many will remain clinically healthy Experts Who May Be Consulted Jim Wellehan DVM PhD DACZM DACVM Department of Small Animal Clinical Sciences University of Florida Phone 352 3922235 wellehanjufledu American Association of Zoo Veterinarians Infectious Disease Manual INCLUSION BODY DISEASE References 1 Banajee KH Chang L Jacobson ER Rich GA Royal AB What is your diagnosis Blood film from a boa constrictor Vet Clin Pathol 20124115159 2 Bodewes R Kik MJ Raj VS Schapendonk CM Haagmans BL Smits SL Osterhaus AD Detection of novel divergent arenaviruses in boid snakes with inclusion body disease in The Netherlands J Gen Virol 2013946120610 3 Chang L Fu D Stenglein MD Hernandez JA DeRisi JL Jacobson ER 2016 Detection and prevalence of boid inclusion body disease in collections of boas and pythons using immunological assays Vet J 2016218138 4 Hetzel U Sironen T Laurinmäki P Liljeroos L Patjas A Henttonen H Vaheri A Artelt A Kipar A Butcher SJ Vapalahti O Isolation identification and characterization of novel Arenaviruses the etiological agent of Boid Inclusion Body Disease J Virol 201387201091835 5 Jacobson ER Viruses and viral diseases of reptiles In Jacobson ER ed Infectious diseases and pathology of reptiles Boca Raton FL CRC Press 2007 p 409474 6 Keller S Hetzel U Sironen T Korzyukov Y Vapalahti O Kipar A Hepojoki J Coinfecting reptarenaviruses can be vertically transmitted in boa constrictor PLOS Pathog 2017131 e1006179 7 Marschang RE Clinical virology In Divers SJ Mader DR Eds Current Therapy in Reptile Medicine and Surgery St Louis MO Elsevier Saunders 2014 p 3252 8 Ossiboff RJ Serpentes In Terio KA McAloose D St Leger J eds Pathology of Wildlife and Zoo Animals Cambridge MA Academic Press 2018 p 897919 9 Schilliger L Selleri P Frye FL Lymphoblastic lymphoma and leukemic blood profile in a redtail boa Boa constrictor constrictor with concurrent inclusion body disease J Vet Diagn Invest 201123159162 10 Schilliger L Rossfelder A Bonwitt J Di Girolamo N Rival F Gandar F Selleri P Nicolier A Antemortem diagnosis of multicentric lymphoblastic lymphoma lymphoid leukemia and inclusion body disease in a boa constrictor Boa constrictor imperator J Herpetol Med Surg 2014241119 11 Stenglein MD Sanders C Kistler A Ruby JG Franco JY Reavill DR Dunker F DeRis JL Identification characterization and in vitro culture of highly divergent arenaviruses from boa constrictors and annulated tree boas candidate etiological agents for snake inclusion body disease MBio 201234e0018012 12 Stenglein MD Guzman DS Garcia VE Layton ML HoonHanks LL Boback SM Kell MK Drazenovich T Hawkins MG DeRisi JL Differential disease susceptibility in experimentally reptarenavirus infected boa constrictors and ball pythons J Virol 20179115e0045117 13 Strik NI Alleman AR Harr KE Circulating inflammatory cells In Jacobson ER ed Infectious diseases and pathology of reptiles Boca Raton FL CRC Press 2007 p 167218 14 Summa NM Guzman DS Hawkins M Grosset C Chen V Goldsmith D Keel K Woolard K Young A Bucy D Steffey M Tracheal and colonic resection and anastomosis in a boa constrictor Boa constrictor with Tcell lymphoma J Herpetol Med Surg 2015258799 15 Hepojoki J Salmenperä P Sironen T Hetzel U Korzyukov Y Kipar A Vapalahti O Arenavirus Coinfections Are Common in Snakes with Boid Inclusion Body Disease J Virol 201589168657 60 16 Stenglein MD Jacobson ER Chang LW Sanders C Hawkins MG Guzman DS Drazenovich T Dunker F Kamaka EK Fisher D Reavill DR Meola LF Levens G DeRisi JL Widespread recombination reassortment and transmission of unbalanced compound viral genotypes in natural arenavirus infections PLoS Pathog 201515e1004900 American Association of Zoo Veterinarians Infectious Disease Manual INFECTIOUS HEMATOPOETIC NECROSIS VIRUS IHNV Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Salmonids Horizontal usually by direct contact with mucus urine feces eggsmilt Vertical transmission is suspected Gills may be important portal of entry as virus survives 1 mo in water and sediment It also is transmitted via insect annelid and crustacean vectors Lethargy with sporadic hyperactivity ascites white fecal casts dorsal darkening petechiation coelomic distension hemorrhage exophthalmia and pale gills Acute mortal ities occur and scoliosis is observed in survivors Varies by strain and temperature Highest mortality in younger fish at 815C Older animals present lower mortality rates and fewer clinical signs Increase temperature to 15C if possible consider euthanasia of affected animals OIE reportable disease Excellent biosecurity isolation and disinfection Egg disinfection Culling and disinfection in the face of an outbreak Increase temperature to 15C No Fact Sheet compiled by Catherine Hadfield Sheet completed on 28 November 2010 updated 5 July 2013 Fact Sheet Reviewed by Brent Whitaker E Scott Weber III Susceptible animal groups Salmonids both freshwater and saltwater and especially rainbow trout Oncorhyncus mykiss Atlantic salmon Salmo salar chinook salmon O tshawytscha sockeye salmon O nerka and chum salmon O keta Generally considered resistant are lake trout Salvelinus namaycush arctic char Salvelinus alpinus and coho salmon O kisutch Causative organism Family Rhabdoviridae genus Novirhabdovirus IHNV Several clades of virus exist with certain clades or strains being isolated within certain geographic regions Zoonotic potential None Distribution Endemic to Pacific coast of North America Alaska to California It is now endemic to Japan and continental Europe Outbreaks in other parts of the US and Asia have occurred Incubation period Temperature dependent 545 days Clinical signs The clinical presentation is more common in fry and fingerlings Lethargy with sporadic hyperactivity is seen Coelomic distension presents due to ascites Pale fecal casts are observed trailing from vent Darkening petechiation erythema exophthalmia and pale gills due to anemia are observed Rapidly escalating mortalities occur which may reach 90 Scoliosis and lordosis are common in 560 of fry and fingerling survivors On hematology leukopenia neutropenia and anemia with increased numbers of bilobed erythrocytes may be observed American Association of Zoo Veterinarians Infectious Disease Manual INFECTIOUS HEMATOPOETIC NECROSIS VIRUS IHNV Post mortem gross or histologic findings Petechiation erythema and pallor may be observed grossly Necrosis of renal hematopoietic tissue and spleen possible focal necrosis in liver and gastrointestinal tract can be seen Degeneration and necrosis of granular cells in the lamina propria stratum compactum and stratum granulosum of the gastrointestinal tract is sometimes considered pathognomonic for IHN Pleiomorphic intracytoplasmic and intranuclear inclusions in the pancreas can be observed Older fish show fewer histologic lesions Diagnosis Presumptive diagnosis is based on species clinical signs age temperature and geographic location Definitive diagnosis for OIE requires viral isolation followed by molecular or immunologic identification Other tests are available eg virus neutralization indirect fluorescent antibody testing RT PCR and staphylococcal coagglutination but are not approved for surveillance Of these tests the staphylococcal coagglutination is the most rapid Material required for laboratory analysis Live fish mucus or eggs Dead fish the same as live and also kidney and spleen by sterile collection or whole fish Pool tissues from up to 10 fish 05 g with viral transport media and antibiotics eg 4ml 10 fetal calf serum and 200 IU penicillin 200 μg streptomycin and 200 μg kanamycin per ml Transport at 4C ASAP Relevant diagnostic laboratories State Fish Health Laboratories university laboratories specializing in fish virology eg UC Davis Fish Health Laboratory Treatment Increase temperature to 15C if possible Prevention and control Excellent biosecurity is important prevention measure For stocking only acquire disinfected eggs commonly iodophor disinfection or from IHNVfree stock Use virusfree water or disinfect with ozone or UV Sterilize feed eg by heat Consider nonsusceptible species in endemic areas surveillance of the youngoftheyear and female broodstock and selective breeding to maintain virusfree stock Commercial vaccine Novartis available in US and several products are under trial In the face of an outbreak cull and disinfect affected animals and increase temperature for remaining animals Suggested disinfectant for housing facilities Virus is inactivated by formalin sodium hypochlorite iodophors gamma and UV irradiation pH 4 or 10 or temperatures 60C for 15 minutes Resistant to ethanol Notification Reportable disease must notify the OIE Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Do not introduce susceptible fish to affected animals Conditions for restoring diseasefree status after an outbreak When the disease is first detected an infected zone is established and a buffer zone is established peripheral to the problem All infected animals are either culled or removed from the infected zone to reduce the risk of disease transmission and the area is disinfected Biosecurity measures are reviewed and modified as needed within the infected zone Surveillance is established until no virus is detected for at least 2 years Experts who may be consulted Dr James R Winton Chief of the Fish Health Section Western Fisheries Research Center United States Geological Survey Seattle WA 206 526 6587 jwintonusgsgov References 1 AFS Suggested Procedures for the Detection and Identification of Certain Finfish and Shellfish American Association of Zoo Veterinarians Infectious Disease Manual INFECTIOUS HEMATOPOETIC NECROSIS VIRUS IHNV Pathogens 2010 Blue Book American Fisheries Society Bethesda MD CDROM 2 Crane M and A Hyatt 2011 Viruses of fish an overview of significant pathogens Viruses 3 20252046 3 Bootland LM and JC Leong 2010 Infectious haematopoietic necrosis virus In Woo PTK ed Fish Diseases and Disorders Volume 3 Viral Bacterial and Fungal Infections CABI Publishing Wallingford UK Pp 66109 4 Kim HJ N Oseko T Nishizawa and M Yoshimizu 2009 Protection of rainbow trout from infectious hematopoietic necrosis IHN by injection of infectious pancreatic necrosis virus IPNV or Poly IC Dis Aquat Org 83 105113 5 McClure CM S Saksida G Karreman J Constantine J Robinson G Traxler and L Hammell 2008 Evaluation of a reverse transcriptase polymerase chain reaction test and virus isolation on field samples collected for the diagnosis of Infectious Hematopoietic Necrosis Virus in cultured Atlantic Salmon in British Columbia J Aquat Anim Health 29 1218 6 Mulcahy D D Klaybor and WN Batts 1990 Isolation of infectious hematopoietic necrosis virus from a leech Piscicola salmositica and a copepod Salmincola sp ectoparasites of sockeye salmon Oncorhynchus nerka Dis Aquat Org 8 2934 7 OIE Manual of Diagnostic Tests for Aquatic Animals 2013 Office International des Epizooties Paris France 554 pp 8 Plumb JA 1999 Trout and salmon viruses In Plumb JA ed Health Maintenance and Principal Microbial Diseases of Cultured Fishes Iowa State University Press Ames Iowa Pp 103 146 9 Purcell MK G Kurath K Garver RP Herwig and JR Winton 2004 Quantitative expression profiling of immune response genes in rainbow trout during IHNV infection or following vaccination with a DNA vaccine against IHNV Fish Shellfish Immunol 17 447462 10 Purcell MK SA Hart G Kurath and JR Winton 2006 Strandspecific realtime RTPCR assays for quantification of genomic and positivesense RNAs of the fish rhabdovirus infectious hematopoietic necrosis virus J Virol Methods 132 1824 11 Purcell MK KM Nichols JR Winton GK Kurath GH Thorgaard P Wheeler JD Hansen RP Herwig and LK Park 2006 Comprehensive gene expression profiling following DNA vaccination against infectious hematopoietic necrosis virus Molec Immunol 43 20892106 12 Smail DA and ALS Munro 2001 The virology of teleosts In Roberts RJ ed 3rd ed Fish Pathology WB Saunders Philadelphia Pennsylvania Pp 169253 American Association of Zoo Veterinarians Infectious Disease Manual KLEBSIELLA Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All vertebrates Environmental sources nosocomial infections fecaloral respiratory cockroach or house fly vector normal intestinal or oropharyngeal flora Wide range of clinical presentation septicemia abscessation multiple organ inflammation Hypermucoviscous phenotype of K pneumoniae is an emerging pathogen of humans primates and freeliving seals Variable hypervirulent strains emerging pathogen of humans domestic animals primates otariid and phocid seals Antibiotics with Gramnegative activity pending appropriate sensitivity testing Multidrug resistant strains of emerging importance in humans and animals Good sanitation disinfection protocols for commissary and medical equipment pest control with emphasis on roach and fly control Potentially zoonotic close genetic relationships exist between humans livestock birds and freeliving seals Fact Sheet compiled by Kelly Helmick Sheet completed on 3 August 2011 updated 17 December 2012 updated 21 February 2018 Fact Sheet Reviewed by June Olds James Steeil Susceptible animal groups All vertebrates are susceptible Epizootics in captive and freeranging primates captive rabbits captive and freeranging rodents freeranging otariid seals domestic carnivores domestic ungulates and humans Isolated reports in captive civet gecko lizard American alligator brown tree frog Isolated from wild and rehabilitated seabirds captive healthy garter snake K pneumoniae hypermucoviscosity phenotype is an emerging disease of humans nonhuman primates and otariid seals associated with increased invasiveness and pathogenicity Multidrug resistant strains of K pneumoniae emerging in human and animal isolates Multidrug resistant pathogenic strains of K pneumoniae isolated from a variety of confiscated psittacine and passerine species Causative organism Klebsiella sp gramnegative bacteria Enterobacteraciae K oxytoca and K pneumoniae Hypervirulent K pneumoniae strains with a generegulated hypermucoviscosity HMV capsular phenotype that is a significant contributing factor to pathogen virulence The HMV phenotype strain is emerging as an important pathogen of humans nonhuman primates and otariid seals Multiantibiotic K pneumonia resistant strains are emerging pathogens of veterinary and human importance Transmission Normal inhabitant of soil and water benign inhabitant of the gastrointestinal tract and oropharynx can colonize medical equipment contamination of foodstuffs Hospital and nosocomial infections in humans and domestic animals Houseflies and cockroaches carry multidrug resistant strains of K pneumoniae Fecal contamination is a common transmission method for cattle with mastitis Human microbial marine pollution is a suspected source for isolates obtained from freeliving seals Dissemination through the respiratory tract occurs in humans African green monkeys Chlorocebus aethiops sabaeus and is suspected in California sea lions Zalophus californianus A hypervirulent K pneumoniae was isolated on oropharyngeal swab of a captive blackandwhite ruffed lemur Varecia variegate that survived infection but no isolates obtained from fecal and oropharyngeal swabs of unaffected conspecifics K oxytoca and hypervirulent K pneumoniae detected on rectal swab from freeliving African green monkeys Chlorocebus aethiops sabaeus Hypervirulent K pneumoniae detected in the oropharyngeal tissues intestine and renal tubules of California sea lions findings may represent normal flora andor other potential routes of transmission for this species Bacterial virulence factors and host factors that promote Klebsiella infection and disease not fully understood Zoonotic potential Zoonotic potential of K pneumoniae HMV phenotype is unknown but is an emerging disease of humans and has been isolated from domestic animals nonhuman primates phocid seals and otariid seals with clinical illness Close genetic relationships between K pneumoniae isolates from humans livestock birds and freeliving seals Distribution Worldwide American Association of Zoo Veterinarians Infectious Disease Manual KLEBSIELLA Incubation period Undetermined Clinical signs Causes a wide range of clinical presentation in affected vertebrates anorexia lethargy pneumonia septicemia hypopyon endophthalmitis mastitis metritis meningitis peritonitis urinary tract infections abscessation Common clinical presentations of domestic animals include mastitis cattle bacteremia calves metritis horses septicemia and pneumonia foals pneumonia urinary tract infection and enteritis dogs polyarthritis goats associated with stomatitis and dermatitis in reptiles suppurative otitis in lemmings Dicrostonyx spp Marine mammals Mortality from natural infection with hypervirulent multidrug resistant K pneumoniae caused acute to subacute respiratory infection in stranded juvenile subadult and adult California sea lions Zalophus californianus meningoencephalitis in New Zealand sea lion Phocarctos hookeri pups cervical abscessation pyothorax omphalitis and peritonitis in stranded common seals Phoca vitulina Primates Mortality from natural infection with hypervirulent multidrug resistant K pneumoniae caused septicemic infection and suppurative meningoencephalitis in a captive cynomolgus monkey Macaca fascicularis suppurative peritonitis in a captive goldhanded tamarin Saguinus midas midas bronchopneumonia and bacteremia in a freeranging goldenheaded lion tamarin Leontopithecus chrysomelas peracute mortality and meningitis in captive lemurs Varecia variegate hepatic and abdominal abscessation in captive African green monkeys Chlorocebus aethiops sabaeus Mortality with multisystemic abscessation African green monkeys Chlorocebus aethiops sabeus noted following experimental infection with a hypervirulent K pneumoniae Post mortem gross or histologic findings Necropsy findings include abscessation of liver lung abdomen or other organs septicemia thoracic or abdominal effusions or other suppurative changes Gramnegative bacilli with a prominent capsule Diagnosis Bacterial culture PCR IHC Culture should include sensitivity testing due to variable antibiotic susceptibility patterns Hyperviscous K pneumoniae produces abundant capsular material on blood agar such that a mucoid string 5mm is lifted off the agar plate string test Phenotyping and molecular characterization for hypervirulent and multidrug resistant strains recommended Material required for laboratory analysis Blood exudate tissue feces sputum urine CSF Relevant diagnostic laboratories Routine microbiology laboratories for culture Genotyping recommended in epizootics Treatment Empirical antibiotic treatment with drugs exhibiting a Gramnegative spectrum of activity modified based on susceptibility testing Resistant strains are emerging resistance to cephalosporins and monobactams through extendedspectrum βlactamases and resistance to almost all β lactams including carbapenems through carbapenemases Hypervirulent strains may also complicate treatment and success rates Prevention and control Good sanitation and biosecurity Fly and cockroach control Appropriate sterilization or disinfection of medical equipment Appropriate food handling and commissary disinfection protocols Suggested disinfectant for housing facilities No special requirements other than good hygiene practices biosecurity and disinfection protocols Notification No special requirements Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal No special requirements animals should be free from clinical illness and reevaluation with culture diagnostics as appropriate Conditions for restoring diseasefree status after an outbreak No special requirements Experts who may be consulted None References 1 Bonney CH Hartfield DA Schmidt RE Klebsiella pneumoniae infection with secondary hypopyon in Tokay gecko lizards J Am Vet Med Assoc 197817311151116 American Association of Zoo Veterinarians Infectious Disease Manual KLEBSIELLA 2 Bueno MG Iovine RO Torres LN CatãoDias JL Pissinatti A Kierulff MC Carvalho VM Pneumonia and bacteremia in a goldenheaded lion tamarin Leontopithecus chrysomelas caused by Klebsiella pneumoniae subsp pneumoniae during a translocation program of freeranging animals in Brazil J Vet Diag Invest 2015 273 387391 3 Burke RL West MW ErwinCohen R Selby EB Fisher DE Twenhafel NA Alterations in cytokines and effects of dexamethasone immunosuppression during subclinical infections of invasive Klebsiella pneumoniae with hypermucoviscosity phenotype in rhesus Macaca mulatta and cynomolgus Macaca fascicularis macaques Comp Med 2010606270 4 Burke RL Whitehouse CA Taylor JK Selby EB Epidemiology of invasive Klebsiella pneumoniae with hypermucoviscosity phenotype in a research colony of nonhuman primates Comp Med 200959589597 5 Castinel A Duignan PJ Pomroy WE LopezVillalobos N Gibbs NJ Chilvers BL Wilkinson IS Neonatal mortality in New Zealand sea lions Phocarctos hookeri at Sandy Bay Enderby island Auckland islands from 1998 to 2005 J Wildl Dis 200743461474 6 Castinel A Kittelberger R Pomroy WE Duignan PJ Chilvers BL Wilkinson I Humoral immune response to Klebsiella spp in New Zealand sea lions Phocarctos hookeri and the passive transfer of immunity to pups J Wildl Dis 200844815 7 Cutlip RC Dennis ED Retrospective study of diseases in a captive lemming colony J Wildl Dis 199329620622 8 Davies YM Cunha MP Oliveira MG Oliveira MC Philadelpho N Romero DC Milanelo L Guimarães MB Ferreira AJ Moreno AM Sá LR Knöbl T Virulence and antimicrobial resistance of Klebsiella pneumoniae isolated from passerine and psittacine birds Avian Pathol 2016452194201 9 Davis GS Price LB Recent research examining links among Klebsiella pneumoniae from food food animals and human extraintestinal infections Curr Environ Health Rep 2016 32128135 10 Duff JP Bidewell CA Williamson SM Teale CJ Stidworthy MF Bexton S AbuOun M Randall L Rogers JP Klebsiella pneumoniae of suspected human origin from freeliving common seals on the east coast of England Vet Rec 2016 7925652 11 Enurah LU Adeniyi KO Ocholi RA Spencer TH Badung JD Klebsiella pneumoniae as a cause of pneumonia and septicemia in a civet kitten Civettictis civetta in the Jos Zoo Nigeria J Wildl Dis 1988 24585586 12 Fotedar R Banerjee U Samantray JC Shirniwas Vector potential of hospital houseflies with special reference to Klebsiella species Epidemiol Infect 1992 109 143147 13 Goldstein EJC Agyare E Vagvolgyi AE Halpern M Aerobic bacterial oral flora of garter snakes development of normal flora and pathogenic potential for snakes and humans J Clin Microbiol 198113954956 14 Guerra MF Teixeira RH Ribeiro VL Cunha MP Oliveira MG Davies YM Silva KC Silva AP Lincopan N Moreno AM Knöbl T Suppurative peritonitis by Klebsiella pneumoniae in captive gold handed tamarin Saguinus midas midas J Med Primatol 2016 4514246 15 Hartman LJ Selby EB Whitehouse CA Coyne SR Jaissle JG Twenhafel NA Rapid realtime PCR assays for detection of Klebsiella pneumoniae with the rmpA or magA genes associated with the hypermucoviscosity phenotype screening of nonhuman primates J Mol Diagn 200911464471 16 Kasuya K Takayama K Bito M Shimokubo N Kawashima R Shibahara T Septicemic invasive Klebsiella pneumoniae infection in a cynomolgus monkey Macaca fascicularis with severe diffused suppurative meningoencephalitis J Vet Med Sci 2017 79711671171 17 Novak SS Seigel RA Gramnegative septicemia in American alligators Alligator mississippiensis J Wildl Dis 1986 22484487 18 Paczosa MK Mecsas J Klebsiella pneumoniae going on the offense with a strong defense Microbiol Mol Biol Rev 2016 803629661 American Association of Zoo Veterinarians Infectious Disease Manual KLEBSIELLA 19 Ranjbar R Izadi M Hafshejani TT Molecular detection and antimicrobial resistance of Klebsiella pneumoniae from house flies Musca domestica in kitchens farms hospitals and slaughterhouses J Infect Public Health 2016 94499505 20 Roe WD Rogers L Pinpimai K Dittmer K Marshall J Chilvers BL Septicaemia and meningitis caused by infection of New Zealand sea lion pups with a hypermucoviscous strain of Klebsiella pneumoniae Vet Microbiol 201517634301308 21 Sasaki E Tokiwa T Tsugo K Higashi Y Hori H Une Y Peracute bacterial neningitis due to infection with Klebsiella pneumoniae in captivebred ruffed lemurs Varecia variegate J Comp Pathol 201715623281285 22 Schadich E Cole ALJ Pathogenicity of Aeromonas hydrophila Klebsiella pneumoniae and Proteus mirabilis to brown tree frogs Litoria ewingii Comp Med 2010 60 114117 23 Seguel M Goggdenker NL Colegrove K Johnson S Struve C Howerth EW Hypervirulent Klebsiella pneumoniae in California sea lions Zalophus californianus pathologic findings in natural infections Vet Pathol 2017 545846250 24 Soto E Dennis MM Beierschmitt A Francis S Sithole F HallidaySimmons I Palmour R Biofilm formation of hypermucoviscous and nonhypermucoviscous Klebsiella pneumoniae recovered from clinically affected African green monkey Chlorocebus aethiops sabeus Microb Pathol 2017 107198201 25 Soto E LaMon V Griffin M Keirstead N Beierschmitt A Palmour R Phenotypic and genotypic characterization of Klebsiella pneumoniae isolates recovered from nonhuman primates J Wildl Dis 201248603611 26 Steele CM Brown RN Botzler RG Prevalence of zoonotic bacteria among seabirds in rehabilitation centers along the Pacific coast of California and Washington USA J Wildl Dis 2005 41 735744 27 Tatfeng YM Usuanlele MU Orukpe A Digban AK Okodua M Oviasogie F Turay AA Mechanical transmission of pathogenic organisms the role of cockroaches J Vect Borne Dis 2005 42 129134 28 Twenhafel NA Whitehouse CA Stevens EL Hottel HE Foster CD Gamble S Abbott S Janda JM Kreiselmeier N Steele KE Multisystemic abscesses in African green monkeys Chlorocebus aethiops with invasive Klebsiella pneumoniae identification of the hypermucoviscosity phenotype Vet Pathol 200845226231 29 Whitehouse CA Keirstead N Taylor J Reinhardt JL Beierschmitt A Prevalence of hypermucoid Klebsiella pneumoniae among wildcaught and captive vervet monkeys Chlorocebus aethiops sabaeus on the island of St Kitts J Wildl Dis 201046971976 American Association of Zoo Veterinarians Infectious Disease Manual KYASANUR FOREST DISEASE Fact Sheet compiled by Owen Slater Sheet completed on 17 August 2013 updated 12 November 2012 and 24 January 2018 Fact Sheet Reviewed by Douglas P Whiteside Susceptible animal groups Mammals Gray langur redfaced bonnet macaque domestic cattle sheep and goats and humans Hosts include whitetailed rat whitebellied rat shrew and bats Causative organism Kyasanur forest disease virus KFDV virus Flaviviridae Zoonotic potential Yes and can be fatal in humans Distribution Enzootic in Karnataka Kerala Maharashtra and Goa States India but also human seropositivity in Andaman and Nicobar islands Debate exists as to whether viruses identified in Saudi Arabia and the Peoples Republic of China are KFDV or closely related viruses Incubation period In humans this period is approximately 38 days Clinical signs Animals Natural infections of monkeys are commonly associated with substantial mortality and evidence of anal hemorrhage Other clinical signs noted include epistaxis diarrhea encephalitis shock and death Humans Fever headache severe muscle pain prostration inflammation of conjunctiva vesicular eruptions on the soft palate tussis vomition diarrhea dehydration and bleeding Decreased platelets red blood cell and white blood cell counts are noted Patients sometimes recover after 12 weeks but usually a biphasic illness with a second wave at three weeks with above clinical signs and for some encephalitis Fatality rate of 310 Post mortem gross or histologic findings Gross Anal hemorrhage epistaxis and diarrhea Histologic Focal liver necrosis with cytoplasmic inclusion bodies sloughing of tubular epithelium in kidney humans small and large intestinal necrosis pallor of the adrenal cortex multiorgan hemorrhage lung kidney brain adrenal nonpurulent encephalitis with focal microgliosis and perivascular cuffing Diagnosis Serology Convalescent phase RTPCR qRTPCR IgM capture ELISA Material required for laboratory analysis Serum whole blood tissue Relevant diagnostic laboratories Centers for Disease Control and Prevention 1600 Clifton Rd Atlanta GA 30329 Treatment No specific treatment for the disease Supportive care for dehydration and hemorrhage Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals primarily rats squirrels porcupine and bats shrews Suncus murinus are reservoir hosts Monkeys are amplication hosts gray langurs Semnopithecus sp and redfaced bonnet macaques Macaca radiata Domestic cattle sheep and goats can be affected Vector Hard ticks primarily nymphal stages of Haemaphysalis spinigera Other Haemaphysalis sp and Ixodes sp soft ticks of Ornithodoros sp and Argas sp Direct contact with an infected animal rodent monkey Biphasic fever tussis dehydration encephalitis epistaxis diarrhea shock death Mild to fatal No specific treatment Supportive care especially for treatment of dehydration and hemorrhage Vector control including insect repellents and protective clothing Yes with mortality for humans living in enzootic areas American Association of Zoo Veterinarians Infectious Disease Manual KYASANUR FOREST DISEASE Prevention and control No vaccine currently available in North America but high success with formalin inactivated virus vaccine was been reported for humans in India Vector tick and rodent control in endemic areas is important Level 34 biosecurity protocols in North America Suggested disinfectant for housing facilities 1 sodium hypochlorite 70 ethanol 2 glutaraldehyde Virus does not survive freezing Notification This is not a notifiable foreign animal disease Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal If importing monkeys rodents or bats from enzootic areas follow normal quarantine measures and strongly consider serologic testing for Kyasanur forest disease virus Conditions for restoring diseasefree status after an outbreak None Experts who may be consulted Dr Stuart T Nichol PhD Chief Molecular Biology Laboratory Special Pathogens Branch Division of Viral and Rickettsial Diseases Centers for Disease Control and Prevention 1600 Clifton Road NE Atlanta GA 30329 References 1 Centers for Disease Control and Prevention Internet Kyasanur Forest Disease KFD 2014 cited 2018 January 24 Available from httpswwwcdcgovvhfkyasanur 2 Kasabi GS Murhekar MV Yadav PD Raghunandan R Kiran SK Sandhya VK Channabasappa GH Mishra AC Mourya DT Mehendale SM Kyasanur Forest Disease India 20112012 Emerg Infect Dis 201319 278281 3 Mehla R Kumar SR Yadav P Barde PV Yergolkar PN Erickson BR Carroll SA Mishra AC Nichol ST Mourya DT Recent ancestory of Kyasanur Forest disease virus Emerg Infect Dis 20091514317 4 Mourya DT Yadav PD Recent scenario of emergence of Kyasansur Forest Disease in Indian and public health importance Curr Trop Med Rep 2016 31713 5 Mourya DT Yadav PD Mehla R Barde PV Yergolkar PN Kumar SR Thakare JP Mishra AC Diagnosis of Kyasanur forest disease by nested RTPCR realtime RTPCR and IgM capture ELISA J Virol Meth 2012186 4954 6 Pathogen Safety Data Sheet Public Health Agency of Canada 1 Government of Canada Internet Pathogen Safety Data Sheets Infectious Substances Kyasanur forest disease virus 2011 cited 2018 January 24 Available from httpswwwcanadacaenpublic healthserviceslaboratorybiosafetybiosecuritypathogensafetydatasheetsriskassessmentkyasanur forestdiseasevirushtml 2 Pattnaik P Kyasanur forest disease an epidemiological view in India Rev Med Virol 20061615165 3 Pavri K Clinical clinicopathologic and hematologic features of Kyasanur forest disease Rev Infect Dis 198911854859 American Association of Zoo Veterinarians Infectious Disease Manual LEPROSY Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Humans 9banded armadillos Unclear Indirect or direct contact Respiratory droplets Consumption of or contact with 9banded armadillos Primarily affects the peripheral nerves skin upper respiratory tract eyes and limbs Sensory loss in skin muscle weakness Long term lack of sensation leads to traumatic injury and potential loss of use in hands and feet Severity of clinical signs based on immunity of host Left untreated it may result in permanent damage to skin nerves eyes limbs Multidrug antibiotic therapy Humans treated early in course of disease are no longer infective Avoid exposure to 9 banded armadillos Cleaning and eating their carcasses may pose increased risk Yes Fact Sheet compiled by Lara M Cusack Sheet completed on 25 May 2011 updated 4 September 2012 Fact Sheet Reviewed by Richard W Truman David M Scollard Susceptible animal groups Humans 9banded armadillos Dasypus novemcinctus Other armadillo species such as 6banded armadillos Euphractus common as exotic pets and 3banded armadillos Tolypeutes are not known to be susceptible to M leprae Causative organism Mycobacterium leprae Zoonotic potential Infectious between people and from 9banded armadillos Distribution Organism is found worldwide Persons in close contact with patients with untreated active predominantly multibacillary disease and persons living in countries with highly endemic disease have higher risk of disease Most 75 of cases originate from Angola Brazil Central African Republic Democratic Republic of Congo India Madagascar Mozambique Nepal and the United Republic of Tanzania In the US cases are documented primarily in Louisiana Texas California New York Massachusetts and Hawaii Infections among wild 9banded armadillos reported in Alabama Arkansas Louisiana Mississippi and Texas as well as in Argentina Brazil Colombia and Mexico Incubation period While typical incubation period is approximately 5 years it can be up to 20 years for clinical signs to appear Clinical signs Humans Majority of healthy individuals will not develop disease Susceptibility to infection appears to be genetic The form of the disease developed depends on host immunity Indeterminate form Earliest clinically detectable form of leprosy found in 10 to 20 of infected people Hypopigmented macules without developed tuberculoid or lepromatous characteristics are present Tuberculoid leprosy paucibacillary leprosy Single or few well demarcated hypopigmented skin lesions frequently with active spreading edges and a clearing center are noted Peripheral nerve swelling or thickening also may occur Acid fast bacilli rare or not visible American Association of Zoo Veterinarians Infectious Disease Manual LEPROSY Lepromatous leprosy multibacillary leprosy Very numerous symmetrically distributed erythematous skin lesions nodules plaques thickened dermis and involvement of the nasal mucosa congestion nose bleeds Acid fast bacilli are always present and may be found in dermal nerves High titer of antibodies to M leprae but little cellular immune response to the bacillus Changes in immunity andor treatment can lead to worsening of clinical signs Borderline Few or several asymmetrical hypopigmented erythematous or coppery skin lesions that are usually positive for acid fast bacilli These cases may be further subdivided according to the number and cellularity of the lesions Borderline Tuberculoid BT are usually well demarcated somewhat dry and few in number Borderline Lepromatous BL have many roughly symmetrical shiny macules nodules or plaques with sloping or poorly defined edges All forms will involve some degree of peripheral neurological damage leading to sensory loss in skin and muscle weakness In long term cases lack of sensation leads to repeated traumatic injury and potential loss of use in hands and feet Left untreated may result in permanent damage to skin nerves eyes and limbs 9Banded Armadillos Cutaneous lesions are discerned only in the late stages One may observe repeated foot ulcers or scrapes around the nose eyes or legs that do not respond well to normal therapies Armadillos generally manifest a diffuse lepromatous form of the disease with systemic involvement of reticuloendothelial tissues Impression smears or swabs of skin lesions can reveal acid fast bacilli or may PCR as M leprae Leprous armadillos have been reported to show an increase in basal metabolic rate With one of the lowest metabolic rates of any placental mammal the cost of infection may represent an important impact but studies to date are undecided as to ecological consequences in wild population It does not appear to infect young animals which may be due to incubation period Post mortem gross or histology findings Mycobacterium leprae is an obligate intracellular acidfast Grampositive bacillus with an affinity for macrophages and Schwann cells Interaction with Schwann cells induces demyelination and stimulates a chronic inflammatory reaction Swelling occurs in the perineurium leading to ischemia fibrosis and axonal loss Sensory fibers are affected prior to motor nerve involvement and the induced insensitivity can contribute to secondary trauma Infection in the armadillo is characterized by an insidious microcytic hypochromic anemia with elevated LDH ALT and AST On gross exam the liver spleen and lymph nodes may be enlarged extensively they may have a granular texture and can contain massive numbers of acid fast bacilli In late stages of disease no organ system is spared and large numbers of bacilli can be found in all tissues Diagnosis Clinical signs Localized skin lesions have demonstrated sensory loss thickened and enlarged peripheral nerves Acidfast bacilli in skin or dermal nerve obtained from the fullthickness skin biopsy of a lepromatous lesion can be demonstrated In many cases rodshaped redstained leprosy bacilli which are diagnostic of the disease may be seen in the smears taken from affected skin when examined under a microscope after appropriate staining weakly acidfast Fite stain better than ZiehlNeelsen Serology and PCR not widely performed fail to reliably detect earlymild forms of the disease 9Banded Armadillos Ear notches preserve in 100 ethanol for genetic screening and in 70 ethanol for PCR analyses to detect M leprae DNA Serum or eluted whole blood ELISA test or immunoglobulin M IgM antibodies to M leprae Confirmation made with PCR Material required for laboratory analysis Skin blood affected tissues spleen liver lymph node dermal swabs and impression smears Relevant diagnostic laboratories Any capable of performing acid fast stain or PCR for M leprae Treatment Hansens disease is a mild disease when treated early and prior to sensory impairment Multidrug therapy MDT with dapsone rifampicin and clofazimine is daily treatment and prolonged multibacillary cases treated for 2 years paucibacillary cases treated for 1 year Drugs provided free of charge by the National Hansens Disease Programs NHDP 18006422477 American Association of Zoo Veterinarians Infectious Disease Manual LEPROSY httpwwwhrsagovhansensdiseaseclinicalcenterhtml Prevention and control Early treatment for atypical skin rashes refractory to treatment should be sought especially if sensory involvement Patients are no longer infective after two weeks of MDT WHONHDP Avoid exposure tocontact with blood or flesh of 9banded armadillos Suggested disinfectant for housing facilities Organism loses infectivity after 30 min exposure to most disinfectants and UV light Disinfectants effective against Mycobacterium tuberculosis are likely also effective against M leprae Notification Nationally it is a Notifiable Disease CDC Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Maintain infected animal in a quarantine situation until treatment initiated Conditions for restoring diseasefree status after an outbreak Disinfection of infected environment Minimize contact with infected persons until treatment is initiated Experts who may be consulted Dr Richard W Truman PhD National Hansens Disease Program LSU School of Veterinary Medicine Tel 2255789848 Fax 2255789856 rtrumanhrsagov Dr David Scollard MD PhD Chief Clinical Branch National Hansens Disease Programs Tel 2257563713 Fax 2257563819 dscollardhrsagov References 1 Deps PD BL Alves CG Gripp RL Aragão BVS Guedes JB Filho MK Andreatta RS Marcari ICA Prates and LC Rodrigues 2008 Contact with armadillos increases the risk of leprosy in Brazil a case control study Ind J Dermatol Venereol Leprol 7433842 2 httpwwwniaidnihgovtopicsleprosyPagesDefaultaspx Accessed 8 July 2013 3 httpwwwhrsagovhansensdisease Accessed 8 July 2013 4 httpwwwcdcgovnczveddivisionsdfbmddiseaseshansensdiseasetechnicalhtml Accessed 8 July 2013 5 httpemedicinemedscapecomarticle1104977overview Accessed 8 July 2013 6 Morgan R and W Loughry 2009 Consequences of exposure to leprosy in a population of wild nine banded armadillos J Mammal 906 13631369 7 Scollard DM LB Adams TP Gillis JL Krahenbuhl RW Truman and DL Williams 2006 The continuing challenges of leprosy Clin Microbiol Rev 192 33881 8 Truman R P Singh R Sharma P Busso J Rougemont A PanizMondolfi and S Cole 2011 Probable zoonotic leprosy in the southern United States New Engl J Med 36417 16261633 9 Truman R 2005 Leprosy in wild armadillos Leprosy Rev 763 198208 10 Walsh G W Meyers C Binford B Gormus G Baskin R Wolf and P Gerone 1988 Leprosy as a zoonosis an update Acta Leprologica 61 5160 American Association of Zoo Veterinarians Infectious Disease Manual LEPTOSPIROSIS Animal Groups Affected Transmission Clinical Signs Fatal Disease Treatment Prevention and Control Zoonotic Mammals Contact with urine of shedding host adapted carrier animal or urine contaminated water organism can penetrate macerated or wounded skin and intact mucous membranes potential but limited transmission transplacental transmammary None or modest in hostadapted carrier animals inapparent to severe in acute infections in non host adapted animals Renal signs most typical and include acute renal failure up to 20 of cases present concurrent hepatitis Fatal disease can occur in non host adapted species Antibiotics usually doxycycline Personal hygiene especially handwashing and prevention of contact with hostadapted carrier animal urine control of freeranging wildlife and pests which are often these host adapted carriers Yes Fact Sheet compiled by Kathryn C Gamble Original date 12 March 2011 updated 14 July 2013 updated 11 February 2018 Fact Sheet Reviewed by Kenneth Harkin June Olds Susceptible animal groups Mammals recent literature assessment published that 1020 prevalence had been reported in most mammalian families although Muridae Canidae and Bovidae were over represented Felidae appear more resilient but recent assessments are that domestic felids are detected more often with subclinical disease than recognized previously and personal author experience with clinical disease in two large exotic felids reservoir situations increasing contact with humans through urbanization and conversion to a omnivorous diet is associated with increased prevalence for some taxa such as Phalangeridae brushtail possum Additional reservoirs including birds and reptiles have been identified Causative organism Leptospira spp 250 serovars are spirochaete bacteria which share a common lipopolysaccharide antigen but differ by surface agglutinating antibodies that allows classification Currently some of the most common pathogenic leptospiral serovars for US mammals are identified as L kirshneri Grippotyphosa and L interrogans Pomona Bratislava Hardjo Icterohemorrhagicae and Autumnalis Zoonotic potential Infectious to people from animals though generally comes from a common point source ie rodents contaminated water when both animal and human are involved Distribution Worldwide distribution with moist environments most conducive especially prevalent in tropical countries occupational and leisure activity risk factors autumn seasonality observed Incubation period 714 days up to 21 days Clinical signs Common reservoir species can have high prevalence of infection up to 50 Generally these individuals do not develop disease or clinical signs except perhaps mild signs at initial infection Fatality would not be expected These animals may shed the organism for a few weeks or intermittently for several years due to chronic infection of the renal tissue Each serovar tends to have certain host associations as potential natural reservoirs wildlife and rodents are often implicated in this role during outbreaks Acute infections can occur in susceptible species and include most captive zoological species and humans following infection with the organism they become ill moderately to severely Fatality can occur especially in untreated individuals These animals generally do not become carriers Once the infection has been resolved especially if these animals are treated prolonged shedding likely does not occur although chronic renal damage may be incurred in survivors Essentially any serovar could infect these individuals and produce disease American Association of Zoo Veterinarians Infectious Disease Manual LEPTOSPIROSIS Endothelial damage is primary source of clinical signs These signs are nonspecific and many infected animals do not become clinically or severely ill The first signs in humans appear as mild to moderate flulike with fever anorexia malaise and fatigue Rash may be present but is inconsistent Other clinical signs are much more severe and related to systemic infection with signs of acute renal disease including the nonspecific but consistent clinical signs of infection in the kidneys Concurrent clinical pathology changes of elevated BUN and creatine and hyperphosphatemia are present and may be accompanied by hemoglobinuria due to vasculitis Some infected animals 1020 progress to concurrent hepatic disease Weils disease with icterus and increasing hepatocellular enzymes Pregnant animals may abort The initial signs may wane with the more serious signs appearing in a biphasic time frame As specific taxon focus equids tend to present with recurrent uveitis rather than renal or hepatic disease however reports of acute pulmonary distress as a result of leptospirosis has been reported in foals Recent studies have also detected leptospiral DNA in vaginal swabs of mares suggesting potential venereal transmission Although original association of this organism with black rhinoceros Diceros bicornis and hemolytic anemia was considered it has not been proven Freeranging California sea lions Zalophus californianus have a marked predisposition to infection with serovar Pomona with severe renal disease limited other serovars have been identified in other pinnipeds but not in cetaceans Post mortem findings These findings are specific to the body system infected and presenting clinical signs at time of illness Usually it is evidence of acute renal failure Acute hepatitis is observed in those animals which had icterus Scarring white spots in affected organs in chronic cases observed macroscopically in the kidneys of pigs and dogs Diagnosis Diagnosis is challenging and treatment must begin before diagnosis is conclusive In the literature since the last review increasing effort to find faster or more pointofcare options was noted Although direct observation with silver or fluorescent antibodies FA or without darkfield microscopy stain enhancement has been reported as useful leptospires must be present in sufficient numbers in the sample evaluated usually urine The defined gold standard of testing is serologic evaluation by microscopic agglutination testing MAT but this testing modality is specific and requires maintenance of the organism with its markedly fastidious culture needs and it cannot differentiate between vaccine and natural antibody production However MAT testing is readily available A positive status is assigned to a test result 1100 in an unvaccinated animal but this low seroconversion requires a fourfold rise in titer over 24 weeks for diagnostic support In a clinically ill animal a single serologic status of 1800 is strongly suggestive of leptospirosis Crossreactivity is quite common so a panel of likely serovars are assessed assigning the serovar with the highest titer as the most likely causative agent Polymerase chain reaction PCR of urine is now available which detects specific gene unique to pathogenic serovars New canine specific tests include indirect ELISA and a commercial lateral flow assay Material required for laboratory analysis Serum is submitted for most testing but urine can be submitted for PCR Whole blood and serum can be submitted for PCR or whole blood for culture Post mortem tissues ideally kidney can be submitted for histology using special silver stains culture PCR or FA Due to the fastidious nature of leptospira cultures are often unrewarding and additional diagnostic methodologies are recommended for confirmatory diagnosis Relevant diagnostic laboratories Leptospire MAT is offered by many commercial and state diagnostic laboratories Michigan State University Diagnostic Laboratory has an excellent serology panel and consultation services available PCR testing now is offered routinely by many laboratories the LipL32 based and 23s rRNAbased PCR have been shown to have false positives from freecatch urine samples Treatment These organisms are generally quite sensitive to most antibiotics except notably chloramphenicol First generation cephalosporins specifically cephalothin historically were considered less successful for treatment but recently these specifically cefazolin and cephalexin have been suggested as effective Best success occurs when the treatment is initiated promptly and as early in the disease course as possible Doxycycline for 14 days is most commonly used successfully to treat clinical signs Supportive care for systemic signs may be needed in more severe cases American Association of Zoo Veterinarians Infectious Disease Manual LEPTOSPIROSIS Prevention and control in zoos Although vaccines as killed whole cell bacterins are available for pigs cattle and dogs it would be necessary to specifically target the serovar of concern in the particular area It may therefore be preferred to leave this option to consideration in outbreak control or in areas with higher risk or increased urban wildlife or domestic stray interactions Serologic testing can be monitored in these situations and during transfers between facilities More importantly pest control and exclusion of other carriers from contact with collection animals would be important Once an animal is confirmed infected prompt treatment will minimize or may eliminate shedding In the treatment interval appropriate staff protection and personal hygiene is to be utilized to prevent spread within the facility or to staff Consideration of drainage of the area should be made in this control measure If the situation were to occur in a contact program area it is recommended to exclude guests until the situation is treated and leptospiruria is confirmed resolved Suggested disinfectant for housing facilities Any standard disinfectant technique would be appropriate for cleaning of this organism Notification In the US Hawaii is the only state currently maintaining this disease as reportable in animals Centers for Disease Control and local health authorities should be alerted for human cases especially clusters USDA apprises WHO of leptospirosis issues in certain production species Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Infected animals should be maintained as isolated as possible from other mammals until treatment interval is completed PCR testing on urine would be helpful to confirm that the infected animal was no longer shedding Serologic monitoring of animals in adjacent areas would be considered prudent Conditions for restoring diseasefree status after an outbreak Serologic monitoring of adjacent areas would be considered prudent following return of infected animal to collection to assess for exposure Experts who may be consulted Michigan State University Diagnostic Center for Population and Animal Health 4125 Beaumont Road Lansing MI 48910 5173531683 Kenneth Harkin DVM Dipl ACVIM Kansas State University Department of Clinical Sciences harkinvetkstateedu References 1 Adler B de la Peña Moctezuma A Leptospira and leptospirosis Vet Microbiol 20101402872962 2 AndersonRanberg EU Pipper C Jensen PM Global patterns of Leptospira prevalence in vertebrate reservoir hosts J Wildl Dis 201652468477 3 Bolin CA Leptospirosis In Fowler ME Miller RE eds Zoo and wild animal medicine Volume 5 Philadelphia PA Elsevier 2005 p699701 4 BrettMajor DM Coldren R Antibiotics for leptospirosis Internet Cochrane Database of Systematic Reviews 2012 Issue 2 Art No CD008264 DOI 10100214651858CD008264pub2 accessed 11 February 2018 5 Chikeka I Dumier JS Neglected bacterial zoonoses Clin Microbiol Inf 201521404408 6 Guerra MA Leptospirosis J Am Vet Med Assoc 20092344472479 7 Gulland FMD Leptospirosis in marine mammals In Fowler ME Miller RE eds Zoo and wild animal medicine Volume 4 Philadelphia PA Elsevier1998 p469471 8 Gyimesi ZS Burns RB Erol E Bolin SR Acute clinical leptospirosis Grippotyphosa serovar in an adult dromedary camel Camelus dromedarius J Zoo Wildl Med 201546605608 9 Harkin KR Roshto YM Sullivan JT Clinical application of a polymerase chain reaction assay for diagnosis of leptospirosis in dogs J Am Vet Med Assoc 200322212241229 10 Harkin KR Roshto YM Sullivan JT Purvis TJ Chengappa MM Comparison of polymerase chain American Association of Zoo Veterinarians Infectious Disease Manual LEPTOSPIROSIS reaction assay bacteriologic culture and serologic testing in assessment of prevalence of urinary shedding of leptospires in dogs J Am Vet Med Assoc 20032222301233 11 Hartmann K Egberink H Pennisi MG Lloret A Addie D Belak S BoucrautBaralon C Frymus T GruffyddJones T Hosie MJ Luzt H Marsilio F Möstl K Radford AD Thiry E Truyen U Horzinek MC Leptospira species infection in cats ABCD guidelines on prevention and management J Fel Med Surg 201315576581 12 Jobbins SE Alexander KA Evidence of Leptospira sp infection among a diversity of African wildlife species beyond the usual suspects Trans R Soc Trop Med Hyg 2015109349351 12 Lizer J Grahlmann M Hapke H Velineni S Lin D Kohn B Evaluation of a rapid IgM detection test for diagnosis of acute leptospirosis in dogs Vet Rec 2017180517 13 Morbidity and Mortality Weekly Report MMWR Internet Centers for Disease Control 2017 cited 2018 February 11 Available from httpswwwcdcgovmmwrvolumes64wrmm6453a1htmscidmm6453a1w 14 Olds JE Sun Y Baum DH Gauger P Serologic survey and results of urinary PCR testing for leptospirosis in captive blacktailed prairie dogs Cynomys ludovicianus J Zoo Wildl Med 201546843 849 15 Sathiyamoorthy A Selvaraju G Palanivel KM Srinivasan P Development of indirect enzymelinked immunosorbent assay for diagnosis of canine leptospirosis Vet World 201710530535 American Association of Zoo Veterinarians Infectious Disease Manual LISTERIOSIS Listeria monocytogenes Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All Fecaloral ingestion inhalation direct contact with affected tissues or indirectly through contaminated milk cheese meat eggs fruits or vegetables in people Common route in animals is hay contamination or unstable silage Three primary forms encephalitic abortion perinatal mortality septicemia but can see ophthalmic form Primarily winter spring disease in US Without aggressive treatment encephalitis and septicemic disease are often fatal or animals recover with permanent brain damage encephalitic form Aggressive and early treatment with antibiotics supportive care Recovery rate often 30 Remove spoiled feed or silage Separate affected animals Good hygiene practices YES At risk groups are pregnant women neonates elderly immune compromised and those handling infected tissues Fact Sheet compiled by Diana Boon DVM Sheet completed on 1 December 2010 updated 21 August 2013 updated 24 Sept 2017 Fact Sheet Reviewed by Clayton Hilton MS DVM Susceptible animal groups Mammals and birds Listeria has been isolated from fish crustaceans and insects but these species are likely carriers Can be cultured from healthy asymptomatic animals humans Causative organism Listeria monocytogenes grampositive bacilli Zoonotic potential Zoonotic potential exists when handling aborted tissues or removing infected brain during necropsy Foodborne illness most common and atrisk groups are pregnant elderly and immune compromised people Distribution Worldwide Incubation period Approximately 10 days 3 weeks but clinical signs have been within 5 hours of exposure in poultry Clinical signs Several forms are possible Encephalitic form adult ruminants aka Circling Disease early signs of depression anorexia disorientation decreased milk production fever which can progress to seizures unilateral trigeminal and facial nerve paralysis circling cerebellar signs ear droop deviated muzzle flaccid lip lowered eyelid on affected sides salivation deviated muzzle flaccid lip and death Abortion adult ruminants fever hypo to anorexia lateterm abortions stillbirths Retained placentas with secondary metritis Septicemic form typically neonates and monogastrics diarrhea focal hepatic necrosis death Septicemic form poultryrare lethargy depressed mentation diarrhea myocardial or hepatic necrosis death Ophthalmic form secondary to nerve damage decreased tear production secondary to changes in special visual efferent SVE system in medulla eyelid paralysis with secondary exposure keratitis or direct contact keratoconjunctivitis retinal changes Postmortem gross or histologic findings Encephalitic form few gross lesions some congestion of meninges histologic lesions consistent with encephalitis or meningoencephalitis with microabscessation and organisms present predilection for pons medulla brain stem and cranial spinal cord Septicemic form evidence of sepsis focal hepatic necrosis and hemorrhagic gastroenteritis Abortion form third trimester abortion common gross lesions are placentitis most severe lesion metritis and subtle fetal infection Histologic lesions are suppurative and necrotizing placentitis and small necrotic foci in any fetal organ especially liver with fetal necrotizing colitis not common but very supportive of listeriosis Gramstain and culture of abomasal contents may be positive for bacteria Maceration of the fetus can be occur American Association of Zoo Veterinarians Infectious Disease Manual LISTERIOSIS Listeria monocytogenes with retained abortions The herd and dam generally do not present with the encephalitic or septicemic forms concurrent with the abortion form Fetal lesions slight to marked autolysis fluid in serous cavities small necrotic hepatic foci often in right half erosion in abomasal mucosa Complete maceration of fetus is common Diagnosis Premortem Clinical signs CSF tap for cytology and culture CSF will have increased protein concentration 0620gL with mild pleocytosis composed of large mononuclear cells Postmortem culture of affected tissues very suggestive if grows at 4C IFA affected tissues gramstain grampositive pleomorphic bacteria not always diphtheroid coccobacillus immunohistochemistry of brain tissues Affected tissues include brain pons medulla nasal discharge placenta associated fluids abortus urine feces milk meat silage and other sources Serology not routinely due to low specificity DDx Trichomoniasis pregnancy toxemia ewes ketosis cattle BSE histophilosis polioencephalomalacia sporadic bovine encephalitis lead poisoning rabies brain abscess cestode Material required for laboratory analysis Aborted fetuses and placentas brain can be submitted and request cold enrichment method for culture Wear gloves and protective clothing when handling tissues Relevant diagnostic laboratories As the diagnosis is mostly postmortem all diagnostic labs should be able to perform testing Remember to request Listeria culture cold enrichment method if initial culture results do not correspond to clinical presentation may take 3 months to get results Treatment Dependent on prompt diagnosis at early stage of disease as death can occur within 2448 hours of onset of clinical signs High doses of penicillin first choice oxytetracycline ceftiofur erythromycin not in dairy cattle trimethoprimsulfonamide Supportive care for clinical signs is needed Prevention and control Reduce fecal contamination of feed and monitor sewage contamination Discard spoiled feed and hay Improve sanitation of pens water supply pasture food refrigerators and housing facilities Limit access of wild birds as possible vector for bacteria if possible Isolate aborting females Pasteurization of milk for human consumption or bottle feeding but may not be 100 effective Listeria vaccine developed for oncology patients Suggested disinfectant for housing facilities No specific disinfectants suggested but good hygiene standards should be maintained including rodent control Notification Reportable to local health authorities within a few days of disease confirmation see specifics for each state Measures required under the Animal Disease Surveillance Plan None defined Most measures are currently for prevention of Listeria introduction into the human food supply Measures required for introducing animals to infected animal Organism can be shed intermittently in milk without signs of mastitis feces and vaginal secretions for 1 month but no recommended measures for reintroduction Conditions for restoring diseasefree status after an outbreak Segregate affected animals remove affected silage or feed Disease may continue to be sporadic as is found in the soils Organism tends to display a seasonal pattern February April of infection Experts who may be consulted Benjamin J Silk PhD MPH Centers for Disease Control and PreventionNCEZD Division of Foodborne Waterborne and Environmental Diseases 1600 Clifton Rd Atlanta GA 30333 4046390536 bsilkcdcgov American Association of Zoo Veterinarians Infectious Disease Manual LISTERIOSIS Listeria monocytogenes References 1 AbdulAziz T Overview of Listeriosis in Poultry Internet Merck Veterinary Manual 2018 cited 2018 November 15 Available from httpswwwmerckvetmanualcompoultrylisteriosisoverviewoflisteriosisinpoultry 2 Bush L Schmidt C Perez M Listeriosis Internet Merck Manual Professional Version 2017 cited 2017 September 24 Available from httpwwwmerckmanualscomprofessionalinfectious diseasesgrampositivebacillilisteriosis 3 Cartwright EJ Jackson KA Johnson SD Graves LM Silk BJ Mahon BE Listeriosis outbreaks and associated food vehicles United States 19982008 Emerg Infect Dis 201319119 DOI PubMed 4 deNoordhout CM Devleesschauwer B Anqulo FJ Verbeke G Haagsma J Kirk M Havelaar A Speybroeck N The global burden of listeriosis a systematic review and metaanalysis Lancet Infect Dis 2014 Nov 1411 10731082 PMCID PMC4369580 Accessed 24 Sept 2017 5 LeiteBrowing M Listeriosis Circling Disease Alabama Cooperative Extension System ACES Alabama AM and Auburn Universities httpwwwacesedupubsdocsUUNP0064 Accessed 24 September 2017 6 Listeriosis Internet Center for Disease Control National Center for Zoonotic VectorBorne and Enteric Diseases 2018 cited 2017 September 24 Available from httpswwwcdcgovlisteriaindexhtml 7 National Enteric Disease Surveillance The Listeria Initiative Internet Center for Disease Control 2016 cited 2017 September 24 Available from httpswwwcdcgovlisteriapdflisteriainitiativeoverview508pdf 8 Scott P Overview of Listeriosis Internet Merck Veterinary Manual 2018 cited 2017 September 24 Available from httpwwwmerckmanualscomvetgeneralizedconditionslisteriosislisterellosiscirclingdisease overviewoflisteriosishtml 9 Ryser ET Marth EH Listeria Listeriosis and Food Safety 3rd edition Boca Raton FL CRC Press Taylor Francis Group 2007 896 p American Association of Zoo Veterinarians Infectious Disease Manual LUMPY SKIN DISEASE Fact Sheet compiled by Jackie Gai Sheet completed on 25 January 2011 updated 1 April 2013 Fact Sheet Reviewed by Carlos Romero Anna Rovid Spickler Susceptible animal groups Cattle Bos taurus European breeds Jersey Guernsey Ayrshire Holstein etc of thin skin are more susceptible than zebu cattle Bos indicus A few cases have been reported in Asian water buffalo Suspected clinical disease has been reported in Arabian oryx Oryx leucocoryx in Saudi Arabia springbok Antidorcas marsupialis in Namibia and oryx Oryx gazelle in South Africa Wildlife probably not important in the epidemiology of the disease Antibodies have been found in 6 out of 44 wildlife species tested in Africa African buffalo Syncerus caffer greater kudu Tragelaphus strepsiceros waterbuck Kobus ellipsiprymnus reedbuck Redunca arundinum impala springbok and giraffe although these may have been due to crossreaction to similar Capripoxviral exposure Experimental infection has been induced in sheep and goats Causative organism Lumpy skin disease virus LSDV of cattle is classified within the genus Capripoxvirus subfamily Chordopoxvirinae family Poxviridae The virus is morphologically identical to the other two known capripoxviruses sheeppox and goatpox viruses to which it is highly antigenically related Zoonotic potential None No evidence exists that capripoxviruses are transmitted to humans Distribution Originally described in 1929 in subSaharan Africa and Madagascar over the last 70 years it has spread north and south of this region Recent outbreaks have occurred in Egypt 1988 2006 Mauritius 2008 Vietnam and Lebanon and Israel 2012 Incubation period Thought to be two to five weeks under natural conditions but this is an estimate Experimentally infected animals developed fever within 69 days and skin lesions at the inoculation site in Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primarily cattle but also African ruminants Mainly via biting insects but less frequently direct contact with infected animal Virus may be present in semen of infected bulls for extended periods of time None to severe fever skin and internal nodules enlarged lymph nodes anorexia rhinitis conjunctivitis brisket and leg edema Typically it is mild but may be severe Most animals slowly recover but may take months Morbidity can be 1 95 within a herd Mortality rate usually low but may be up to 25 Subject to regulatory approval as infected animals outside endemic area may be destroyed Supportive care as virus runs its course Appropriate antibiotics for secondary bacterial infections Import restrictions mainly shipments from Africa proper quarantine and testing of animals imported from endemic areas Live and attenuated vaccines exist in endemic areas No American Association of Zoo Veterinarians Infectious Disease Manual LUMPY SKIN DISEASE 420 days However not all experimentally infected cattle develop clinical signs or skin lesions indicating that there are other unknown factors involved in the pathogenesis of the disease Clinical signs Signs may range from inapparent to severe clinical disease Pyrexia followed by the development of multiple painful nodules 25 cm in diameter over entire body especially on head neck udder perineum and legs Nodules involve the full thickness of the skin and may initially exude serum developing into necrotic plugs Rhinitis conjunctivitis and hypersalivation may be seen Agalactia or marked reduction in milk yield may occur Generalized lymphadenopathy and limb edema that makes animals reluctant to move Pox lesions may develop on mucous membranes of mouth Pregnant cattle may abort and aborted fetuses may have skin nodules Anorexia and emaciation Post mortem gross or histologic findings Greyish pink skin nodules may turn into conical necrotic plugs which penetrate the full thickness of the hide sitfasts Flat or ulcerative lesions may be found in mucous membranes of the oral and nasal cavities epiglottis and trachea Nodules may also be found in the gastrointestinal tract especially abomasum udder urinary bladder lungs kidneys and reproductive organs Pleuritis and enlargement of mediastinal lymph nodes in severe cases Enlargement of lymph nodes that drain affected areas with lymphoid proliferation edema congestion and hemorrhage Synovitis or tendosynovitis with fibrin in synovial fluid Temporary or permanent sterility may occur in bulls and cows Diagnosis Confirmation of LSD in a new area requires virus isolation and identification Biopsy or scrapes of skin lesions and nasal and oral swabs are the most useful samples for virus isolation and rapid identification by PCR and sequencing or by staining of infected cell cultures with specific labeled antiserum Intracytoplasmic inclusion bodies can be seen on electron microscopy The gold standard for detecting specific antibodies to capripoxviruses is the virus neutralization test Material required for laboratory analysis Scrapings and biopsies of skin lesions and nasal pharyngeal and conjunctival swabs Lymph node biopsies may be useful when there is generalized adenopathy Relevant diagnostic laboratories Within the US Foreign Animal Disease Diagnostic Laboratory USDAAPHIS 40550 Route 25 Orient NY 11957 6313233256 International shipments USDA Attn FADDL Lab Director co Port Veterinarian APHIS VS 23059 Rockaway Blvd 101 Jamaica NY 11413 7185531727 Outside the US Institute for Animal Health Pirbright Laboratory Ash Road Woking Surrey GU24 ONF Great Britain American Association of Zoo Veterinarians Infectious Disease Manual LUMPY SKIN DISEASE Treatment Subject to regulatory approval as infected animals outside endemic area may be destroyed No specific treatment provide supportive care Antibiotics such as sulfonamides to prevent or control secondary infection Prevention and control Stringent import restrictions on livestock carcasses hides and semen are in place When importing animals from endemic countries adhere to regulatory preshipment and quarantine requirements Report all suspected cases to the appropriate regulatory agency in your area immediately The disease is mainly transmitted mechanically by biting arthropods contrary to sheep pox and goat pox that are mainly transmitted by direct contact with infected animals The infection may also be transmitted by contaminated semen Animals that recover from the natural disease are immune for life Liveattenuated sheepgoat pox vaccine Kenya SGPV strain as well as South African LSD live vaccine Neethling strain are used in cattle in endemic countries Suggested disinfectant for housing facilities Sodium hypochlorite 23 iodine compounds 133 dilution Virkon 2 quaternary ammonium compounds Notification Lumpy Skin Disease is a reportable disease which must be reported immediately to the appropriate regulatory body ie Department of Food and Agriculture USDAAPHIS or State Veterinarian Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected areas None this is a reportable disease and animals with confirmed infection outside of endemic area will be destroyed Conditions for restoring diseasefree status after an outbreak To be determined by governmental authority Lifelong immunity occurs in recovering individuals Buffalo may serve as viral reservoirs Experts who may be consulted Douglas Gregg DVM PhD Foreign Animal Disease Diagnostic Laboratory NVSL APHIS USDA Greenport NY 11944 USA Dr Eeva Tuppurainen Institute for Animal Health Pirbright Laboratory Ash Road Pirbright Woking Surrey GU24 ONF UNITED KINGDOM 441483 232441 Fax 441483 232448 eevatuppurainenbbsrcacuk Dr Baratang Alison Lubisi Onderstepoort Veterinary Institute Agricultural Research Council Private Bag X5 Onderstepoort 0110 SOUTH AFRICA Tel 2712 5299233 Fax 2712 5299418 Lubisiaarcagricza References 1 httpwwwcfsphiastateeduDiseaseInfodiseasephpnamelumpyskindisease Center for Food Security Public Health at Iowa State University Accessed 8 August 2013 2 httpwwwoieintfileadminHomeengAnimalHealthintheWorlddocspdfLUMPYSKIN DISEASEFINALpdf World Organization for Animal Health Accessed 8 August 2013 American Association of Zoo Veterinarians Infectious Disease Manual LUMPY SKIN DISEASE 3 Babiuk S TR Bowden DB Boyle DB Wallace and RP Kitching 2008 Capripoxviruses an emerging worldwide threat to sheep goats and cattle Transbound Emerg Dis 55 263272 4 Greth A JM Gourreau NguyenBaVy M Wyers and PC Lefevre 1992 Capripoxvirus disease in an Arabian oryx Oryx leucoryx from Saudi Arabia J Wildl Dis 282 295300 5 Kitching P 2008 Capripoxvirus In Committee on Foreign and Emerging Diseases of the United States Animal Health Association ed Foreign Animal Diseases 7th edition Revised 2008 Boca Publishing Group Inc Boca Raton Florida Pp 189 196 httpwwwaphisusdagovemergencyresponsedownloadsnahemsfadpdf Accessed 10 September 2013 6 Tuppurainen ES and CA Oura 2012 Review Lumpy Skin Disease an emerging threat to Europe the Middle East and Asia Transbound Emerg Dis 591 40 48 7 Tuppurainen ES WH Stoltsz M Troskie DB Wallace CA Oura PS Mellor JA Coetzer and EH Venter 2011 A potential role for Ixodid hard tick vectors in the transmission of Lumpy Skin Disease virus in cattle Transbound Emerg Dis 582 93104 8 Kahn C and S Line eds 2005 The Merck Veterinary Manual 9th Edition Merck Co Inc Whitehouse Station New Jersey Pp 699700 9 MacLachlan N and J Stott 2004 Poxviridae In Hirsh DC NJ MacLachlan and RL Walker eds Veterinary Microbiology 2nd Edition Blackwell Publishing Professional Ames Iowa Pp 336 337 10 McNamara T and D Gregg 1994 A novel pox infection in pudus Pudu puda Proceedings from the Association of Reptilian And Amphibian Veterinarians Pp 225 231 American Association of Zoo Veterinarians Infectious Disease Manual LUNG MITES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Marine Mammals Birds Snakes Nonhuman primates Canids Direct In many cases animals are asymptomatic however in severe infections they may show signs of upper or lower respiratory disease depending on the host and species of parasite involved Dependent on the intensity of infection Mortality is low but can be higher if bacterial or fungal co infection develops Ivermectin Reduce population density hand rear young No Fact Sheet compiled by Sara ChildsSanford Sheet completed on updated 2017 Fact Sheet Reviewed by Rich Sim Susceptible animal groups Marine Mammals Pinnipeds phocid seals otariids walrus sea otters Birds Numerous species including companion passerines especially exotic finches wild passerines and galliformes Snakes reported in Elaphe schrencki Russia Crotalus and Pituophis spp southern United States Natrix trigrinal Korea Nonhuman Primates Old World monkeys esp Macaca mulatta apes Canids reported in a fox Norway only documentation in a species other than the domestic dog Causative organism Pinnipeds Phocid seals Halarachne spp including H halichoeri Otariids walrus Orthohalarachne spp including O attenuata and O diminuata Sea otters Halarachne miroungae Birds Sternostoma tracheacolum Captive birds primarily finches and canaries Also reported in numerous wild passerine species as well as wild Gouldian finches in Australia following introduction via domestic canaries Numerous other species of Sternostoma have been reported in wild passerines Cytodites nudus pheasants chickens turkeys ruffed grouse canaries finches cockatiels budgerigars pigeons Numerous Ptilonyssus spp have been reported in wild passerines in North and South America and in captive canaries Snakes Entonyssus spp including E squamatus E halli E koreansis E vitzthumi Primates Pneumonyssus spp including P simicola P duttoni P africanus Canids Pneumonyssoides caninum Zoonotic potential One report describes a case of human ophthalmic acariasis after getting sneezed on by a walrus which resulted in ophthalmalgia and corneal abrasion Distribution Worldwide Incubation period Unknown Clinical signs Marine mammals American Association of Zoo Veterinarians Infectious Disease Manual LUNG MITES Pinnipeds nasal discharge sneezing facial pruritus head shaking and if lung involvement dyspnea Sea otters may be predisposed to sinus or turbinate infections Birds wheezing gasping openmouth breathing head shaking loss of or change in voice cessation of singing dyspnea Nonspecific signs such as weight loss weakness and sudden death may occur Snakes usually asymptomatic Primates usually asymptomatic but may be predisposed to other pulmonary diseases due to bronchiolar epithelial changes and sneezing and coughing In advanced cases especially in aged or immunocompromised animals death may occur Canids in domestic dogs sneezing is common but may also have facial pruritus excessive lacrimation and nasal discharge Post mortem gross or histologic findings Marine mammals histologically erosion and inflammation of the nasal turbinates and nasopharynx may be seen associated with mites Sinusitis rhinitis bronchopneumonia O attenuata adults primarily occupy the nasopharynx while O diminuata are found in the lungs Birds Sternostoma Black mites can be found in trachea air sacs and lungs Histologically tracheitis air sacculitis multifocal pneumonia Cytodites Mites can be visualized macroscopically as small white spots within bronchi lungs and air sacs Severe infections may result in granulomatous pneumonia Ptilonyssus Mites within the trachea with mucosal sloughing epithelial deciliation and necrosis and tracheal cartilage degradation Primates Small 15mm pale yellow foci containing mites throughout the lungs In advanced cases cavitation of the lungs may be present Gross lesions may resemble those of tuberculosis May be a cause of pulmonary bullae Histologically presence of macrophages containing brown to black pigment and multifocal eosinophilic granulomatous bronchiolitis with intralesional arthropods Diagnosis Antemortem diagnosis is difficult Marine mammals identification of larval mites in sputum or nasal exudate or at necropsy Rhinoscopy may be useful Birds following wetting of the cervical feathers with alcohol tracheal illumination may reveal the mites as small black spots within the lumen Failure to visualize mites with this method does not rule out infection On necropsy mites can be identified macroscopically in the tracheal lumen lungs or air sacs Snakes lung wash necropsy Primates tracheobronchial lavage necropsy Radiographic lesions may include an interstitial pattern with increased bronchial thickness pleural thickening pleural adhesions and cavitating pulmonary lesions Pneumothorax is a common complication of pulmonary acariasis and is frequently unilateral Canids nasal swabbing rhinoscopy necropsy use of an antibody ELISA has been reported Material required for laboratory analysis Depending on the species and location of infection sputum nasal discharge lung wash lung tissue Relevant diagnostic laboratories Any veterinary diagnostic laboratory with a parasitologist on staff Treatment Ivermectin Marine mammals 200µgkg twice 2 weeks apart Birds ivermectin or doramectin Can be given as an injection or in small birds can be applied topically on the bare skin at the base of the neck dilute 110 with propylene glycol and apply 1 drop per bird up to 50g repeat in 710 days Primates Canids 200µgkg subcutaneously Prevention and control Antemortem diagnosis and prevention are difficult since infected animals are often asymptomatic and identification of those with a low mite burden is unlikely Can consider American Association of Zoo Veterinarians Infectious Disease Manual LUNG MITES prophylactic treatment of newly acquired captive animals during quarantine High population density facilitates transmission Animals can be raised free of infection if they are separated from the mother soon after birth and handreared Suggested disinfectant for housing facilities Appropriate acaricides eg pyrethroids Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Infected animals should be treated prior to introduction to diseasefree animals Conditions for restoring diseasefree status after an outbreak Successful treatment of all potentially exposed susceptible animals Experts who may be consulted While no specific researchers are currently reporting expertise in this parasite parasitology staffs at veterinary colleges would be a good option References 1 AlonsoFarre JM Diaz DSilva JI Gestal C Nasopharyngeal mites Halarachne halichoeri Allman 1847 in grey seals stranded on the NW Spanish Atlantic coast Vet Parasit 20121833 4317322 2 Altman RB Clubb SL Dorrestein GM Quesenberry K eds Avian Medicine and Surgery Philadelphia PA WB Saunders Co 1997 p 464 575 1026 1195 3 Andrade MCR Marchevsky RS Histopathologic findings of pulmonary acariasis in a rhesus monkeys breeding unit Brazil J Vet Parasitol 2007164229234 4 Arabkhazaeli F Madani SA Ghavami S 2016 Outbreak of an unusual tracheal mite Ptilonyssus morofskyi Acarina Rhinonyssidae in canaries Serinus canaria with concurrent infection with Staphylococcus aureus and Macrorhabdus ornithogaster J Av Med and Surg 303269273 5 Bowman DD Georgis Parasitology for Veterinarians Bowman DD St Louis MO Saunders Elsevier 2009 p 63 6 Bredal WP Gjerde BK Kippenes H Pneumonyssoides caninum the canine nasal mite reported for the first time in a fox Vulpes vulpes Vet Parasit 19977334 291297 7 Dierauf LA Gulland MD CRC Handbook of Marine Mammal Medicine 2nd ed New York NY CRC Press 2001 p 372 8 Hrapkiewicz K Medina L Holmes D eds 1998 Clinical Medicine of Small Mammals and Primates An Introduction 2nd ed Ames IA Iowa State University Press 1998 304 p 9 Johnson AL Simonek GD Keesler RI Fatal pulmonary acariasis in an aged indoor rhesus macaque Macaca mulatta J Med Primatol 201746 9092 10 Kim JM Han S Shin JS Min BH Jeong WY Lee GE Kim MS Kim JE Chung H Park CG Computed tomography or necropsy diagnosis of multiple bullae and the treatment of pneumothorax in rhesus macaques Macaca mulatta J Med Primatol 201746 260262 11 Kim KC Haas VL Keyes MC Populations microhabitat preference and effects of infestation of two species of Orthohalarachne Halarachnidae Acarina in the northern fur seal J Wildl Dis 19801614551 12 Mascarenhas CS Coimbra MA Muller G Brum JG Nasal mites Gamasida Rhinonyssidae of Paroaria coronata Miller Passeriformes Emberezidae Neotrop Entomol 2011404507508 13 Rohde K ed 2005 Marine Parasitology Collingwood Australia CSIRO Publishing 2005 14 Seguel M Gutiérrez J Hernández C Montalva F Verdugo C Respiratory mites Orthohalarachne diminuata and βhemolytic Streptococciassociated bronchopneumonia outbreak in South American Fur seal pups Arctocephalus australis J Wildl Dis 2018542380 5 15 Webb JP Furman DP Wang S A unique case of human ophthalmic acariasis caused by Orthohalarachne attenuata Banks 1910 Acari Halarachnidae J Parasitol 1985713 388 389 American Association of Zoo Veterinarians Infectious Disease Manual LUNG MITES 16 WolfeCoote S ed The Laboratory Primate San Diego CA Elsevier Academic Press 2005 650 p American Association of Zoo Veterinarians Infectious Disease Manual LYMPHOCYTIC CHORIOMENINGITIS VIRUS CALLITRICHID HEPATITIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic New World nonhuman primates NHP Platyrrhini of the families Callitrichidae and Callimiconidae humans and rodents Horizontal due to ingestion of infected mice with LCMV including wild rodents Vertical transmission of LCMV to an aborted nonhuman primate fetus Lethargy jaundice anorexia weakness dyspnea High fatality rate morbidity and mortality None Rodent control avoid feeding primates on mice Yes Fact Sheet compiled by Enrique YartoJaramillo Sheet completed on 4 August 2011 updated 4 February 2018 Fact Sheet Reviewed by Salomé Cabrera Lilian Silva Catenacci Rosalia Pastor Pierre Rollin Susceptible animal groups The common house mouse Mus musculus is the natural host and principal reservoir of LCMV Several genera of families Callitrichidae especially Callithrix sp Saguinus sp and Callimiconidae especially Callimico goeldii are susceptible to the infection with LCMV In captive golden lion tamarins Leontopithecus rosalia and pygmy marmoset Cebuella pygmaea the virus accounted for 43 and 71 of deaths of animals respectively Humans and wild laboratory and pet rodents especially mice hamsters gerbils rats and guinea pigs are susceptible Infections to humans from pet rodents have been reported Although rodents can potentially become infected they often do not show any signs of illness Hamsters are not the natural reservoir so in young hamsters it causes a chronic fatal wasting disease Infected mice and hamsters have proven to shed the virus in large quantities through their lives in saliva feces urine and nasal secretions Humans may also acquire this virus from nesting materials from infected pet rodents Causative organism Lymphocytic choriomeningitis virus LCMV which is a lipid enveloped single stranded RNA virus family Arenaviridae genera Mammarenavirus of the Old Worlds Arenavirus group is considered the prototypic arenavirus This group of viruses utilize rodents as their principal reservoirs LCMV is a virus with high mutation rates and important strain variations Rodent reservoirs pass the virus to their offspring and shed the virus in urine and oral secretions which are additional routes of transmission to zoo animals The other route of transmission to zoo animals has been the domestic mice used to feed non human primates Animals not eating mice neither became ill nor seroconvert to LCMV even after close contact with sick primates Thus direct primateprimate transmission of LCMV was not observed yet although such a mode of transmission remains a possibility Vertical transmission of LCMV to an aborted tamarin fetus however was demonstrated in a US zoo Zoonotic potential LCMV is a prevalent human pathogen infecting large numbers of humans according to serological studies which indicate that approximately 5 of adult humans in the USA show antibodies to this virus Seroconversion with no evidence of clinical disease has been reported in handlers of infected animals although the infection has been reported to cause substantial neurological disease especially in immunocompromised humans In humans the LCMV causes influenzalike clinical signs occasionally with neurologic complications alike manifestations of aseptic meningitis Since this virus has a strong American Association of Zoo Veterinarians Infectious Disease Manual LYMPHOCYTIC CHORIOMENINGITIS VIRUS CALLITRICHID HEPATITIS neurotropism LCMV is recognized as an important cause of neurologic disease in humans Infection may be asymptomatic in up to one third of patients although serious complications often occur in intrauterine infection Less severe cases of adult human infection are likely underreported and often misdiagnosed It is also a potential emerging neutoteratogen causing congenital defects in children Several reports of LCMV acquired during pregnancy have demonstrated severe disruption of brain development In 2009 the Center for Disease Control and Prevention confirmed a case of LCMVassociated congenital hydrocephalus and chrorioretinitis in a child from New York The mothers history referred exposure to mice during pregnancy LCMV is recognized as a zoonotic disease associated with exposure to infected hamsters and gerbils Child neurologists should be more familiar with this virus due to its potential to cause severe neurologic birth defects and so to promote its inclusion within the TORCHS acronym In April 2012 the CDC was notified about a patient diagnosed with aseptic meningitis who was an employee at a rodent breeding facility in Indiana and whose testing revealed LCMV Further testing showed evidence of prevailing or past LCMV infection in 13 out of 52 employees at the same facility Distribution LCMV is found worldwide probably because of its association with its natural Old Worlds host the house mouse Mus musculus Although antibodies have also been detected in other rodent species arenaviruses are known to be serologically crossreactive Outbreaks have been reported in zoo colonies of callitrichid primates in US and Europe UK and Germany Incubation period In nonhuman primates it is from one to three weeks but deaths which can reach 100 in an outbreak may occur over a period of weeks to months Clinical signs In infected callitrichid primates marmosets tamarins and Goeldis monkeys clinical findings are acute onset of lethargy anorexia anemia weakness fever dyspnea and mucuscovered feces along with jaundice and sometimes hemorrhage It was also reported abortion and dystocia in captive tamarins and marmosets Animals having a longer course of the disease may present jaundice and inguinal petechiae Some authors have reported grand mal seizures or sudden death without prior clinical signs Clinical laboratory findings elevated levels of aspartate aminotransferase alkaline phosphatase and bilirubin but none of them are specific Serologic evidence of LCMV in marmosets without clinical signs has been documented In experimentallyinfected rhesus macaques LCVMWE strain has led to fatal liver disease which was formerly described as Lassa fever LF hepatitis Postmortem gross or histologic findings Gross necropsy findings in NHP may include hepatitis hepatomegaly splenomegaly pleural and pericardial effusions lymphadenopathy jaundice subcutaneous and intramuscular hemorrhages Histologic findings include multifocal hepatocyte necrosis with infiltration by lymphocytes and neutrophils and portal vein vasculitis necrosis of spleen lymph nodes adrenal cortex and intestinal tract Acidophilic bodies Councilman bodies that represent apoptotic hepatocytes have been observed in affected liver tissues Brain tissues may show encephalitis minimal meningitis and vasculitis Diagnosis In NHP clinical signs clinical findings and husbandry history exposure to rodent species or history of being fed suckling mice are consistent with diagnosis In humans confirmatory diagnosis is usually by virus isolation in cerebrospinal fluid CSF by PCR on tissues or CSF antiLCMV IgM and IgG by ELISA in blood serum or CSF In human genetic analysis LCVM strains have demonstrated these viruses are genetically and biologically highly diverse Histopathology virus isolation electron microscopy nucleic acid hybridization analysis immunofluorescence and immunoblot in liver biopsy and other tissues spleen lung adrenal glands lymph nodes intestine kidneys urinary bladder heart and brain are the reported diagnostic methods for LCMV in NHP In rodents few isolates of LCMV have been obtained from wild rodents so little is known about its genetic diversity Confirmatory diagnosis is by viral isolation or PCR and antibody detection in the bloodserum by ELISA In recent experimental studies using different types of macrophages and American Association of Zoo Veterinarians Infectious Disease Manual LYMPHOCYTIC CHORIOMENINGITIS VIRUS CALLITRICHID HEPATITIS hepatocytes it has been validated that AML12 hepatocytes are useful in studying the mechanisms of arenavirusinduced hepatitis Material required for laboratory analysis Serum for serology tissue samples especially liver and brain frozen at 70ºC for PCR or virus isolation Formalinfixed tissues for pathology and immunohistochemistry Relevant diagnostic laboratories Virus Reference Laboratories Inc 7540 Louis Pasteur Road San Antonio Texas 78229 Phone 210 614 7350 Fax 210 614 7355 Treatment No effective treatment known although supportive therapy with fluids to correct hypovolemia and electrolyte imbalances might be of benefit The antiviral agent ribavirin has been used in infected primates 150mgkg intramuscularly once daily for 6 days but all of them were in an advanced stage of the disease and a clinical response was not observed Prevention and control Avoid feeding callitrichid primates on mice pinkies and stringent rodent control programs in zoos and primate centers particularly in areas housing callitrichids People using frozen or live rodents to feed other animals should follow safety precautions including wearing gloves when handling animal products Washing hands with soap and water after handling animal products is warranted Once an outbreak has been detected the animal enclosure should be cleaned and disinfected Proper snap traps of rats and mice as well as spraying dead rodents with disinfectants double bagging the carcasses and waste disposal should reduce the risk for people Suggested disinfectant for housing facilities A 110 bleach solution is effective in killing LCMV Hypochlorite solution 1 and ½ household bleach 1 gallon of water is indicated as a disinfectant for contaminated areas Notification Due to some reports on human patients contracting the virus from transplanted organs as well as LCMVassociated congenital defects LCMV is a reportable disease in three US states Wisconsin Massachusetts and Arizona and one city New York New York Increased physician awareness should improve disease recognition and reporting in human patients Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal It appears that most NHP that become clinically infected succumb to the disease Horizontal transmission has not been reported in people however vertical transmission can occur Conditions for restoring diseasefree status after an outbreak Strict pest control and removal and control of all rodents and their droppings urine and bedding Disinfection of all premises with 110 bleach solution Experts who may be consulted CDC Viral Special Pathogens Branch 4046391115 or 4046391510 Dvd1spathcdcgov httpwwwcdcgovnceziddhcppvspbindexhtml References 1 Centers for Disease Control and Prevention Internet Lymphocytic Choriomeningitis LCM 2014 cited 2019 September 24 Available from httpswwwcdcgovvhflcm 2 Centers for Disease Control and Prevention Internet Lymphocytic choriomeningitis virus LCMV at a rodent breeding facility in Indiana MayJune 2012 c2012 cited 2019 September 24 Available from httpswwwcdcgovmmwrpreviewmmwrhtmlmm6132a5htmscidmm6132a5w American Association of Zoo Veterinarians Infectious Disease Manual LYMPHOCYTIC CHORIOMENINGITIS VIRUS CALLITRICHID HEPATITIS 3 Asper M Hofmann P Osmann C Funk J Metzger C Bruns M Kaup FJ Schmitz H Günther S First outbreak of callitrichid hepatitis in Germany genetic characterization of the causative lymphocytic choriomeningitis virus strain Virol 2001284203213 4 Beier JI Jokinen JD Holz GE Whang PS Martin AM Warner NL Arteel GE Lukashevich IS Novel mechanism of Arenavirusinduced liver pathology PLOS One Internet 2015 cited 2019 September 24103e0122839 5 Bielitzki JT Emerging viral diseases of nonhuman primates In Fowler ME Miller RE eds Zoo and Wild Animal Medicine Current Therapy 4 Philadelphia PA Saunders 1999 p 377382 6 Blasdell KR Becker SD Hurst J Begon M Bennett M Host range and genetic diversity of arenoviruses in rodents United Kingdom Emerg Infect Dis 200814914551458 7 Bonthius DJ Lymphocytic choriomeningitis virus An underrecognized cause of neurologic disease in the fetus child and adult Semin Pediatr Neurol 20121938995 8 CatãoDias JL Infectious diseases in Order Primates In Fowler ME Cubas ZC eds Biology Medicine and Surgery of South American Wild Animals Ames IA Iowa State University Press 2001 p 269272 9 Fischer SA Graham MB Kuehnert MJ Kotton CN Srinivasan A Marty FM Comer JA Guarner J Paddock CD DeMeo DL Shieh WJ Erickson BR Bandy U DeMaria Jr A Davis JP Delmonico FL Pavlin B Likos A Vincent MJ Sealy TK Goldsmith CS Jernigan DB Rollin PE Packard MM Patel M Rowland C Helfand RF Nichol ST Fishman JA Ksiazek T Zaki SR Transmission of lymphocytic choriomeningitis virus by organ transplantation N Engl J Med 2006354212235 10 Gog J Woodroffe R Swinton J Disease in endangered metapopulations the importance of alternative hosts In Proc R Soc Lond B 2002 p 671676 11 Holz Gretchen E Proinflammatory cytokines promote viral replication and cell cycle mediators in arenavirusinduced hepatitis University of Louisville Electronic Theses and Dissertations Internet 2016 cited 2019 September 24 Available from httpsirlibrarylouisvilleeducgiviewcontentcgirefererhttpsscholargooglecomhttpsredir1 article3652contextetd 12 Knust B Macneil A Wong SJ Backenson PB Gibbons A Rollin PE Nichol ST Exposure to lymphocytic choriomeningitis virus New York USA Emerg Infect Dis 201117713241325 13 Lavergne A de Thoisy B Tirera S Donato D Bouchier C Catzeflis F Lacoste V Identification of lymphocytic choriomeningitis mammarenavirus in house mouse Mus musculus Rodentia in French Guiana Infec Genet and Evol 201637225230 14 Ludlage E Mansfield K Clinical care and diseases of the common marmoset Callithrix jacchus Comp Med 2005534369382 15 Mello MA Toscano C Muniz JAPC Torres MAN de Oliva OP da Costa Vasconcelos PF del Rio do Valle R da Silva VLC de Barros VLRS Svoboda WK Pereira WLA Costa ZGA Manual de Vigilância de Epizootias em Primatas nãohumanos Ministério da Saúde Internet 2005 cited 2019 September 24 Available from httpbvsmssaudegovbrbvspublicacoesmanualvigepizootiaspdf 16 Montali RJ Bush M Diseases of callitrichidae In Fowler ME Miller RE eds Zoo and Wild Animal Medicine Current Therapy 4 Philadelphia PA Saunders 1999 p 369376 17 Montali RJ Connolly BM Armstrong DL Scanga CA Holmes KV Pathology and immunohistochemistry of callitrichid hepatitis an emerging disease of captive New World primates caused by lymphocytic choriomeningitis virus Am J Pathol 199514714411449 18 Montali RJ Scanga CA Pernikoff D Wessner R Ward R Holmes KV A commonsource outbreak of callitrichid hepatitis in captive tamarins and marmosets J Infect Dis 1993167946950 American Association of Zoo Veterinarians Infectious Disease Manual LYMPHOCYTIC CHORIOMENINGITIS VIRUS CALLITRICHID HEPATITIS 19 Rensing S Oerke AK Husbandry and management of New World species marmosets and tamarins In WolfeCoote S ed The Handbook of Experimental Animals The Laboratory Primate San Diego CA Elsevier 2005 p 145162 20 Setzer AP Hepatites virais In Cubas ZC Silva JCR CatãoDias JL eds Tratado de Animais Selvagens medicina veterinária Rio de Janeiro Brazil Editora Roca LTDA 2007 p 815825 21 Scanga CA Holmes KV Montali RJ Serologic evidence of infection with lymphocytic choriomeningitis virus the agent of callitrichid hepatitis in primates in zoos primate research centers and a natural reserve J Zoo Wildl Med 199324469474 22 Stephensen CB Jacob JR Montali RJ Holmes KV Muchmore E Compans RW Arms ED Buchmeier MJ Lanford RE Isolation of an arenavirus from a marmoset with callitrichid hepatitis and its serologic association with disease J Virol 19916539954000 23 Udofin LU Lymphocytic choriomeningitis In Rabinowitz PM Conti LA eds HumanAnimal Medicine Clinical Approaches to Zoonoses Toxicants and Other Shared Health Risks Maryland Heights MO Saunders 2010 p 204209 24 Wissman MA Husbandry and medical care of callitrichids J Exot Pet Med 201423347362 American Association of Zoo Veterinarians Infectious Disease Manual MARBURG HEMORRHAGIC FEVER Fact Sheet compiled by Aubrey M Tauer Sheet completed on 1 April 2011 15 August 2013 Fact Sheet Reviewed by Christine Fiorello Pierre E Rollin Susceptible animal groups Primates including humans African fruit bat Rousettus aegyptiacus is a natural reservoir for Marburg Causative organism Lake Victoria Marburgvirus Filovirus Zoonotic potential Yes Distribution Natural virus circulation and human cases isolated or during outbreak are restricted to Africa geographical range of the reservoir although imported monkeys caused an human outbreak in Europe in 1967 and several infected travelers have imported the disease outside the endemic zone Incubation period Generally it is 810 days range 521 days Clinical signs Early signs are similar to influenza and malaria and the onset of disease is sudden Humans Fever headache chills and myalgia sometimes followed around the fifth day by possible maculopapular rash on the chest abdomen and back As the illness progresses nausea vomiting abdominal pain diarrhea chest pain sore throat jaundice weight loss and pancreatitis are observed Many patients develop some form of bleeding and often from multiple sites Shock renal failure liver failure and multiple organ dysfunctions occur in the most severe cases and usually preceded death Case fatality rate ranges from 23 to more than 80 in recent outbreaks In recovered humans complications such as orchitis recurrent hepatitis uveitis transverse myelitis have been reported Animals Lymphopenia and elevation of liver enzymes are characteristic Thrombocytopenia is frequent Although duikers are susceptible to Ebola virus a related filovirus little is known about the host range of Marburg virus Complications in the few recovering animals are not reported Post mortem gross or histologic findings In laboratory nonhuman primates maculopapular rash pulmonary congestion and edema enlarged friable fatty liver enlarged congested andor hemorrhagic lymphoid tissue pericardial effusion pyloric and duodenal congestion andor hemorrhage fibrinous interstitial pneumonia and lymphocytolysis and lymphoid depletion in lymph nodes and spleen have been observed Diagnosis Antigencapture enzymelinked immunosorbent assay ELISA polymerase chain reaction PCR and virus isolation on acutephase blood or tissue specimens from deceased individuals Recovering animals or human develop IgM capture ELISA and IgG ELISA Immunohistochemistry can be used on tissue specimens from deceased individuals PCR method has been used on bone marrow samples of primate carcasses in poor condition in the field for the related Ebola virus The virus has also been visualized in organ tissues by Electron Microscopy Material required for laboratory analysis Like for Ebola hemorrhagic fever although the virus could be Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primates including humans Direct contact with body fluids sexual activity droplets and aerosolized virus Fever rash malaise vomiting diarrhea shock multiple organ dysfunction syndrome hemorrhage High morbidity and mortality No specific treatment Personal protective equipment strict quarantine Yes American Association of Zoo Veterinarians Infectious Disease Manual MARBURG HEMORRHAGIC FEVER detected in a large variety of biological samples saliva throat swabs urine semen excrement vomit and potentially skin biopsies and bone samples blood and tissues spleen liver are the most important specimens to collect for acute case diagnosis Protective safety equipment and safe collection methods are mandatory Relevant diagnostic laboratories Marburg diagnosis can only be undertaken at BSL4 laboratories such as Viral Special Pathogens Branch in the Centers for Disease Control and Prevention Atlanta Treatment No specific treatment for this disease exists Supportive care such as maintaining fluid and electrolyte balance blood pressure and oxygenation is the currently recommended practice for human patients Whole blood and freshfrozen plasma transfusions can be beneficial for the subset of patients that develop hemorrhage Culling may be the practice of choice in outbreak situations with animals Prevention and control Strict quarantine procedures for mammals imported from Central Africa should be observed Follow CDC guidelines if importing species suspected to be reservoirs such as the Egyptian fruit bat Caution should be observed when handling or shipping blood or tissue samples from known affected species and follow CDC and WHO guidelines The CDC has detailed instructions regarding disinfection quarantine and personal protective equipment Suggested disinfectant for housing facilities Viruses in the Filoviridae family are readily inactivated by several virucidal products 05 sodium hypochlorite 10 solution household bleach glutaraldehyde 2 and phenolic disinfectants 053 are recommended by the CDC Soaps and detergents can also be used liberally and also inactivate the virus Care should also be taken to prevent aerosolization of the virus Notification All suspected cases must immediately be reported to the CDC Special Pathogens Branch 404 6391115 as well as local and state health departments Prior to collecting and sending any laboratory samples for Marburg virus testing consult with the Special Pathogens Branch as well as the local state health department Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Inadvisable Conditions for restoring diseasefree status after an outbreak Under advisement of the CDC and state health department Expert who may be consulted Pierre E Rollin MD Viral Special Pathogens Branch Centers for Disease Control and Prevention 1600 Clifton Road Atlanta Georgia 30333 4046391124 office prollincdcgov References 1 httpwwwcdcgovncidoddvrdspbmnpagesdispagesmarburghtm Accessed 26 August 2013 2 Alves DA AR Glynn KE Steele MG Lackemeyer NL Garza JG Buck C Mech and DS Reed 2010 Aerosol exposure to the Angola strain of Marburg virus causes lethal viral hemorrhagic fever in Cynomolgus Macaques Vet Pathol 475 831851 3 Amman BR SA Carroll ZD Reed TK Sealy S Balinandi R Swanepoel A Kemp BR Erickson JAC Comer S Campbell DL Cannon ML Khristova P Atimnedi CD Paddock RJ Kent Crockett TD Flietstra KL Warfield R Unfer E KatongoleMbidde R Downing JW Tappero SR Zaki PE Rollin TG Ksiazek ST Nichol and JS Towner 2012 Seasonal pulses of Marburg virus circulation in juvenile Rousettus aegyptiacus bats coincide with periods of increased risk of human infection PLoS Pathogens 810e1002877 American Association of Zoo Veterinarians Infectious Disease Manual MARBURG HEMORRHAGIC FEVER 4 Centers for Disease Control 1988 Viral hemorrhagic fever initial management of suspected and confirmed cases MMWR 32 2S 27S39S 5 Formenty P 2008 EbolaMarburg viral diseases In Heyman DL ed Control of Communicable Diseases Manual American Public Health Association Washington DC Pp 204207 6 Geisbert TW KM DaddarioDiCaprio JB Geisbert HA Young P Formenty EA Fritz T Larsen and LE Hensley 2007 Marburg virus Angola infection of rhesus macaques pathogenesis and treatment with recombinant nematode anticoagulant protein c2 J Infect Dis 196Suppl 2S372 S381 7 Interim guidance for managing patients with suspected viral hemorrhagic fever in US hospitals 2005 Center for Disease Control httpwwwcdcgovHAIpdfsbbpVHFinterimGuidance051905pdf Accessed 26 August 2013 8 Rouquet P JM Froment M Bermejo A Kilbourn W Karesh P Reed B KumulunguiP Yaba A Délicat PE Rollin and EM Leroy 2005 Wild animal mortality monitoring and human Ebola outbreaks Gabon and Republic of Congo 20012003 Emerg Infect Dis 112 283290 American Association of Zoo Veterinarians Infectious Disease Manual MEASLES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primates including humans especially susceptible are colobus monkeys macaques and callitrichids Aerosol Fever conjunctivitis cough and characteristic rash Other signs of encephalitis and gastroenteritis colitis Highly contagious with variable species morbidity and mortality None aside from symptomatic care Proper quarantine of animals wearing proper protective equipment especially when known exposure to disease Vaccination can be considered for nonhuman primates Yes Fact Sheet compiled by Natalie D Mylniczenko Sheet completed on 29 January 2011 updated 10 September 2013 19 April 2018 Fact Sheet Reviewed by Erika TravisCrook Susceptible animal groups All primates human and nonhuman are affected although humans are the only known reservoir in humans usually young children or immunocompromised adults infected Nonhuman primates are susceptible with variable morbidity and mortality that is species specific and affected by individual animal health status With some nonhuman primate species only seroconversion occurs Causative organism Measles paramyxoviridaemorbillivirus also known as rubeola It is an enveloped single stranded RNA virus Zoonotic potential Yes Distribution Worldwide but now it is considered a foreign disease in the US as it was eliminated in 2000 Despite this status a number of outbreaks occur each year usually secondary to travel abroad and then spread due to lack of vaccination in groups of children Incubation period Infectious 521 d post exposure Clinical signs Disease is often asymptomatic When clinical signs are present they resemble influenza such as nasal and ocular discharge and conjunctivitis Diarrhea may be present especially in New World monkeys Occasionally dermatitis is present and rarely Koplick spots or stomatitis Facial edema blepharitis and erythema have been documented Measles is immunosuppressive therefore other diseases may confound diagnosis Encephalitis although rare occurs acutely and has a rapid clinical course Rarely further in macaques abortion can be observed Post mortem gross or histologic findings Exanthematous rash is noted grossly In callitrichids gastritis and enterocolitis is observed Evidence of encephalitis is observed with acute measles Syncytial cell formation and giant cell pneumonia is observed histologically In macaques that abort endometritis can be rarely observed Diagnosis Serology IgM and IgG paired titers with 4 fold increase in IgG titer or if IgM is found immunofluorescence urine viral isolation Material required for laboratory analysis Serum is preferred frozen or fresh although plasma is accepted at some labs Tissue samplessee specific labs for their requirements are usually oropharyngeal swabs nasal lavage or urine Relevant diagnostic laboratories PCR and ELISA testing on varying sample types contact each group for their requirements can be done at the following facilities Centers for Disease Control and Prevention Measles Virus Laboratory Unit 81 1600 Clifton Road Atlanta Georgia 30333 American Association of Zoo Veterinarians Infectious Disease Manual MEASLES 4046391156 or 4046393512 Fax 4046394187 jrotacdcgov httpwwwcdcgovmeasleslabtoolsindexhtml Primate Diagnostic Services Laboratory PDSL Washington National Primate Research Center University of Washington Seattle Washington 981957330 richardgrantwanprcorg httpswwwwanprcorgprimateresourcespdsl Primate Assay Laboratory PAL Formerly PDL California National Primate Research Center University of California Davis Phone 5307528242 Email cnprcpdlucdavisedu httpwwwcnprcucdaviseduprimateassaylaboratorycore Virus Reference Laboratories Inc VRLSan Antonio USA PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 Office 8776157275 Fax 2106157771 httpwwwvrlsatcom Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 913113800 8187178880 Fax 8187178881 infozoologixcom httpwwwzoologixcom Treatment Supportive or symptomatic care as no specific treatments are available Prevention and control Vaccination has minimum age for humans of 1 year and booster is recommended to booster at least 4 weeks later although can be administered up to 46 years after the initial vaccinations See httpwwwcdcgovvaccinesrecsscheduleschildschedulehtmhcp Vaccination in gorillas has shown positive serologic responses Colobus have been vaccinated without adverse effects per SSP veterinary advisor reports Vaccination against canine distemper virus in macaques has shown effective protection against measles Human handlers should be properly vaccinated against disease According to human guidelines set by the CDC pregnant women should not be vaccinated with MMR however this concern is based on miscarriage or premature birth occurring in women with actual disease httpwwwcdcgovvaccinespubspregguidehtm American Association of Zoo Veterinarians Infectious Disease Manual MEASLES Infant macaques are vaccinated at 3 mo of age or older with a modified live vaccine A second dose is given no sooner than 6 weeks produces protective antibody levels Adult macaques in quarantine are vaccinated with a single dose Note monovalent measles vaccine is no longer available in the US so can only be obtained in polyvalent combinations particularly MMR Measles Mumps Rubella Suggested disinfectant for housing facilities Short lived virus so routine disinfection is usually sufficient Notification While this disease is not notifiable in animals it is a human reportable disease Measures required under the Animal Disease Surveillance Plan While this disease is not notifiable in animals it is a human reportable disease Measures required for introducing animals to infected animal Once exposed the animal has a natural immunity and will not become reinfected Typically primates contract disease from human handlers Conditions for restoring diseasefree status after an outbreak The disease has a rapid spread and short course with no animal reservoirs Experts who may be consulted Centers for Disease Control and Prevention 1600 Clifton Road Atlanta GA 303294027 USA 800CDCINFO 8002324636 TTY 8882326348 References 1 Albrecht P Lorenz D Klutch MJ Vickers JH Ennis FA Fatal measles infection in marmosets pathogenesis and prophylaxis Infect Immun 1980273969978 2 Bailey C Mansfield K Emerging and reemerging infectious diseases of nonhuman primates in the laboratory setting Vet Pathol 2010473462481 3 Centers for Disease Control and Prevention Internet Measles Rubeola 2018 cited 2018 April 10 Available from httpwwwcdcgovmeaslesaboutindexhtml 4 Choi YK Simon MA Kim DY Yoon BI Kwon SW Lee KW Seo IB Kim DY Fatal measles virus infection in Japanese macaques Macaca fuscata Vet Pathol 1999366594600 5 Christe KL McChesney MB Spinner A Rosenthal AN Allen PC Valverde CR Roberts JA Lerche NW Comparative efficacy of a canine distempermeasles and a standard measles vaccine for immunization of rhesus macaques Macaca mulatta Comp Med 200252546772 6 de Swart RL Measles What we have learned from nonhuman primate models Drug Discov Today Dis Models 201723 3134 7 Hall WC Kovatch RM Herman PH Fox JG Pathology of measles in rhesus monkeys Vet Pathol 197184307319 8 Hime JM Keymer IF Baxter CJ Measles in recently imported colobus monkeys Colobus guereza Vet Rec 19759720392 9 Kobune F Takahashi H Terao K Ohkawa T Ami Y Suzaki Y Nagata N Sakata H Yamanouchi K Kai C Nonhuman primate models of measles Lab Anim Sci 1996463315320 10 Levy BM Mirkovic RR An epizootic of measles in a marmoset colony Lab Anim Sci 197121133 39 11 Lorenz D Albrecht P Susceptibility of tamarins Saguinus to measles virus Lab Anim Sci 1980304 Pt 1661665 12 MacArthur JA Mann PG Oreffo V Scott GB The effect of measles vaccination in rhesus monkeys Macaca mulatta Lab Anim 1982163267270 13 Mansfield K King N Viral Diseases Viral Diseases In Bennett BT Abee CR Henrickson R eds Nonhuman Primates in Biomedical Research San Diego CA Academic Press 1998 p 157 American Association of Zoo Veterinarians Infectious Disease Manual MEASLES 14 Montrey RD Huxsoll DL Hildebrandt PK Booth BW Arimbalam S An epizootic of measles in captive silvered leafmonkeys Presbytis cristatus in Malaysia Lab Anim Sci 1980304 Pt 1694 697 15 Munson L Measles In Williams ES Barker IK eds Infectious Diseases of Wild Mammals Ames IA Iowa University Press 2001 p 6364 16 Remfry J A measles epizootic with 5 deaths in newlyimported rhesus monkeys Macaca mulatta Lab Anim 19761014957 17 Renne RA McLaughlin R Jenson AB Measles virusassociated endometritis cervicitis and abortion in a rhesus monkey J Am Vet Med Assoc 19731636 639641 18 Scott GB Keymer IF The pathology of measles in Abyssinian colobus monkeys Colobus guereza a description of an outbreak J Pathol 19751174229233 19 Willy ME Woodward RA Thornton VB Wolff AV Flynn BM Heath JL Villamarzo YS Smith S Bellini WJ Rota PA Management of a measles outbreak among Old World nonhuman primates Lab Anim Sci 19994914248 American Association of Zoo Veterinarians Infectious Disease Manual MELIOIDOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Humans Most common routes of infection are contamination of wounds ingestion of contaminated soil water or carcasses and inhalation Skin lesions pneumonia internal organ miliary abscesses Mimics many other diseases Can vary widely depending on the site of infection Antibiotic therapy multiple drugs for septicemic cases pulmonary resection may be considered for chronic cases Chlorinate or filter water Minimize exposure to diseased animals Yes rare Fact Sheet compiled by Angkana Sommanustweechai Tanit Kasantikul Karn Lekagul Sheet completed on 3 February 2011 updated 1 April 2013 Fact Sheet Reviewed by Ronald Mitchell Bush Rasana Wongratanachewin Susceptible animal groups Infection with B pseudomallei is seen most often in many species of domestic animals especially goats and sheep While cattle pig dog and cat have higher resistance to melioidosis Although incidences of melioidosis in wildlife are rarely reported cases have been documented in marine mammals camels alpacas mules zebra deer kangaroos bear and various nonhuman primates Reptiles such as crocodiles snakes softshelled turtles birds including parrots penguin and tropical fish can also become infected with the bacteria Hamsters and guinea pigs can be infected in the laboratory Causative organism Gram negative flagellated bipolarshaped saprophytic bacteria called Burkholderia pseudomallei Zoonotic potential Humans can be infected by ingesting contaminated food inhalation or direct contact of the contaminant with open wound Intrauterine and mammary transmissions have also been observed Arthropod borne transmission has also been described Horizontal transmission between human to human or animal to human by aerosol is unclear Distribution The organism is ubiquitous throughout southeast Asia northern Australia and the South Pacific Its distribution is predominantly tropical and subtropical with hyperendemicity in the top end of the Northern Territory of Australia and northeast Thailand The true boundaries of its endemicity are ambiguous due to movement of the organism and its ability to travel to and exist in temperate regions southwest Australia and France where it may cause sporadic disease and outbreaks Reports of possible autochthonous melioidosis have also come from India Pacific islands Central and South America the Caribbean Africa and the Middle East Incubation period In natural infections the incubation period in humans can vary from days to months or years The medical onset time of the disease is usually in the range of 121 days means 9 days Abscesses may be carried without clinical signs which can be found in some resistant animal species such as pigs and cattle The incubation period in animal particularly in wildlife is uncertain due to lack of clinical history Clinical signs Called The Great Mimicker melioidosis has a wide range of clinical presentation including fulminating septicemia and chronic and local suppurative infections Moreover relapsing melioidosis can also American Association of Zoo Veterinarians Infectious Disease Manual MELIOIDOSIS cause the fulminating sepsis in patient who underwent insufficient eradication phase of treatment The most common site of infection is acute respiratory form and sepsis through hematogenous dissemination The chronic septicemia can present as intermittent febricula with chronic respiratory infection Local infection can be seen as lameness osteomyelitis mastitis orchitis aortic aneurysms which may possibly induce fulminating septicemia or chronic infection Subclinical infections are common in animals The animals mostly undergo chronic illness Abscesses may be found in asymptomatic animals at slaughter or died shortly after show the clinical signs The clinical presentation also varies by species In goat and sheep a severe febrile reaction accompanied by anorexia lameness and yellow thick exudate from the nose and eyes Mastitis is sometimes seen in goats and the superficial lymph nodes and udder may contain palpable abscesses In horses neurologic disease respiratory symptoms or colic and diarrhea have been described Neurological signs include walking in circles nystagmus blindness hyperaesthesia and mild tetanic convulsions have been reported in cows goats camels and horses Septicemia or extensive involvement of the vital organs can be fatal Camels are highly susceptible and can present symptoms of pyrexia severe depression septic arthritis anorexia mucopurulent nasal discharge with nervous signs Nonhuman primates mostly show generalized lethargy progressive cachexia and respiratory distress with nasal purulent discharge Most cases in captive marine mammals have been characterized by acute septicemia with anorexia and lethargy followed by death Pyrexia was often recorded in the last few days preceding death but respiratory distress was noticed only in a few animals immediately before death Although birds may be relatively resistant to melioidosis fatal cases with lethargy anorexia and diarrhea have been reported in various avian species in Australia Post mortem gross or histologic findings At necropsy the major findings are multiple abscesses containing thick caseous greenishyellow or offwhite material These abscesses are generally not calcified The regional lymph nodes lungs spleen liver and subcutaneous tissues are most often involved but abscesses can occur in most organs In animals with respiratory disease fibrinous pleuritis and exudative bronchopneumonia consolidation andor abscesses may be found in the lungs Suppurative lesions including nodules and ulcers may also be found on the nasal mucosa and septum as well as on the turbinate bones These nodules may coalesce to form irregular plaques Meningoencephalitis severe enteritis suppurative polyarthritis and other syndromes have also been reported Aortic aneurysms and mastitis are common in goats Splenic abscesses are often found in asymptomatic pigs at slaughter Diagnosis The gold standard method is isolation and identification of the organism from lesions and discharges The organism is readily cultured on routine diagnostic media such as MacConkeys agar and blood agar The selective media Ashdowns agar can help increase the sensitivity and specificity of this technique The unique characteristic of Burkholderia pseudomallei colony is earth odor Effective serologic screening tests include complement fixation and indirect hemagglutination In some species agglutination tests indirect hemagglutination immunofluorescence and enzyme immunoassays can be used for diagnosis However serological end points are not available for each wildlife species Crossreactions may occur in serologic tests with avirulent strain Burkholderia thailandensis which causes a false positive outcome in exposed animals Although antibody titers cannot be detected in chronically infected animals new tests using DNA probes and PCR have recently been developed The specific primers that are designed for conserved regions to 16s rRNA 16S23S rRNA intergenic spacer flagellin and lipopolysaccharide can differentiate between B pseudomallei B mallei and B thailandensis Material required for laboratory analysis Culture swab from lesions or exudates infected tissue or organs serum for serologic testing Relevant diagnostic laboratories Any lab is capable of culturing the organism Currently there is no reference lab in the world for Melioidosis listed with the Office International des Epizootics OIE This list can be checked at httpwwwtestoieintourscientificexpertisereferencelaboratorieslistoflaboratories American Association of Zoo Veterinarians Infectious Disease Manual MELIOIDOSIS Treatment The medical treatment which will take at least 4 months can be divided into 3 phases including post exposure prophylaxis induction and eradication phases Treatment of septicemic melioidosis in wildlife is difficult and challenging due to the need for extended continuous intravenous antibiotics and extralabel use of medicine Moreover pharmaceutical treatment can lose their effectivenesss after prolonged treatment often resulting in an unsuccessful cure with risks of recrudescence once treatment is discontinued in animals Prevention and control In endemic or contaminated areas contact between the animal and soil should be minimized Providing safe drinking water is important in endemic areas Chlorine 1ppm in the water for 30 minutes is effective in inhibiting bacterial activity in the water supply Carnivores and omnivores should not be allowed to eat contaminated carcasses Although there is no effective vaccine promising vaccine candidates are currently being researched and developed A routine environment collection for bacteriology will help in the disease surveillance and control Suggested disinfectant for housing B pseudomallei can survive for months to years in soil and water but can be readily destroyed by heat Moist heat of 121C for at least 15 min or dry heat of 160170C for at least 1 hour is recommended for disinfection The organism is also susceptible to numerous disinfectants including 1 sodium hypochlorite 70 ethanol glutaraldehyde and formaldehyde SPILLS Allow aerosols to settle wear protective clothing gently cover spill with paper towels and apply 1 sodium hypochlorite starting at perimeter and working towards the centre allow sufficient contact time 30 min and clean the area 40 WW calcium oxide is proved to be effective in preventing bacterial activity in the environment for 1 year Notification Public health officials and state veterinarians will need to be notified if zoonotic transmission occurs Measures required under the Animal Disease Surveillance Plan Melioidosis is not listed under this plan Measures required for introducing animals to infected animal An infected animal should be maintained in a quarantine situation until the wound has healed Do not introduce infected animal to an animal with a compromised immune system Conditions for restoring diseasefree status after an outbreak Follow the suggestions above for disinfection of facilities and maintaining uncontaminated water sources Decontaminate waste before disposal steam sterilization incineration chemical disinfection Quarantine any affected individuals until lesions resolved Experts who may be consulted There are no listed OIE experts for Burkholderia pseudomallei That said the following people deal with Melioidosis routinely and would be willing to respond to questions from professionals dealing with confirmed or suspect cases Bart Currie Professor and Head Tropical and Emerging Infectious Diseases Division Menzies School of Health Research Northern Territory Clinical School and Infectious Diseases Department Royal Darwin Hospital PO Box 41096 Casuarina Northern Territory 0811 Australia Phone 61889228056 Fax 61889275187 bartmenzieseduau copied to Mark Mayo program manager MarkMayomenzieseduau Mindy Glass Bacterial Special Pathogens Branch Division of HighConsequence Pathogens and Pathology CDC Zoonoses and Select Agent Laboratory American Association of Zoo Veterinarians Infectious Disease Manual MELIOIDOSIS 1600 Clifton Rd MS G34 Atlanta GA 30333 Phone 4046394055 Fax 4046393023 Email mglasscdcgov References 1 Ashdown LR 1979 An improved screening technique for isolation of Pseudomonas pseudomallei from Clinical Specimens Pathol 11 293297 2 Centers for Disease Control and Prevention CDC httpwwwcdcgovmelioidosis Accessed 3 July 2013 3 Choy JL M Mayo A Janmaat and BJ Currie Animal melioidosis in Australia Acta Tropica 2000 74 153158 4 Haase A M Brennan S Barrett Y Wood S Huffam DO Brien and B Currie 1998 Evaluation of PCR for diagnosis of melioidosis JClin Microbiol 36 10391041 5 Howard K and Inglis TJJ The effect of free chlorine on Burkholderia pseudomallei in potable water Water Res 2003 37 44254432 6 Inglis TJJ Review the Treatment of melioidosis Pharmaceuticals 3 12961303 7 Lee MA D Wang and EH Yap 2005 Detection and differentiation of Burkholderia pseudomallei Burkholderia mallei and Burkholderia thailandensis by Multiplex PCR FEMS Immunol Med Microbiol 43 413417 8 Limmathurotsakul D and SJ Peacock 2011 Melioidosis a clinical overview British Med Bull 99125139 9 Peacock SJ HP Schweizer DAB Dance TL Smith JE Gee V Wuthiekanun D DeShazer ISteinmetz PTan and P J Currie 2008 Management of accidental laboratory exposure to Burkholderia pseudomallei and B mallei Emerg Infect Dis 147 e2 doi 103201eid1407071501 10 Puthucheary SD ASS Anuar and TS Tee 2010 Burkholderia thailandensis whole cell antigen crossreacts with B pseudomallei antibodies from patients with melioidosis in an immunofluorescent Assay Southeas Asian J Trop Med Public Health 412 395400 11 Sirisinha S N Anuntagool T Dharakul P Ekpo S Wongratanacheewin P Naigowit B Petchclai V Thamlikitkul Y Suputtamonkol 2000 Recent development in laboratory diagnosis of melioidosis Acta Tropica 74235245 12 Sprague LD Neubauer H Melioidosis in animals A review on epidemiology diagnosis and clinical presentation J Vet Med 2004 B51 305320 American Association of Zoo Veterinarians Infectious Disease Manual MRSA METHICILLINRESISTANT Staphyloccus aureus Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals including Humans Contact with contaminated surfaces Minor to severe skin redness pustule red lesions boils rash fever headache malaise Typically mild but may be fatal in the immune compromised No mortality rates are reported in animals but disease increasingly common in ICU foals Wound care susceptible antibiotics as determined by testing when needed Personal environmental hygiene Wear gloves when handling known infected animal and equipment Yes Fact Sheet compiled by Tara M Harrison Sheet completed on 29 November 2009 updated 7 September 2012 updated 2018 Fact Sheet reviewed by Dalen Agnew Christine Fiorello Donald Janssen Susceptible animal groups Mammals avian Causative organism Methicillinresistant Staphylococcus aureus also Methicillinresistant Staphylococcus pseudointeritidis Zoonotic potential Yes Distribution Crowded living conditions group work and gyms closely shared work and locker spaces long term care or rehabilitation facilities hospitals A captive chimpanzee colony was found to have 69 prevalence of MRSA There was also a wide variety of asymptomatic mammals that cultured positive at a Copenhagen zoo MRSA was also isolated from clinical and nonclinical animals at a Belgium zoo An elephant skin infection was also caused by MRSA in a California Zoo Incubation period Generally is requires 110 days People 7 in hospitals and in the community 2 can have MRSA colonization with no clinical signs It is thought that 10 to up to 90 of dogs and cats can be nonclinical carriers as well Clinical signs Healthy people and animals typically do not develop disease under normal circumstances Humans Skin redness pimplelike red lesions boils rash fever headache malaise Animals Primarily skin infections or skin wounds although necrotizing pneumonia or other general infection may occur Post mortem gross or histologic findings This bacterium can produce a wide spectrum of clinical disease particularly of the skin In humans these diseases including impetigo folliculitis furunculosis cellulitis abscesses and wound infections Other diseases include necrotizing pneumonia endocarditis septic arthritis osteomyelitis meningitis and septicemia In animals abscesses dermatitis fistulas have been reported as well as pneumonia rhinitis bacteremia septic arthritis osteomyelitis omphalophlebitis metritis and mastitis Postmortem lesions are similar to any other purulent bacterial infection and vary with the organ or tissue involved in the infection Diagnosis Bacterial culture and antibiotic susceptibility testing Material required for laboratory analysis Culture swab or tissue sample of the affected area Relevant diagnostic laboratories Any laboratory capable of bacteriologic culturing is capable of diagnosing MRSA Treatment Typically it is resistant to all ßlactam agents including cephalosporins and carbapenems Hospitalassociated MRSA isolates often are resistant to multiple commonly used antimicrobial agents including erythromycin clindamycin and tetracycline while communityassociated MRSA isolates are often resistant only to ßlactam agents and erythromycin Treatment specifically depends on the specific MRSA isolate and its antibiotic sensitivity profile This will require sensitivity testing on ALL isolates and possibly repeated testing on isolates from a single case In humans Vancomycin if not resistant linezolid and daptomycin quinupristindalfopristin rifampin American Association of Zoo Veterinarians Infectious Disease Manual MRSA METHICILLINRESISTANT Staphyloccus aureus tetracycline and tigecycline are used for severe MRSA infections or MRSA infections resistant to vancomycin Prevention and control Minimization of indiscriminate antibiotic use would help prevent the development of additional antibioticresistant strains Follow all wound care procedures recommended by veterinarian or physician Practice good hygiene wash hands often Keep cuts and scrapes clean and cover with bandages avoid direct contact with cuts and scrapes use gloves to treat wounds replace and disinfect items in holding or exhibit frequently Porous surfaces such as blankets need to be washed in hot water using bleach and a hot air dryer to help kill bacteria Alcoholbased hand cleaners are effective when hands arent dirty Isolate the patient if possible to minimize staff contact and exposure Animal enclosures should be clearly marked with the diagnosis and preventative measures required Maintain infected animal in isolation or away from other animals until wounds are healed or cultures are negative If treatment of the animal is not possible humane euthanasia of infected animal may be warranted to minimize risk of infection to staff and other animals Suggested disinfectant for housing facilities After cleaning gross contamination 1 tablespoon of bleach to one quart of water fresh daily leave solution on to dry or wipe dry after 10 minutes Other disinfectants effective against Staphylococcus aureus or Staph are also most likely also effective against MRSA Check the disinfectant products label on the back of the container to verify it is effective against it Notification Public health officials may need to be notified if zoonotic transmission occurs depending on the state Notification to the state may be required if the person is admitted to an acute care ICU or person dies from MRSA or it is not associated with the following been hospitalized had surgery had dialysis been in long term care within the last year has an indwelling catheter or has a percutaneous medical device at the time of culture Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Maintain infected animal in a quarantine situation until the wound is healed Do not introduce infected animal to an animal with a compromised immune system Conditions for restoring diseasefree status after an outbreak Clean infected environment with diluted bleach to the extent possible Minimize contact of infected staff with animal Experts who may be consulted J Scott Weese DVM DVSc DipACVIM Dept of Pathobiology Ontario Veterinary College University of Guelph Guelph Ontario N1G2W1 5198244120 ext 54064 jsweeseuoguelphca httpwwwwormsandgermsblogcom References 1 Bortolami A Verin R Chantrey J Corrò M Ashpole I Lopez J Timofte D Characterization of LivestockAssociated MethicillinResistant Staphylococcus aureus CC398 and mecCpositive CC130 from Zoo Animals in the United Kingdom Microb Drug Resist 2017237908914 2 Centers for Disease Control Methicillin resistant Staphylococcus aureus skin infections from an elephant calf San Diego California 2008 MMWR Morbid Mortal Weekly Report 20095881948 3 Diana A Guglielmini C Pivetta M Sanacore A DiTommaso M Lord PF Cipone M Infection with methicillinresistant Staphylococcus pseudointermedius masquerading as cefoxitin American Association of Zoo Veterinarians Infectious Disease Manual MRSA METHICILLINRESISTANT Staphyloccus aureus susceptible in dogs J Am Vet Med Assoc 2009235 10641066 4 Dvorak G RovidSpickler A Roth J eds Handbook for Zoonotic Diseases of Companion Animals The Center for Food Security and Public Health Ames IA Iowa State University College of Veterinary Medicine 2008 p 177184 5 EspinosaGongora C Chrobak D Moodley A Bertelsen MF Guardabassi L Occurrence and distribution of Staphylococcus aureus lineages among zoo animals Vet Microbiol 20121581 2228231 6 Finks J Wells E Dyke TL Husain N Plizga L Heddurshetti R Wilkins M Rudrik J Hageman J Patel J Miller C Vancomycinresistant Staphylococcus auerus Michigan USA 2007 Emerg Inf Dis 2009156 7 Hanley PW Barnhart KF Abee CR Lambeth SP Weese JZ Methicillinresistant Staphylococcus aureus prevalence among captive chimpanzees Texas USA Emerg Infect Dis 201521122158 2160 8 Janssen DL Lamberski N Donovan T Sugerman DE Dunne G Methicillinresistant Staphylococcus aureus infection in an African elephant Loxodonta africana calf and caretakers In 2009 Proceedings AAZV AAWV Conference 2009200201 9 Liu C Bayer A Cosgrove SE Daum RS Fridkin SK Gorwitz RJ Kaplan SL Karchmer AW Levine DP Murray BE Rybak MJ Talan DA Chambers HF Clinical practice guidelines by the infectious diseases society of America for the treatment of Methicillinresistant Staphylococcus aureus infections in adults and children Clin Infect Dis 2011138 10 Methicillinresistant Staphylococcus Aureus MRSA Infections Internet Centers for Disease Control c20162018 cited 2013 July 2 Available from httpwwwcdcgovmrsaindexhtml 11 Methicillinresistant Staphyococcus aureus skin infections from an elephant calf San Diego California MMWR 200858194198 12 MRSA What you should know Michigan Department of Community Health MRSA control and prevention at home for people with pets County of San Diego Community Epidemiology Branch 13 National Association of Public Health Veterinarians Compendium of veterinary standard precautions for zoonotic disease prevention in veterinary personnel J Am Vet Med Assoc 2008233415430 14 Vercammen F Bauwens L De Deken R Brandt J Prevalence of methicillinresistant Staphylococcus aureus in mammals of the Royal Zoological Society of Antwerp Belgium J Zoo Wildl Med 2012431159161 American Association of Zoo Veterinarians Infectious Disease Manual MONKEYPOX Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Humans nonhuman primates rodents especially prairie dogs CDC recommends that all mammals be considered susceptible Contact with an infected animal human or contaminated materials through broken skin respiratory tract or mucous membranes Papulovesicular dermatitis upper respiratory disease blepharophlebitis prairie dogs fever lethargy decreased foodwater lymphadenopathy asymptomatic High case fatality rate in prairie dogs variable mortality in other species African rodents are suspected reservoir No specific treatment Guidelines available from the CDC Yes Fact Sheet compiled by Kelly Helmick Sheet completed on 21 February 2018 Fact Sheet Reviewed by Jennifer Kilburn Chris Hanley Susceptible animal groups The reservoir and full host range is unknown but African rodents are suspected in transmission Old and New World primates and rodents have shown susceptibility to experimental and natural infection Virus recovery from naturally infected animals outside of the US has been limited to a clinically ill rope squirrel Funiscuirus sp 1985 Democratic Republic of Congo and a dead infant mangabey Cercocebus atys 2012 Tai National Park Cote dIvoire Viral testing during the 2003 US outbreak identified infection in imported rope squirrels Funiscuirus sp dormice Graphiurus sp and African giant pouched rats Cricetomys sp and in exposed prairie dogs Cynomys sp Prairie dogs appear very susceptible to infection Chinchillas Chinchilla lanigera and coatimundis Nasua nasua developed antibodies after exposure Serological evidence of monkeypox virus infection has been detected in nonhuman primates rodents and squirrels in Africa Experimentally infected rope squirrels and Gambian pouched rats shed large quantities of virus Experimentally infected marmosets Callitrhix jaccus and ground squirrels Marmota bobak developed typical clinical signs Currently the CDC recommends that veterinarians consider all mammals susceptible to monkeypox virus Causative organism Monkeypox virus Orthopoxvirus family Poxviridae Two clades Central African and West African Transmission Contact with an infected animal human or contaminated materials through broken skin respiratory tract or mucous membranes Animaltohuman bite scratch bush meat preparation needle sticks direct contact with infected fluids or lesion material indirect contact contaminated bedding Cutaneous transmission implicated in the 2003 US outbreak Humantohuman respiratory droplets shared via prolonged facetoface contact direct contact with infected fluids or lesion material indirect contact contaminated clothing bedding Zoonotic potential Yes Rare zoonotic viral disease endemic to central and west Africa The West African clade is associated with limited humantohuman transmission milder symptoms and lower mortality compared to the Central African clade Humantohuman transmission of the Central African clade is welldocumented The most recent human cases occurred in Sierra Leone 2014 and Sudan 2005 Monkeypox is endemic in the Democratic Republic of Congo 2003 US outbreak A human outbreak involving the West African clade of monkeypox occurred in the US in 2003 Introduction of monkeypox virus occurred through a shipment of small mammals originating in Ghana CDC testing isolated virus from rope squirrels Funiscuirus sp dormice Graphiurus sp and African giant pouched rats Cricetomys sp Prairie dogs Cynomys sp housed in proximity to imported American Association of Zoo Veterinarians Infectious Disease Manual MONKEYPOX animals were also infected and sold as pets prior to developing signs of infection All human cases were associated with contact with infected prairie dogs Distribution Monkeypox virus is endemic to central and west Africa A 2003 outbreak occurred in the US involving prairie dogtohuman transmission traced to contact with newly imported infected African rodents Incubation period The incubation period in humans is typically 714 days but can range from 521 days Clinical signs Humans Fever headache muscle aches lethargy chills and swollen lymph nodes appear first A rash develops approximately 13 days later usually on the face and then spreading to other areas of the body Lesion progression is macules papules vesicles pustules then scab formation Symptoms last approximately 24 weeks In Africa human mortality occurs in approximately 1 of 10 cases Symptoms mimic smallpox lymphadenopathy occurs in monkeypox but not smallpox Rodents In naturally infected prairie dogs and experimentally infected rope squirrels fever respiratory symptoms of coughing nasal discharge ocular discharge rash beginning as papules progressing to pustules then crusts affecting head extremities trunk oral ulcers blepharophlebitis naturally infected prairie dogs lymphadenopathy may or may not be present experimentally infected rodents lethargy reduced foodwater intake elevated serum liver enzymes Some animals exhibited minimal clinical symptoms while others died Nonhuman primates Fever rash beginning as papules progressing to pustules then crusts typically on the face limbs hands feet tail respiratory symptoms of coughing nasal discharge dyspnea anorexia facial edema lymphadenopathy Similar symptoms to rodents observed in experimentally infected nonhuman primates Cynomolgus sp Postmortem gross or histologic findings Lymphadenitis skin rash and evidence of upper and lower respiratory disease on gross postmortem exam Lower respiratory epithelium is the target cell for virus replication with lymphoid tissue a secondary site for replication and lymphatogenous spread Trachea nasal mucosa skin hepatocytes and macrophages can demonstrate high levels of monkeypox virus presence marmosets ground squirrels Infected epithelial cells show prominent ballooning degeneration and dense eosinophilic intracytoplasmic granules prairie dogs Eosinophilic cytoplasmic granules Guarnierilike inclusions require IHC or EM to confirm orthopoxviral inclusions Necrotizing bronchopneumonia conjunctivitis and tongue ulceration prairie dogs Bronchopneumonia papulovesciular dermatitis ulcerative stomatitis colitis gastritis secondary bacterial septicemia experimentally infected Cynomolgus monkeys Use appropriate PPE when examining or collecting diagnostic samples from animals known or suspected to have monkeypox virus Diagnosis Clinical symptomology in rodents animals originating from endemic regions or animals housed in proximity to African rodents originating from endemic regions In humans monkeypox differs from smallpox by the presence of lymphadenopathy RTPCR immunohistochemistry virus isolation and electron microscopy There is no commercial assay to detect monkeypox virus Material required for laboratory analysis Tonsillar swab nasopharyngeal swab aspirate of vesicles biopsy of lesions scab or crust collection serum or whole blood EDTA collection Wear appropriate PPE and practice appropriate biosecurity Formalinfixed samples can be held and shipped at room temperature All other samples are held and shipped at 40C Do not use viral transport media Pack and ship according to IATA rules and regulations for diagnostic specimens Use appropriate PPE when examining or collecting diagnostic samples from animals known or suspected to have monkeypox virus Relevant diagnostic laboratories Veterinarians should contact their local or state health departments regarding monkeypox virus testing before contacting the CDC There is no commercial assay to detect monkeypox virus Culture based testing for monkeypox virus should be limited to the CDC American Association of Zoo Veterinarians Infectious Disease Manual MONKEYPOX Treatment There is no specific treatment for monkeypox virus in humans or animals Provide supportive treatment with appropriate biosecurity and PPE guidelines Prevention and control Foster good hygiene practices hand washing utilize PPE gloves masks and follow biosecurity protocols Limit contact by humans or mammals with known or suspected infected animals and bedding material especially animals arising from regions where monkeypox virus is endemic Utilize practices to limit or eliminate animal bites scratches needle sticks or other injuries Isolate suspected animals The CDC bans importation of all African rodents into the US Suggested disinfectant for housing facilities Contact state or local health authorities for guidelines when monkeypox virus infection is known or suspected Consult with state or local public health officials for proper waste disposal do not dispose of contaminated waste in a dump landfill or by routine hospital waste disposal methods Conduct environmental cleaning using any EPAregistered hospital disinfectant used for health care facilities or environmental sanitation Laundry can be cleaned using hot water detergent and bleach using a standard washing machine Notification Report suspected or confirmed cases to the appropriate local or regional animal and public health authorities Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal None not recommended Conditions for restoring diseasefree status after an outbreak Euthanasia quarantine andor disinfection and incineration protocols as recommended by local state andor federal health and regulatory agencies Experts who may be consulted Center for Disease Control httpswwwcdcgovpoxvirusmonkeypoxindexhtml State animal health officials httpwwwusahaorgfederalandstateanimalhealth Local public health agencies References 1 Croft DR Sotir MJ Williams CJ Kazmierczak JJ Wegner MV Rausch D Graham MB Foldy SL Wolters M Damon IK Karem KL Davis JP Occupational risks during a monkeypox outbreak Wisconsin 2003 Emerg Infect Dis 20071311501157 2 Doty JB Malekani JM Kalemba LN Stanley WT Monroe BP Nakazawa YU Mauldin MR Bakambana TL Diyandja Dja Liyandia T Braden ZH Wallace RM Malekani DV McCollum AM GallardoRomero N Kondas A Peterson AT Osorio JE Rocke TE Karem KL Emerson GL Carroll DS Assessing monkeypox virus prevalence in small mammals at the humananimal interface in the Democratic Republic of Congo Viruses Internet 2017 cited 2018 February 02 910 283 Available from doi103390v9100283 3 Falendysz EA Lopera JG Doty JB Nakazawa Y Crill C Lorenzsonn F Kalemba Ronderos MD Mejia A Malekani JM Karem K Carroll DS Osorio JE Rocke TE Characterization of monkeypox virus infection in African rope squirrels Funisciurus sp PLoS Negl Trop Dis Internet 2007 cited 2018 February 02118 e0005809 Available from doi101371journalpntd0005809 4 Falendysz EA Lopera JG Lorenzsonn F Salzer JS Hutson CL Doty J GallardoRomero N Carroll DS Osorio JE Rocke TE Further assessment of monkeypox virus infection in Gambian pouched rats Cricetomys gambianus using in vivo bioluminescent imaging PLoS Negl Trop Dis Internet 2015 cited 2018 February 02 910 e0004130 Available from doi 101371journalpntd0004130 5 Guarner J Johnson BJ Paddock CD Shieh W Goldsmith CS Reynolds MG Damon IK Regnery RL Zaki SR and the Veterinary Monkeypox Virus Working Group Monkeypox transmission and pathogenesis in prairie dogs Emerg Infect Dis 200410 426431 6 Hutson CL Nakazawa YJ Self J Olson VA Regnery RL Braden Z Weiss S Malekani J Jackson E Tate M Karem KL Rocke TE Osorio JE Damon IK Carroll DS Laboratory investigations of American Association of Zoo Veterinarians Infectious Disease Manual MONKEYPOX African pouched rats Cricetomys gambianus as a potential reservoir host species for monkeypox virus PLoS Negl Trop Dis Internet 2015 cited 2018 February 02 910e0004013 Available from doi 101371journalpntd0004013 7 Langohr IM Stevenson GW Thacker HL Regnery RL Extensive lesions of monkeypox in a prairie dog Cynomys sp Vet Pathol 200441 702707 8 Monkeypox Internet Centers for Disease Control 2018 cited 2018 February 2 Available from httpswwwcdcgovpoxvirusmonkeypoxindexhtml 9 Mucker EM Chapman J Huzella LM Huggins JW Shamblin J Robinson CG Hensley LE Susceptibility of marmosets Callithrix jacchus to monkeypox virus a low dose prospective model for monkeypox and smallpox disease PLoS One 2015107e0131742 Available from doi 101371journalpone0131742 10 Nagata N Saijo M Kataoka M Ami Y Suzaki Y Sato Y IwataYoshikawa N Ogata M Kurane I Morikawa S Sata T Hasegawa H Pathogenesis of fulminant monkeypox with bacterial sepsis after experimental infection with West African monkeypox virus in a cynomolgus monkey Int J Clin Exp Pathol 20147743594370 11 Radonić A Metzger S Dabrowski PW CouacyHymann E Schuenadel L Kurth A MätzRensing K Boesch C Leendertz FH Nitsche A Fatal monkeypox in wildliving sooty mangabey Côte dIvoire Emerg Infect Dis 2014 20610091011 Available from doi 103201eid2006131329 12 Sergeev AA Kabanov AS Bulychev LE Sergeev AA Pyankov OV Bodnev SA Galahova DO Zamedyanskaya AS Titova KA Glotova TI Taranov OS Omigov VV Shishkina LN Agafonov AP Sergeev AN Using the ground squirrel Marmota bobak as an animal model to assess monkeypox drug efficacy Transbound Emerg Dis 2017641226236 13 Tree JA Hall G Pearson G Rayner E Graham VA Steeds K Bewley KR Hatch GJ Dennis M Taylor I Roberts AD Funnell SG Vipond J Sequence of pathogenic events in cynomolgus macaques infected with aerosolized monkeypox virus J Virol 201589843354344 14 Zaucha GM Jahrling PB Geisbert TW Swearengen JR Hensley L The pathology of experimental aerosolized monkeypox virus infection in cynomolgus monkeys Macaca fascicularis Lab Invest 20018115811600 American Association of Zoo Veterinarians Infectious Disease Manual ATYPICAL MYCOBACTERIOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Fish Amphibians Reptiles Birds Mammals Ingestion inhalation waterborne environmental exposure via defects in respiratory integumentary or urogenital systems direct extension via bite wounds Variable to none Cutaneous lesions ascites pneumonia mastitis lymphadenopathy lameness emaciation lethargy Asympto matic to chronic disease or acute death May not be advised Antibiotics amino glycoside quinolone macrolide Good sanitation good wound care prevent contact with contaminated water soil or feed Yes Fact Sheet compiled by Elizabeth Manning Sheet completed on 15 April 2011 updated 21 July 2013 updated 2018 Fact Sheet Reviewed by Kurt Volle Shannon Cerveny Susceptible animal groups Fish amphibians reptiles birds mammals Causative organisms This group includes all Mycobacteria except M tuberculosis complex and M leprae Nontuberculous mycobacteria Mycobacterium avium M intracellulare M marinum M fortuitum M chelonae M porcinum M farcinogenes M smegmatis M scrofulaceum M xenopi M kansasii M simiae M genavense and others are slender nonmotile acidfast bacilli that are classified as slow growing or rapidly growing Zoonotic potential Yes Many of these bacteria species may infect people who have a genetic predisposition or diminished immune function Typically they are not transmitted between humans or between animals and humans Most infections are acquired from environmental sources but infection may result secondary to abrasions cuts or similar disruption to surfaces Distribution Ubiquitous worldwide Incubation period Typically two weeks to greater than 2 months however the Runyon Group IV M chelonae fortuitum smegmatis are rapid growing and need less than 7 days for incubation Clinical signs Variable clinical signs are observed which depend on species infected and site of infection Asymptomatic to acute death presentations are possible Other signs include lethargy emaciation and other nonspecific signs of illness cutaneous ulcers abscesses and granulomas enlarged abdomen and ascites cough dyspnea pneumonia mastitis lymphadenopathy and lameness due to bone infections Post mortem gross or histologic findings Gross Granulomas in multiple organs cutaneous ulcers andor abscesses ascites pneumonia mastitis lymphadenitis osteomyelitis tenosynovitis arthritis Histologic Granulomatous inflammation Diagnosis From cytology or histopathology samples acidfast bacilli can be demonstrated and tissue culture can be followed by biochemical identification of the bacteria Polymerase chain reaction PCR is available Material required for laboratory analysis For culture fresh tissue samples are required For histopathology formalinfixed tissue samples are submitted which can then can be used for PCR Direct lesion sampling by swabs can also be used with PCR Relevant diagnostic laboratories National Veterinary Services Laboratories 1920 Dayton Avenue Ames Iowa 50010 USA 5153377266 NVSLConcernsaphisusdagov httpwwwaphisusdagovanimalhealthlabinfoservices Treatment Due to possibility for development of antibiotic resistance and safety concerns for personnel in close contact with affected animals treatment may not be recommended Treatment when attempted should be based on antimicrobial susceptibility testing but empirical treatment options include aminoglycosides American Association of Zoo Veterinarians Infectious Disease Manual ATYPICAL MYCOBACTERIOSIS quinolones and macrolides Radical surgical excision of cutaneous lesions in conjunction with longterm antibiotic therapy has been described Prevention and control Once diagnosed excellent sanitation measures and permanent quarantine of known positive animals should be introduced Appropriate wound care and prevention of wound contact with potentially contaminated water soil and feed will minimize these infections Suggested disinfectant for housing facilities Tuberculocidal products as listed by the US EPA httpwwwepagovoppad001listbtuberculocidepdf Notification Not required Measures required under the Animal Disease Surveillance Plan None required Measures required for introducing animals to infected animal None required Conditions for restoring diseasefree status after an outbreak Due to ubiquitous nature of the etiologic agents chronic profile and inability to diagnose carrier state diseasefree status is not possible Experts who may be consulted Nicole M Parrish PhD Associate Director of Mycobacteriology Division of Medical Mycobacteriology The Johns Hopkins Hospital Meyer B1193 600 North Wolfe Street Baltimore Maryland 21287 USA 4105503525 nparrishjhmiedu Nontuberculous Mycobacterial Infections Program National Jewish Health 1400 Jackson Street Denver Colorado 80206 USA 8004238891 x1279 mycoconsultsnjhealthorg References 1 Bercovier H Vincent V Mycobacterial infections in domestic and wild animals due to Mycobacterium marinum M fortuitum M chelonae M porcinum M farcinogenes M smegmatis M scrofulaceum M xenopi M kansasii M simiae and M genavense Rev Sci Tech Off Int Epiz 200120 265290 2 Cook J L Nontuberculous mycobacteria opportunistic environmental pathogens for predisposed hosts Br Med Bull 201096 4559 3 Hoop RK Public health implications of exotic pet mycobacteriosis Semin Avian Exot Pet 199763 8 4 Jernigan JA Farr BM Incubation period and sources of exposure for cutaneous Mycobacterium marinum infection case report and review of the literature Clin Infect Dis 200031439443 5 Kramer MH Granulomatous osteomyelitis associated with atypical mycobacteriosis in a bearded dragon Pogona vitticeps Vet Clin Exot Anim 20069 563568 6 Lee EY Ip JW Fung BKK Ted EU Mycobacterium chelonae hand infection a review Hand Surg 200914 713 7 Markey B Leonard F Archambault M Cullinane A Maguire D Clinical Veterinary Microbiology Mosby 2013 p 163 8 Passantino A Macri D Coluccio P Foti F Marino F Importation of mycobacteriosis with ornamental fish medicolegal implications Travel Med Infect Dis 20086 240244 9 US Environmental Protection Agency Office of Pesticide Programs Internet List B EPAs registered tuberculocide products effective against Mycobacterium tuberculosis 2009 cited 2013 July 23 Available at httpwwwepagovoppad001listbtuberculocidepdf American Association of Zoo Veterinarians Infectious Disease Manual AVIAN MYCOBACTEROSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All birds some mammals Fecaloral environment inhalation Emaciation weakness lethargy hepatosplenomegaly Rarely skin lesions and respiratory disease Variable Severe in the individual with end stage disease Not recommended as this organism is resistant to most if not all human antimycobacterial drugs Euthanasia may need to be considered Cleaning of the environment Decreasing load in the environment Maintaining good immune systems and good husbandry Yes but humans have a high resistance to M avium unless immune compromised Treatment may be difficult Fact Sheet compiled by Nancy Carpenter Sheet completed on 1 February 2011 updated 1 March 2013 Fact Sheet Reviewed by Erika TravisCrook M Scott Echols Susceptible animal groups Birds some mammals such as pigs mink and rabbits Causative organism Mycobacterium avium complex MAC consisting of M avium and M intercellularae M genavense can also cause disease in birds Zoonotic potential There is potential however humans appear to be highly resistant unless immune compromised Distribution Worldwide However in North America the distribution favors the North Temperate Zone Incubation period There is not a definitive incubation period because the resultant disease is dependant upon immune response to exposure Exposure does not guarantee disease Typically an animal suffering from disease caused by Mycobacteria may have had the disease for many years before signs are recognized or more likely it is an incidental finding on necropsy Clinical signs Emaciation weakness lethargy hepatosplenomegaly Post mortem gross or histologic findings Emaciated carcasses hepatosplenomegaly nodular disease in affected organs Nodules are typically white to yellow and solid to soft or crumbly in consistency Liver spleen lung and intestines are most commonly affected but joints skin and respiratory tract may also show lesions Diagnosis Elevated white blood cell counts 60000 can be an indicator of mycobacteriosis Antemortem screening can be performed via coelomoscopic examination focusing on the liver spleen and intestines Biopsy any plaque like lesions or the liver for histopathological screening Diagnosis is attained through the identification or culture of acid fast organisms or histopathology as the most common route However acid fast staining of prepared feces can also be done but is not a definitive test since other organisms can be acid fast positive confounding results Tuberculin testing is not recommended PCR assays detect the actual disease causing organism and are considered to be the fastest most sensitive method for detecting M avium ELISA assays detect specific antibodies for M avium and help determine exposure These assays can be performed on whole blood feces serum vent and throat swabs depending upon the laboratory and the test to be run Feces for Zoologix whole blood serum vent and throat swabs for Avian Biotech International American Association of Zoo Veterinarians Infectious Disease Manual AVIAN MYCOBACTEROSIS Material required for laboratory analysis Acid Fast staining of slides from a suspect nodule feces or touch prep of affected tissues formalinized tissue for histopath examination culture swab for acid fast testing and culture Lowenstein Jensen media required for culture Feces for PCR by Zoologix or whole blood serum vent and oral swabs for Avian Biotech International for PCR or ELISA Post mortem sampling includes liver spleen and lungs andor suspect areas Relevant diagnostic laboratories Avian Biotech International wwwavianbiotechcom Zoologix wwwzoologixcom See the Avian and Livestock Assay Data Sheet Treatment Typically control is more desired as treatment can be unrewarding and possibly cause further spread of the disease Some antibiotic resistance can be expected The ethics of treatment must be considered as treatment may be life long and may not prevent shedding Prevention and control Try to maintain a clean environment and be diligent in screening via necropsy and testing for acid fast bacteria Maintain a thorough quarantine protocol Suggested disinfectant for housing facilities Cidex appears to be the product that is the standard efficacy comparison in most studies Equivalent disinfectants include Sactimed sinald a quaternary ammonium compound Steris 20 a peracetic acid compound and Pentapon DC1 a betaene compound are equally effective Persafe a tertiary amine that is classified as an HLD High Level Disinfectant is also reported to be as effective as Cidex Virkon was NOT effective Roccal D does not list M avium as being susceptible to that product Some of these may not be applicable for premise application Sukusept Plus Ecolab is a glucoprtoamin based disinfectant and has effectiveness against all mycobacteria at 2500 ppm for 15 minutes It is also effective against a glutaraldehyde resistant M chelonae but at a concentration of 5000 ppm for 15 minutes or at 2500 ppm for 60 minutes Note that this product may not be available in the US 1 Stroke Environ B Vestal Labs Virostat TBQ Steris TBQ Husky QT 814 are other premise disinfectants with efficacy against mycobacteria During premise disinfection it is recommended that a protective face covering ie respirator is worn due to the route of infection for these organisms is through aerosolization Notification Check your individual state for reporting requirements Measures required under the Animal Disease Surveillance Plan This is not one of the listed diseases as of 2013 Measures required for introducing animals to infected animal If an animal is known to be infected euthanasia may need to be considered It is not recommended to mix a known infected animal with a healthy animal unless the risk for infection is considered acceptable Studies show that there is an increased incidence of disease when an animal is housed with a known positive Conditions for restoring diseasefree status after an outbreak As this bacterium is ubiquitous this condition is unachievable Efforts should be concentrated on decreasing the environmental load of this bacterium and enhancing the immune response for those living in the contaminated environment through good nutrition and proper husbandry Screening of all deaths for mycobacteria having sentinel animals in the enclosureand periodic liver biopsies have all been done American Association of Zoo Veterinarians Infectious Disease Manual AVIAN MYCOBACTEROSIS Experts who may be consulted Scott Larsen DVM MS Dipl ACZM Denver Zoo 2300 Steele St Denver Colorado 80205 Phone 303 3764996 Fax 303 3764991 slarsendenverzooorg Jim Wellahan DVM MS PhD DACZM DACVM Zoological Medicine Service College of Veterinary Medicine Gainesville Florida 32610 Phone 3523922226 wellahanjufledu Shannon Ferrell DVM Dept of Companion Animals Atlantic Veterinary College UPEI 550 University Avenue Charlottetown PE C1A 4P3 Canada Email sferrellupeica Bruce Rideout DVM PhD San Diego Zoo Global Institute for Conservation Research Director Wildlife Disease Laboratories PO Box 120551 San Diego California 92112 619 2311515 brideoutsandiegozooorg American Association of Zoo Veterinarians Infectious Disease Manual AVIAN MYCOBACTEROSIS References 1 Avian Services Center Avian Tuberculosis Mycobacterium avium httpwwwavianbiotechcomdiseasesAvianTuberculosishtm Accessed 3 July 2013 2 Gerlach H 1994 Mycobacterium In Ritchie BW GJ Harrison and LR Harrison eds Avian Medicine Wingers Publishing Lake Worth FL Pp 971975 3 Beehler BA 1990 Management of Mycobacterium Avium in a Mixed Species Aviary In Proceedings of the AAZV Pp 138142 4 Friend M 1999 Tuberculosis In Friend M and JC Franson eds Field Manual of Wildlife Diseases US Dept of the Interior US Geological Survey Washington DC Pp 9398 5 Hernandez A E Martro L Matas L and V Ausina 2003 Invitro evaluation of Perasafe compared with 2 alkaline glutaraldehyde against Mycobacterium spp J of Hosp Inf 541 5256 6 Kearns K 2003 Avian Mycobacteriosis In Kearns KS and B Loudis eds Recent Advances in Avian Infectious Diseases International Veterinary Information Service Ithaca New York Pp XXX 7 Meyer B and C Kluin 1999 Efficacy of glucoprotamin containing disinfectants against different species of mycobacteria J of Hosp Inf 422151154 8 Napier JE SH Hinrich F Lampen PC Iwen RS Wickert JL Garrett TA Aden E Restis TG Curro LG Simmons and DL Armstrong 2009 An outbreak of avian mycobacterosis caused by Mycobacterium intracellulare in little blue penguins Eudyptula minor J Zoo Wildl Med 4046806 9 Pollock CJ W Carpenter and N Antinoff 2004 Protocols used in treating mycobacteriosis in birds In Carpenter JW ed Exotic Animal Formulary 3rd ed Saunders Elsevier St Louis Missouri Pp 303304 10 Tell LA STF Ferrell and PMGibbons 2004 Avian mycobacteriosis in freeliving raptors in California 6 cases 19972001 J of Avian Med and Surg 1813040 11 Zoologix Mycobacterium avium and other Mycobacteria species httpzoologixcomavianDatasheetsMycobacteriahtm Accessed 3 July 2013 American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN ELEPHANTS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals including elephants Aerosol of infectious droplets Chronic weight loss excessive mucus discharge from the trunk and respiratory system Variable Most infected elephants have no clinical signs after many years of chronic infection At least three drugs should be used when initiating treatment Toxicity related to drug treatment has been reported including hepatopathy icterus bone marrow suppression and anorexia Quarantine testing while culture is the only definitive test ancillary tests include elephant STAT Pak and other in vitro assays Yes Fact Sheet compiled by Gary West and Charles O Thoen Sheet completed on 31 January 2011 updated 31 January 2013 Fact Sheet Reviewed by Linda Peddie Dennis Schmitt Paul P Calle Michele Miller Susceptible animal groups Mammals including elephants Causative organism Predominantly Mycobacterium tuberculosis and rarely M bovis have been associated with these infections M avium complex and certain other mycobacteria M szulgai and M elephantishave been isolated from elephants Zoonotic potential Yes Distribution Worldwide distribution in captive animals and in freeranging animals in close contact with humans ie working elephants in Asia Chronically infected and shedding elephants and their caretakers have been noted Animals traditionally have been relocated without rigorous quarantine Trunk washes should be collected from animals for mycobacteriologic examinations ie PCR and culture before integration into new herds Incubation period Weeks to years Clinical signs The most commonly observed sign is chronic weight loss Elephants may also have mucoid sputum discharge from trunk and partial anorexia However often no premonitory signs of illness are present until the disease is in the very advanced stages Post mortem gross or histologic findings Primarily lung and associated thoracic lymph nodes are observed with chronic granulomas with caseocalcaerous and cavitated lesions Lesions often are paucibacillary on acid fast staining Diagnosis Laboratory examinations on trunk wash by acid fast staining and culture of the fluid Ancillary tests include Elephant TBstatPAK and MAPIA for serology In the US elephant TBstatPAK testing should coincide with the trunk wash collection per current USDA guidelines Although not permitted for the official USDA testing sputum samples or mucus from the trunk can also be cultured and may be useful Additionally mycobacterial organisms rarely have been isolated from other body fluids such as vaginal secretions Postmortem cultures should be performed NOTE Some elephants with chronic inflammatory conditions have tested positive on the Elephant American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN ELEPHANTS TBstatPAK and have not been positive on culture for Mycobacteria species Trunk wash should be collected from these animals if they originate in a herd with a history of tuberculosis or of unknown source as the animals could be infected and not shedding the tubercle bacillus Intradermal tuberculin testing is not recommended for elephants due to the nonspecific reactions observed in this species Material required for laboratory analysis Saline wash of the trunk for mycobacteriologic examination Culture PCR on lesions collected at necropsy or on biopsy Blood may be collected for Elephant TBstatPAK and MAPIA and other in vitro supplemental tests Consult the current Guidelines to Control Tuberculosis in Elephants for additional information httpwwwaphisusdagovanimalwelfaredownloadselephantelephanttbpdf Relevant diagnostic laboratories NVSL National Veterinary Services Laboratory Ames IA in the US or similar reference laboratories in other countries Treatment Empirical treatment with at least three drugs isoniazied rifampin ethambutol and pyrazinamide while susceptibility tests are pending Drug resistance has been a concern in a few cases therefore fluoroquinolones can also be used in combination with other medications Pyrazinamide is ineffective against M bovis Toxicity related to drug treatment has been observed and may include signs of gastrointestinal discomfort hepatopathy bone marrow suppression malaise and joint stiffness Prior to beginning treatment it is recommended that clinicians consult with others with experience in elephant mycobacterial treatment to ensure that the latest information is incorporated into the treatment plan Prevention and control Elephants with chronic unexplained weight loss and identified shedders should be isolated from other animals Quarantine and test new arrivals to the institution Antituberculocidal disinfectants should be used for cleaning Consideration for staff should be given to wearing HEPAfilter masks that are certified to protect against tuberculosis when collecting trunk wash samples or when in close contact with infected elephants Suggested disinfectant for housing facilities EPA approved tuberculocidal agent Notification USDA in the US appropriate regulatory officials in other countries Measures required under the Animal Disease Surveillance Plan Specific guidelines are in place in the US httpwwwaphisusdagovanimalwelfaredownloadselephantelephanttbpdf Measures required for introducing animals to infected animal Follow USDAAPHIS or similar guidelines as above under surveillance Animals that are not actively shedding Mycobacteria and are undergoing treatment may be considered for reintroduction to the herd which may decrease the stress of the animal Conditions for restoring diseasefree status after an outbreak see USDAAPHIS Guidelines to Control Tuberculosis in Elephants httpwwwaphisusdagovanimalwelfaredownloadselephantelephanttbpdf Experts who may be consulted James Peddie DVM 4201 Faria Road Ventura California 93001 805 6521429 Dennis Schmitt DVM PhD Karis Hall 20 Missouri State University Springfield Missouri USA 417 8365091 American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN ELEPHANTS dennisschmittmissouristateedu Charles O Thoen DVM PhD 2152 Vet Med Veterinary Microbiology and Preventive Medicine Iowa State University Ames Iowa USA 515 2947608 cthoeniastateedu Gary West DVM Phoenix Zoo 455 N Galvin Parkway Phoenix Arizona 85008 6022731341 gwestthephxzoocom References 1 httpwwwaphisusdagovanimalwelfaredownloadselephantelephanttbpdf 2010 Guidelines to Control Tuberculosis in Elephants Accessed 23 July 2013 2 Ball RL G Dumonceaux JH Olsen MS Burton and K Lyashchenko 2006 Comparison of trunk wash results matched to multiantigen print immunoassay MAPIA in a group of captive Asian elephants Elephas maximus 2006 Proceedings of the American Association of Zoo Veterinarians Tampa FL Pp 303304 3 Bhandara M and CO Thoen 2014 Zoonotic tuberculosis in humans elephants and other animals in Nepal In Thoen CO J H Steele and J B Kaneene eds Zoonotic Tuberculosis Mycobacterium bovis and other pathogenic mycobacteria WileyBlackwell Publishing In press 4 Fowler ME 2006 Infectious diseases In Fowler ME and SK Mikota eds Biology Medicine and Surgery of Elephants Blackwell Publishing Ames IA Pp 131158 5 Greenwald R O Lyashchenko J Esfandiari M Miller S Mikota JH Olsen R Ball G Dumonceaux D Schmitt T Moller JB Payeur B Harris D Sofranko WR Waters and KP Lyashchenko 2009 Highly accurate antibody assays for early and rapid detection of tuberculosis in African and Asian elephants Clin Vaccine Immunol 16 605612 6 Lyashchenko K R Greenwald J Esfandiari J Olsen R Ball G Dumonceaux F Dunker C Buckley M Richard S Murray JB Payeur P Anderson JM Pollock SK Mikota M Miller D Sofranko and WR Waters 2006 Tuberculosis in elephants antibody responses to defined antigens of Mycobacterium tuberculosis potential for early diagnosis and monitoring of treatment Clin Vacc Immunol 13722732 7 Michalak K C Austin S Diesel MJ Bacon P Zimmerman and JN Maslow 1998 Mycobacterium tuberculosis infection as a zoonotic disease transmission between humans and elephants Emerg Infect Dis 4 283287 8 Mikota SK L Peddie J Peddie R Isaza F Dunker G West W Lindsay RS Larsen MD Salman D Chatterjee J Payeur D Whipple C Thoen S Davis C Sedgwick RJ Montali M Ziccardi and J Maslow J 2001 Epidemiology and diagnosis of Mycobacterium tuberculosis in captive Asian elephants Elephas maximus J Zoo Wildl Med 32 116 9 Murphree R J Warkentin JR Dunn W Schaffner and TF Jones 2010 Outbreak of Mycobacterium tuberculosis infection among employees of an elephant refuge Presentation at the American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN ELEPHANTS National Tuberculosis Conference 2224 June 2010 10 Murphree R JV Warkentin JR Dunn W Schaffner and TF Jones 2011 Elephanttohuman transmission of tuberculosis Emerg Infect Dis 173 366371 11 West G 2006 Tuberculosis in captive exotic animals In Thoen CO JH Steele and MJ Gilsdorf eds Mycobacterium bovis infection in Animals and Humans Blackwell Publishing LTD Oxford UK Pp 248257 12 American Association of Zoo Veterinarians Infectious Disease Manual MYCOBACTERIUM AVIUM SUBSP PARATUBERCULOSIS JOHNES DISEASE Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Ruminants Fecaloral Raw colostrum In utero Weakness Weight loss Diarrhea in some species Eventually fatal None Quarantine or cull infected animals Regular herd testing Good sanitation Incon clusive Fact Sheet compiled by Elizabeth Manning Sheet completed on 19 April 2011 updated 21 July 2013 Fact Sheet Reviewed by Genevieve Dumonceaux Patrick Pithua Susceptible animal groups Ruminants are affected and though other mammals and birds may become infected they rarely develop clinical disease Causative organism Mycobacterium avium subspecies paratuberculosis MAP which is a Grampositive acidfast positive small rodshaped bacterium that grows in clumps of 10100 cells and a member of the Mycobacterium avium complex MAC Zoonotic potential As an opportunistic pathogen in immunocompromised individuals zoonotic status is possible but it is very unlikely in the zoo setting as organism must be swallowed by immunosusceptible human Much controversy exists regarding the relationship between MAP and Crohns disease in humans Distribution Global Incubation period Months to years Clinical signs These signs are observed primarily in adults although animals are usually infected in the first months of life or in utero if dam is infected Early course of infection is asymptomatic Severe and abrupt weight loss occurs as disease progresses with weakness secondary to emaciation Some species present with chronic diarrhea Post mortem gross or histologic findings Gross These findings range from none to many including corrugated reddened thickened gastrointestinal tract enlarged mesenteric lymph nodes and enlarged lymphatic vessels and emaciation with lack of fat stores Histologic These findings range from minimal to extensive granulomatous inflammation Variable numbers of acidfast positive rods in giant cells of the ileum and mesenteric lymph nodes can be found and in some species aortic mineralization is noted Diagnosis Organismbased culture feces tissue samples environmental samples PCR feces paraffin blocks of tissue samples culture isolate identification histopathology acidfast positive rods within macrophages infiltrating the caudal gastrointestinal tract and mesenteric lymph nodes Serology ELISA for cattle sheep goats bison deer Material required for laboratory analysis Antemortem Feces serum milk colostrum and environmental samples soil water grass Postmortem Fresh mesenteric lymph node ileum samples for culture in formalin for histopathology Relevant diagnostic laboratories Animal and Plant Health Inspection Service APHISApproved Laboratories are listed at httpwwwaphisusdagovanimalhealthlabinfoservicesapprovedlabsshtml Lab familiarity with zoo collection diagnostics and husbandry is helpful American Association of Zoo Veterinarians Infectious Disease Manual MYCOBACTERIUM AVIUM SUBSP PARATUBERCULOSIS JOHNES DISEASE Treatment None Prevention and control Adherence to principles driving guidelines in the Voluntary Johnes Disease Herd Status Program httpwwwaphisusdagovanimalhealthanimaldiseasesjohnesdownloads johnes umrpdf and including Screening incoming adult ruminants during quarantine period if 1yr old test dam Feed only pasteurized colostrum or approved commercial colostrum replacers to neonatal ruminants Bottle feed neonatal ruminants with pasteurized milk or commercial milk replacer Prevent exposure of ruminants less than 6 months of age to adult manure including through water drainage or feed contamination Use sod from pastures grazed by Johnes diseasefree ruminants Establish ruminant enclosure status all adults in enclosurebarn Establish and use a dedicated maternity area separate from lactating cows to reduce the risk of transmission Examine all adult ruminants dying on site for Johnes disease even if other cause of death known including culture of mesenteric lymph node Learn MAP status of source herds for petting zoofarm animals as high prevalence in domestic ruminants Institute excellent sanitation measures Suggested disinfectant for housing facilities Tuberculocidal products as listed by the US EPA httpwwwepagovoppad001listbtuberculocidepdf Notification Reportable to the World Organisation for Animal Health OIE USDA APHIS and many state veterinarians Measures required under the Animal Disease Surveillance Plan None required although voluntary program participation exists Measures required for introducing animals to infected animal It is not recommended Conditions for restoring infectionfree status after an outbreak Following quarantine or cull infected animals and environmental decontamination it would be useful to demonstrate negative test results in adult ruminants over multiple years Experts who may be consulted Michael T Collins DVM PhD University of Wisconsin School of Veterinary Medicine 2015 Linden Drive Madison Wisconsin 53706 USA 6082628457 mcollin5wiscedu Pam Dennis MSL DVM PhD DACZM Cleveland Metroparks Zoo 3900 Wildlife Way Cleveland Ohio 44109 USA 2166352520 pmdclevelandmetroparkscom References 1 Behr M A and D M Collins eds 2010 Paratuberculosis Organism Disease Control 1st ed CABI Cambridge Massachusetts Pp 1375 2 Burgess T C Witte and B Rideout 2012 Understanding the spread of Johnes disease in zoo animals who should we worry about Proceedings of the AAZV Oakland CA P 53 3 Collins M and E Manning 2001 Johnes Information Center httpjohnesorg Accessed 23 July American Association of Zoo Veterinarians Infectious Disease Manual MYCOBACTERIUM AVIUM SUBSP PARATUBERCULOSIS JOHNES DISEASE 2013 4 Manning EJB and JM Sleeman 2012 In Fowler E and R E Miller eds Fowlers Zoo and Wild Animal Medicine Current Therapy 7th ed Elsevier Saunders St Louis Missouri Pp 628635 5 National Advisory Committee on Microbiological Criteria for Foods 2010 Assessment of food as a source of exposure to Mycobacterium avium subspecies paratuberculosis MAP J Food Prot 73 13571397 6 Pithua P LA Espejo SM Godden and SJ Wells 2013 Is an individual calving pen better than a group calving pen for preventing transmission of Mycobacterium avium subsp paratuberculosis in calves results from a field trial Res Vet Sci 95 2 398404 7 Pithua P SM Godden SJ Wells and MJ Oakes 2009 Efficacy of feeding plasmaderived commercial colostrum replacer for the prevention of transmission of Mycobacterium avium subsp paratuberculosis in Holstein calves J Am Vet Med Assoc 234 9 11671176 8 Proceedings of the Workshop on Diagnosis Prevention and Control of Johnes Disease in Non Domestic Hoofstock Yulee FL 2628 June 1998 9 Singh S V A V Singh P K Singh A Kumar and B Singh 2011 Molecular identification and characterization of Mycobacterium avium subspecies paratuberculosis in free living nonhuman primate Rhesus macaques from North India Comp Immunol Microbiol Infect Dis 34326771 10 US Environmental Protection Agency Office of Pesticide Programs 2009 List B EPAs registered tuberculocide products effective against Mycobacterium tuberculosis httpwwwepagovoppad001listbtuberculocidepdf Accessed 23 July 2013 11 USDA APHIS 2010 Uniform program standards for the voluntary bovine Johnes disease control program httpwwwaphisusdagovanimalhealthanimaldiseasesjohnesdownloadsjohnesupspdf Accessed 19 September 2013 American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN NONHUMAN PRIMATES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Non human primates Inhalation and ingestion predominates fomite potential documented Varies rough hair coat weight loss cough lymph adenopathy Highly variable asymptomatic to severely debilitating disease Limited efficacy even with multi modal treatment but may be considered for extremely valuable animals However culling of positive animals highly recommended Skin test is routine and gold standard but nonspecific responses occur Yes and anthroponotic Fact Sheet compiled by Patrice Frost Heather Cole Charles O Thoen Sheet completed on 3 August 2011 updated 31 January 2013 Fact Sheet Reviewed by Paul P Calle Hilton Klein Ana Cristina Leandro Susceptible animal groups All primates including humans Causative organisms Mycobacterium tuberculosis M bovis M avium ss avium Zoonotic potential Yes Distribution Old World nonhuman primates and great apes usually with typical mycobacterial infection New World nonhuman primates usually with other mycobacterial infections Incubation period Variable from weeks to months animals can develop latent infections with reactivation in weeks months or even years later Development of disease is dependent on organism route of infection dose and immunologic status of animal Susceptibility morbidity and mortality are variable for different species Clinical signs The clinical signs are often nondescript and illdefined Tuberculosis can imitate a multitude of diseases such as pneumonia neoplasia or fungal infections The clinical spectrum of signs range from asymptomatic to multisymptomatic the profile is highly dependent on the route of exposure the system involved and the infecting agent General signs can include a roughened hair coat anorexia depression lethargy fever low grade intermittent or persistent weight loss hepatomegaly splenomegaly and local or general lymphadenopathy which may or may not have draining tracts A chronic or paroxysmal cough and dyspnea indicate pulmonary involvement which mirrors acute bronchitis or pneumonia Neurological presentation with signs including anisocoria or ataxia may implicate meningitis or central nervous system involvement and paresis to paralysis can indicate a peripheral neurological component that may be a result of spondylitis Post mortem gross or histologic findings At necropsy tuberculosis indications vary with the duration and degree of disease Organs of predilection are the lung and adjacent hilar lymph nodes Dissemination occurs to the spleen kidney liver and associated lymph nodes Additional sites less frequently seen include omentum ovary cerebrum spinal column peripheral lymph nodes skin and mammary gland The extent of the lesions can range from no detectable lesions to wide dissemination of caseous granulomas varying in size from pinpoint to large coalescing lesions Appearance of lesions within the lung can be focal coalescing or cavitary American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN NONHUMAN PRIMATES Lesions in parietal pleural with adjacent adhesion maybe caused by collapse of large granulomas expelling contents into the adjacent airway in this process referred to as cavitation Diagnosis Intradermal tuberculin skin test TST Using Mammalian Old Tuberculin mOT produced by Symbiotics Inc is currently the only USDA approved tuberculin for nonhuman primates Intradermal injection of 01 ml of MOT using a 26 gauge needle in the palpebrae In small primates reduced dose 005ml can be used Injection sites are observed at 24 48 and 72 hours post injection for hyperemia edema and induration Grading systems can be found in the Guidelines for the Prevention and Control of Tuberculosis in Nonhuman Primates The test is interpreted as positive when palpebral swelling is present in conjunction with droop A minimum of two weeks should occur between skin tests Detection of positive animals is difficult in early infections and in advanced stages of disease animals may be nonresponsive An immunologically competent animal is required for the test to be effective False positives may occur due to trauma during administration of antigen or nonspecific response caused by cross reactivity with nonpathogenic Mycobacteria or previous exposure to Freunds Complete adjuvant A comparative TST using biologically balanced purified protein derivatives PPD of M bovis and of M avium placed into separate palpebrae or at separate sites on the abdomen is useful in differentiating nonspecific sensitization Limitations to testing can be challenged by the quality and purity and volume of the tuberculin injected skill in administration thorough recording of bruise or palpebral trauma visual access in group settings accurate interpretation at all time periods inadequate interval between tests or lack of documentation All of these can jeopardize a surveillance program Thoracic radiographs facilitate diagnosis in conjunction with additional diagnostics Laboratory testing This methodology can augment TST PRIMAGAM Prionics USA Inc Cell mediated Immunity IFNγ assayfully licensed by USDA in 2007 for in vitro testing of cynomologus and Rhesus macaques and tests for M tuberculosis M bovis and M avium No antigen is administered to the animals so retesting can be conducted immediately Questionable ability to detect latenc TSPOTTB Oxford Immunotec Oxford UK Cell Mediated Immunity IFNγ assay for use in macaques Response is to M tuberculosisspecific antigens and shows some promise for the diagnosis of latent and active infections PrimaTB STATPAK Assay Chembio Diagnostic Systems Inc Medford NY which detects IgM and IgG antibodies rapid 20 minute lateral flow immunoassay Licensed by USDA in 2007 for use in nonhuman primates Advantage test uses serum plasma or whole blood and requires small quantity 30µl although interpretation is difficult due color of blood Test is used to detect M tuberculosis and M bovis A combination of diagnostic techniques may provide for an improved diagnosis Material required for laboratory analysis Antemortem Polymerase chain reaction PCR may be conducted on lesion or granuloma feces bronchoalveolar and gastric lavage Culture and speciation To optimize isolation of organisms from specimens it is recommended that the samples be centrifuged at 3500 rpm for 30 minutes in sterile polypropylene conical tubes Success of isolation is dependent on quality of specimen appropriate processing and culture techniques in the laboratory The process requires 4 8 weeks for isolation and longer to speciate Microbiological staining Specimens include lesions or granulomas in lymph nodes ie bronchoalveolar and gastric lavage Fine needle aspirates impression smears or tissue suspensions that are air dried in a thin layer on slides that is heat fixed and stained for the appearance of acid fast bacilli Postmortem All primates euthanized or found dead should receive complete necropsies to include gross examination and histological examination of lesions including acid fast stains PCR culture and staining for organism blood lesion or granuloma feces lymph nodes and bronchial or American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN NONHUMAN PRIMATES gastric lavage Products Available AFB Kinyoun Kit Polysciences Inc stain of slides for acidfast bacilli PRIMAGAM Prionics USA Inc heparinized whole blood TSPOTTB Oxford Immunotec Oxford UK heparin PBMCs Relevant diagnostic laboratories National Veterinary Services Laboratories NVSL 1920 Dayton Ave Ames Iowa 50010 Provides IFNγ Histopathology Isolation and PCR NVSL is the reference center for US animal health and contribute to public health by ensuring that timely and accurate laboratory support is provided by their nationwide animalhealth diagnostic system PCRZoologix Primate Diagnostics Zoologix Inc 9811 Owensmouth Ave Suite 4 Chatsworth CA 913113800 infozoologixcom Treatment Isoniazid ethambutol and rifampin is usual starting point However even this combination has limited efficacy and is not recommended for tuberculous animals Prevention and control Nonhuman primate colonies should be maintained closed and have minimal direct contact with public Establish a routine surveillance program using the skin testing to identify infected animals additional diagnostics may augment TST Segregate or cull positive animals during confirmation Identify designated quarantine area for all new nonhuman primates hold animals for a minimum of 30 days and retest using TST Animals of unknown source or high risk animals should be quarantined for longer duration for retest Suggested disinfectant for housing facilities All primate primary housing clinics and caging should incorporate tuberculocidal products The Environment Protection Agency Antimicrobials Division Test oversees the testing of these products for efficacy Consideration for product selection will depend on surfaces caging and equipment needing tuberculocidal products Notification USDA Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal It is not recommended to introduce new animals to collections holding tuberculous animals Conditions for restoring diseasefree status after an outbreak Cull all positive animals or treat all extremely valuable animals in isolation Continue to conduct routine surveillance testing to include TST and other diagnostic testing Maintain proper PPE and Occupational Health Program for all people in contact with nonhuman primates Experts who may be consulted Charles O Thoen DVM PhD Diplomate AVES 2152 Vet Med Veterinary Microbiology and Preventive Medicine Iowa State University Ames Iowa USA 515 2947608 cthoeniastateedu Hilton J KleinVMD MS Dipl ACLAM Dipl ECLAM American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN NONHUMAN PRIMATES Global VP Science and NPI Harlan Laboratories Retired Indianapolis Indiana USA Hkleinvmdaolcom Southwest National Primate Research CenterSouthwest Foundation for Biomedical Research Tuberculosis Laboratory cleandrosfbrgeneticsorg References 1 NIH Guidelines for the Prevention and Control of Tuberculosis in Nonhuman primates httpoacuodnihgovARACdocumentsNHPTBPreventionpdf Accessed 23 July 2013 2 PRIMAGAM Prionics USA Inc httpwwwprionicscomdiseasessolutionstuberculosisPRIMAGAM Accessed 23 July 2013 3 Zoologix httpzoologixcomprimateDatasheetsMycobacteriahtm Accessed 23 July 2013 4 Frost PA P Calle H Klein and CO Thoen 2014 Zoonotic tuberculosis in nonhuman primates In Thoen CO J H Steele and J B Kaneene eds Zoonotic Tuberculosis Mycobacterium bovis and other pathogenic mycobacteria WileyBlackwell Publishing In press 5 Lerche NW JL Yee SV Capuano and JL Flynn 2008 New approaches to tuberculosis surveillance in nonhuman primates ILAR 49 2 170178 6 Simsek H S Alpar N Ucar F Aksu I Ceyhan A Gozalan S Cesur and M Ertek 2010 Comparison of tuberculin skin testing and TSpottb for diagnosis of latent and active tuberculosis Japan J Infect Dis 632 99102 7 Thoen C O 2010 Tuberculosis and other mycobacterial infections In Kahn CM and S Line eds The Merck Veterinary Manual 10th ed Merck and Co Inc Whitehouse Station NJ httpwwwmerckmanualscomvetgeneralizedconditionstuberculosisandothermycobacterialinfe ctionsoverviewoftuberculosisandothermycobacterialinfectionshtml Accessed 23 July 2013 American Association of Zoo Veterinarians Infectious Disease Manual MYCOBACTERIOSIS piscine Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Fish Mammal includes humans Reptile Amphibian Ingestion is probably the major route of infection in fishes other species direct contact with infected individuals or contaminated objects Bacteria may be found in aquatic biofilm Fishes hyperemia pale to dark coloration morbidity mortality granuloma or ulcers of the skin and subcutaneous tissues Mild to severe in fishes causing a wide range of gross and microscopic lesions Mild to moderate in humans usually restricted to extremities Fishes generally not attempted due to systemic nature of disease at diagnosis poor response to treatment and zoonotic potential longterm antimicrobial therapy with appropriate compounds can be tried Humans appropriate antimicrobial therapy accompanied by surgical debridement in some cases Proper hygiene disinfection biosecurity quarantine protective apparel Manage environment to reduce stressors on fish Yes Fact Sheet compiled by Gregory A Lewbart and Melanie L Church Sheet completed on 16 March 2011 updated 20 August 2012 Fact Sheet Reviewed by Stephen A Smith Leigh A Clayton Susceptible animal groups Fishes mammals including humans reptiles amphibians Causative organism Mycobacterium spp with approximately more than 120 species recognized in the genus Mycobacterium Common isolates include M marinum M chelonae M neoaurum M fortuitum and M haemophilum The organisms are Grampositive and acidfast staining Zoonotic potential Yes moderate Distribution Global and most commonly associated with aquatic environments The optimal temperature range is 2428º C 7682º F The bacteria can survive for up to 2 years in the environment Incubation period Varied weeks to months in fishes 2 days to 6 weeks in humans Clinical signs Fishes Chronic progressive infection is most typically reported and may include skin hemorrhage ulcerations and granulomas andor white nodules on viscera hyperemia of fins exophthalmos corneal ulcer granulomatous endophthalmitis lethargy anorexia weight loss abdominal edema cutaneous edema reduced pigmentation loss of scales Acute mortalities may occur with more virulent strains and animals American Association of Zoo Veterinarians Infectious Disease Manual MYCOBACTERIOSIS piscine may lack substantial gross changes such as granulomas Animals may be infected without evidence of disease Humans Usually causes a chronic infection that is limited to the extremities such as fingers and hands A localized skin nodule or granuloma may ulcerate and start to exude a serosanguinous or purulent discharge Depending on immunological status of infected individual nodular cutaneous lesions can progress to tenosynovitis arthritis and osteomyelitis Post mortem gross or histologic findings Gross changes presented in clinical signs Microscopically acidfast organisms are frequently detected in tissues and within granulomas but not all acidfast organisms are Mycobacteria species Acidfast bacilli may be detected in both granulomatous and nongranulomatous tissues Staining intensity can vary Diagnosis History signalment clinical signs gross lesions acidfast staining of tissue touch impressions histopathology with granulomatous inflammation and acidfast staining microbial culture PCR and DNA sequencing Material required for laboratory analysis Tissue samples for touch impressions culture histopathology and in some cases PCR Relevant diagnostic laboratories Many National Veterinary Services Diagnostic Laboratory Ames Iowa for culture and sensitivity Treatment Treatment often considered unrewarding for eliminating infection in individual fish or fish populations Longterm antibiotic including rifampin erythromycin streptomycin as examples may be considered Surgical excision and long term antibiotics are usually recommended in humans Prevention and control The disease can be difficult to eradicate Wear gloves when cleaning aquariums or handling fish Hands should be washed thoroughly afterwards with 70 isopropyl alcohol and a bactericidal soap In exhibit settings may manage certain populations as positive particularly if animals presenting infrequently with chronic disease in older individuals consistent with opportunistic infection Reducing environmental stressors may help reduce clinical disease Suggested disinfectant for housing facilities Ethanol or methanol 70 Notification None required by law Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Introductions to infected animals should be avoided Conditions for restoring diseasefree status after an outbreak Depopulate disinfect the environment and then monitor and test sentinel animals Experts who may be consulted Andrew Kane PhD Emerging Pathogens Institute Aquatic Pathobiology Laboratory University of Florida PO Box 100188 Gainesville Florida 326100188 Phone 352 2739090 Email Kaneufledu Stephen A Smith MS DVM PhD Aquatic MedicineFish Health Department of Biomedical Sciences Pathobiology American Association of Zoo Veterinarians Infectious Disease Manual MYCOBACTERIOSIS piscine VirginiaMaryland College of Veterinary Medicine VMRCVM Duck Pond Drive Virginia Tech 0442 Blacksburg Virginia 24061 540 2317666 Email stsmith7vtedu Dr Roy Yanong University of FloridaIFAS Tropical Aquaculture Laboratory 1408 24th Street SE Ruskin FL 33570 Phone 813 6715230 x104 Email rpyifasufledu References 1 Anonymous 2006 Mycobacteriosis Institute for International Cooperation in Animal Biologics and the Center for Food Security Public Health Iowa State University and the OIE wwwcfsphiastateeduFactsheetspdfsmycobacteriummarinumpdf 4 pp 2 FrancisFloyd R and R Yanong Mycobacteriosis in fish 2002 University of Florida Extension Fact Sheet VM96 httpedisufledu 3 Gauthier DT and MW Rhodes 2009 Mycobacteriosis in fishes a review Vet J 1803347 4 Mainous ME and SA Smith 2005 Efficacy of common disinfectants against Mycobacterium marinum J Aquatic Anim Health 17284288 5 Passantino A D Macri P Coluccio F Foti and F Morino 2008 Importation of mycobacteriosis with ornamental fish medicolegal implications Travel Med Infect Dis 64240244 6 Ramsay JM V Watral CB Schreck and ML Kent 2009 Husbandry stress exacerbates mycobacterial infections in adult zebrafish Danio rerio Hamilton J Fish Dis 3211 931941 7 Reavill D and R Schmidt R 2012 Mycobacterial lesions in fish amphibians reptiles rodents lagomorphs and ferrets with reference to animal models Vet Clin N Amer Exot Anim Pract 1512540 8 Shivaprasad H and C Palmieri 2012 Pathology of mycobacteriosis in birds Vet Clin N Amer Exot Anim Pract 15 1 4155 9 Slany M P Jezek V Fiserova M Bodnarova J Stork M Havelkova F Kalat and I Pavlik 2012 Mycobacterium marinum infections in humans and tracing of its possible environmental sources Can J Microbiol 5813944 10 Whipps CM C Lieggi and R Wagner 2012 Mycobacteriosis in zebrafish colonies ILAR J 532 95102 11 Yanong RP DB Pouder and JO Falkinham III 2012 Association of Mycobacteria in recirculating aquaculture systems and mycobacterial disease in fish J Aquatic Anim Health 224219223 12 Zanoni RG D Florio ML Fioravanti M Rossi and M Prearo 2008 Occurrence of Mycobacterium spp in ornamental fish in Italy J Fish Dis 31433441 13 Zerihun M D Cloquhoun and T Poppe 2012 Experimental mycobacteriosis in Atlantic cod Gadus morhua L J Fish Dis 355365377 American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN UNGULATES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Ungulates Primarily aerosol and ingestion fomites are a potential Labored breathing coughing lymph adenopathy wasting Highly variable generally slowly progressive to severely debilitating and fatal Not recommended except in extraordinary cases with endangered species wide range of antimicrobial combinations utilized based on sensitivity Isolation and quarantine test and cull Yes Fact Sheet compiled by Douglas Armstrong and Charles O Thoen Sheet completed on 13 February 2011 updated 31 January 2013 Fact Sheet Reviewed by Claude Turcotte John Kaneene Paul P Calle Susceptible animal groups All ungulates ruminants and camelids are susceptible However very rare in North American zoo populations due to ongoing monitoring via necropsy programs and tuberculin skin testing during interzoo animal transfer It is more common in some farmed exotics such as cervids Pockets of endemic infection in the US in wildlife including white tail deer elk and bison specifically in Michigan Causative organism Mycobacterium bovis Zoonotic potential Significant zoonotic potential Distribution Global Incubation period Variable generally slowly progressive Clinical symptoms Dyspnea coughing lymphadenopathy lethargy weight loss Post mortem gross or histopathologic findings Gross Lesions typically will be yellowish caseous necrotic areas within nodules of firm white fibrous tissue Tuberculous lesions may be accompanied by cavitation and calcification Miliary patterns of granulomas may be present in some species Primarily affected organs are lungs and lymphoid system especially retropharyngeal lymph nodes However virtually any organ may be affected Histology Tubercles are granulomatous lesions with a caseous necrotic center bordered by epithelioid cells some of which may form multinucleated giant cells Histologic lesions may vary substantially with species Culture of affected tissue and polymerase chain reaction detection are useful tools in diagnosis Diagnosis All zoo ungulate deaths should be necropsied with the intent to detect this disease if present See above post mortem description Ante mortem Primary assessment is by delayed hypersensitivity to M bovis PPD tuberculin 01 ml injected intradermally using a 26 gauge needle 38 inch in length In the US procedures and sites are defined and regulated by United States Department of Agriculture Veterinary Services as well as other regulations in the US and other countries Defined testing procedures and sites for accredited veterinarians for preshipment testing or screening programs include single site caudal tail fold in true cattle species and bison single site mid cervical region in cervids and antelope species dorsal lateral edge of base of ear in suidae species and the axillary region for camelidae In the US comparative tuberculin skin tests can be conducted by USDA approved veterinarians using biologically balanced PPDs prepared from M bovis and from M avium injected in the cervical region In vitro antibody tests have been described however the validity of these tests for detecting TB in early stages of American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN UNGULATES infection has not been confirmed Interferon gamma assay is validated and approved only for use in domestic cattle Material required for laboratory analysis Mycobacteriologic examination of material from post mortem lesions lesions or enlarged lymph nodes harvested at necropsy are needed Relevant diagnostic laboratories National Veterinary Service Laboratory USDA httpwwwaphisusdagovanimalhealth and some state veterinary diagnostic laboratories in the US or similar reference laboratories in other countries Treatment This route is not recommended as it is both ineffective and expensive Particularly it is difficult in ruminants since most recommended medications are administered by the oral route If undertaken for animals of substantial conservation or genetic value initial protocol of some combination of antimicrobials should be modified subsequently based on culture and sensitivity of organism from tracheal wash possible Normally use multidrug regimen includes combinations of isoniazid ethambutol and rifampin Prevention and control Isolation of suspected infected animals is recommended For captive populations and aggressive test and cull program in recommended with depopulation if disease is widespread Suggested disinfectant for housing facilities Cresylics phenolics and gluteraldehyde based disinfectants labeled to kill pathogenic Mycobacteria Notification Reportable disease to state and federal authorities Measures required under the Animal Disease Surveillance Plan Determined by state and federal authorities may vary by region Consult state and regional federal authorities in the US or similar regulatory authorities in other countries Measures required for introducing animals to infected population Not recommended Conditions for restoring diseasefree status after an outbreak Repeated tuberculin skin testing to identify reactors and depopulate Consult state and area federal APHIS livestock disease veterinary authorities in the US or similar regulatory authorities in other countries Experts who may be consulted John B Kaneene DVM MPH PhD Room A109 Veterinary Medical Center Center for Comparative Epidemiology College of Veterinary Medicine Michigan State University East Lansing Michigan 48824 5173552269 kaneenecvmmsuedu Michael Gilsdorf DVM 1910 Sunderland Place NW Washington DC 20036 Phone 202 2234878 Fax 2022234877 Mgilsdorfnafvorg Charles O Thoen DVM PhD Dipl AVES Department of Veterinary Microbiology and Preventive Medicine College of Veterinary Medicine Iowa State University Ames Iowa 50011 American Association of Zoo Veterinarians Infectious Disease Manual TUBERCULOSIS IN UNGULATES cthoeniastateedu References 1 Gilsdorf MJ and JB Kaneene 2014 The importance of M bovis infection in cervids on the eradication of bovine tuberculosis in the USA In Thoen CO J H Steele and J B Kaneene eds Zoonotic Tuberculosis Mycobacterium bovis and other pathogenic mycobacteria WileyBlackwell Publishing In press 2 Himsworth C G BT Elkin JS Nishi T Epp KP Lyashchenko O Surujball C Turcotte J Esfandiari R Greenwald and FA Leighton 2010 Comparison of test performance and evaluation of novel immunoasays for tuberculosis of wood bison naturally infected with Mycobacterium bovis J Wildlife Dis 461 7886 3 OBrien D J SM Schmitt KP Lyashchenko WR Waters DE Berry MV Palmer J McNair R Greenwald J Esfandiari and MK Cosgrove 2009 Evaluation of blood assays for detection of Mycobacterium bovis in white tailed deer Odocoileus virginianus in Michigan J Wildlife Dis 451 153164 4 Stevens J B CO Thoen EB Rohanczy S Tessaro HA Kelly and JR Duncan 1998 Experimental tuberculosis in lamas Llama glama Canad Vet J 62 102109 5 Thoen C O KJ Thorlson LD Miller EM Himes and RL Morgan 1988 Pathogenesis of Mycobacterium bovis infection in American bison Am J Vet Res 49 18611865 6 Thoen CO PA LoBue DA Enarson JB Kaneene and IN de Kantor 2009 Tuberculosis a re emerging disease in animals and humans Vet Ital 45135181 7 Thoen C O WJ Quinn LD Miller LL Stackhouse BF Newcomb and JM Ferrel 1992 Mycobacterium bovis infection in North American elk Cervus elephas J Vet Diagn Invest 4 423 427 American Association of Zoo Veterinarians Infectious Disease Manual MYCOPLASMOSIS Mycoplasma ovipneumoniae M gallisepticum M agassizi and others Fact Sheet compiled by Anne JusticeAllen Sheet completed on 25 February 2011 updated 1 April 2013 updated 2 January 2018 Fact Sheet Reviewed by Tom Besser Bruce Rideout Susceptible animal groups M ovipneumoniae bighorn sheep mountain goats musk oxen M gallisepticum birds especially passerines house finches and galliformes M agassizii M testudineum tortoises Many other Mycoplasma spp exist and new ones are being identified in connection with disease syndromes in mammals birds and reptiles Mycoplasma mycoides cluster sheep goats cattle others M bovis bison and bovids Other Mycoplasma spp may be minimally or nonpathogenic Causative organism Mycoplasma spp are bacteria with no cell wall and complex growth requirements making traditional culture mediated isolation difficult Many of the organisms associated with disease have not been fully characterized because identification has been by molecular methods Mycoplasma mycoides cluster organisms cause contagious bovine pleuropneumonia contagious agalactia of sheep and goats and contagious caprine pleuropneumonia and are considered foreign animal diseases in the United States M agalactiae is the major cause of contagious agalacia of sheep and goats but has only been reported sporadically in the United States Within a species some strains may vary in pathogenicity as well as in the clinical syndrome that develops For example some strains M bovis are linked to calf pneumonia while others will generally cause mastitis A subcategory of mycoplasmas is the hemoplasmas obligate red blood cell pathogens such as Mycoplasma ovis in sheep M suis in swine and novel species in raccoons Disease caused by hemoplasmas is not considered to be mycoplasmosis Zoonotic potential Marine mammal workers have acquired skin infections suspected to be Mycoplasma spp Humans have their own complement of Mycoplasma pathogens and many of those may infect nonhuman primates Distribution Worldwide often host species specific Incubation period 2 to 4 weeks possibly longer Clinical signs Generally mycoplasmas cause one or more of three clinical syndromes lymphocytic pneumonia where secondary infection with additional bacteria is common Pasteurellas for example polyarthritis mastitis Additionally otitis media and conjunctivitis may occur with some species In bighorn sheep and mountain goats signs typically consist of coughing respiratory distress otitis sinusitis loss of body condition death is possible in all age classes on first exposure death in neonates and weanlings in subsequent years population declines and poor recruitment In birds the predominant sign is mild to severe conjunctivitis death in some cases In tortoises the predominant signs are nasal discharge clear to mucopurulent conjunctivitis edema of the eyelids infection often becomes chronic and may end in death A fatal multisystemic disease attributed to M alligatoris has been identified in American alligators and related caimans Additional species black vultures skunks crocodiles signs consist of polyarthritis Post mortem gross or histologic findings Epithelial hyperplasia is observed in the affected tissues lymphoid aggregates and infiltrates which can progress to fibrosis Lesions can become suppurative and necrotizing with secondary bacterial invasion Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Sheep goats birds and tortoises most important others possible Direct contact between animals most important fomites possible Respiratory pneumonia coughing conjunctivitis polyarthritis Tends to be chronic can be severe and result in death Macrolides and fluoroquinolones may be effective early in the disease but ineffective for polymicrobial secondary pneumonia Vaccination generally not effective Health screening by culture and PCR Prevent close contact Maybe American Association of Zoo Veterinarians Infectious Disease Manual MYCOPLASMOSIS Mycoplasma ovipneumoniae M gallisepticum M agassizi and others Diagnosis PCR is most reliable with several protocols available Culture with specialized media PPLO SP4 Friis modified Hayflick may be utilized Serology is unreliable for individual animal diagnosis but can be used for screening groups of animals When comparing disease risk between populations straintyping is recommended as pathogenicity has been shown to vary between strains and crossprotection appears to be incomplete Material required for laboratory analysis Tissues especially lung trachea and retropharyngeal lymph nodes deep nasal or oropharyngeal swabs or washes middle ear swabs and sinus swabs joint fluid or tissue Swabs dacron or polyester with a plastic shaft should be transported in PPLO TSB with 10 glycerin or specialized mycoplasmalviral transport media consult the laboratory and should be sent to the lab promptly should arrive within 72 hours on gel ice For PCR testing swabs may be shipped without media in cryovials Relevant diagnostic laboratories Colorado Veterinary Diagnostic Laboratory Colorado State University httpcsucvmbscolostateeduvdlPagesdefaultaspx 9702971281 National Veterinary Services Laboratory httpwwwaphisusdagovanimalhealthlabinfoservicesaboutnvslshtml 515 3377266 Mycoplasma Research Lab Dr Mary Brown University of Florida 352 2944029 Lab Telephone 352 2944094 or 2944071 Texas Veterinary Medical Diag Lab TAMU httptvmdltamuedu 979 8453414 Washington Animal Disease Diagnostic Laboratory Washington State Univ httpwwwvetmedwsuedudeptsWADDL 5093359696 Treatment Azithromycin erythromycin tulathromycin enrofloxacin beta lactam antibiotics are not effective due to an absent cell wall Prevention and control Population testing with blocking or competitive ELISA is most appropriate for non domestic species where other serology methods such as AGID or SN have not been validated Prolonged quarantine as stress increases shedding and repeated attempts at isolation during this interval are recommended For positive populations straintyping should be conducted as isolates can vary in pathogenicity Suggested disinfectant for housing facilities Mycoplasmas are susceptible to most commonly used disinfectants including Virkon S quaternary ammonium compounds or household bleach 120 in water Bleach and to a lesser extent quaternary ammonium compounds are inactivated in the presence of organic matter so are preferably used on clean surfaces Mycoplasma doesnt survive well in dry conditions or with exposure to sunlight Some species of Mycoplasma will have increased survival in conditions where biofilms develop Notification Mycoplasma mycoides cluster organisms cause contagious bovine pleuropneumonia contagious agalactia of sheep and goats and contagious caprine pleuropneumonia all of which are foreign animal diseases in the United States Immediate notification of USDA and state agencies is required for any suspected cases Measures required under the Animal Disease Surveillance Plan None American Association of Zoo Veterinarians Infectious Disease Manual MYCOPLASMOSIS Mycoplasma ovipneumoniae M gallisepticum M agassizi and others Measures required for introducing animals to infected animal Multiple negative culturesPCR tests from infected animal Chronic and subclinical carriers highly likely Conditions for restoring diseasefree status after an outbreak Difficult to impossible longterm treatment with appropriate systemic antibiotic see above Testandcull showing promise experimentally for M ovipneumoniae in bighorn sheep and has been used in other species Multiple tests should be conducted on individual animals as shedding of organisms is inconsistent Experts who may be consulted Thomas E Besser DVM PhD Professor and Rocky Crate D V M and Wild Sheep Foundation Chair in Wild Sheep Disease Research Washington State University College of Veterinary Medicine Phone 5093356075 tbesservetmedwsuedu References 1 Besser TE Cassirer EF Potter KA VanderSchalie J Fischer A Knowles DP Herndon DR F R Rurangirwa FR Weiser GC Srikumaran S Association of Mycoplasma ovipneumoniae infection with populationlimiting respiratory disease in freeranging Rocky Mountain bighorn sheep Ovis canadensis canadensis J Clin Microbiol 20084642330 2 Brown MB McLaughlin GS Klein PA Crenshaw BC Schumacher IM Brown DR Jacobson ER Upper respiratory tract disease in the gopher tortoise is caused by Mycoplasma agassizii J Clin Microbiol 19993722629 3 Cassirer FE Manlove KR Almberg ES Kamath PL Cox M Wolff P Roug A Shannon J Robinson R Harris RB Gonzoles BJ Plowright RK Hudson PJ Cross PC Dobson A Besser TE Pneumonia in bighorn sheep Risk and resilience J Wildl Management 2018823245 4 Cassirer FE Manlove KR Plowright RK Besser TE Evidence for strainspecific immunity to pneumonia in bighorn sheep J Wildl Management 201781133143 5 Fischer JR Stallknecht DE Luttrell P Dhondt AA Converse KA Mycoplasmal conjunctivitis in wild songbirds the spread of a new contagious disease in a mobile host population Emerg Infect Dis 19973 6972 6 Ossiboff R J Raphael BL Ammazzalorso AD Seimon TA Niederriter H Zarate B Newton AL McAloose D A Mycoplasma species of Emydidae turtles in northeastern USA J Wildl Dis 20155146670 7 Ostrowski S Thiaucourt F Amirbekov M Mahmadshoev A MansoSilván AL Dupuy V Vahobov D Ziyoev O Michel S Fatal outbreak of Mycoplasma capricolum pneumonia in endangered markhors Emerg Infect Dis 201117233841 8 Rettenmund C L Boyer DM Orrico WJ Parker SG Wilkes RP Seimon TA Paré JA Longterm oral clarithromycin administration in chelonians with subclinical Mycoplasma spp infection J Herpet Med and Surg 2017275861 9 Sumithra TG Chaturvedi VK Susan C Siju SJ Rai AK Harish C Sunita SC Mycoplasmosis in wildlife a review Eur J Wildl Res 201359769781 10 Tardy F Baranowski E Nouvel LX Mick V MansoSilvàn L Thiaucourt F Thébault P Breton M SirandPugnet P Blanchard A Garnier A Gibert P Game Y Poumarat F Citti C Emergence of atypical Mycoplasma agalactiae strains harboring a new prophage and associated with an alpine wild ungulate mortality episode Appl Environ Microbiol 201278465968 11 Volokhov DV Hwang J Chizhikov VE Danaceau H Gottdenker NL Prevalence Genotype Richness and Coinfection Patterns of Hemotropic Mycoplasmas in Raccoons Procyon lotor on Environmentally Protected and Urbanized Barrier Islands Appl Environ Microbiol 201783e0021117 American Association of Zoo Veterinarians Infectious Disease Manual OESOPHAGOSTOMIASIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Old World monkeys great apes ruminants camelids and suids Fecaloral ingestion of thirdstage larvae L3 direct life cycle Diarrhea anorexia weight loss lethargy and abdominal pain Variable but severe infection can result in death Ivermectin pyrantel pamoate or a benzimidazole Surgical removal of mass effect Quarantine of new individuals isolation of affected animals parasite monitoring programs Yes only for some parasite species that infect non human primates Fact Sheet compiled by Ginger L Takle updated by Karen Terio Sheet completed on 21 June 2011 updated 13 September 2013 updated 24 May 2018 Fact Sheet Reviewed by Stephanie McCain Susceptible animal groups Great apes Old World monkeys suids camelids ruminants Causative organism Primates Oesophagostomum bifurcum O Conoweberia apiostomum O Conoweberia stephanostomum O aculeatum Ruminants O columbianum O venulosum O radiatum and other species may be found in wild ruminants New and Old World camelids O venulosum Oesophagostomum sp Suids Odentatum O brevicaudum O quadrispinulatum and other species may be found in wild suids Zoonotic potential Yes Oesophagostomum bifurcum and O stephanostomum Distribution Worldwide but most commonly occurs in the tropics and subtropics Incubation period Ova passed in feces hatch and develop into infective L3 in approximately 27 days depending on environmental conditions After ingestion the L3 burrow into the intestinal wall forming cystic nodules to granulomas within the submucosa muscularis and mesentery in which the nematodes molt into fourthstage larvae L4 The L4 can then remain in the nodules or return to the intestinal lumen where they develop to the adult stage Generally prepatent period is considered 3242 days Clinical signs Primates Clinical signs can range from intermittent diarrhea to inappetence severe mucoid bloody diarrhea pale mucous membranes weakness lethargy weight loss vomiting abdominal pain and death Ruminants and Suids fetid diarrhea anorexia weakness emaciation and death If chronic infection is present clinical signs may be seen that are consistent with decreased intestinal motility stenosis or intussusception Post mortem gross or histologic findings Oesophagostomins are also known as nodular worms due to their gross appearance The L3 penetrate deep into and encyst in the lamina propria submucuosa muscularis of the small and large intestine and in some cases the adjacent mesentery Granulomas nodules form around the larvae and can be 550mm in diameter These granulomas may contain reddish brown fluid and a central nematode In some sections inflammation is associated with migration tracts and abdominal adhesions or peritonitis may be present Mesenteric lymph nodes are often enlarged Diagnosis Identification of ova on fecal examination but these are confused easily with hookworm eggs identification of larvae or adults during intestinal biopsy morphological identification of adult specimens collected at necropsy PCR PCRRFLP seminested PCR Material required for laboratory analysis Fecal sample larvae or adult worms nodular intestinal tissues American Association of Zoo Veterinarians Infectious Disease Manual OESOPHAGOSTOMIASIS Relevant diagnostic laboratories Any diagnostic laboratory with routine parasitologic capabilities should be able to diagnose this infection These diagnostics are readily available as inhouse fecal flotation or any laboratory performing fecal exams Treatment Ivermectin pyrantel pamoate or benzimidazole can be administered Where possible surgical excision of the nodules may be performed Prevention and control Quarantine of new animals parasite monitoring program isolation and treatment of affected animals proper sanitation and waste removal can assist with prevention Freeliving larval stages L1 infective L3 survive in the environment moisture and temperature dependent Suggested disinfectant for housing facilities Commonly used disinfectants can be used after removal of feces from the area Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Treat infected or potentially infected animals prior to introduction to noninfected animals Conditions for restoring diseasefree status after an outbreak Negative fecal examinations can be used to identify persistent infections that should be resolved before introductions Experts who may be consulted Parasitologists are well versed in this disease and should be consulted References 1 Oesophagostomiasis Internet Center for Disease Control c 2017 cited 24 May 2018 Available from httpwwwdpdcdcgovdpdxhtmloesophagostomiasishtm 2 Boomker J Parasites of South African wildlifeV A description of the males of Oesophagostomum mocambiquei Ortlepp 1964 from warthogs Phacochoerus aethiopicus Pallas 1766 Onderstepoort J Vet Res 199057169173 3 Helminths In Bowman DD ed Georgis Parasitology for Veterinarians 8th ed St Louis MO Saunders 2003 p 115118 4 Gasser R De Gruijter J Polderman A Insights into the epidemiology and genetic makeup of Oesophagostomum bifurcum from human and nonhuman primates using molecular tools Parasitol 2006132453460 5 Krief S Jamart A Mahé S Leendertz F MätzRensing K Crespeau F Bain O Guillot J Clinical and pathologic manifestation of oesophagostomosis in African great apes does selfmedication in wild apes influence disease progression J Med Primatol 200837188195 6 Krief S Vermeulen B Lafosse S Kasenene J Nieguitsila A Berthelemy M LHostis M Bain O Guillot J Nodular worm infection in wild chimpanzees in western Uganda a risk for human health PLoS Negl Trop Dis 20104e630 7 Terio KA Lonsdorf EV Kinsel MJ Raphael J Lipende I Collins A Li Y Hahn BH Travis DA Gillespie TR Oesophagostomiasis in nonhuman primates of Gombe National Park Tanzania Am J Primatol 2018801 Available from doi 101002ajp22572 American Association of Zoo Veterinarians Infectious Disease Manual OPHIDIAN PARAMYXOVIRUS OPMV Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All snakes especially Viperidae Primarily airborne but fomite waterborne fecal oral transmission can occur Vertical transmission may occur but uncertain at this time Respiratory compromise neurologic signs anorexia regurgitatio n and chronic poor doer and sudden death Severe animals can survive infection with supportive care but death is common Supportive care including broad spectrum antibiotics fluid and nutritional support and ensure proper husbandry especially correct thermal gradient Strict quarantine with separate airspace and utensils PCR testing on tracheal lavage and proper husbandry No Fact Sheet compiled by Christopher S Hanley Sheet completed on 19 November 2011 updated 1 April 2013 updated 8 Feb 2018 Fact Sheet Reviewed by Randy Junge Susceptible animal groups All snakes especially Viperidae Causative organism Ophidian paramyxovirus Zoonotic potential None Distribution Outbreaks have been documented in multiple private and zoological collections worldwide seroconversion has been documented in wild specimens and importance of which remains uncertain Outbreaks are more common from January through May Incubation period Seroconversion takes at least 8 weeks but the incubation period has been documented to be at least 10 months in some specimens Clinical signs Acute death respiratory compromise blood in the oral cavity or nares neurologic signs including head tremors star gazing flaccid paralysis convulsions and loss of righting reflex In more chronic cases anorexia regurgitation cachexia lethargy and abnormal feces are common As with other paramyxoviruses OPMV causes immunosuppression so secondary infections are common Post mortem gross or histologic findings No pathognomonic lesions occur with this disease Gross findings range from no lesions to respiratory lesions including pulmonary congestion hemorrhage respiratory exudates and pneumonia pancreatic hyperplasia and hepatic necrosis and granulomas may all be macroscopically evident Histologic lesions include hyperplasia of the respiratory epithelium thickening of the pulmonary septa inflammatory cell infiltration evidence of exudates and edema and rarely eosinophilic intracytoplasmic inclusions If the CNS is involved there can be encephalitis with multifocal gliosis moderate ballooning of axon fibers in the brain stem and spinal cord Hepatic necrosis or multifocal pyogranulomatous inflammation is often observed Hyperplasia of pancreatic ducts and acinar cells with cystic dilatation has been observed The salivary glands can be affected by ductular dilatation flattening of the ductular epithelium and accumulation of cellular debris and secretory material in the lumen Diagnosis Definitive diagnosis requires viral isolation from tissues PCR for viral nucleic acid immunohistochemical staining for viral antigen andor electron microscopy Tracheal lavages submitted for PCR analysis may provide an antemortem diagnosis Material required for laboratory analysis Tracheal lavage fluid can be submitted for PCR analysis as a screening tool and tissue samples collected at necropsy especially lung liver and pancreas both formalin fixed and frozen depending on test Relevant diagnostic laboratories University of Florida 2015 SW 16th Avenue Bldg 1017 Room V2238 Gainesville FL 32608 352 3924700 ext 5775 American Association of Zoo Veterinarians Infectious Disease Manual OPHIDIAN PARAMYXOVIRUS OPMV Treatment Supportive care including broad spectrum antibiotics fluid and nutritional support and ensure proper husbandry especially correct thermal gradient Prevention and control Maintain proper husbandry especially correct thermal gradients Quarantine all new animals for a minimum of 6090 days using separate utensils and supplies disinfection or destruction of all materials at the end of quarantine and usage of a footbath Obtain OPMV PCR via tracheal wash during quarantine period Monitor animals closely for abnormal behaviors Necropsy all animals that die While OPMV serology is available from multiple laboratories question has been raised as to the value of this method of testing especially when comparing results between different laboratories If used as with any other antibody titer serial sampling is required to confirm infection versus just exposure Suggested disinfectant for housing facilities Bleach is recommended for disinfection at 12 cupgallon of water 120mlL Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Due to the fact that PCR positive animals would be actively shedding the virus it is not recommended to introduce new animals to those that are infected A minimum of 60 days and ideally longer after the last OPMV death should pass before the introduction of new specimens Conditions for restoring diseasefree status after an outbreak PCR positive animals should be isolated and those that are PCR negative should appear healthy and have negative tracheal washes at least 90 days after diagnosis before new animals are introduced into the collection Experts who may be consulted Jim Wellehan DVM MS PhD DACZM DACVM Virology BacteriologyMycology Zoological Medicine Service University of Florida College of Veterinary Medicine Gainesville Florida 326100126 wellehanjufledu References 1 Allender MC Mitchell MA Dreslik MJ Phillips CA Beasley VR Measuring agreement and discord among hemagglutination inhibition assays against different ophidian paramyxovirus strains in the Eastern massasauga Sistrurus catenatus catenatus J Zoo Wild Med 2008 39358361 2 Bronson E Cranfield MR Paramyxovirus In Mader DR ed Reptile medicine and surgery 2nd ed St Louis MO Elsevier 2006 p 851861 3 Ophidian Paramyxovirus OPMV Internet Microbiology Parasitology Serology UF Diagnostic Laboratories College of Veterinary Medicine c2018 cited 2018 February 08 Available from httplabsvetmedufleduavailabletestszoomedinfectionsopm 4 Pees M Schmidt V Marschang RE Heckers KO KrautwaldJunghanns ME Prevalence of viral infections in captive collections of boid snakes in Germany Vet Rec 2010166422425 American Association of Zoo Veterinarians Infectious Disease Manual OXYURIASIS pinworm Alaeuris Aspiculuris Dentostomella Enterobius Oxyuris Probstmayria Passalurus Skrjabinema Syphacia and Trypanoxuria spp Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals including humans reptiles Fecaloral by ingestion of eggs retroinfection by anal entry possible with some species and short pre patent period Asymptomatic to substantial irritability as anusitis and pruritus Equids with severe infection often present with broken tail hairs or perianal excoriation or trauma Typically mild but may become highly aggravatin g to horses and humans Anthelminthics eg ivermectin fenbendazole Hygiene to prevent re infection Personal environmental hygiene quarantine of new arrivals and treatment as necessary Enterobius is probably transmissible between apes and humans Zoonotic potential of others are not known Fact Sheet compiled by Christopher J Bonar Sheet completed on 14 February 2011 updated 16 April 2013 updated 2018 Fact Sheet Reviewed by Kate Pritchett Christie Hicks Susceptible animal groups Mammals including humans reptiles avian Causative organism Enterobius spp infects humans and chimpanzees Trypanoxuria and Enterobius can also cause disease in New World primates Probstmayria vivipara Skrjabinema ovis and S caprae in sheep and goats Oxyuris equi infects equids and Oxyuris karamoja infects African rhinoceroses and elephants Passalurus ambiguous is common in the colon and cecum of lagomorphs Dentostomella spp Syphacia sppand Aspiculuris tetraptera infect laboratory rodents although no oxyurid is described in guinea pigs Alaeuris brachylophi has been described in reptiles Oxyuronema atelophorum has been reported in monkeys of the genus Ateles Zoonotic potential Yes Distribution Parasite is found occasionally in wild and captive chimpanzees elephants rhinos equids reptiles domestic and laboratory rodents and humans Incubation Period Aspiculuris tetraptera prepatent period 23 days Enterobius vermicularis prepatent period 30 days Passalarus ambiguous prepatent period 5664 days Syphacia muris prepatent period 8 days Syphacia obvelata prepatent period 1115 days Clinical signs Humans Perineal and anal pruritus often worse in the evenings when oxyurids emerge to lay eggs on the perineum Animals Irritability anal pruritus occasionally gastrointestinal impaction in reptiles Post mortem gross or histologic findings Parasites are most commonly found incidentally on routine fecal ova and parasite examination but rarely do they occur in large enough numbers to cause noticeable gross pathology Occasional reports of infections in lizards and turtles severe enough to cause gastrointestinal impaction Hemorrhagic enteritis has been reported in Ateles spp infected with Oxyuronema atelophorum Diagnosis Scotch tape preparation from anusperineum routine fecal OP examination floatation Examination of cecal and colonic contents at necropsy PCR amplified DNA has recently been demonstrated to be more sensitive than fecal OP examination Material required for laboratory analysis Egg masses from perineum or from fecal examination or worms and eggs recovered from cecal or colonic contents at necropsy Relevant diagnostic laboratories Any laboratory equipped with light microscopy and basic supplies for fecal OP examination can detect oxyurids PCR capabilities are a useful adjunct Treatment Pyrantel avermectins and benzimidazoles are all effective against oxyurids Fenbendazole American Association of Zoo Veterinarians Infectious Disease Manual OXYURIASIS pinworm Alaeuris Aspiculuris Dentostomella Enterobius Oxyuris Probstmayria Passalurus Skrjabinema Syphacia and Trypanoxuria spp medicated feed is commonly used for laboratory rodents Prevention and control Detection on routine fecal ova and parasite examinations and on scotchtape preparations on symptomatic individuals and followup treatment on infected individuals should allow for control of the organisms Good hygiene of enclosures should help to prevent reinfection Eggs have been shown to be present on laboratory workers hands as well as in the dust found around cages on air vents and in animal room ventilation systems Filtertop cages or individually ventilated cages therefore may be useful to prevent airborne transmission in laboratory rodent facilities Strict sanitation and hygienic measures should be adequate to prevent zoonotic transmission of Enterobius spp between apes and man Suggested disinfectant for housing facilities Eggs may be resistant to routine disinfectants Heat disinfection of cages and cleaning implements 100oC is effective in killing eggs Chlorhexidine 05 formaldehyde vapors and 75 mgL chlorine dioxide have also been recommended Mechanical removal by washing and scrubbing of enclosures and heat disinfection where possible is recommended Notification This disease is not ordinarily reportable Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Routine anthelminthic treatments Conditions for restoring diseasefree status after an outbreak Repeated treatment of individual animals and conspecifics as well as sanitation measures to prevent reinfection via the fecaloral route should eventually be effective Experts who may be consulted KR Pritchett DVM DACLAM MRCVS Charles River Laboratories Wilmington MA katepritchettcrlcom References 1 Adeoye GO Ogunbanwo OO Helminth parasites of the African lizard Agama agama Squamata Agamidae in Lagos Nigeria Rev Biol Trop Int J Trop Biol 2007552417425 2 Dole VS Zaias J KricopoulosCleasby DM Banu LA Waterman LL Sanders K Henderson KS Comparison of traditional and PCR methods during screening for and confirmation of Aspiculuris tetraptera in a mouse facility J Am Assoc Lab An Sci 201150904909 3 Jacobson ER Parasitic diseases of reptiles In Fowler ME ed Zoo and Wild Animal Medicine 2nd edition Philadelphia PA WB Saunders 1986 p 162181 4 Georgi JR Parasitology for Veterinarians 4th Edition Philadelphia PA WB Saunders 1985 p 121122 5 Pritchett KR and NA Johnston A review of treatments for eradication of pinworm infections in laboratory rodent colonies J Am Assoc Lab An Sci 20024123646 6 Lytvynets A Langrova I Lachout J Vadlejch J Detection of pinworm eggs in the dust of laboratory animals breeding facility in the cages and on the hands of the technicians Lab Anim 2013477173 7 Wallach JD Boever WR 1983 Diseases of Exotic Animals Medical and Surgical Management Philadelphia PA WB Saunders 1983 p 435795 1020 8 Wolff PL Parasites of New World Primates In Fowler M E and RE Miller Zoo and Wild Animal Medicine Current Therapy 3rd Edition Philadelphia PA WB Saunders 1993 p 378389 American Association of Zoo Veterinarians Infectious Disease Manual MENINGEAL WORM Parelaphostrongylus tenuis Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Ungulates notably cervids Oral Ingestion of infected intermediate host which includes numerous terrestrial mollusk species ie snails and slugs Neurologic Ranges from mild lameness to recumbency and death Severity is typically worse in young animals and may vary between species High doses of anthelmintics combined with antiinflammatories supportive therapy Prophylactic anthelmintic administered every 46 wks exclusion of the natural host whitetailed deer elimination or control of mollusk population No Fact Sheet compiled by Rae Gandolf and Julie Ter Beest Sheet completed on 1 January 2011 updated 9 October 2012 Fact Sheet Reviewed by Priya Bapodra Susceptible animal groups Natural host The whitetailed deer Odocoileus virginianus serves as the natural host and is rarely clinically affected they can shed numerous dorsalspined larvae in their feces Approximately 80 of whitetailed deer are infected in endemic regions Aberrant or deadend hosts Other cervid species moose caribou mule deer elk Sika deer camelids camels llamas alpacas pronghorn some bovids many antelope species bighorn sheep Angora goats bison rarely domestic cattle and rarely equids reported in domestic horses may show severe clinical signs Overall these species rarely shed larvae in their feces Disease significance Mortalities in captive species failed reintroduction of cervid species such as caribou suppression of elk and moose populations suspected cause of moose population declines in central and eastern North America Causative organism Parelaphostrongylus tenuis an extrapulmonary lungworm nematode Life cycle The natural host whitetailed deer acquires the infection through accidental ingestion of mollusks infected with 3rd stage larvae The larvae migrate from the gastrointestinal tract along spinal nerves and into the spinal cord where they develop to the last larval state Adult worms then locate on the meninges and in the cranial venous sinuses where they lay eggs The eggs pass into the venous circulation develop into 1st stage larvae in lung capillaries and then migrate into the lung tissue These larvae are expectorated swallowed and passed in the feces Mollusks acquire larval infection when crawling over feces and the parasite develops into the infective 3rd stage larvae within this intermediate host In the aberrant host infection is acquired by the same route However migration of the larvae in the spinal cord tends to be nondirectional and larvae often die before reaching the brain The aimless migration and larval death result in more local tissue damage as compared to the natural host Larvae infrequently develop into reproductive adults in the aberrant host Zoonotic potential None reported Distribution Predominantly associated with deciduous and deciduousconiferous forests of eastern and central North America concurrent with whitetail deer populations It is uncertain why deer of the southeast coastal plains region and of western North America are not infected American Association of Zoo Veterinarians Infectious Disease Manual MENINGEAL WORM Parelaphostrongylus tenuis Incubation period Natural host prepatent period 82137 days inversely proportional to infection dose Aberrant host signs typically appear in 3060 days as short as 5 days reported in experimental infections Clinical signs Neurologic signs are associated with intracranial or spinal cord inflammatory lesions caused by parasite migration Signs may range from single limb lameness or rear limb weakness to head tilt ataxia circling blindness progressive loss of motor function and death Ocular symptoms associated with migration of larvae into the uvea have been reported Post mortem gross or histologic findings Lesions in the aberrant host consist primarily of histologic changes in the brain and spinal cord They may include meningitis and encephalitis perivascular cuffing and infiltrations of eosinophils lymphocytes and plasma cells calcified remains of worms worm tracks focal traumatic malacia caused by developing nematodes gliosis disruption of the ependyma neuronal and myelin degeneration Eggs and larvae may be found associated with the eyes or the roots of cranial nerves on the leptomeninges and in brain tissue Diagnosis Natural host Modified Baermann technique for retrieving 1st stage larvae from feces Larvae must then be differentiated from related species using PCR However there are limited species of dorsalspined larvae and they are easy to retrieve allowing for presumptive diagnosis In addition to whitetailed deer moose and elk may shed the larvae in low numbers Aberrant hosts Antemortem diagnostic testing is currently unavailable a serum ELISA is under development at the University of Tennessee aimed at detecting antibodies against 3rd stage larvae in cervid species Post mortem diagnostics include PCR on tissues collected at necropsy postmortem recovery of adult worms or identification of larvae in neurologic tissue Material required for laboratory analysis Post mortem spinal cord and brain Antemortem plasma or serum aberrant hosts feces whitetailed deer moose and elk Relevant diagnostic laboratories ELISA in development or PCR tissue University of Tennessee College of Veterinary Medicine Department of Biomedical and Diagnostic Sciences Knoxville Tennessee USA Treatment High dose fenbendazole 2050mgkg orally once daily for 5 days and or high dose ivermectin 0304mgkg SC daily for 35 days or levamisole in addition to supportive therapies including nonsteroidal or steroidal antiinflammatory drugs vitamin E and vitamin B complex Early initiation of treatment is key to success Prevention and control Captive species Administration of anthelmintics every 4 6 weeks to target 3rd stage larvae before they migrate to neural tissue minimize exposure of captive animals to mollusks by establishing gravel roads or other vegetation breaks to act as snail and slug barriers use molluscicides with caution due to potential for environmental toxicity allow nonsusceptible species to initiate grazing on new or overgrown pastures reduce whitetailed deer population and build fences to exclude them Freeranging species Control of whitetailed deer population to reduce exposure Suggested disinfectant for housing facilities Molluscicides copper sulfate metaldehyde sodium pentachlorophenate may be used against the intermediate host with caution as they are potential environmental toxins Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal As no direct transmission of the parasite occurs and species susceptible to clinical disease do not typically pass larvae infected animals do not pose a direct threat to uninfected animals However whitetailed deer should generally be considered as infected and exposure of susceptible species to whitetailed deer should be avoided as possible American Association of Zoo Veterinarians Infectious Disease Manual MENINGEAL WORM Parelaphostrongylus tenuis Conditions for restoring diseasefree status after an outbreak This disease is endemic in whitetailed deer populations of eastern North America Experts who may be consulted Dr Murray Lankester Lakeland University Department of Biology CB 4026 955 Oliver Road Thunder Bay Ontario Canada P7B 5E1 Phone 250 4659019 mlankesterlakeheaduca Dr Richard Gerhold University of Tennessee College of Vet Medicine Department of Biomedical and Diagnostic Sciences 2407 River Drive Knoxville TN 37996 USA Phone 865 9745819 Fax 865 9745640 rgerholdutkedu References 1 Kocan AA The use of ivermectin in the treatment and prevention of infection with Parelaphostrongylus tenuis Dougherty Nematoda Metastrongyloidea in whitetailed deer Odocoileus virginianus J Wildl Dis 198521454455 2 Lankester MW Extrapulmonary lungworms of cervids In Samuel WM Pybus MJ Kocan AA eds Parasitic diseases of wild mammals 2nd ed Ames IA Iowa State University Press 2001 p 228278 3 Lankester MW Understanding the impact of meningeal worm Parelaphostrongylus tenuis on moose populations Alces 2010465370 4 Lankester MW Peterson WM Ogunremi O Diagnosing parelaphostrongylosis in moose Alces 2007434959 5 Nichols DK Montali RJ Phillips LG Alvarado TP Bush M Collins L Parelaphostrongylus tenuis in captive reindeer and sable antelope J Am Vet Med Assoc 1986188619621 6 Ogunremi O Lankester M Gajadhar A Immunodiagnosis of experimental Parelaphostrongylus tenuis infection in elk Can J Vet Res 20026617 7 Purdy SR Gagliardo LF Lefman S Hamel PJ Ku S Mainini T Hoyt G Justus K DaleyBauer LP Duffy MS Appleton JA Analysis of heavychain antibody responses and resistance to Parelaphostrongylus tenuis in experimentally infected alpacas Clin Vaccine Immunol 2012197101926 8 Tanabe M Gerhold RW Beckstead RB de Lahunta A Wade SE Molecular confirmation of Parelaphostrongylus tenuis infection in a horse with verminous encephalitis Vet Pathol 201047759 9 Tyler GV Hibler CP Experimental infection of mule deer with Parelaphostrongylus tenuis J Wildl Dis 198016533541 10 Wasel S Samuel WM Crichton V Distribution and ecology of meningeal worm Parelaphostrongylus tenuis Nematoda in north central North America J Wildl Dis 200339338346 11 Weiss RB Sarver CF Thilsted J Wolfe BA Clinical Parelaphostrongylus tenuis infection in two captive American bison Bison bison J Amer Vet Med Assoc 200823311271130 American Association of Zoo Veterinarians Infectious Disease Manual PARVOVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Carnivores including felids mink canids procyonids viverrids mustelids ursids hyaenids and possibly sea lions other species are affected by speciesspecific parvoviruses but the diseases differ substantially from the carnivores Ingestion primarily fecaloral Canine parvovirus2 CPV2 and panleukopenia virus most common signs are vomiting and diarrhea that can result in dehydration and death immune suppression is also common In some cases no clinical signs occur Respiratory or neurologic signs also can be seen with panleukopenia virus Nonclinical or mild to severe including death depends on immune status of animal Symptomatic treatment to prevent dehydration and prevent or treat secondary bacterial infections Vaccination when possible environmental sanitation prevention of contamination of environment strict isolation of naïve populations control can be managed with quarantine for at least 30 days No Fact Sheet compiled by Tara M Harrison Sheet completed on 3 August 2011 updated 7 September 12 updated 6 February 2018 Fact Sheet Reviewed by Dalen Agnew Rebecca Smedley Roger Maes Susceptible animal groups Carnivores such as felids canids procyonids mustelids ursids hyaenids and viverrids are affected by those parvoviruses described on this fact sheet Many other groups of animals are affected by various parvoviruses but the disease differs significantly from these disease presentations Causative organism Canine parvovirus type2 and Feline parvovirus panleukopenia virus are discussed here Other parvoviruses include but are not limited to canine parvovirus type 1 minute virus of canines mink enteritis virus mink Aleutian disease parvovirus ferret Aleutian disease virus raccoon parvovirus Zoonotic potential None Distribution Worldwide distribution Incubation period Typically 57 day incubation period but can range from 410 days Clinical signs For canine and other enteric parvoviruses puppies are most likely to suffer severe disease and death However any unvaccinated canid of any age can become infected with CPV2 Clinical signs range from nonclinical to profound depression lethargy and inappetence enteric parvoviruses cause signs of gastroenteritis such as vomiting and severe diarrhea that can be foulsmelling and include mucus fibrin casts and blood may also see pyrexia and dehydration Other parvorviruses cause variable disease syndromes such as chronic wasting or neurologic disease seen with mink Aleutian disease or respiratory neurological andor gastrointestinal disease seen with panleukopenia Most parvoviruses also cause immunosuppression Most animals that succumb do so within 45 days of infection juveniles have a higher fatality rate than adults Clinical pathological gross and histopathological findings Feline parvovirus panleukopenia total white counts of 10002000ml and neutrophils 200ml Canine feline and other enteric parvoviruses anemia and hypoproteinemia possibly due to blood and protein loss through the gastrointestinal tract segmental reddening hemorrhage and a granular appearance of the serosa of the small intestine lymphoid depletion necrosis and loss of crypts with subsequent villous atrophy blunting and fusion in the small intestine involution of the lymphoid tissues in the small intestine lymph nodes spleen and thymus bone marrow may be hypocellular Diagnosis Testing should be performed on acutely infected or recently exposed or high risk canines Inhouse fecal ELISA tests are quite specific and sensitive for currently circulating strains of canine parvovirus and are reportedly useful for feline panleukopenia Some strains of CPV2 can infect domestic cats as well as dogs As American Association of Zoo Veterinarians Infectious Disease Manual PARVOVIRUS with any test false results are possible and negative results can occur later in the course of disease Weak false positives may also reportedly occur due to recent vaccination However this is uncommon so positive results should be taken seriously even in recently vaccinated dogs Shedding can be intermittent therefore testing more than one animal or one animal on sequential days is suggested Other possible tests are latex agglutination and hemagglutination which is not a specific test Virus can be detected in serum by hemagglutination and IgG IFA virus may be detected in tissues using virus isolation hemagglutination PCR immunohistochemistry IHC and electron microscopy Serology is a useful tool to assess risk or to further clarify the need for quarantine of individual dogs Necropsy both gross and histopathology are very useful especially in a herd health situation when mortality is present A presumptive diagnosis may be made from characteristic gross and histologic lesions and confirmed with positive IHC labeling within the damaged small intestinal crypts and in the epithelial cells of the tongue tongue can be useful for PCR IHC or FA testing in canines and felines if there is marked autolysis in the small intestine Material required for laboratory analysis Enteric parvoviruses feces small intestine tongue systemic lymphoid tissues Serum can also be used but may not be helpful Relevant diagnostic laboratories Most diagnostic laboratories can test for enteric parvoviruses several in house diagnostic tests are also available for enteric parvovirus Treatment Enteric parvoviruses isolate infected animal provide supportive care to treat dehydration and electrolyte imbalance prevent secondary bacterial infections especially in animals with leukopenia Prevention and control Parvoviruses can survive for months in cool moist areas protected from sunlight and are very stable when frozen can persist in feces for 6 months at room temperature and may remain viable in the natural environment for 912 months Vaccination is the cornerstone of parvovirus prevention In the absence of maternal antibody interference a single modified live vaccine can confer protection within 35 days Re vaccination must be performed especially in high risk situations such as shelters Both inactivatedadjuvanted and modified live vaccines are available although the use of modified live vaccines in nondomesticated animals may produce disease and is typically not recommended Although modified live vaccines against parvovirus were used in red wolves and produced titers for three years and no adverse reactions Suggested disinfectant for housing facilities Parvovirus must be mechanically removed or can be killed by one of the few effective disinfectants Disinfection using formaldehyde glutaraldehyde potassium peroxymonosulfate Trifectant or VirkonS or chlorine solutions such as 01755 sodium hypochlorite solution for bleach 5 household bleach can be used but should be freshly diluted at 132 12 cup per gallon Foot baths can also be used with sodium hypochlorite solutions to prevent spread Like all disinfectants bleach must be used and stored correctly to be effective Application should be only to precleaned surfaces free of organic matter Independent studies have shown that quaternary ammonium disinfectants do not reliably kill parvovirus Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Do not introduce noninfected animal to infected animal noninfected animal should be vaccinated prior to exposure to previously infected animal whenever possible Conditions for restoring diseasefree status after an outbreak Adequate husbandry practices using an approved disinfectant in many environments parvovirus may be endemic and it may be difficult to restore a diseasefree environment If the virus is present endemically in other wildlife vectors or in a captive setting appropriate vaccination and disinfection may assist in controlling potential outbreaks Quarantine of infected animals for a minimum of 30 days may also help to control an outbreak and restore a diseasefree state References below include information for less common parvoviruses Experts who may be consulted Patricia Pesavento DVM PhD Department of Pathology Microbiology and Immunology American Association of Zoo Veterinarians Infectious Disease Manual PARVOVIRUS 5323 Vet Med 3A School of Veterinary Medicine University of California Davis CA 95616 530 7521166 papesaventoucdavisedu Department of Virology Veterinary Diagnostic Laboratory 4125 Beaumont Rd Lansing Michigan 48910 5173531683 References 1 AbdEldaim M Beall M Kennedy M Detection of feline panleukopenia virus using a commercial ELISA for canine parvovirus Vet Ther 200910 E16 2 Alexandersen S Pathogenesis of disease caused by Aleutian mink disease parvovirus APMIS Suppl 199014 132 3 Anderson K Case A Woodie K Waddell W Reed HH Duration of immunity in red wolves Canis rufus following vaccination with a modified live parvovirus and canine distemper vaccine J Zoo Wildl Med 20144535504 4 Appel M Parrish CR Canine Parvovirus type 2 In MJ Appel ed Virus infections of carnivores Amsterdam Elsevier Science 1987 p 6992 5 Barker IK Parrish CR Parvovirus infections In E S Williams and IK Barker eds Infectious Diseases of Wild Mammals 3rd ed Ames IA Iowa State University Press 2001 p 131146 6 Burger D Gorham JR Mink virus enteritis In JW Davis LH Karstad and DO Trainer eds Infectious diseases of wild mammals Ames IA Iowa State University Press 1970 p 7684 7 Demeter Z Gal J Palade EA Rusvai M Feline parvovirus infection in an Asian palm civet Paradoxurus hermaphroditus Vet Rec 2009164213216 8 Duarte MD Barros SC Henriques M Fernandes TL Bernardino R Monteiro M Fevereiro M Fatal infection with feline panleukopenia virus in two captive wild carnivores Panthera tigris and Panthera leo J Zoo Wildl Med 200940354359 9 Eleraky NZ Potgieter LN Kennedy MAVirucidal efficacy of four new disinfectants J Am Anim Hosp Assoc 200238231234 10 Gjeltema J Murphy H Rivera S Clinical canine parvovirus type 2C infection in a group of Asian smallclawed otters Aonyx cinerea J Zoo Wildl Med 2015461120123 11 Godard A Leisewitz AL Canine parvovirus Vet Clin North Am Small Anim Pract 201040 1041 1053 12 Hoelzer K Parrish CR The emergence of parvoviruses of carnivores Vet Res 201041 39 13 Hurley K Feline Panleukopenia Internet UC Davis Shelter Health Portal cited 2013 July 2 Available from httpwwwsheltermedicineorg 14 Hurley K Canine parvovirus Internet UC Davis Shelter Health Portal cited 2013 July 2 Available from httpwwwsheltermedicineorg 15 McKnight CA Maes RK Wise AG Kiupel M Evaluation of tongue as a complementary sample for the diagnosis of parvoviral infection in dogs and cats J Vet Diagn Invest 200719 40913 16 Pollock RVH Experimental canine parvovirus infection in dogs Cornell Vet 198272 103119 17 Pollock RVH Parrish CR Canine parvovirus In RG Olsen S Krakowa and J R Blakeslee eds Comparative pathobiology of viral diseases Boca Raton FL CRC Press 1985 p 145177 18 Sassa Y Yamamoto H Mochizuki M Umemura T Horiuchi M Ishiguro N Miyazawa T Successive deaths of a captive snow leopard Uncia uncia and a serval Leptailurus serval by infection with feline American Association of Zoo Veterinarians Infectious Disease Manual PARVOVIRUS panleukopenia virus at Sapporo Maruyama Zoo J Vet Med Sci 2011734491494 19 Scott FW Virucidal disinfectants and feline viruses Am J Vet Res 198041 410414 20 Uttenthal A Lund E Hansen M Mink enteritis parvovirus Stability of virus kept under outdoor conditions APMIS 1999107353358 21 Wasueru J Schmiedeknecht G Forster C Konig M Reinacher M Parvovirus infection in a Eurasian lynx Lynx lynx and in a European wildcat Felis silvestris silvestris J Comp Pathol 2009140203 207 22 de Welchman D Oxenham BM Done SH Aleutian disease in domestic ferrets diagnostic findings and survey results Vet Record 1993132479484 American Association of Zoo Veterinarians Infectious Disease Manual PASTEURELLOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Avian Aerosol mechanical via bite or scratch wounds or environmental food water Colonization of lungs by endogenous nasopharyngeal bacteria is described in ruminants and swine due to environmental stressors andor primary infections due to viruses or Mycoplasma spp Primarily depression fever coughing nasal and oral discharge increased respiratory rates tachypnea Arthritis gastrointestinal disease otitis media mastitis bite wound abscesses and other signs are possible Variable Ranges from subclinical to peracute and fatal Supportive care early intervention with antibiotics ideally based on antibiotic sensitivity Drainage of localized abscesses Organ specific treatment for systemic infections Peracute systemic infections may be unresponsive Sanitation quarantine optimization of animal health and management and minimization of environmental and social stressors Vaccination for viral respiratory agents that can predispose to pasteurellosis Some strains may be responsive to vaccination Yes but rare Fact Sheet compiled by Glen C Weiser David S Miller and Susan M Lindstedt Sheet completed on 1 March 2011 updated 1 October 2012 Jan 2018 Fact Sheet Reviewed by Robert E Briggs James J England Jack C Rhyan Susceptible animal groups Most notably ruminants and birds but members of the Pasteurellaceae family can cause disease in many farm companion and wild animals Causative organism Members of the Pasteurellaceae family In ruminant pneumonia mostly Mannheimia haemolytica Bibersteinia trehalosi Histophilus somni and Pasteurella multocida are involved While each organism is capable of causing systemic and septicemic disease prominently P multocida in association with avian cholera or hemorrhagic septicemia In some cases the incidence of M haemolytica may be underestimated due to proximity dependent inhibition by other organisms Dassanayake et al 2010 Bavananthasivam et al 2012 although this has only been shown in vitro It can be a primary infection particularly in avians or secondary to viral or Mycoplasma spp infections and stress Recent data from free ranging bighorn sheep suggest that Mycoplasma ovipneumoniae rather than Pasteurellaceae may play a primary role in epizootic pneumonia and predispose to secondary Pasteurellaceae infection Besser et al 2012 In free ranging bighorn sheep lambs appeared more susceptible to pasteurellosis than adults and βhemolytic isolates were more likely to be associated with respiratory disease in adults Miller et al 2012 Zoonotic potential Yes but rare primarily in severely immunocompromised individuals Cat bite infections are more common Distribution Ubiquitous Incubation period Various reports indicate 18 days although some strains are carried asymptomatically for prolonged periods Clinical signs Serous oculonasal discharge cough depression anorexia fever pneumonia tachypnea dyspnea Arthritis otitis media gastrointestinal disease and other signs are possible particularly with chronic and systemic infections Localized abscesses in rabbits and cats due to bite wounds American Association of Zoo Veterinarians Infectious Disease Manual PASTEURELLOSIS Postmortem gross or histologic findings Highly variable but lesions are most common in the thoracic cavity Gross signs include pleural effusion fibrinous adhesions hemorrhage necrosis pulmonary consolidation thickened interlobular septa hydropericardium multifocal liver lesions and abscesses Histopathologic lesions include hyperemia pneumonitis fibronopurulent bronchopneumonia coagulative necrosis and fibrinous pleuritis Diagnosis Bacterial culture PCR detection methods are available Laboratories with specific expertise in pasteurellosis for disease investigations Concurrent testing for respiratory viruses and Mycoplasma spp is recommended Material required for laboratory analysis Nasal andor oropharyngeal swabs tonsilar tissue lung tissue or other infected tissues Relevant diagnostic laboratories Most veterinary diagnostic laboratories can complete analysis In cases involving wildlife labs with specific wildlife experience should be consulted Wildlife Pasteurellaceae can differ from domestic animal isolates Treatment Rapid quarantine of infected individuals prompt administration of appropriate antibiotics ceftiofur oxytetracycline penicillins florfenicol enrofloxacin tilmicosin azithromycin or based on susceptibility testing reduction of stressful environmental and social conditions general supportive care Drainage of abscesses or other therapy specific to the clinical presentation Prevention and control Sound management practices including minimization of stressors nutritional and environmental control and vaccination for viral respiratory agents quarantine of affected animals that prevents fence line and close aerosol contact quick treatment or in advanced cases euthanasia Specific vaccination is practiced for septicemic disease avian cholera atrophic rhinitis and bovine respiratory disease Suggested disinfectant for housing facilities Thorough physical cleaning chlorhexidine bleach or other effective disinfectants Notification None required Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Quarantine do not introduce animals with recent or observed clinical disease Optimize animal health prior to introduction with appropriate nutrition and similar measures minimize environmental extremes ensure social compatibility Conditions for restoring diseasefree status after an outbreak Absence of apparent respiratory disease Persistent subclinical infections are difficult to determine Experts who may be consulted Any licensed veterinarian with appropriate experience or university animal extension specialists Glen C Weiser Caine Veterinary Teaching Center University of Idaho may be able to provide reference laboratory support also including Mycoplasma isolation and PCR detection of some species and isolation and characterization of Pasteurellaceae Thomas E Besser College of Veterinary Medicine Washington State University may be able to provide strain typing of Mycoplasma spp References 1 Adlam C and Rutter JM eds Pasteurella and Pasteurellosis San Diego CA Academic Press Inc 1989 341 p 2 Bavananthasivam J Dassanayake RP Kugadas A Shanthalingam S Call DR Knowles DP Srikumaran S Proximitydependent inhibition of growth of Mannheimia haemolytica by Pasteurella multocida Appl Environ Microbiol 20127866836688 3 Besser TE Highland MA Baker K Cassirer EF Anderson NJ Ramsey JM Mansfield K Bruning DL Wolff P Smith JB Jenks JA Causes of pneumonia epizootics among bighorn sheep Western United States 20082010 Emerg Infect Dis 201218406414 American Association of Zoo Veterinarians Infectious Disease Manual PASTEURELLOSIS 4 Blackall P NørskovLauritsen N Pasteurellaceae the view from the diagnostic laboratory In Kuhnert P Christensen H eds Pasteurellaceae Biology Genomics and Molecular Aspects Norfolk UK Caister Academic Press 2008 p 227259 5 Dassanayake RP Call DR Sawant AA Casavant NC Weiser GC Knowles DP Srikumaran S Bibersteinia trehalosi inhibits the growth of Mannheimia haemolytica by a proximitydependent mechanism Appl Environ Microbiol 20107610081013 6 Franco KH Pollock C Internet Pasteurellosis in rabbits 2010 cited 2019 September 24 Available from httpslafebercomvetpasteurellosisinrabbits 7 Friend M Avian cholera In Friend M ed Field Guide to wildlife diseases Washington DC Department of the Interior Fish and Wildlife Service 1987 p 6982 8 Miller DS Weiser GC Ward ACS Drew ML Chapman PL Pasteurellaceae isolated from bighorn sheep Ovis canadensis from Idaho Oregon and Wyoming Amer J Vet Res 20127310241028 9 Miller MW Pasteurellosis In Williams ES Barker IK eds Infectious Diseases of Wild Mammals 3rd ed Ames AI Iowa State University Press 2001 p 330349 10 Ward ACS Weiser G Anderson BC Cummings PJ Arnold KF Corbeil LB Haemophilus somnus Histophilus somni in bighorn sheep Can J Vet Res 200670 3442 American Association of Zoo Veterinarians Infectious Disease Manual PESTE des PETITS RUMINANTS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Goats sheep small ruminants Direct contact with ocular nasal oral secretions urine and feces of affected animals indirect via fomites is possible virus fragile in environment so long distance transmission is unlikely Fever erosive stomatitis conjunctivitis gastroenteritis pneumonia abortion Can be mild to severe with up to 100 morbidity and 20 100 mortality Supportive care antibiotics for secondary bacterial infections anthelmintics for parasitic complications Vaccination w PPR modified live vaccine Eradication from newly infected areas No Fact Sheet compiled by Andrea Goodnight Sheet completed on 4 June 2018 Fact Sheet Reviewed by Douglas P Whiteside Susceptible animal groups Goats most susceptible and most severely affected 80100 morbidity and mortality sheep small ruminants less severe disease Whitetailed deer are susceptible experimentally A few outbreaks in camels and water buffalo Isolated clinical cases reported in gazelles Dorcas Thomsons Rheem Arabian bushbuck impala springbuck gemsbok bharal Sindh ibex bezoar ibex Afghan Markhor goat Nubian ibex Barbary sheep Laristan sheep and Indian buffalo Cattle pigs subclinical infection deadend hosts Causative organism Peste des petits ruminants virus Genus Morbillivirus family Paramyxoviridae Four lineages recognized Zoonotic potential No Distribution Historically subSaharan Africa north of the equator more recently cases spreading including into North Africa Middle East Turkey Iraq Iran Pakistan Afghanistan southern Asia including India Bangladesh and Vietnam moving into Nepal and China as well Incubation period 210 days typically 36 days for clinical signs to appear Clinical signs Acute most common High fever 4041oC crusting lip scabs nasal discharge serous to mucopurulent eventually occludes nares purulent ocular discharge conjunctivitis profuse catarrhal discharge matting palpebrae closed necrotizing stomatitis including lips gingiva dental pad hard palate cheeks anterior tongue gray necrotic foci over shallow erosions profuse nonhemorrhagic diarrhea bronchopneumonia with dyspnea anorexia dehydration emaciation abortion death in 510 days long convalescence in survivors Peracute mortality Frequent in goats high fever severe depression death Subacute and chronic Pneumonia inconsistent signs develops over 1015 days Post mortem gross or histologic findings Gross Erosions not ulcerations inside of lower lip including gingiva cheeks near commissures tongue hard palate pharynx upper 13 of esophagus abomasum and small intestine moderate erosions Peyers patches extensive necrosis large intestine has most severe lesions extensive congestion zebra stripes on mucosal folds of colon and rectum pneumonia generalized lymphadenopathy Histologic Degeneration necrosis of epithelial cells of mucous membranes eosinophilic intracytoplasmic and intranuclear inclusions in epithelial cells lymphoid cell depletion in Peyers patches necrotichemorrhagic enteritis bronchointerstitial pneumonia eosinophilic intracytoplasmic and intranuclear inclusions in giant cells and alveolar macrophages American Association of Zoo Veterinarians Infectious Disease Manual PESTE des PETITS RUMINANTS Diagnosis Clinical signs are only presumptive so must have laboratory confirmation especially to differentiate from rinderpest although rinderpest is considered eradicated worldwide Material required for laboratory analysis Virus neutralization serum 10 mL Virus isolation or PCR RTPCR whole blood in EDTA or heparin 10 mL tissue bronchial or mesenteric lymph nodes tonsil spleen lung intestinal mucosa Virus isolation nasal ocular oral fecal swabs Ship samples fresh on ice within 12 hours Histopathology on formalin fixed tissue Relevant diagnostic laboratories National Veterinary Services Laboratories NVSL Foreign Animal Disease Diagnostic Laboratory FADDL Plum Island NY httpwwwaphisusdagovanimalhealthlabinfoservicesdiagnostestsshtml FAO Reference Laboratory for PPR CIRADEMVT Campus International de Baillarguet MontferriersurLez BP 5034 34032 Montpellier Cedex 1 France diallociradfr Treatment Supportive care antibiotics for secondary infections anthelmintics for parasitic complications PPR hyperimmune bovine serum may decrease severity of clinical signs if given early in course of disease quarantine infected animals surviving animals have circulating neutralizing antibodies up to 4 years post infection with likely lifelong immunity Prevention and control Eradication quarantine and slaughter proper carcass disposal incineration or burial decontamination of housing facilities proper disposal of contact fomites restrict importation of sheep and goats from endemic areas Vaccination if approved by the government strategically or for high risk population with a homologous PPR vaccine is protective for 3 years No current evidence of virus circulation in wild ruminants unless introduced from domestic sheep and goats Suggested disinfectant for housing facilities PPR virus killed by most common disinfectants UV light and desiccation likely inactivate the virus within 34 days Virus survives long periods in chilled or frozen tissues Notification In the US and Canada this is a foreign animal disease which must be reported to state or federal veterinarian Measures required under the Animal Disease Surveillance Plan In the US and Canada this is a foreign animal disease which must be reported to state or federal veterinarian Measures required for introducing animals to infected animal It is not recommended to introduce new animals to infected animals however vaccination of introduced animals is recommended if must introduce Conditions for restoring diseasefree status after an outbreak Eradication of infected flock and decontamination of facility Experts who may be consulted Jeremiah T Saliki DVM PhD College of Veterinary Medicine University of Georgia Athens GA 30602 jsalikivetugaedu Peter Wohlsein Dr Med Vet School of Veterinary Medicine Hannover Germany PeterWohlseintihohannoverde American Association of Zoo Veterinarians Infectious Disease Manual PESTE des PETITS RUMINANTS References 1 World Organization for Animal Health Internet Peste des Petits Ruminants 2013 cited 2018 Jun 5 Available from httpwwwoieintfileadminHomeengAnimalHealthintheWorlddocspdfDiseasecardsPESTE DESPETITSRUMINANTSpdf 2 Balamurugan V Hemadri D Gajendragad MR Singh RK Rahman H Diagnosis and control of peste des petits ruminants a comprehensive review Virusdis 2014353956 3 Abu Elzein EME Housawi FMT Bashareek Y Gameel AA AlAfaleq AI Anderson E Severe PPR infection in gazelles kept under semifree range conditions J Vet Med B Infect Dis Vet Public Health 2004516871 4 Cebra C Cebra M Peste des Petits Ruminants Pseudorinderpest In Pugh D Baird N eds Sheep and Goat Medicine 1st ed Philadelphia PA Saunders 2002 p 384685 5 United States Department of Agriculture Animal and Plant Inspection Service Internet Disease Response Strategy Peste des Petits Ruminants 2013 cited 2018 Jun 5 Available from httpswwwaphisusdagovanimalhealthemergencymanagementdownloadspprdiseasestrategyp df 6 Kinne J Kreutzer R Kreutzer M Wernery U Wohlsein P Peste des petits ruminants in Arabian wildlife Epidemiol Infect 201013812111214 7 Munir M Abubakar M Zohari S Berg M Serodiagnosis of Peste des petits ruminants virus In Al Moslih M ed Serological Diagnosis of Certain Human Animal and Plant Diseases IntechOpen Internet 2012 cited 2018 Jun 5 Available from httpwwwintechopencombooksserological diagnosisofcertainhumananimalandplantdiseasesserodiagnosisofpestedespetitsruminants virus 8 The Center for Food Security and Public Health and Institute for International Cooperation in Animal Biologics Iowa State University College of Veterinary Medicine Internet Peste des Petits Ruminants c20082015 cited 2018 Jun 5 Available from wwwcfsphiastateeduFactsheetspdfspestedespetitsruminantspdf 9 Roeder PL Obi TU Recognizing Peste des Petits Ruminants A field manual Rome Italy Food and Agriculture Organization of the United Nations 1999 cited 2018 Jun 5 Available from httpwwwfaoorgdocrep003x1703ex1703e00htm 10 Saliki JT Wohlsein P Peste des petits ruminants Internet US Animal Health Association Committee on Foreign Animal Disease Foreign animal diseases the gray book Ed 7 Part III chap 36 Richmond Virginia US Animal Health Assoc 200835764 cited 2018 Jun 5 Available from httpwwwaphisusdagovemergencyresponsedownloadsnahemsfadpdf 11 Santhamani R Singh RP Njeumi F Peste des petits ruminants diagnosis and diagnostic tools at a glance perspectives on global control and eradication Arch Virol 201616129532967 American Association of Zoo Veterinarians Infectious Disease Manual PHOCINE DISTEMPER VIRUS Fact Sheet compiled by Laurie J Gage Sheet completed on 3 August 2011 updated 19 March 2013 Fact Sheet Reviewed by Ariana Finkelstein Kimberly Rainwater Susceptible animal groups Phocids and possibly northern sea otters Causative organism Morbillivirus Phocine Distemper Virus PDV Zoonotic potential None Distribution North Sea North America Atlantic coast and North Pacific Ocean Incubation period 5 to 12 days Clinical signs Variable body condition lethargy fever coughing dyspnea oculonasal discharge conjunctivitis keratitis diarrhea neurologic signs increased buoyancy abortion inability to dive Post mortem gross or histologic findings Bronchointerstitial pneumonia interstitial and purulent pneumonia alveolar and interstitial emphysema alveolitis generalized lymphodepletion Less common findings are nonsuppurative encephalitis and eosinophilic intracytoplasmic and intranuclear viral inclusion bodies in the brain and predominantly eosinophilic intracytoplasmic inclusion bodies in various organs including lungs liver kidneys pancreas intestine and brain Lymphoid depletion is marked in acute infection In two pinniped cases of morbilliviral dermatitis syncytia and eosinophilic intracytoplasmic inclusions were prominent in the epidermis follicular epithelium and sebaceous glands Diagnosis Presence of characteristic histopathological lesions immunohistochemistry PCR RTPCR ELISA Paired serum samples with increasing antibody titer Material required for laboratory analysis Fresh or fixed tissue serum Relevant diagnostic laboratories University of Georgia Marine Mammal Diagnostics Saliki Treatment Supportive Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Phocids primarily harbor seals but also gray seals Virus isolated from northern sea otters Primarily aerosolization of respiratory secretions but also possible via fecal urinary and ocular secretions via direct or indirect transmission Lethargy fever coughing dyspnea oculonasal discharge conjunctivitis keratitis diarrhea generalized body tremors and spasms neurologic signs increased buoyancy abortion inability to dive Acute to subacute Mortality is high in susceptible populations Supportive treat secondary infections Vaccination with MLV or killed canine distemper CD vaccine or subunit CD vaccine Vaccination of freeranging pinnipeds is controversial and difficult to implement effectively Virus is enzootic in arctic seals No American Association of Zoo Veterinarians Infectious Disease Manual PHOCINE DISTEMPER VIRUS Prevention and control Vaccination with canine distemper vaccine Vaccination with a subunit vaccine is practiced in European rescue centers and appears to be protective Suggested disinfectant for housing facilities No special requirementsstandard disinfection protocol Notification Not required Measures required under the Animal Disease Surveillance Plan None required Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak No special requirements Experts who may be consulted Jeremiah T Saliki jsalikiugaedu References 1 Duignan PJ O Nielsen C House KM Kovacs N Duffy G Early S Sadove DJ St Aubin BK Rima and JR Geraci 1997 Epizootiology of morbillivirus infection in harp hooded and ringed seals from the Canadian Arctic and western Atlantic J Wildl Dis 33 719 2 Duignan PJ S Sadove JT Saliki and JR Geraci 1993 Phocine distemper in harbor seals Phoca vitulina from Long Island New York J Wildl Dis 29 465469 3 Duignan PJ J T Saliki DJ St Aubin G Early S Sadove JA House K Kovacs and JR Geraci 1995 Epizootiology of morbillivirus infection in North American harbor seals Phoca vitulina and gray seals Halichoerus grypus J Wildl Dis 31 491501 4 Goldstein T JA Mazet VA Gill AM Doroff KA Burek and JA Hammond 2009 Phocine distemper virus in northern sea otters in the Pacific Ocean Alaska USA Emerg Infect Dis 15 925 927 5 Grant RJ AC Banyard T Barrett JT Saliki and CH Romero 2009 Realtime RT PCR assays for the rapid and differential detection of dolphin and porpoise morbilliviruses J Virol Meth 156 117 123 6 Härkönen T R Dietz P Reijnders J Teilmann K Harding A Hall S Brasseur U Siebert SJ Goodmand PD Jepson T Dau Rasmussen and P Thompson 2006 The 1988 and 2002 phocine distemper virus epidemics in European harbour seals Dis Aquat Organ 68 115130 7 Kennedy S 1998 Morbillivirus infections in aquatic mammals J Comp Pathol 119320125 8 Lawson B and PD Jepson eds 2004 UK phocine distemper virus epizootic investigation report 20022003 Department for Environment Food and Rural Affairs London 9 Phillip Earle JA MM Melia NV Doherty O Nielsen and S L Cosby 2011 Phocine distemper virus in seals east coast United States 2006 Emerg Infect Dis 17 215220 10 Saliki JT EJ Cooper and JP Gustavson 2002 Emerging morbillivirus infections of marine mammals development of two diagnostics approaches Ann N Y Acad Sci 96951 59 11 Stanton JB CC Brown S Poet TP Lipscomb J Saliki and S Frasca Jr 2004 Retrospective differentiation of canine distemper virus and phocine distemper virus in phocids J Wildl Dis 40 53 59 12 Taubenberger JK MM Tsai TJ Atkin TG Fanning AE Krafft RB Moeller SE Kodsi MG Mense and TP Lipscomb 2000 Molecular genetic evidence of a novel morbillivirus in a longfinned pilot whale Globicephalus melas Emerg Infect Dis 61425 13 Zarnke RL JT Saliki AP Macmillan SD Brew CE Dawson JM Ver Hoef KJ Frost and RJ Small 2006 Serologic survey for Brucella spp phocid herpesvirus1 phocid herpesvirus2 and phocine distemper virus in harbor seals from Alaska 19761999 J Wildl Dis 42 290300 American Association of Zoo Veterinarians Infectious Disease Manual PLASMODIUM Fact Sheet compiled by Dennilyn Parker updated by Gediminas Valkiûnas Sheet completed on 7 June 2011 updated 3 August 2013 Fact Sheet Reviewed by Sam Telford Jr Arnaud Van Wettere Susceptible animal groups The parasite is reported in birds of the majority of avian orders Species that have been relocated from habitats without vector or parasite or in areas where the vector or parasite have been introduced are especially vulnerable eg penguins other captive Arctic or Antarctic species species from Hawaii or other islands Infection of mammals is most common in tropical countries diversity is greatest in Africa where Plasmodium parasites have been reported in primates rodents ungulates and bats One report in wild and captive capybaras in South America has been documented Humans and nonhuman primates are infected mainly in tropical Africa Asia and South America Reptiles have been seen infected mainly in tropical countries primarily lizards some snakes and reported anecdotally in tortoises but has not been reported in turtles or crocodiles Causative organism Plasmodium spp Plasmodiidae Haemosporida 200 species Zoonotic potential No zoonotic risk exists from avian or reptilian species Although no evidence of zoonotic risk from nonhuman primate species primates can carry the same species that infect humans so reservoir exists Distribution Worldwide except Antarctica due to absence of mosquitoes and low temperature Incubation period Avian usually 57 days Clinical signs Cases in most species of adapted hosts are often of low virulence Importantly the same lineages of Plasmodium sp cause diseases of markedly different severity in different avian hosts that should be taken in consideration in conservation projects Susceptible nonadapted avian species eg penguins and some endemic Hawaiian birds present lethargy dyspnea anorexia vomiting ruffled feathers anemia where hematocrits may fall by more than 50 and regenerative hemolytic anemia is observed Biliverdinuria may occur Partial or total paralysis and convulsions can present terminally Post mortem gross or histologic findings Avian Blood and reticuloendothelial system hemolysis splenomegaly hepatomegaly and pulmonary edema Macrophages lymphocytes and plasma infiltrate in liver and spleen Exoerythrocytic meronts in endothelial cells with possible blockage of brain and lung capillaries Hemozoin pigment in Kupffer cells and splenic macrophages Primates virulence of different species and strains markedly vary in different hosts Macroscopic pathology of the brain and endocardium might show hemorrhages and the liver and spleen often are enlarged Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Reptiles birds especially penguins and some mammals including nonhuman primates and humans Mosquitoes of different genera in reptiles also other biting flies Lethargy anorexia minor to severe anemia neurologic signs paralysis Typically of low virulence in adapted hosts mild to severe possibly fatal disease in nonadapted hosts Various anti malarial drugs can be used but are unlikely to eliminate infection at tissue stage resulting in relapses of parasitemia Vector control and mosquito proof enclosures Generally no in endemic areas primates can act as a reservoir for humans American Association of Zoo Veterinarians Infectious Disease Manual PLASMODIUM Microscopic pathology usually shows sequestration of pigmented parasitized red blood cells in the vessels of the cerebrum cerebellum heart kidney and other organs The spleen and liver contains abundant pigment containing macrophages and parasitized red blood cells During acute infections the kidney often has evidence of tubular necrosis Diagnosis Identification of intracellular red blood cell parasite on a smear but difficult to detect low intensity chronic infections by microscopy gold standard Giemsa stained blood smear erythrocytic meronts and gametocytes with pigment granules PCR is more sensitive but may still not identify low level parasitemias and often does not read coinfections small subunit ribosomal ribonucleic acid and mitochondrial cytochrome b genes are definitive targets for malarial parasite ID and used to determine genetic relationships Immunoblotting can be used to ID antibiodies to Plasmodium but only to the level of parasite genus ELISA available for P relictum in penguins Material required for laboratory analysis Giemsa stained blood films microscopy and whole blood or tissue ie liver andor spleen PCR are most often used Relevant diagnostic laboratories Any laboratory performing complete blood counts is capable of diagnosis Plasmodium spp on blood smears DNA testing is not widely performed commercially at this time but is available in many research laboratories that manage wildlife parasites Treatment Avian Chloroquine phosphate primaquine phosphate pyrimethaminesulfadoxine combinations mefloquine and atovaquone proguanil hydrochloride canaries penguins raptors and wild passerines Sulfamonomethoxine suppresses parasitemia but does not protect from mortality if given after circulating parasites are present sulfachloropyrazine reduces mortality but has no effect of parasitemia Halofuginone delays parasitiemia but only minor suppression of it turkeys Mefloquine and atovaquone proguanil hydrochloride are highly efficient for blood stages but does not affect exoerythrocytic tissue stages Primates drugs which are used for human malaria treatment can be used for treatment of malaria in primates chloroquine phosphate quinine sulfate plus doxycycline or malarone and other drugs Prevention and control Housing susceptible species indoors Vector mosquito control Prophylactic treatment of highly susceptible species can be considered Vaccines development is under trial Preventive treatment for primates has not been used extensively Suggested disinfectant for housing facilities Disinfection is not appropriate for this disease Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Isolate infected animals with vector control to prevent spread to susceptible animals Conditions for restoring diseasefree status after an outbreak Difficult or impossible as wildlife acts as a reservoir Experts who may be consulted Centers for Disease Control and Prevention Center for Global Health Division of Parasitic Diseases and Malaria 1600 Clifton Road Mailstop A06 Atlanta Georgia 30333 7704887788 or 8558564713 tollfree Fax 4047184815 malariacdcgov wwwcdcgovmalaria American Association of Zoo Veterinarians Infectious Disease Manual PLASMODIUM References 1 Atkinson CT 2008 Avian malaria In Atkinson CT NJ Thomas and D B Hunter eds Parasitic Diseases of Wild Birds 1st ed WileyBlackwell Ames Iowa Pp 3553 2 Grim KC E Van der Merwe M Sullivan N Parsons T F McCutchan and M Cranfield 2003 Plasmodium juxtanucleare associated with mortality in blackfooted penguins Spheniscus demersus admitted to a rehabilitation center J Zoo Wildl Med 34 250255 3 Grim KC T McCutchan J Li M Sullivan TK Graczyk G McConkey and M Cranfield 2004 Preliminary results of an anticircum sporozoite DNA vaccine trial for protection against avian malaria in captive African blackfooted penguins Spheniscus demersus J Zoo Wildl Med 35 154161 4 Palinauskas V G Valkiūnas A Križanauskienė S Bensch and CV Bolshakov 2009 Plasmodium relictum lineage PSGS1 further observation of effects on experimentally infected passeriform birds with remarks on treatment with Malarone Exp Parasitol 123 2 134 139 5 Telford Jr SR 2009 Hemoparasites of the Reptilia CRC Press Boca Raton Florida 198 pp 6 Valkiūnas G 2005 Avian malaria parasites and other haemosporidia Boca Raton Florida 946 pp American Association of Zoo Veterinarians Infectious Disease Manual PNEUMOCOCCOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primates including humans multiple domestic and lab mammal species dolphins Aerosol direct contact Primarily respiratory neurologic and septic Asymptomatic to severe Antibiotics and symptomatic treatment Vaccine is available for humans No vaccines have been used routinely for animals Prevent contact with sick animals or people Theoretical Fact Sheet compiled by Ellen Wiedner Sheet completed on 3 August 2011 updated 18 September 2013 Fact Sheet Reviewed by Jim Wellehan Ramiro Isaza Steve Unwin Susceptible animal groups Humans multiple nonhuman primate species both wild and captive dogs cats rats mice guinea pigs cattle horses dolphins Causative organism Streptococcus pneumonia is an alphahemolytic strep encapsulated facultative anaerobe optochin sensitive and bile soluble with more than 90 serotypes Zoonotic potential This risk is theoretical but unproven Animals have developed disease both from human serotypes as well as animalspecific serotypes One report documented in a human included several clinically ill house pets with S pneumoniae Suspected reverse zoonosis from a keeper to zoo chimpanzees have occurred Distribution Worldwide Incubation period Carrier status confirmed With asymptomatic but infective carriers it is unknown in animals how long carrier state lasts Clinical disease can occur within 96 hours of exposure Clinical signs Pneumonia meningitis sepsis conjunctivitis sinusitis otitis media other respiratory disease polyarthritis endocarditis pericarditis and sudden death Clinical disease often more severe with a viral coinfection Post mortem gross or histologic findings Fibrinous bronchopneumonia pericarditis necrotizing cerebral vasculitis Diagnosis Bacterial identification of isolates using DNA sequencing latex agglutination tests and others Positive Gram staining of respiratory samples with lancetshaped diplococci Serotyping recommended Material required for laboratory analysis Respiratory secretions CSF or blood If immediate 1hr transport to laboratory is not possible samples should be inoculated into growth media and kept cool The laboratory should be consulted first about appropriate media Relevant diagnostic laboratories Any laboratory that performs cultures and sensitivities on a routine basis can complete testing for this organism PCR testing can be found at many major commercial and veterinary diagnostic laboratories Streptococcus Laboratory Centers for Disease Control and Prevention 1600 Clifton Rd American Association of Zoo Veterinarians Infectious Disease Manual PNEUMOCOCCOSIS Atlanta GA 30333 4046391237 Treatment Historically penicillins were recommended However severe multidrug resistance reported in many serotypes to betalactam fluoroquinolone and macrolide antibiotics so culture and sensitivity should be collected and submitted prior to treatment Prevention and control Vaccination programs for humans have decreased rates of S pneumoniae severe and fatal disease cases No vaccines have been tested in animal species Prevention of contact with infected animals and good hygiene is recommended in zoos and similar animal facilities If vaccination considered bacterial typing required before vaccination to confirm polyvalent vaccine applicable Suggested disinfectant for housing facilities The bacteria is susceptible to many disinfectants 70 ethanol 2 glutaradehyde 1 sodium hypochlorite and others However it can live in sputum at room temperature for one week and in dust particles for up to 25 days Notification The disease is reportable nationally CDC and several states currently conducting surveillance of resistant strains Measures required under the Animal Disease Surveillance Plan None at this time Measures required for introducing animals to infected animal Do not introduce new animals to an infected animal Conditions for restoring diseasefree status after an outbreak In human nursing homes vaccination and treatment of close contacts with prophylactic antibiotics is done However no studies on this approach have been documented in animals Experts who may be consulted Streptococcus Laboratory Centers for Disease Control and Prevention 1600 Clifton Rd Atlanta GA 30333 4046391237 Fabian Leendertz Robert Koch Institute Postbox 650280 D13302 Berlin Germany Nordufer 20 13353 Berlin Germany 49 030 187542592 leendertzfrkide References 1 Adam D 2009 Issues in pneumococcal disease and pneumococcal conjugate vaccines Highlights of the 27th meeting of ESPID Brussels Belgium June 913 2009 Vaccine 27 71337137 2 Chi F M Leider F Leendertz C Bergmann C BoeschS Schenk G Pauli H Ellerbrok and R Hakenbeck 2007 New Streptococcus pneumoniae clones in deceased wild chimpanzees J Bact 18916 60856088 3 Dagan R 2009 New insights on pneumococcal disease what we have learned over the past decade Vaccine 275 C3C5 4 GAO 2004 Emerging infectious diseases Review of state and federal disease surveillance efforts U S G A Office httpwwwgaogovnewitemsd04877pdf Accessed 23 July 2013 5 Haber M A Barskey W Baughman L Barker CG Whitney KM Shaw W Orenstein and DS Stephens 2007 Herd immunity and pneumococcal conjugate vaccine a quantitative model American Association of Zoo Veterinarians Infectious Disease Manual PNEUMOCOCCOSIS Vaccine 25 53905398 6 Hicks L A D L Monnet and RM Roberts 2010 Increase in Pneumococcus macrolide resistance USA Emerg Infect Dis 165 896897 7 Jenkins T C J Sakai BC Knepper CJ Swartwood JS Haukoos LA Long CS Price and WJ Burman 2012 Risk factors for drugresistant Streptococcus pneumonia and antibiotic prescribing practices in outpatient communityacquired pneumonia Acad Emerg Med 196 703 706 8 McCullers J A J L McAuley S Browall AR Iverson KL Boyd and B Henriques Normark 2010 Influenza enhances susceptibility to natural acquisition of and disease due to Streptococcus pneumoniae in ferrets J Inf Dis 2028 12871295 9 Office of Laboratory Security Public Health Agency of Canada 2011 Streptococcus pneumoniae Material Safety Data Sheets MSDS DOIhttpwwwphacaspcgccalabbiorespsds ftssstreptococcuspneumoniaeengphp Accessed 23 July 2013 10 Reinert R R M R Jacobs and SL Kaplan 2010 Pneumococcal disease caused by serotype 19A review of the literature and implications for future vaccine development Vaccine 28 4249 4259 11 Solleveld HA MJ van Zwieten PJ Heidt and PM van Eerd 1984 Clinicopathologic study of six cases of meningitis and meningoencephalitis in chimpanzees Lab Anim Sci 341 8690 12 Unwin S J Chatterton and J Chantrey 2013 Management of severe respiratory tract disease caused by human respiratory syncytial virus and Streptococcus pneumoniae in captive chimpanzees Pan troglodytes J Zoo Wildl Med 441 105115 13 Van der Linden M A AlLahham W Nicklas and R R Reinert 2009 Molecular Characterization of Pneumococcal Isolates from Pets and Laboratory Animals PLoS ONE 4 httpwwwplosoneorgarticleinfo3Adoi2F1013712Fjournalpone0008286 Accessed 23 July 2013 American Association of Zoo Veterinarians Infectious Disease Manual PNEUMOCYSTIS Fact Sheet compiled by Brenda Tesini and Zachary Hoy Sheet completed on 3 June 2011 updated 10 September 2013 Fact Sheet Reviewed by Francis Gigliotti Remo Lobetti Susceptible animal groups Humans primates and numerous mammalian species The organism is presumed to be ubiquitous in the environment Serological evidence shows that most healthy children have had exposure to the organism by 4 years of age Studies screening numerous zoological wildlife and laboratory mammalian species have also shown a high prevalence of exposure to the organism The organism proliferates in the lungs of host species with compromised immune systems Studies have found an absence of the organism in animals with body temperatures below 35oC and above 41oC Studies conducted in birds reptiles amphibians and fish have not identified the organism Causative organism Human derived Pneumocystis jirovecii formally known as P carinii Multiple other mammalian hostspecific species exist For example P carinii in the rat and P murina in the mouse The organism was previously thought to be a protozoan but in 1988 through DNA analysis it was determined to be a yeastlike fungus It is unusual when compared to other fungi in that the cell membrane lacks ergosterol and currently is unable to be grown in culture Genomic and phenotypic differences exist between the organisms that infect different mammalian species indicating that the organisms are hostspecies specific Zoonotic potential Pneumocystis organisms infecting each mammalian species are host specific No animal reservoir for P jiroveci has been identified and no animal strains have been identified as human pathogens Distribution Worldwide in humans and animals Incubation period 3 to 12 weeks but unclear if this includes carriage time in healthy individuals as compared to immunocompromised hosts Clinical signs Immunocompetent individuals are most often asymptomatic Immunodeficient individuals develop Pneumocystis pneumonia PcP a chronic progressive pneumonia The most common clinical signs include dyspnea an unproductive cough cyanosis pyrexia and weight loss Severe cases can lead to respiratory failure and death Extrapulmonary lesions occur in a minority 3 of patients involving most frequently the lymph nodes spleen liver and bone marrow The organisms reside in the alveoli and stimulate both a humoral and cellular immune response The hosts inflammatory response leads to alveolar damage impaired gas exchange and decreased respiratory function which results in the common clinical signs of this disease Post mortem gross or histologic findings Lungs show evidence of interstitial pneumonia Grossly the lungs will be edematous and heavy They will have a pale gray or tan granular firm consolidated cut surface Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Humans nonhuman primates and numerous mammalian species especially immune compromised individuals Aerosol transmission environmental exposure or direct contact with infected individuals Dyspnea dry cough cyanosis pyrexia weight loss Can be fatal in immuno compromised individuals Trimethoprim sulfa methoxazole TMPSMX is the drug of choice Prophylactic treatment with TMP SMX No as human strain is believed to be host specific American Association of Zoo Veterinarians Infectious Disease Manual PNEUMOCYSTIS Histological examination of lung tissue often reveals a foamy eosinophilic exudate within the alveolar spaces and interstital fibrosis of the alveolar septa Basophilic dots within the exudate represent the Pneumocystis cysts With special stains the cysts can be identified as ovoid bodies Additional stains can also be used to identify isolated trophozoites The organism can be specifically identified using immunohistochemistry immunofluorescense and PCR assay Studies have also identified the organism in a large percentage of asymptomatic infants on postmortem Diagnosis Specific diagnosis is by the recovery and identification of the organism in samples obtained through transtracheal aspirate TTA bronchoalveolar lavage BAL induced sputum or lung tissue obtained through biopsy or necropsy Identification of the organism via PCR assay immunohistochemistry immunofluorescence or special stains that stain the cyst wall of the organism Gomoris methanamine silver GMS toluidine blue O or those that stain the nuclei of the trophozoites and sporozoites Geimsa Wright DiffQuick polychrome methylene blue and Grams stain Material required for laboratory analysis Bronchopulmonary secretions obtained via TTA BAL or induced sputum Lung tissue obtained via biopsy or necropsy Relevant diagnostic laboratories Laboratories with the capability to perform nested PCR assay are used to identify the organism Immunohistochemical methods require the host speciesspecific monoclonal antibody used to identify the organism to avoid false negative results Identification of the organism using special stains requires reviewer expertise Treatment Since the organism lacks ergosterol common antifungal treatments are not effective Trimethoprimsulfamethoxazole TMPSMX is the drug of choice for both the treatment of infection and prophylaxis Alternative drugs used for the treatment of infection include pentamidine trimethoprim plus dapsone atovaquone and primaquine plus clindamycin Alternative drugs used for prophylaxis include dapsone dapsone plus pyrimethamine pentamidine and atovaquone Recurrence is common if the immunosuppressive condition of the host persists Prevention and control Avoidance of the organism is impractical since the natural reservoir is unknown and the organism is presumed to be ubiquitous in the environment TMPSMX or other chemoprophylaxis can be used as a preventative treatment in susceptible individuals Suggested disinfectant for housing facilities A study found the following chemical disinfectants to be effective in the inactivation of Pneumosytis cysts 70 ethyl alcohol 10 iodoform 1 quaternary ammonium salts 3 hydrogen peroxide sodium chlorite and 1 cresol soap Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Prevent exposure of healthy animals to animals exhibiting clinical signs of pneumocytosis Conditions for restoring diseasefree status after an outbreak This approach may not be possible since a large percentage of humans and other mammalian species harbor this organism while remaining asymptomatic Testing can be used to screen individuals for the presence of the organism Serological screening is not effective since a large percentage of humans and other mammalian species are shown to have had exposure to the organism Sterilization of any air filters in the area of the outbreak is an important measure to reduce the number of cysts in the environment Disinfecting the area of the outbreak with appropriate disinfectants will help to inactivate any remaining cysts Experts who may be consulted Brenda L Tesini MD University of Rochester Medical Center Department of Pediatrics Infectious Diseases American Association of Zoo Veterinarians Infectious Disease Manual PNEUMOCYSTIS Rochester New York USA BrendaTesiniURMCRochesteredu Zachary Hoy MD University of Rochester Medical Center Department of Pediatrics Infectious Diseases Rochester New York USA Zacharyhoyurmcrochesteredu Francis Gigliotti MD University of Rochester Medical Center Department of Pediatrics Infectious Diseases Rochester New York USA FrancisGigliottiURMCRochesteredu References 1 httpdpdcdcgovdpdxHTMLpneumocystishtm Accessed 16 September 2013 2 Armstrong MYK and MT Cushion 1994 Animal models In Walzer PD ed Pneumocystis carinii Pneumonia 2nd ed Marcel Dekker Inc New York New York Pp 181203 3 Cailliex JC N Seguy CM Denis EM Aliouat E Mazars L Polonelli D Camus and E Dei Cas 1996 Pneumocystis carinii an atypical fungal microorganism J Med Vet Mycol 344 227 239 4 DeiCas E M BrunPascaud V BilleHansen A Allaert and EM Aliouat 1998 Animal models of pneumocystosis FEMS Immunol Med Microbiol 2212 163168 5 Demanche C M Berthelemy T Petit B Polack AE Wakefield E DeiCas and J Guillot 2001 Phylogeny of Pneumocystis carinii from 18 primate species confirms host specificity and suggests coevolution J Clin Microbiol 396 21262133 6 Edman JC JA Kovacs H Masur DV Santi HJ Elwood and ML Sogin 1988 Ribosomal RNA sequence shows Pneumocystis carinii to be a member of the fungi Nature 3346182 519522 7 Haque AK and PA Adegboyega 2008 Pneumocystis jiroveci pneumonia In Tomashefski JF ed Dail and Hammars Pulmonary Pathology Volume I Nonneoplastic lung disease 3rd ed Springer New York New York Pp 487514 8 Joffrion TM and MT Cushion 2010 Sterol biosynthesis and sterol uptake in the fungal pathogen Pneumocystis carinii FEMS Microbiol Lett 3111 19 9 Kaneshiro ES and JN Maiorano 1996 Survival and infectivity of Pneumocystis carinii outside the mammalian host J Eukaryot Microbiol 435 35S 10 Kuramochi T K Hioki and M Ito 1997 Pneumocystis carinii cysts are susceptible to inactivation by chemical disinfectants Exp Anim 46 3 241245 11 Laakkonen J 1998 Pneumocystis carinii in wildlife Int J Parasitol 282 241252 12 Poelma FG 1975 Pneumocystis carinii infections in zoo animals Z Parasitenkd 46 6168 13 Ponce C A M Gallo R Bustamante and SL Vargas 2010 Pneumocystis colonization is highly prevalent in the autopsied lungs of the general population Clin Infect Dis 503 347353 14 Sakura A AK Jarvnen M Olsson M Karkkainen and T Ilvesniemi 1996 Pneumocystis carinii pneumonia in dogs a diagnostic challenge J Vet Diagn Invest 81 124130 15 Settnes OP PB Nielsen R Bucala MJ Linke and MT Cushion 1994 A survey of birds in Denmark for the presence of Pneumocystis carinii Avian Dis 381 110 16 Stringer JR Beard CB Miller RF and Wakefield AE 2002 A new name for Pneumocystis American Association of Zoo Veterinarians Infectious Disease Manual PNEUMOCYSTIS from humans and new perspectives on the hostpathogen relationship Emerg Infect Dis 89 891 896 American Association of Zoo Veterinarians Infectious Disease Manual POLIOVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Humans non human primates Fecaloral and respiratory routes Rapidly spread through feces contaminated food and water sources Range from asymptomatic to paresis and death Most severe clinical signs include permanent flaccid paralysis of one or more limbs or muscle groups Paralysis of respiratory muscles can lead to death Symptomatic supportive care based on clinical presentation No effective antiviral medications currently advocated Vaccination used extensively in humans To control spread of infection use isolation standard cleaning and disinfection methods and PPE Yes and humans are the primary reservoir Fact Sheet compiled by Wynona C Shellabarger Sheet completed on 8 August 2011 updated on 30 August 2018 Fact Sheet Reviewed by Jennifer DAgostino Susceptible animal groups Humans and nonhuman primates are affected although cases in NHPs are rare with great apes in particular chimps most frequently reported in literature Macaques and chimpanzees assisted in vaccine development in early 1950s1960s Causative organism Poliovirus types 1 2 and 3 family Picornaviridae subgroup Enteroviridae Zoonotic potential Yes humans are the primary reservoir Distribution Historically the disease was present worldwide Western Hemisphere declared free of indigenous poliovirus since September 1991 and the last case of endemic polio in the US was in 1979 This status was achieved through the global efforts of WHO UNICEF and an international contingent spearheading the Global Polio Eradication Initiative GPEI and widespread use of vaccines in humans Global eradication is still an active goal of these organizations and incidence and transmission have continued to dramatically decline with continued use and distribution of vaccine Currently three countries maintain an endemic status Afghanistan Nigeria and Pakistan an additional four African countries have continued incidence of importedwild type polio Incubation period Differs depending on type of polio but ranges from 3 to 35 days Nonparalytic disease has incubation period of 3 to 6 days paralytic disease has incubation period of 7 to 21 days Virus can be shed in the feces for 3 to 6 weeks post exposure or after vaccination with oral polio vaccine OPV Clinical signs Although flaccid paralysis is the most noteworthy and potentially severe of the clinical signs described poliovirus infection in humans can be highly variable and clinical signs are categorized based on presentation The majority of human infections are asymptomatic 72 About 24 of infections result in minor disease including those of the upper respiratory tract gastrointestinal disturbances and flulike signs with associated fever and muscle aches In 12 of cases signs are more severe including meningitis muscle weakness or flaccid paralysis of a single limb to quadriplegia and respiratory failure with 01 of all reported polio cases resulting in the paralytic form in humans Death occurs but rarely at 25 in children and 1530 in adults that contract the paralytic form of this disease A postpolio syndrome may occur in 25 to 40 of human cases as well which develops decades after the initial infection Although rare poliovirus infection has been described in chimpanzees orangutans gorillas macaques and colobus monkeys in human care laboratory and wild settings and manifests with similar clinical signs to those of human infections Postmortem gross or histological findings Most severe lesions are associated with paralytic disease and include muscle wasting inflammation demyelination apoptosis destruction of interior horn cells of spinal cord brain stem andor lower motor neurons Diagnosis Culture intratypic differentiation genome sequencing and serology are used for poliovirus American Association of Zoo Veterinarians Infectious Disease Manual POLIOVIRUS testing Viral detection via cell culture or PCR of throat fecal or occasionally CSF cultures may be positive within the first week of illness in humans Realtime reverse transcription PCR is used to distinguish wild strain from vaccine induced strain from cell culture isolates Retrospectively serologic titers can be used to confirm diagnosis since IgM and IgG titers may take weeks to develop and become detectable Material required for laboratory analysis Diagnostic samples include pharyngeal swabs feces CSF fluids urine and serum Contact local and state public health and epidemiology officials for specific NHP sample submissions and guidance Relevant diagnostic laboratories Diagnosis isolation and characterization of polioviruses from submitted human samples are coordinated by Center for Disease Control Global Polio Laboratory NetworkPolio and Picornavirus Laboratory Division of Viral Diseases 1600 Clifton Rd Atlanta GA 303294027 USA 800CDCINFO 8002324636 TTY 8882326348 EmailCDCINFO 404 6392749 Fax 404 6394011 wwwcdcgov Treatment Symptomatic treatment is based on severity of clinical signs including pain relief and physical therapy Mechanical ventilation used in humans with permanent respiratory muscle paralysis Prevention and control Infected animals should be isolated and standard disinfection measures used with personnel protective equipment to minimize exposure to humans or other animals Vaccines are used extensively in humans to prevent disease and vaccine use has reduced incidence of disease worldwide by 99 Inactivated IPV and oral polio OPV vaccines are currently available for human use but since 2000 only IPV has been used in the US to minimize vaccineassociated paralytic polio VAPP incidence The World Health Organization recommends that all children be fully vaccinated Current recommendations for childhood coverage are a series of 4 IPV vaccines at 2 4 618 months and 4 6 years of age Naïve adult vaccine recommendations and vaccine information for travelers to endemic countries are also available through the CDC website OPV is still used in a number of other countries Routine polio vaccination with OPV or IPV of great apes in human care has been recommended historically but is currently at the discretion of the animals holding facility Risk of exposure is low due to human vaccine eradication efforts Type and schedule of vaccination in NHPs is extrapolated from human ACIP recommendations and vaccines available Suggested disinfectant for housing facilities Poliovirus is known to be susceptible to heat chlorine formaldehyde and UV light Standard disinfection using a dilute bleach solution or one of the above products should be adequate Removal of feces and bodily fluids before disinfection is required for effective disinfection Notification If polio is suspected veterinarians should work closely with local and state public health officials and epidemiologists Contact CDC directly if local or state authorities are not available Measures required under the Animal Disease Surveillance Plan Currently no measures are required However polio is epidemiologically important to monitor due to extensive worldwide eradication efforts in the human population Measures required for introducing animals to infected animal Maintain potentially infected animals in isolation and quarantine conditions until presentation is resolved Vaccination of conspecific naïve NHPs should be considered Conditions for restoring diseasefree status after an outbreak Minimize fecal contamination and clean and disinfect potentially contaminated areas thoroughly for at least 36 weeks post infection and vaccination series Source of infection should be determined and NHP staff vaccination history should be reviewed and updated if necessary American Association of Zoo Veterinarians Infectious Disease Manual POLIOVIRUS Experts who may be consulted Center for Disease Control Global Polio Laboratory NetworkPolio and Picornavirus Laboratory Division of Viral Diseases 1600 Clifton Rd Atlanta GA 303294027 USA 800CDCINFO 8002324636 TTY 8882326348 EmailCDCINFO 404 6392749 Fax 404 6394011 wwwcdcgov References 1 AZA Ape TAG 2010 Preventative Medicine In Chimpanzee Pan troglodytes Care Manual Association of Zoos and Aquariums Silver Spring MD 20096653841 2 AZA Gorilla Species Survival Plan 2017 Preventative Medicine In Gorilla Gorilla gorilla gorilla Care Manual Association of Zoos and Aquariums Silver Spring MD 2016 774 5659 3 Centers for Disease Control and Prevention Internet Epidemiology of VaccinePreventable Diseases Polio c20152018 cited 2018 August 29 Available from httpswwwcdcgovvaccinespubspinkbookpoliohtml 4 Centers for Disease Control and Prevention Internet Morbidity and Mortality Weekly Report MMWR Polio Reports c20122019 cited 2018 August 29 Available from httpswwwcdcgovmmwrpolioreportshtml 5 Centers for Disease Control and Prevention Internet Travelers Health Polio c20132018 cited 2018 August 29 Available from httpswwwnccdcgovtraveldiseasespoliomyelitis 6 Centers for Disease Control and Prevention Internet Updates on CDCs Polio Eradication Efforts 2016 cited 2018 August 29 Available from httpswwwcdcgovpolioupdates 7 Centers for Disease Control and Prevention Internet Vaccine Recommendations and Guidelines of the ACIP Polio ACIP Vaccine Recommendations 2014 cited 2018 August 29 Available from httpswwwcdcgovvaccineshcpaciprecsvaccspecificpoliohtml 8 Douglas JD Spoike KF Raynor J The incidence of poliovirus in chimpanzees Pan troglodytes Lab Anim Care 197020265268 9 Global Polio Eradication Initiative Internet Global Polio Eradication Initiative cited 2018 August 29 Available from httppolioeradicationorg 10 The Global Polio Eradication Initiative Stop Transmission of Polio STOP Program 19992013 MMWR Morb Mortal Wkly Rep 20136224501503 11 Guilloud NV Allmond BW Froeschle JE Fitzgerald FL Paralytic poliomyelitis in laboratory animals J Am Vet Med Assoc 196915511901193 12 Mugisha L Pauli G OpudaAsibo J Joseph O Leendertz F Diedrich S Evaluation of poliovirus antibody titers in orally vaccinated semicaptive chimpanzees in Uganda J Med Primatol 2010392123128 13 OttJoslin JE Zoonotic diseases of nonhuman primates In Fowler ME ed Zoo and Wild Animal Medicine Volume 3 Current Therapy Philadelphia PA WB Saunders Co 1993 p 358373 14 Seibil VB Malyshkina LP Khishtova SN Lesnikova MV Baryshnikova AS Konopleva TN Mnozhina EG Agafonova TV and Vladimirova LA State of collective immunity against poliomyelitis in some regions of Russia Zh Mikrobiol Epidemiol Immunobiol 201325664 American Association of Zoo Veterinarians Infectious Disease Manual PSITTACINE BEAK AND FEATHER DISEASE Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Psittacines Old World more than New World species Direct contact with infected animals with virus presented by inhalation or ingestion Indirect contact with contaminated excretions secretions and feather dust Virus remains in contaminated environments particularly air handling systems for years Peracute Particularly common in African grey parrots with pancytopenia and death Acute Depression followed by appearance of dystrophic feathers and death Chronic Progressive appearance of dystrophic feathers Necrotic beak and ulcerations in some long term infected birds Death occurs in months to years Aggressive disease most common in African grey vasa and eclectus parrots and cockatoos PCV1 associated disease is fatal in most Old World psittacines Chronic and less severe disease in lovebirds lories and lorikeets particularly those birds infected with PCV2 Supportive care should be provided in isolated environments where even caretakers have no contact with other birds Prevention PCRbased testing has reduced spread in managed populations Developed vaccine has reached government al approval stage Control Testing and isolation of infected birds strict entry quarantine protocols None known Fact Sheet compiled by Branson W Ritchie Sheet completed on 15 November 2011 updated 19 August 2013 Fact Sheet Reviewed by Thomas N Tully Lauren V Powers Susceptible animal groups All psittacines are susceptible to infection Most New World species develop a rapid immune response and clear the virus although classic disease has been documented in some New World species ie macaws and Amazon parrots Classic disease associated with PCV1 can occur in any Old World psittacine but is most common in cockatoos African grey parrots ringnecked parakeets and eclectus parrots PCV2 causes less severe disease and affected birds may recover from disease infections with this pathotype are most common in lories and lorikeets Lovebirds may be infected with PCV1 alone or with both PCV1 and PCV2 Disease progression appears to vary in lovebirds infected with both pathotypes Causative organism Psittacine circovirus a nonenveloped icosahedral DNA virus belonging to the family Circoviridae Two pathotypes PCV1 and PCV2 must be distinguished for accurate prognosis and patient management Circovirus infections have also been documented in Anseriformes Columbiformes Passeriformes Galliformes and gulls Zoonotic potential No known human transmission has occurred American Association of Zoo Veterinarians Infectious Disease Manual PSITTACINE BEAK AND FEATHER DISEASE Distribution Virus likely evolved in Australia and has been disseminated globally through transcontinental movement of infected birds Virus could be found on any continent with a sufficient population of freeranging or captive psittacine birds to support virus survival and transmission Virus will continue to spread in untested or until available unvaccinated psittacine birds Incubation period Experimentally signs appear in 34 weeks However variation in disease progression can make the incubation period appear longer Clinical signs Most birds infected with PCV1 develop a transient infection that can be detected by finding viral DNA in whole blood Most infected birds subsequently respond with an appropriate immune response and clear the virus with no recognizable clinical changes In unmanaged untested populations infection should be considered relatively common while disease is comparatively uncommon PeracuteAcute Form These forms most commonly occur in young chicks and may begin with signs unrelated to the beak or feathers Affected birds are often depressed and regurgitate due to crop stasis They may develop a diarrheacausing enteritis or pneumonia and die without displaying any lesions of the feathers or beak This peracute form of the disease is particularly common in African grey parrots that frequently die with acute hepatic necrosis In the acute form feather abnormalities in already developed feathers from causes other than PCV should be distinguished from abnormalities associated with the developing feather from the pulp cap to the feather base Visible developmental feather abnormalities include retention of the feather sheath hemorrhage of the pulp cavity shortened deformed feathers and circumferential constrictions at the feather base Stress lines are common in affected feathers Affected feathers are often loose break easily may bleed and elicit a pain response with minimal manipulation Some chicks die within days to weeks of the first signs of feather abnormalities and others survive with progression to chronic disease Chronic Form Newly developing powder down and contour feathers are the first to show clinical changes in birds that exhibit feather abnormalities after their remiges and rectrices are developed The visible changes in these feathers are similar to those described above In psittacines other than lovebirds feather lesions associated with PCV1 become progressively worse with each successive molt and if the bird survives for years it may become mostly or completely featherless as feather follicle damage prevents replacement In some affected birds beak abnormalities may occur that typically start as a brownish necrotic area on the inside of rhinotheca Affected beaks may elongate becoming progressively deformed and fracture Secondary beak and oral infections are common in necrotic areas of the beak Some affected birds may develop beak elongation in the absence of necrosis In some birds the nails can also be deformed or slough Birds with the chronic form of the disease may live for months to years Progressive disease is associated with organopathies that are likely associated with immune suppression and birds usually die from secondary bacterial fungal parasitic or other viral infections Birds with PBFD shed substantial quantities of extremely environmentally stable virus in their feather dander and should not be maintained in environments aviaries or hospitals or by care takers that have direct or indirect contact with other birds Recovery of Old World psittacines with the chronic disease associated with PCV1 has not been documented Comparatively PCV2 appears clinically less virulent and lories and lorikeets with moderate feather abnormalities have been shown to recover as indicated by a return to normal feather plumage and no detectable viral DNA in their blood The PCV2 pathotype has only been documented as a monotypic infection in lories and lorikeets Comparatively other psittacines particularly lovebirds have been documented with both PCV1 and PCV2 and the role that coinfection may play in altering the virulence of PCV1 and thus the progression of classic disease is unknown Post mortem gross or histologic findings Gross feather and less often beak changes described above are associated with the circovirus infection In chronic cases other lesions related to the secondary infections that actually lead to the birds death will be found at necropsy American Association of Zoo Veterinarians Infectious Disease Manual PSITTACINE BEAK AND FEATHER DISEASE Predominant histological lesions include necrosis and ballooning degeneration of epithelial cells in the epidermal collar and epidermal basal and intermediate zones of the developing feather shaft The follicular epithelium also may be necrotic but this lesion is reported less commonly Feather sheath hyperkeratosis prevents the feather from exsheathing resulting in retention of the feather sheath Feather pulp lesions are characterized by suppurative inflammation including perivascular accumulations of heterophils plasma cells macrophages and rarely lymphocytes The characteristic basophilic intracytoplasmic and less commonly intranuclear inclusions are usually but not always present in diseased feathers Granulomatous dermatitis with vesicle formation was described in a group of infected lovebirds Histologic lesions in the beak of PBFD birds are similar to those described in their feathers including necrosis and hyperplasia of epithelial cells in the basal and intermediate epithelial layers Hyperkeratosis and separation of the cornified outer layer from the underlying tissues and bone may also be evident and are often accompanied by secondary necrosis and osteitis of associated tissues In peracute cases histologic lesions may be limited to severe bursal or thymic necrosis with the presence of viral inclusion bodies Feather pathology in these cases may not occur or may be limited to edema in the follicular epithelium if present In birds with beak disease necrosis and inflammation of the epithelial lining of the tongue beak cavity and crop have also been reported Secondary Gramnegative bacteria and fungi are commonly isolated from beak lesions and may be associated with acute or chronic inflammatory reactions Diagnosis PBFD should be considered in any bird presenting abnormal feather loss or developmental abnormalities PBFD can only be diagnosed by detection of the virus using in situ hybridization immunohistochemistry or electron microscopy to document the virus or viral components in diseased tissues For antemortem diagnosis a biopsy of 34 diseased feathers and their associated follicle is recommended It is critical for the clinician to biopsy diseased feathers Both diseased and normal feathers can be present directly next to each other and failure to obtain a biopsy of diseased feathers can result in an inaccurate diagnosis Birds with the peracute and early acute forms of the disease may die before the development of feather abnormalities and disease is documented by histopathologic evaluation of internal organs including the bursa thymus and liver PCRbased testing can be used to detect target segments of viral DNA in the blood of suspect birds before feather abnormalities develop but this condition does not confirm the presence of disease Most birds infected with PCV develop a transient infection that can be detected by finding viral DNA in whole blood Most infected birds subsequently respond with an appropriate immune response and clear the virus with no recognizable clinical changes A bird that is PCR positive for PCV1 and does not have dystrophic feathers must be retested in 90 days to determine if the bird has cleared the virus It is important that birds be maintained in a virus free environment during this 90 day period The author has placed vaccinated protected birds in the same room with PBFD positive birds and viral DNA can be intermittently detected in the vaccinated birds because of persistent environmental exposure to the virus and the subsequent clearing of the virus through the blood that is necessary for any inhaled or ingested virus A bird that is PCR positive for PCV2 and does not have dystrophic feathers must be retested in 180 days to determine if the bird has cleared the virus Lories with PCV2 and with dystrophic feathers have been documented to recover from disease but should be maintained in strict isolation during any convalescent period Virus is being shed in the dystrophic feathers until they are replaced even though viral DNA can no longer be detected in the blood For the most current recommendations on testing and interpretation of PCRbased assays see wwwvetugaeduSAMSIDL Material required for laboratory analysis Biopsy of dystrophic feathers and their associated follicle in formalin for histologic diagnosis Whole blood collected by venipuncture Blood samples collected by toe nail American Association of Zoo Veterinarians Infectious Disease Manual PSITTACINE BEAK AND FEATHER DISEASE clipping should be considered environmental samples and not a bird specific sample Feathers submitted for PCRbased testing should also be considered environmental samples and are not bird specific Viral DNA can be detected by PCRbased testing in environmental swabs These can be used to document the extent of environmental contamination air filters fan motors nest boxes etc and for evaluating cleaning efforts following an outbreak Postmortem samples include bursa thymus liver spleen kidney and dystrophic feathers if present in formalin Swabs of tissues collected from the cut surface of the bursa thymus or liver can be used for rapid detection of viral DNA Only disposable scalpel blades should be used for collecting postmortem samples or swab may be positive because of transfer to the cut surface of the organ from viral contaminated instruments Prior to shipping blood samples should be stored refrigerated 4oC392oF Samples must be shipped in a padded envelope or box In cooler seasons samples may be sent by regular mail but overnight is recommended For the most current recommendations on sample submission see wwwvetugaedu SAMSIDL Relevant diagnostic laboratories Infectious Disease Laboratory College of Veterinary Medicine University of Georgia 110 Riverbend Rd Riverbend North Room 150 Athens GA 306027390 706 5428092 Fax 706 5830843 wwwvetugaeduSAMSidl Treatment No known specific antiviral treatment Prevention and control Transmission of the virus is primarily through inhalation or ingestion of air or food containing viral contaminated feather or fecal dust Contaminated clothing hair and body surfaces of care takers can also serve to disseminate the virus as can contaminated bird carriers feeding utensils nest boxes and nesting materials Two of the most severe modern post PCRbased testing outbreaks the author investigated were associated with use of a contaminated grinder for nail grooming and the sale of a contaminated egg incubator Maternal transmission has been documented The virus is extremely environmentally stable and for the safety of birds any contaminated environment should always be considered a source of infectious virus Any diseased birds should be maintained in strict isolation and the care takers of these birds should always be considered contaminated with the virus Maintain strict quarantine and testing protocols for new birds prior to entering the collection PCRbased testing should be used during entry quarantine to detect viral DNA in the blood See the recommendations above for testing procedures and interpretation Because of the difficulty in decontaminating a typical clinic it is not recommended that known diseased birds by evaluated or maintained in the hospital PCRbased testing of environmental swabs can be used to document the severity of viral contamination in the environment A PCV vaccine has been developed by the Emerging Diseases Research Group at the University of Georgia and the vaccine awaits a USDA approved manufacturer to take the necessary steps to register the vaccine for commercial use Suggested disinfectant for housing facilities While specific data on the susceptibility of PCV to disinfectants is unknown it is known that other circovirus are among the most environmentally stable and disinfectant resistant of all viruses The goal in a contaminated facility is to wash the virus out of the environment expose contaminated surfaces to prolong drying and direct sunlight and then seal any remaining virus to a substrate American Association of Zoo Veterinarians Infectious Disease Manual PSITTACINE BEAK AND FEATHER DISEASE with paint or equivalent Any contaminated surface that is porous not made of metal or plastic should be discarded All metal concrete and plastic surfaces should be washed with a sodium hypochlorite eg Clorox containing detergent rinsed and allowed to dry in direct sunlight The procedure should be repeated 34 times Air handling systems should be professionally cleaned by a company experienced with decontaminating hospital air systems Once repeated cleaning has been accomplished a pressure painter should be used to coat all remaining surfaces floor walls and ceiling If a diseased bird has been maintained in an incubator one should make certain that the fan and motor housing are decontaminated and PCR negative for viral DNA before the fan is returned to service PCRbased testing can be used to evaluate the success for virus removal from the environment Notification Not needed Measures required under the Animal Disease Surveillance Plan Not applicable Measures required for introducing animals to infected animal It is not recommended to mix infected and noninfected birds Conditions for restoring diseasefree status after an outbreak Remove any birds with feather dystrophy and maintain in isolation while conducting additional diagnostic testing Remove birds without feather dystrophy from any potentially contaminated environment wash the birds if feasible and wait 90 days one could also blood test these birds for the presence of viral DNA immediately but many will be blood positive and clear the virus Waiting 90 days with the birds in a noncontaminated environment will reduce the number of birds that require additional testing Follow the current testing recommendations based on the detected pathotype provided at wwwvetugaeduSAMSIDL PCRbased testing of environmental samples collected during and after the cleaning and decontaminated process as detailed above Experts who may be consulted Branson W Ritchie DVM PhD Diplomate ABVP and ECZM University of Georgia College of Veterinary Medicine 706 2067931 britchieugaedu Chris Gregory DVM PhD Emerging Diseases Research Group University of Georgia 7065830742 crgugaedu References 1 httpwwwvetugaeduSAMSidl Accessed 26 August 2013 2 Khalesi B 2007 Studies of beak and feather disease virus infection Doctoral dissertation httpresearchrepositorymurdocheduau126101Frontpdf Accessed 26 August 2013 3 Ritchie BW 1995 Circoviradae In Avian Viruses Function and Control Wingers Publishing Inc Lake Worth Florida Pp 223251 4 Reed H H 2000 Circovirus in lories and lorikeets Proc Am Assoc Zoo Vet International Assoc Aquatic An Med Joint Meeting New Orleans Louisiana Pp 317321 5 Strunk A V Lester BW Ritchie D Pesti KS Latimer P Ciembor CR Gregory H Wilson and J Sherrill 2002 Pathobiology and testing recommendations for psittacine circovirus 2 in lories Proc Assoc Avian Vet Monterey California Pp 4547 6 Ritchie BW and PD Lukert 2008 Psittacine circovirus In DufourZavala L DE Swayne JR Glisson JE Pearson WM Reed MW Jackwood and PR Woolcock eds A Laboratory Manual American Association of Zoo Veterinarians Infectious Disease Manual PSITTACINE BEAK AND FEATHER DISEASE for the Isolation and Identification of Avian Pathogens 5th edition American Association of Avian Pathologists Kennett Square Pennsylvania 249 pp American Association of Zoo Veterinarians Infectious Disease Manual PYTHIOSIS Fact Sheet compiled by Roberto Aguilar updated by Leonel Mendoza and Raquel Vilela updated by Charles O Cummings Sheet completed on 31 January 2011 updated 9 September 2013 updated 11 November 2019 Fact Sheet Reviewed by Amy Grooters Susceptible animal groups Essentially all mammals are susceptible Small mammals cats and dogs have been reported Horses cattle sheep and camelids present pythiosis with some frequency Captive wild felids and ursids have been reported although all mammals are potentially susceptible In zoo species specifically primary pulmonary pythiosis in a jaguar in Louisiana spectacled bears in South Carolina and a lion in Florida have been reported Mandibular bulbar gastric and vulvar infections in captive camels In birds a cutaneous infection in a whitefaced ibis and esophageal infection in an ostrich have been described Ocular and vascular pythiosis is reported in humans Causative organism Pythium insidiosum pathogenic water mold Zoonotic potential Humans would get pythiosis from the environment but infection is rare No evidence had been documented that pythiosis can be transmitted from an animal to a person Distribution Globally pythiosis is most often encountered in Southeast Asia especially Thailand and Indonesia eastern coastal Australia New Zealand and South America but has also been recognized in Korea Japan and the Caribbean In the United States it is most often found in the southeastern US but it also has been identified in Wisconsin New Jersey New York Virginia Kentucky Arizona California Illinois Indiana Oklahoma Missouri Kansas and Tennessee Incubation period Unknown but clinical disease likely develops weeks to months after exposure Clinical signs Gastrointestinal weight loss vomiting diarrhea and hematochezia Laboratory abnormalities include eosinophilia anemia hyperglobulinemia hypoalbuminemia and rarely hypercalcemia Abdominal Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals canids felids equids felids cattle camelids and sheep Birds limited Motile biflagellate zoospore P insidiosum released into aquatic environments Gastrointestinal weight loss vomiting diarrhea and hematochezia Other mucosal eg vulvar weight loss masses Cutaneous Nonhealing wounds naso pharyngeal lesions invasive subcutaneous masses draining nodular lesion or ulcerated plaque like lesions Often fatal unless resectable with wide margins Surgical resection or amputation of infected tissues with wide margins Postoperative treatment with antifungals may decrease recurrence when incomplete resection occurs Addition of corticosteroids to antifungals may be of benefit for nonresectable lesions Immunotherapy has also been seen to be effective in humans and horses As it is environmental exposure control is difficult No although humans can get it from the environ ment infection is rare American Association of Zoo Veterinarians Infectious Disease Manual PYTHIOSIS radiography and sonography usually reveal severe segmental thickening of the gastrointestinal tract an abdominal mass andor mesenteric lymphadenopathy Cutaneous Nonhealing wounds and invasive masses that contain ulcerated nodules and draining tracts In horses the formation of hard masses kunkers within the lesions may occur Nasopharyngeal lesions invasive subcutaneous masses draining nodular lesion and ulcerated plaquelike lesions are found in cats Pythium insidiosum has been also reported affecting bones lungs lymph nodes eyes and blood vessels Post mortem gross or histologic findings Histologically pythiosis is characterized by eosinophilic pyogranulomatous inflammation associated with broad 47 micron poorly septate hyphae Affected tissues contain multiple foci of necrosis surrounded and infiltrated by neutrophils eosinophils and macrophages In addition there are discrete granulomas composed of epithelioid macrophages plasma cells multinucleate giant cells Hyphae stain well with GMS but less well with PAS Histologically pythiosis other oomycoses and zygomycosis have a similar appearance Diagnosis Veterinarians and physicians with expertise in this disease could suspect pythiosis because the clinical features of the disease However a clinical specimen biopsy kunkers is always recommended to support the findings Confirmation is usually histopathology followed by PCR confirmation of pythiosis in paraffinembedded tissues Serology has been performed successfully in canids exotic felids and several species of ursids but this frequently requires speciesspecific antibodies Cytologic evaluation of exudates from draining tracts or fineneedle aspirates of enlarged lymph nodes may be suggestive of fungal infection Material required for laboratory analysis Paraffinembedded tissue infected tissue fineneedle aspirates serum Gomoris methenamine silver stain GMS selective media containing streptomycin and ampicillin for culture Relevant diagnostic laboratories Panfungal PCR and Sequencing from Paraffinembedded Tissue Texas AM Dermatopathology Specialty Service TVMDL Shipping Address FedEx UPS LSO 483 Agronomy Rd College Station TX 778434471 USPS Mailing Address PO Drawer 3040 College Station TX 778413040 Pythium Serology Canine and Equine 158 Greene Hall Auburn University AL 36849 334 8442694 Fax 334 8442652 Fungal Culture Immunotherapy Consultation Leonel Mendoza Michigan State University North Kedzie Hall 354 Farm Lane Rm 322 East Lansing MI 488241031 517 4321234 Fax 517 4322006 mendoza9msuedu American Association of Zoo Veterinarians Infectious Disease Manual PYTHIOSIS Treatment Surgical resection of infected tissues with wide margins or amputation for distal cutaneous lesions Postoperative treatment with itraconazole and terbinafine may decrease the chance of recurrence in lesions that are not completely resected For inoperable pythiosis the addition of corticosteroids to terbinafine and itraconazole had resulted in lesion resolution and decreased titers in dogs Immunotherapy Pan American Veterinary Laboratories httpspavlabcompavlabpythiosisinsidiosum is often effective for treatment in horses especially when it is combined with aggressive surgical resection It is infrequently effective in dogs Prevention and control As it is transmitted via environmental exposure control is difficult Suggested disinfectant for housing facilities No special requirements for disinfection Standard disinfection protocols may be used Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal None Conditions for restoring diseasefree status after an outbreak None Experts who may be consulted Most internal medicine specialists DACVIMs and dermatologists DACVDs practicing in the American Southeast are familiar with the intricacies of treating pythiosis and other oomycoses References 1 Bissonnette KW Sharp NJ Dykstra MH Robertson IR Davis B Padhye AA Kaufman L Nasal and retrobulbar mass in a cat caused by Pythium insidiosum J Med Vet Mycol 19912939 2 Camus AC Grooters AM Aguilar RF Granulomatous pneumonia caused by Pythium insidiosum in a Central American jaguar Panthera onca J Vet Diag Invest 200416567571 3 Foil CSO Short BG Fadock VA Kunkle GA A report of subcutaneous pythiosis in five dogs and a review of the etiologic agent Pythium spp J Am Anim Hosp Assoc 198420959 4 Gaastra W Lipman LJA DeCock AWAM Exel TK Pegge RB Scheurwater J Vilela R Mendoza L Pythium insidiosum an overview Vet Microbiol 2010146116 5 Grooters AM Pythiosis lagenidiosis and zygomycosis in small animals Vet Clin North Am Small Anim Pract 200333695 6 Grooters AM Gee MK Development of a nested PCR assay for the detection and identification of Pythium insidiosum J Vet Intern Med 200216147 7 Grooters AM Leise BS Lopez MK Gee MK OReilly KL Development and evaluation of an enzymelinked immunosorbent assay for the serodiagnosis of pythiosis in dogs J Vet Intern Med 2002a16142 8 Grooters AM Whittington A Lopez ML Boroughs MN Roy AF Evaluation of microbial culture techniques for the isolation of Pythium insidiosum from equine tissues J Vet Diagn Invest 2002b14288 9 Grooters AM Pythiosis and zygomycosis In Sellon DC Long MT eds Equine Infectious Diseases St Louis MO Elsevier 2007 p 412419 10 Heck LC Bianchi MV Pereira PR Lorenzett MP de Lorenzo C Pavarini SP Driemeier D Sonne L Gastric Pythiosis in a Bactrian Camel Bactrianus camelus J Zoo Wildl Med 20184978487 11 Hilton RE Tepedino K Glenn CJ Merkel KL Swamp Cancer A Case of Human Pythiosis and Review of the Literature Brit J Derm 201617539497 12 Mendoza L Vilela R 2013 The mammalian pathogenic Oomycetes Curr Fungal Infect Rep 20137198208 13 Mendoza L Newton JC Immunology and immunotherapy of the infections caused by Pythium insidiosum Med Mycol 200543477486 14 Pereira IB Botton SA Azevedo MI Motta MA Lobo RR Soares MP Fonseca AO Jesus FP Alves American Association of Zoo Veterinarians Infectious Disease Manual PYTHIOSIS SH Santurio JM Canine gastrointestinal pythiosis treatment by combined antifungal and immunotherapy and review of published studies Mycopathologia 2013176309315 15 Pesavento PA Barr B Riggs SM Eigenheer AL Pamma R Walker RL Cutaneous pythiosis in a nestling whitefaced ibis Vet Pathol 200845538541 16 Rakich PM Grooters AM Tang KN 2005 Gastrointestinal pythiosis in two cats J Vet Diagn Invest 200517262 17 Reagan KL Marks SL Pesavento PA Maggiore AD Zhu BY Grooters AM Successful Management of 3 Dogs with Colonic Pythiosis Using Itraconzaole Terbinafine and Prednisone J Vet Int Med 201933143439 18 Schemiedt CW StrattonPhelps M Torres BT Bell D Uhl EW Zimmerman S Epstein J Cornell KK Treatment of intestinal pythiosis in a dog with a combination of marginal excision chemotherapy and immunotherapy J Am Vet Med Assoc 2012241358363 19 Souto EPF Pessoa CRM Pessoa AFA Trost ME Kommers GD Correa FR Dantas AFM et al Esophageal Pythiosis in an Ostrich Struthio camelus Arq Brasil Med Vet Zootec 201971108184 20 Videla R van Amstel S ONeill SH Frank LA Newman SJ Vilela R Mendoza L Vulvar Pythiosis in Two Captive Camels Camelus dromedarius Med Mycol 20125021224 21 Wellehan JFX Farina LL Keoughan CG Lafortune M Grooters AM Mendoza L Brown M Terrell SP Jacobson ER Heard DJ Pythiosis in a dromedary Camelus dromedarius J Zoo Wildl Med 200435564568 American Association of Zoo Veterinarians Infectious Disease Manual RABBIT HEMORRHAGIC DISEASE RHD RABBIT CALICIVIRUS DISEASE RCD Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic RHDV1RHDVa European rabbit Oryctolagus cuniculus viral RNA found in deceased wood mice Apodemus sylvaticus and Algerian mice Mus spretus RHDV2 European rabbit Oryctolagus cuniculus Cape hare Lepus capensis var mediarraneus Italian hare Lepus corsicanus Black tail jackrabbit Lepus californicus and Cottontail rabbit Sylvilagus audubonii Rabbit caliciviruses circulate in healthy rabbits Direct contact with infected rabbits rabbit products or secretions insect or animal vectors fomites fecal excretion of virus from predators or scavengers Importation of infected rabbit meat or rabbits that survive infection as they can shed virus for at least 4 weeks Climate may be important many outbreaks occur in winter or spring Often sudden death with no obvious signs In symptomatic animals depression coma nervous signs paddling ataxia convulsions opisthotonos reluctance to move prostration serosanguineous discharge from nostrils congested conjunctivitis edema external genitalia Often high morbidity up to 100 and high mortality 50100 None Avoid contact with infected or contaminated animals animal products fomites or vectors Perform disinfection depopulation surveillance and quarantine under supervision of state and federal agencies Vaccinate in countries where available and legal not so in US No Fact Sheet compiled by Denise McAloose updated by Tess Rooney Sheet completed on 12 January 2011 updated 6 March 2013 updated 15 December 2019 updated 24 April 2020 Fact Sheet Reviewed by Alisa Newton Ken Conley Diana Boon Susceptible animal groups RHDV1 European rabbit Oryctolagus cuniculus some rodent species viral RNA found in deceased wood mice Apodemus sylvaticus and Algerian mice Mus spretus other lagomorph species are not affected RHDV2 European rabbit Oryctolagus cuniculus Cape hare Lepus capensis var mediarraneus Italian hare Lepus corsicanus blacktail jackrabbit Lepus californicus and cottontail rabbit Sylvilagus audubonii Both virus subtypes typically affect animals 2 months of age animals that survive infection become immune American Association of Zoo Veterinarians Infectious Disease Manual RABBIT HEMORRHAGIC DISEASE RHD RABBIT CALICIVIRUS DISEASE RCD Causative organism Rabbit Hemorrhagic Disease Family Caliciviridae Genus Lagovirus Species Rabbit hemorrhagic disease virus two serotypes One serotype contains RHDV classical RHVD andRHDVa antigenic variant other serotype is associated with RHDV2 also called RHDVb Rabbit Calicivirus Disease Family Caliciviridae Genus Lagovirus Species Rabbit calicivirus Michigan rabbit calicivirus Zoonotic potential No Distribution Disease has been reported in 40 countries and is endemic in Australia New Zealand Cuba parts of Asia and Africa and most of Europe will likely be endemic in British Columbia Washington and New Mexico as of 2020 Sporadic reports in several countries including Mexico now eradicated Canada 2011 Uruguay 2004 and the United States Iowa 2000 Utah 2001 Illinois 2001 New York 2001 Indiana 2005 Minnesota 2010 RHDV2 Ohio 2018 RHDV2 San Juan Islands WA 2019 RHDV2 in wild rabbits New Mexico Arizona Texas Colorado 2020 although was thought to have been eradicated in the US in 2019 It also has been reported in China Republic of Korea India and the Middle East It is more likely to be detected in large congregations than in single eg individual pet rabbits disease spread exacerbated in crowded conditions Incubation period Incubation 13 days death often occurs within 1236 hours of fever onset Clinical signs Classical RHDVRHDVa Often subclinical especially in young rabbits less than 48 weeks of age In older animals peracute and acute disease are common presentations Peracute clinical signs may include fever and sudden death within 1236 hours of fever onset Sometimes terminal squeals are the only clinical sign followed by subsequent collapse and death Acute clinical signs may include depression dullness anorexia congested conjunctiva prostration reluctance to move congested genitalia neurologic signs incoordination inappropriate excitement opisthotonos and paddling and respiratory signs dyspnea cyanosis and in final stages hemorrhagic frothy discharge from mouth or nostrils may be seen In animals that survive infection jaundice weight loss and lethargy may be seen RHDV2 Affects both old and young animals experimentally infected animals generally survive longer with fewer peracuteacute presentations of disease Clinical signs are otherwise similar to classical RHDV RCD Typically circulates subclinically in healthy animals Michigan rabbit calicivirus was isolated from an outbreak in Michigan that clinically resembled RHDV acute fatalitites with clinical signs including vulvar hemorrhage in pregnant does inappetence neurological signs diarrhea ocular discharge vocalizations and death but was not reproducible in experimentally infected animals clinical signs were raremild Post mortem gross or histologic findings Gross findings The primary lesion identified in animals infected with RHDV RHDVa and RHDV2 is hepatic necrosis Most commonly identified lesions include friable liver splenomegaly congested dark brown kidneys evidence of DIC hemorrhage andor infarcts in various organs especially thymus and pulmonary congestion edema andor petechiae multifocal petechiae in other organs or serosanguineous tracheal fluid may be present trachea often hyperemic American Association of Zoo Veterinarians Infectious Disease Manual RABBIT HEMORRHAGIC DISEASE RHD RABBIT CALICIVIRUS DISEASE RCD Histologic findings More common lesions mild to more often severe hepatic necrosis disseminated intravascular coagulopathy DIC splenic congestion multifocal lymphocytolysis Less frequently multifocal acute pulmonary edema congestion or hemorrhage and multifocal hemorrhage in other sites may be present Diagnosis Serologic tests hemagglutination inhibition HI indirect ELISA IELISA competitive ELISA CELISA Pathogen identification hemagglutination test HA electron microscopy negative staining EM immunoEM immunogold EM virus detection ELISA RTPCR RTLAMP Western blot histology immunostaining inoculation study RHDV never grown in cell cultures in situ hybridization liver contains highest viral titers and has been proposed as most diagnostic organ to submit for virus identification Material required for laboratory analysis Serum HI IELISA CELISA Fresh liver preferred sample spleen or lung HA RTPCR inoculation study 10 neutral buffered formalinfixed paraffin embedded liver spleen lung histology immunostain Fresh or fixed liver depending on procedure EM Relevant only diagnostic laboratory USDAAPHISVSNVSLFADDL 40550 Route 25 for packages Orient Point NY 11957 PO Box 848 for letters Greenport NY 119440848 631 3233256 Fax 631 3233366 Treatment Currently there is no treatment for this disease beyond supportive care Passively acquired immunity such as hyperimmune antiserum has been shown to protect animals that have not developed clinical signs but has not been effective in symptomatic animals Prevention and control Biosecurity is highly important for prevention and control restrict importation of live rabbits or rabbit products from endemic areas especially in the event of an outbreak Other biosecurity measures to employ include avoid contact with imported rabbits and rabbit products prevent contact between healthy and ill animals quarantine new animals or animals that have been in contact with other rabbits With input from State and Federal agencies control will include disinfection depopulation surveillance and quarantine elimination of fomites including insects other animal vectors incineration of dead animals feedstuff feces limit or ban animalanimal derivative product movement in face of outbreak Animals that survive infection are immune but may shed virus for at least 4 weeks Three vaccines are available in UK no vaccine available in US or Canada as of April 2020 Some states have been provisionally licensed for use of Filavac Vaccinated rabbits are protected from disease but due to low mucosal immunity can still develop intestinal infection and shed virus in the absence of clinical disease Suggested disinfectant for housing facilities This process is to be performed in collaboration with and under supervision of State and Federal Agencies RHDV is inactivated by 1 sodium hydroxide lye or 12 formalin OIE recommends 3 for disinfecting pelts Recommended disinfectants are substituted phenolics eg 2 Onestroke Environ and 05 sodium hypochlorite bleach Notification Reportable to State and Federal USDA agencies OIE reportable disease Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Due to highly infectious nature significance of disease and persistence in the environment introduction to infected animals is not recommended and may not be permitted by State and Federal agencies American Association of Zoo Veterinarians Infectious Disease Manual RABBIT HEMORRHAGIC DISEASE RHD RABBIT CALICIVIRUS DISEASE RCD Conditions for restoring diseasefree status after an outbreak State and Federal agencies will make recommendations that may include addition of sentinel animals on treated premises to monitor for persistent virus minimum post depopulation disinfection period prior to new animal addition Experts who may be consulted Preparedness and Incident Coordination Veterinary Services US Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services Emergency Management 4700 River Road Unit 41 Riverdale MD 207371231 Telephone 301 7348073 Fax 301 7347817 Email FADPRePCommentsaphisusdagov References 1 McIntosh MT Behan SC Mohamed FM Lu Z Moran KE Burrage TG Neilan JG Ward GB Botti G Capucci L Metwally SA A pandemic strain of calicivirus threatens rabbit industries in the Americas Virol J 2007496109 2 Marcato PS Benazzi C Vecchi G Galeotti M Salda LD Sarli G Lucidi P Clinical and pathological features of viral haemorrhagic disease of rabbits and the European brown hare syndrome Rev Sci Tech 199110371392 3 Rabbit Hemorrhagic Disease Internet OIE c2019 cited 2020 April 24 Available from httpswwwoieintfileadminHomeengAnimalHealthintheWorlddocspdfDiseasecardsRHDp df 4 Rabbit Hemorrhagic Disease Standard Operating Procedures Foreign Animal Disease Preparedness Response Plan United States Department of Agriculture c2013 cited 2020 April 24 Available from httpswwwaphisusdagovanimalhealthemergencymanagementdownloadssopsoprhdeepdf 5 Hoehn M Kerr PJ Strive T In situ hybridization assay for localization of rabbit calicivirus Australia1 RCAA1 in European rabbit Oryctolagus cuniculus tissues J Virol Meth 201218812148152 6 Abrantes J van der Loo W Le Pendu J Esteves PJ Rabbit haemorrhagic disease RHD and rabbit haemorrhagic disease virus RHDV a review Vet Res 201243112 7 Filavac vaccine monologue Internet HarcourtBrown cited 2020 April 24 Available from httpswwwharcourtbrowncoukmediadocumentsfilavacdoc American Association of Zoo Veterinarians Infectious Disease Manual RABIES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Major reservoirs in the US include dogs raccoons skunks foxes and bats Internationally vampire bat Latin America mongoose species the Caribbean southern Africa and parts of Asia jackals parts of Africa wolves parts of northern Europe marmosets Brazil ferret badgers China Bites or scratches of infected animals saliva into open wounds and mucous membranes Paresthesia or pain at bite site fever myalgia malaise behavior changes paresis seizures and other CNS signs Nearly always fatal Once clinical signs present no treatment in humans and animals is available although an experimental procedure has been used in humans with limited success Eliminating exposure to rabid animals including vaccination of species for which an approved vaccine exists providing exposed persons local treatment of wounds and human or equine rabies immune globulin if not previously vaccinated vaccinating persons in at risk professions Yes Fact Sheet Compiled by Erica Lipanovich Completed on updated 12 January 2019 Fact Sheet Reviewed by Donna Ialeggio Susceptible Animal Groups All mammals are susceptible Causative Organism The disease rabies is caused by the rabies virus Family Rhabdoviridae Genus Lyssavirus and nonrabies lyssaviruses such as Australian Bat Lyssavirus Duvenhage virus European Bat Lyssavirus and Mokola virus Zoonotic Potential Bites or scratches of infected animals saliva into open wounds and mucous membranes Distribution Worldwide Several countries have been declared canine rabiesfree However the of such declaration is to facilitate waiving the rabies vaccination requirement as these are countries that have not reported recent cases of rabies in land animals and that have adequate disease surveillance for rabies cases as determined by the CDC Countries on the list might still have circulating bat lyssaviruses which can cause the disease in people Incubation Period Incubation is prolonged and variable The virus typically remains at the inoculation site for a considerable time In domestic animals it is generally 112 weeks but can range from several days to months rarely exceeding 6 months Virus can be shed for a few days prior to the onset of clinical signs and during illness Clinical Signs Animals will show inappetence cranial nerve deficits ataxia salivating drooping of lower jaw acute behavioral changes such as altered vocalization aggression docility coma and progressive paralysis Humans experience pain paresthesia and intense pruritus at the bite site fever myalgia malaise and mood changes that progress to paresthesia paresis seizures coma and many other neurologic signs Survival is extremely rare in humans and animals Post mortem Gross or Histological Findings Gross lesions are often undetectable Necrotic tonsillitis necrotic bronchitis bronchiolitis and alveolitis are commonly seen Focal areas of necrosis are often found in American Association of Zoo Veterinarians Infectious Disease Manual RABIES the liver spleen lymph nodes and adrenal glands Histologically nonsuppurative meningoencephalitis is a characteristic lesion in the gray and white matter Negri bodies intracytoplasmic eosinophilic inclusions may be seen in neurons Mononuclear perivascular cuffing and neuronal necrosis may also be present Diagnosis Rabies diagnosis should be performed in accordance with the established national standardized protocol for postmortem rabies testing by a qualified laboratory that has been designated by the local or state health department Euthanasia should be accomplished in such a way as to maintain the integrity of the brain so that the laboratory can recognize the anatomical parts Rabies viral antigen is typically widespread in the brain of rabid animals though may spread unilateral It is therefore critical to examine a complete cross section of the brainstem Rabies diagnosis in animals is accomplished through the direct fluorescent antibody test Brain tissues examined must include medulla oblongata and cerebellum Serological tests are used to monitor antibody titers in response to rabies vaccination Human antemortem testing requires a minimum of four samples to rule out rabies Samples required include saliva nuchal skin biopsy serum and cerebral spinal fluid and brain biopsy Nuchal skin biopsy for immunofluorescent antibody staining is the most reliable test of rabies infection during the first week Reverse transcription polymerase chain reaction immunofluorescent staining for viral antigen virus neutralization assays and isolation of infectious virus in cell culture can be performed Material Required for Laboratory Analysis Except in the case of very small animals such as bats in which whole animals should be collected only the head or brain including brain stem should be submitted to the laboratory httpswwwcdcgovrabiesresourcesspecimensubmissionguidelineshtml Brain tissues examined must include multiple regions To facilitate laboratory processing and prevent a delay in testing any animal specimen being submitted for testing should preferably be stored and shipped under refrigeration and not be frozen httpwwwcdcgovrabiesspecificgroupslaboratoriesindexhtml Chemical fixation of tissues should be avoided to prevent significant testing delays and because it may preclude reliable testing Relevant Diagnostic Laboratories State and Local laboratories and Centers for Disease Control and Prevention Rabies Laboratory DASH Bldg 18 Room SSB218 1600 Clifton Road NE Atlanta GA 30333 404 6391050 httpswwwcdcgovrabiespdfspecimensubmissionguideline508pdf Treatment No known antivirals currently effective A few cases of human recovery have been documented following utilization of the Milwaukee protocol an experimental procedure but failures significantly outnumber successes using this protocol Prevention and Control Vaccination is primary means of prevention Rabies in humans can be prevented either by eliminating exposures to rabid animals or by providing exposed persons without a prior history of vaccination with prompt local treatment of wound washing for 15 minutes combined with the administration of human rabies immune globulin and a series of 4 doses of vaccine Though not nationally notifiable some state health departments have made animal bites and use of postexposure prophylaxis PEP reportable within their jurisdictions Individuals that have been previously vaccinated and have a potential rabies exposure require prompt wound care and a series of 2 doses of vaccine These recommendations along with information concerning the current local and regional epidemiology of animal rabies and the availability of human rabies biologics are available from state health departments American Association of Zoo Veterinarians Infectious Disease Manual RABIES Suggested Disinfectant for Housing Facilities Lyssaviruses are not stable in the environment and are inactivated by common disinfectants The best disinfectants are detergents hypochlorites alkalis Virkon and glutaraldehyde Notification Rabies is rare in vaccinated animals If such an event is suspected it should be reported to state public health officials the vaccine manufacturer and USDA Animal and Plant Health Inspection Service Center for Veterinary Biologics at 8007526255 or httpswwwaphisusdagovaphisourfocusanimalhealthveterinarybiologics The laboratory diagnosis should be confirmed and the virus variant characterized by a rabies reference laboratory A thorough epidemiologic investigation should be conducted Because of the risk of rabies in wild animals especially raccoons skunks coyotes foxes and bats the AVMA CSTE NACA and NASPHV strongly recommend the enactment and enforcement of state laws prohibiting their importation distribution translocation and private ownership Other biting animals which might have exposed a person to rabies should be reported immediately to the local health department Management of animals other than dogs cats and ferrets depends on the species the circumstances of the bite epidemiology of rabies in the area and biting animals history current health status and potential exposure to rabies Prior vaccination of these animals may not preclude the necessity for euthanasia and testing merely quarantining Measures Required under the Animal Disease Surveillance Plan The National Association of State Public Health Veterinarians NASPHV Guidelines for dogs and the Compendium of Animal Rabies Control Guidelines are updated regularly by the NASPHV and provide recommendations httpwwwnasphvorgdocumentsCompendiahtml However these guidelines do not supersede state and local laws Measures Required for Introducing Animals to Infected Animal See below Conditions for Restoring DiseaseFree Status after an Outbreak Unvaccinated animals exposed to a rabid animal should be euthanized immediately If the owner is unwilling the animal should be placed in strict isolation for 6 months Rabies vaccine should be administered upon entry into isolation or 1 month prior to release to comply with preexposure vaccination recommendations Animals maintained in USDA licensed research facilities or accredited zoological parks should be evaluated on a casebycase basis Rabies virus may be excreted in the saliva of infected animals during illness andor for only a few days prior to illness or death A healthy animal which was previously vaccinated that bites a person should be confined and observed daily for 10 days administration of rabies vaccine is not recommended during the observation period to avoid confusing signs of rabies with possible side effects of vaccine administration Animals should be evaluated by a veterinarian at the first sign of illness during confinement If signs suggestive of rabies develop the animal should be euthanized and the head submitted for testing Any stray that bites a person may be euthanized immediately and the head submitted for rabies examination Other biting animals which might have exposed a person to rabies should be reported immediately to the local health department Management of animals other than dogs cats and ferrets depends on the species the circumstances of the bite epidemiology of rabies in the area and the biting animals history current health status and potential for exposure to rabies Prior vaccination of these animals may not preclude the necessity for euthanasia and testing Experts Who May Be Consulted Public Health Veterinarians can be found at Other state and local rabies consultations can be found at httpwwwnasphvorgDocumentsStatePublicHealthVeterinariansByStatepdf last updated 12 Sept 2018 httpswwwcdcgovrabiesresourcescontactshtml last updated 31 July 2018 References 1 American Veterinary Medical Association Internet AVMA Guidelines for the Euthanasia of Animals 2013 Edition 2013 cited 2019 January 12 Available from httpswwwavmaorgKBPoliciesDocumentseuthanasiapdf 2 American Veterinary Medical Association Internet Ownership or possession of wild animals or their hybrids 2019 cited 2019 January 12 Available from American Association of Zoo Veterinarians Infectious Disease Manual RABIES httpswwwavmaorgKBPoliciesPagesOwnershipandorPossessionandAppropriate DispositionofWildandExoticPetSpeciesorTheirHybridsaspx 3 Brown CM Slavinski S Ettestad P Sidwa TJ Sorhage FE Compendium of Animal Rabies Prevention and Control 2016 2016 cited 2019 January 12 Available from httpwwwnasphvorgDocumentsNASPHVRabiesCompendiumpdf 4 Centers for Disease Control and Prevention Morbidity and Mortality Weekly Report Human rabies preventionUnited States 2008 Recommendations of the Advisory Committee on Immunization Practices 2008 cited 2019 January 12 Available from httpswwwcdcgovmmwrPDFrrrr5703pdf 5 Greene CE Rabies and other Lyssavirus Infections In Greene CE ed Infectious Diseases of the Dog and Cat 4th ed St Louis MO Saunders Elsevier 2011 6 Hanlon CA Childs JE Nettles VF Recommendations of the working group on rabies Article III rabies in wildlife J Am Vet Med Assoc 199921516121618 7 Hanlon CA Smith JS Anderson GR Recommendations of the working group on rabies Article II laboratory diagnosis of rabies J Am Vet Med Assoc 199921514441446 8 Ma X Monroe BP Cleaton JM Orciari LA Li Y Kirby JD Chipman RB Petersen BW Wallace RM Blanton JD Rabies surveillance in the United States during 2017 J Am Vet Med Assoc 20182531215551568 9 Rupprecht C Internet Merck Veterinary Manual Overview of Rabies 2019 cited 2019 January 12 Available from httpswwwmerckvetmanualcomnervoussystemrabiesoverviewofrabies 10 United States Department of Agriculture Animal and Plant Health Inspection Service Internet Terrestrial Animal Health Standards Commission September 2010 Report Chapter 810 Rabies 2010 cited 2019 January 12 Available from httpswwwaphisusdagovimportexportanimalsoiedownloadstahcsep10tahcrabies79sep10 pdf 11 Vora NM Clippard JR Stobierski MG Signs K Blanton JD Animal Bite and Rabies Postexposure Prophylaxis Reporting United States 2013 J Pub Health Mgmt Prac Internet 2015 cited 2019 January 12 213E24E27 httpsinsightsovidcomcrossrefan0012478420150500000017 12 Wisconsin Division of Public Health Internet Rabies Algorithm Rabies Prevention Flowchart Introduction 2018 cited 2019 January 12 Available from httpswwwdhswisconsingovrabiesalgorithmindexhtm 13 World Health Organization Internet Rabies 2018 cited 2019 January 12 Available from httpwwwwhointmediacentrefactsheetsfs099en American Association of Zoo Veterinarians Infectious Disease Manual RANAVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Amphibians especially larvae and metamorphs fish and reptiles Transmission can occur through direct contact with infected animals contact with contaminated water or substrates ingestion of infected tissues or fomites Largescale die offs especially of larval stages of amphibians Infection can be subclinical Subtle to severe hemorrhages in the ventral skin especially at the base of the hind limbs and around the vent opening fluid accumulation under the skin or within the coelom hemorrhages within serosa of heart stomach and liver Chelonians show swollen eyelids oral plaques ulcers on feet Infection with Ranavirus is an important cause of mortality in wild amphibians and chelonia only occasional reports of this infection in captive animals None Quarantine any infected animals Screen incoming amphibians for history of clinical signs consistent with disease Disinfect all equipment and effluent water No Fact Sheet compiled by Ann E Duncan Sheet completed on 15 January 2011 updated 19 August 2013 updated 2018 Fact Sheet Reviewed by Allan P Pessier Amanda Duffus Susceptible animal groups All types of amphibians including urodeles salamanders and newts and anurans frogs and toads Larvae and metamorphs are most often associated with morbidity and mortality Adult morbidity and mortality occurs less often Some species may have covert infections and be able to shed and transmit virus to other susceptible animals without ever exhibiting clinical signs Ranaviruses are also found in other poikilothermic vertebrates including reptiles and fish Has been associated with mortality events in wild and captive chelonia Sporadic mortality in captive snakes and lizards Amphibians may serve as a reservoir Causative organism Ranaviruses are members of the Iridoviridae a group of double stranded DNA viruses Numerous strains are identified however viruses related to the Ambystoma tigrinum virus ATV and Frog virus 3 FV3 appear to be the most important in North America The Bohle iridovirus BIV from Australia also is of concern as it has recently been identified in a zoological collection in the USA Some ranaviruses are able to infect animals from more than one class eg amphibians and reptiles or amphibians and fish Zoonotic potential None Distribution Worldwide although hotspots have been identified in recurrent mortality events Ranaviruses are considered to be globally emerging infections Incubation period Variable Less than 5 days to several weeks Incubation is affected by ambient temperatures dose of virus exposure immunosuppression developmental stage and species differences in susceptibility to different Ranavirus strains Clinical signs In amphibians subtle to severe hemorrhages in the ventral skin especially at the base of the hind limbs and around the vent opening fluid accumulation under the skin or within the coelom hemorrhages within serosa of heart stomach and liver Skin ulceration andor epithelial proliferation may be seen Infection does not always cause clinical disease Longterm nonclinical carriers have been identified In chelonian nasal discharge conjunctivitis caseous plaques in the oral cavity and subcutaneous edema of the palpebra and neck have been seen Post mortem gross or histologic findings In amphibians necrosis andor hemorrhage is present in multiple tissues especially skin liver kidney spleen hematopoietic tissue and gastrointestinal tract In chelonians necrotizing and fibrinous stomatitisesophagitis splenitis and vasculitis are seen Histologically intracytoplasmic inclusion bodies may be seen however they are difficult to identify are not always due to the virus and may be absent or inconspicuous in many cases Diagnosis PCR is the most useful test and is becoming more widely available Realtime PCR techniques American Association of Zoo Veterinarians Infectious Disease Manual RANAVIRUS allow detection of smaller amounts of virus but to identify the group type ATV or FV3 viruslike of Ranavirus present conventional PCR with DNA sequencing is required Determining the specific species of Ranavirus usually requires cell culture virus isolation and molecular characterization These techniques are not widely available outside of research laboratories Conventional PCR may not detect low level infections and can provide falsepositive results if confirmatory DNA sequencing or Southern blot analysis is not performed Histopathology is helpful to screen for lesions in sick animals but lesions tend to be nonspecific unless intracytoplasmic inclusion bodies are seen Virus isolation immunohistochemistry transmission electron microscopy cell culture and serology not widely available or validated for most species have also been used to identify infected animals Material required for laboratory analysis The best choice is tissue samples collected at necropsy especially liver kidney and if lesions are present skin Frozen tissues are required for virus isolation and are generally best for molecular analysis however freezing is not acceptable for histology For histology tissues should be submitted fresh or fixed in 70 ethanol or 10 neutral buffered formalin Ethanolpreserved tissues may be used for some molecular testing Formalinfixed tissues may also be used for some molecular testing if the length of time in formalin is minimal at days to weeks but it is possible to perform PCR on paraffin embedded tissues Samples can also be collected from clinically ill living animals such as cloacal or pharyngeal swabs tissue biopsy tail clips or blood Contact the laboratory to determine the best swab choice for testing as some can inhibit detection If living animals are tested results should be interpreted with caution recognizing test limitations eg a positive test result is more meaningful than a negative test result Test sensitivity for antemortem PCR increases with time postexposure and development of clinical signs of illness Contact individual laboratories for more information regarding screening Relevant diagnostic laboratories For an overall list httpswwwranavirusorgresourcestestinglabs Amphibian Disease Laboratory Taqman PCR for Ranavirus Conventional PCR and MCP sequencing 15600 San Pasqual Valley Road Escondido CA 92027 760 7478702 x 5471 httpwwwsandiegozooglobalorgNewsAmphibianDiseaseLaboratory Diagnostic or research Coventional PCR qPCR virus culture MCP sequencing histopathology University of Tennessee Center for Wildlife Health 274 Ellington Plant Sciences Building 2431 Joe Johnson Drive Knoxville Tennessee 379964563 865 9747948 dmill42utkedu or mgray11utkedu qPCR cell culture genomic sequencing and speciation Zoo Medicine Infectious Disease Lab co April Childress University of Florida 2015 SW 16th Ave Building 1017 Room V2186 Gainesville FL 32608 Phone 3522944420 ChildressAufledu httplabsvetmedufledusamplerequirementsmicrobiologyparasitologyserologyzoomedinfections American Association of Zoo Veterinarians Infectious Disease Manual RANAVIRUS qPCR Zoologix 9811 Owensmouth Avenue Suite 4 Chatsworth CA 913113800 Phone 8187178880 Fax 8187178881 Email infozoologixcom Treatment None in amphibians is available Antiviral therapy and supportive care have been attempted in reptiles Prevention and control The major concerns in captive programs are that mortality will occur in a valuable species or population or that subclinically infected animals will expose naïve wild populations The prevalence of infection in captive animals is not yet known Disease has likely gone unrecognized due to clinical and pathological similarities to other diseases in amphibians Captive amphibian populations can be surveyed continuously for disease by histopathology testing of samples collected at necropsy and PCR Once a population or individual has been found positive by PCR the disposition of these animals will depend on careful risk assessment A positive test does not distinguish between a lethal infection and a subclinical carrier Factors to be considered include their importance to the survival of the species the presence or absence of pre existing infection in captive and wild populations and results of followup histologic and PCR testing In some cases the animals or a population may be managed in permanent isolation from the general amphibian population Further prevention measures include quarantining all incoming animals The health history of animals being brought into a population needs to be reviewed if there have been deaths or illness due to confirmed or suspected Ranavirus in the prior 6 months the risk of disease transmission with introduction is considered higher Animals dying during quarantine can be screened using PCR and histopathology Strict biosecurity measures must be followed to avoid transmission of infection to other amphibians or susceptible classes of animals fish turtles tortoises Suggested disinfectant for housing facilities 1 Potassium peroxymonosulfate Virkon 3 sodium hypochlorite and 1 chlorhexidine have been reported to be effective at inactivating Ranavirus after 1 min contact duration Some ranaviruses were found to remain viable for 113 days on dry surfaces and up to 2 weeks in water Amphibians are sensitive to disinfectant residues thorough rinsing is required after use Biosecurity measures must include treatment of waste and effluent from Ranavirus infected animals Notification Infection by a Ranavirus is classified as a reportable disease by the OIE requiring proof of Ranavirusnegative results before commercial shipment of amphibians OIE 2008 httpwwwoieintengnormesfcodefcode2008enchapitre242htm A reporting mechanism eg via USDAAPHIS has not been announced for the US at this time Measures required under the Animal Disease Surveillance Plan Currently none See httpwwwoieintengnormesfcodefcode2008enchapitre242htm as Article 24210 states that importation of live aquatic animals intended for use in zoos from a country not declared free from Ranavirus should be followed by lifelong holding of the animals in biosecure facilities for continuous isolation from the local environment and treatment of all effluent and waste materials in a manner that inactivates Ranavirus Measures required for introducing animals to infected animals Animals should not be introduced to those showing clinical signs of disease or with exposure to known infected animals Conditions for restoring diseasefree status after an outbreak None established See httpwwwoieintengnormesfcodefcode2008enchapitre242htm Experts who may be consulted Allan P Pessier Department of Veterinary Microbiology and Pathology Washington State University apessierwsuedu 5093353877 American Association of Zoo Veterinarians Infectious Disease Manual RANAVIRUS Debra L Miller Center for Wildlife Health The University of Tennessee 274 Ellington Plant Sciences Building 2431 Joe Johnson Drive Knoxville Tennessee 379964563 865 9747948 dmille42uktedu References 1 Global Ranavirus Consortium Internet Global Ranavirus Consortium cited 2018 November 15 Available from wwwranavirusorg 2 Miller DL Pessier AP Hick P Whittington RJ Comparative Pathology of Ranaviruses and Diagnostic Techniques In Gray M Chinchar V eds Ranaviruses Springer Cham 2015 p 178 201 3 United States Geological Survey Internet USGS National Wildlife Health Center cited 2018 November 26 Available from httpswwwusgsgovcentersnwhc 4 Bryan LK Balwin CA Gray MJ Miller DL Efficacy of select disinfectants at inactivating Ranavirus Dis Aquat Org 2009848994 5 Cheng K Jones ME Jancovich JK Burchell J Schrenzel MD Reavill DR Imai DM Urban A Kirkendall M Woods LW Chinchar VG Isolation of a Bohlelike iridovirus from boreal toads housed within a cosmopolitan aquarium collection Dis Aquat Org 2014111139152 6 Driskell EA Miller DL Swist SL Gyimesi ZS PCR detection of Ranavirus in adult anurans from the Louisville Zoological Garden J Zoo Wildl Med 200940355963 7 Johnson AJ Pessier AP Wellehan JFX Childress A Norton TM Stedman NL Bloom DC Belzer W Titus VR Wagner R Brooks JW Spratt J Jacobson ER Ranavirus infection of freeranging and captive box turtles and tortoises in the United States J Wild Dis 2008444851863 8 Pessier AP Mendelson JR eds 2010 A Manual for Control of Infectious Diseases in Amphibian Survival Assurance Colonies and Reintroduction Programs IUCNSSC Conservation Breeding Specialist Group Apple Valley Minnesota cited 2013 September 26Available from wwwcbsgorg 9 OIE Internet OIE Aquatic Animal Health Code Chapter 242 OIE Paris cited 2013 September 26 Available from httpwwwoieintindexphpid171L0htmfilechapitre182htm American Association of Zoo Veterinarians Infectious Disease Manual CHIMPANZEE CORYZARESPIRATORY SYNCYTIAL VIRUS RSV Fact Sheet compiled by Allison Wack Sheet completed on 26 December 2010 updated 19 March 2013 Fact Sheet Reviewed by Kay A Backues Elizabeth Hammond Susceptible animal groups Chimpanzees one fatal case report in a muriqui experimental infection with clinical signs in owl and bonnet monkeys serologic evidence of exposure in orangutans possible disease in other great apes and redcapped mangabeys Causative organism Respiratory Syncytial Virus Family Paramyxoviridae Genus Pneumovirus 2 antigenic subgroups A and B Zoonotic potential Yes but transmission generally from human to primate not primate to human Distribution Worldwide in temperate areas frequently presenting in fallwinter months Incubation period 45 days Clinical signs coughing sneezing rhinorrhea ocular discharge anorexia lethargy which may progress to pneumonia Peracute death has been reported Recovery typically in 12 weeks in humans Post mortem gross or histologic findings Bronchopneumonia bronchiolitis pneumonitis rhinitis hyperplasia of pulmonary lymph nodes and lymphadenitis Multinucleate syncytial cells with eosinophilic cytoplasmic inclusion bodies may be seen Diagnosis RTPCR DIA IFA ELISA Material required for laboratory analysis nasalnasopharyngeal swab aspirate or wash PCR serum DIA IFA ELISA Relevant diagnostic laboratories VRL Labs BioReliance wwwvrlsatcom wwwbioreliancecom RTPCR DIA IFA ELISA Treatment Symptomatic Palivizumab hRSV IgG has been used in high risk human children to prevent severe disease although it cannot treat already advanced disease Antibiotics for secondary bacterial infections NSAIDs may control some clinical signs Prevention and control Prevent sick humanprimate contact and transmission via fomites appropriate use of Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Chimps most commonly Muriqui other primate spp may be infected experimentally or have seroevidence of exposure Aerosol direct or indirect contact fomites both respiratory secretions and feces contain virus Cough sneeze rhinorrhea lethargy anorexia progression to lower respiratory disease peracute death possible High morbidity low to moderate mortality limited reported fatalities in juvenile chimps with pneumonia outbreak in chimp group with 10 mortality Symptomatic Palivizumab has been used to reduce risk of infection in high risk children Avoidance of contact with sick humans proper hygiene and staff PPE Yes American Association of Zoo Veterinarians Infectious Disease Manual CHIMPANZEE CORYZARESPIRATORY SYNCYTIAL VIRUS RSV masks gloves and hand washing Highly transmissible No vaccine is available Suggested disinfectant for housing facilities Virus is readily inactivated by most disinfectants ie quaternary ammonium compounds phenols It usually lasts only hours in environment although can persist longer in cool shady areas or in serum or tissue debris transmission via fomites ie enrichment items cage furniture Notification Reportable in humans in many states check individual state regulations Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal No long term immunity and no carriers Introduction after clinical signs have resolved and area is disinfected would be optimal Conditions for restoring diseasefree status after an outbreak Resolution of clinical signs some immunocompromised humans can shed for up to 4 weeks though usual time of shedding is 38 days Experts who may be consulted CDC References 1 httpwwwcdcgovrsvindexhtml Accessed 3 July 2013 2 httpwwweazanetactivitiestdfactsheets05120Respiratory20Syncytial20Virusdocpdf Accessed 3 July 2013 3 Belshe RB Richardson LS London WT Sly DL Lorfeld JH Camargo E Prevar DA and RM Chanock 1977 Experimental respiratory syncytial virus infection of four species of primates J Med Virol 1 157162 4 Byrd LG and GA Prince 1997 Animal models of respiratory syncytial virus infection Clin Infect Dis 25 13631368 5 Clarke CJ Watt NJ Meredith A McIntyre N and SM Burns 1994 Respiratory syncytial virus associated bronchopneumonia in a young chimpanzee J Comp Path 110 207212 6 Kilbourn AM Karesh WB Wolfe ND Bosi EJ Cook RA and M Andau 2003 Health evaluation of freeranging and semicaptive orangutans Pongo pygmaeus pygmaeus in Sabah Malaysia J Wild Dis 39 7383 7 McCarthy CA and C B Hall 2003 Respiratory syncytial virus concerns and control Ped Rev 24 301308 8 Mansfield K and N King 1998 Viral diseases In Bennett BT Abee CR and R Henrickson eds Nonhuman Primates in Biomedical Research Academic Press San Diego California Pp 148 9 Santos SV Strefezzi RF Pissinatti A Takakura CFH Kanamura C Duarte MIS and JL CatãoDias 2012 Respiratory syncytial virus RSV pneumonia in a southern muriqui Brachyteles arachnoides J Med Primatol 42 6 403406 10 Simoes EAF Hayward AR Ponnuraj EM Straumanis JP Stenmark KR Wilson HL and PG Babu 1999 Respiratory syncytial virus infects the bonnet monkey Macaca radiata Ped Develop Path 2 316326 11 Szentiks CA Kondgen S Silinski S Speck S and F H Leendertz 2009 Lethal pneumonia in a captive juvenile chimpanzee Pan troglodytes due to humantransmitted human respiratory syncytial virus HRSV and infection with Streptococcus pneumoniae J Med Primatol 38 236240 12 Takanori K Okamoto M Yoshida T Nishida T Tsubota T Saito A Tomonaga M Matsuzawa T Akari H Nishimura H and T MiyabeNishiwaki 2013 Epidemiological study of zoonoses derived from humans in captive chimpanzees Primates 541 8998 13 Unwin S Chatterton J and J Chantrey 2013 Management of severe respiratory tract disease caused by human respiratory syncytial virus and Streptococcus pneumoniae in captive chimpanzees Pan troglodytes J Zoo Wild Med 441 105115 American Association of Zoo Veterinarians Infectious Disease Manual RICKETTSIOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Vectorborne primarily ticks but some species are transmitted by fleas Nonspecific Nonclinical or mild to severe including death Doxycycline Avoid contact with ticks and other ecto parasites No vaccine available Many species are zoonotic Fact Sheet compiled by Michael J Yabsley Sheet completed on 1 August 2013 updated 2018 Fact Sheet Reviewed by Edward B Breitschwerdt Kristina M Delaski Gail Miriam Moraru Susceptible animal groups For those Rickettsia species that are tickborne ticks serve as the definitive and reservoir hosts for these bacteria but numerous vertebrate hosts are important as they serve as bloodmeals for ectoparasites and some can serve as amplifying hosts for Rickettsia spp Antibodies to Rickettsia spp have been reported in a wide range of wildlife and domestic animal species Causative organism The four main Rickettsia species that are known to cause disease in people andor animals in the United States are Rickettsia rickettsii the causative agent of Rocky Mountain Spotted Fever is transmitted by ticks primarily Dermacentor spp and rarely by Amblyomma americanum In Arizona USA transmission to dogs and people has been documented by Rhipicephalus sanguineus Rickettsia parkeri causative agent of Parkeri Rickettsiosis or American Boutonneuse Fever is transmitted by ticks primarily Amblyomma maculatum and rarely A americanum and frequently causes an eschar Rickettsia philipii Rickettsia 364D causative agent of Pacific Coast tick fever an escharassociated febrile disease in people is transmitted by Dermacentor occidentalis Rickettsia typhi endemic or murine typhus is transmitted by Xenopsylla cheopis usually infesting rats Rickettsia felis commonly referred to as cat flea typhus which is transmitted by Ctenocephalides felis is endemic to all continents except Antarctica Other species of Rickettsia have been detected in the US but most are considered endosymbionts of ticks ie these species arent known to induce disease in vertebrate hosts However in recent years some of these endosymbionts eg Rickettsia amblyommatis have been associated with mild disease in people Outside of the US numerous of Rickettsia species exist many of which are zoonotic Zoonotic potential Many species but not all are zoonotic Distribution Rickettsia spp have been reported worldwide R rickettsii and R felis are distributed throughout the Americas while R parkeri is found in the southeastern US and R philipii occurs in California R typhi and R felis are widely distributed throughout the world Incubation period Typically 314 days Clinical signs People Wide range of symptoms from asymptomatic to severe potentially fatal disease Mild or asymptomatic cases rarely diagnosed Some individuals develop a fever muscle pain headache and rash due to damage of vascular endothelial cells but importantly a rash is not always observed with rickettsioses Multiorgan disease results in high mortality rate if not treated Infections with R parkeri and R philipii tend to be less severe than R rickettsii and often present with an eschar at the site of tick attachment Neurologic signs may develop in people infected with R typhi or R felis Canines Canines are susceptible to R rickettsii and can develop severe disease rapidly although most infections are asymptomatic or mild Dogs can develop similar clinical signs as people The most common clinical signs include fever lethargy anorexia ataxia rash swollen lymph nodes and localized edema American Association of Zoo Veterinarians Infectious Disease Manual RICKETTSIOSIS Other animals Most other animals only have shortterm infections with no associated disease These animals as well as others that dont become ill develop antibodies that can be detected by serologic testing Clinical pathological gross and histopathological findings Thrombocytopenia is common Leukopenia followed by a leukocytosis and mild anemia may develop Petechiae and ecchymoses are common due to damage to endothelial cells Diagnosis These diseases can be difficult to diagnose but diagnosis is based on clinical signs exposure to ectoparasites ticksfleas and supporting data from laboratory findings serology andor molecular assays Ideally acute and convalescent serum samples are tested for antibodies Molecular testing of petechial skin biopsies or blood although this sample is less rewarding can be used Fluorescent antibody FA or molecular testing of tissues can be used to diagnoses cases postmortem Because clinical signs may develop quickly lack of a serologic response doesnt preclude infection PCR testing has not been widely used to document active infection in wildlife species Material required for laboratory analysis Serum EDTA blood for PCR skin biopsy andor tissue samples Relevant diagnostic laboratories Humans Many state diagnostic labs have testing capabilities Animals North Carolina State University College of Veterinary Medicine Vector Borne Disease Diagnostic Laboratory 1060 William Moore Drive Room 462A Raleigh NC 27607 9195138279 httpwwwcvmncsueduvhccsdsticklabhtml serology and PCR Antech Diagnostics Corporate Headquarters 17672B Cowan Avenue Irvine CA 92614 ANTECH West 18007454725 ANTECH East 18008721001 ANTECH Canada 18003413440 ANTECH Test Express 18883978378 serology Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth CA 913113800 Phone 8187178880 Fax 8187178881 Email infozoologixcom This PCR does not differentiate among Rickettsia spp Treatment The most common treatment is doxycycline usually 10 20 mgkg every 12 hours for 7 days A lower dose 5 mgkg every 12 hours can also be given for 14 days Chloramphenicol can also be used Prevention and control Because Rickettsia spp are vectorborne limiting exposure to vectors is necessary to prevent transmission Transmission doesnt occur from animal to animal but can occur through blood American Association of Zoo Veterinarians Infectious Disease Manual RICKETTSIOSIS inoculation of wounds Habitat modification to limit ticks in areas where animal frequent Some birds are known hosts for certain tick species and while they may not be competent hosts of the rickettsial pathogens they can aid in distribution of vectors Suggested disinfectant for housing facilities Rickettsia spp are not viable outside of the host Prevent vector exposure Application of acaricides and removal of leaf litter can decrease tick abundance Notification CDC Reportable Disease for human cases in US Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal These bacteria are vectorborne so direct contact between animals is not a risk factor for infection However ectoparasite prevention should be implemented Conditions for restoring diseasefree status after an outbreak na Experts who may be consulted Ed Breitschwerdt DVM NCSU College of Veterinary Medicine Vector Borne Disease Diagnostic Laboratory 1060 William Moore Drive Room 462A Raleigh NC 27607 EdBreitschwerdtncsuedu Susan Little Oklahoma State University Center for Veterinary Health Sciences 250 McElroy Hall Stillwater OK 74078 susanlittleokstateedu References 1 Allison RW Little SE Diagnosis of rickettsial diseases in dogs and cats Vet Clin Pathol 201342127 144 2 Apperson CS Engber B Nicholson WL Mead DG Engel J Yabsley MJ Dail K Johnson J Watson DW Tickborne diseases in North Carolina is Rickettsia amblyommii a possible cause of rickettsiosis reported as Rocky Mountain spotted fever Vector Borne Zoonotic Dis 20088597606 3 Bayliss DB Morris AK Horta MC Labruna MB Radecki SV Hawley JR Brewer MM Lappin MR Prevalence of Rickettsia species antibodies and Rickettsia species DNA in the blood of cats with and without fever J Feline Med Surg 200911266270 4 Breitschwerdt EB Hegarty BC Maggi RG Lantos PM Aslett DM Bradley JM Rickettsia rickettsii transmission by a lone star tick North Carolina Emerg Infect Dis 201117873875 5 Cohen SB Yabsley MJ Garrison LE Freye JD Dunlap BG Dunn JR Mead DG Jones TF Moncayo AC Rickettsia parkeri in Amblyomma americanum ticks Tennessee and Georgia USA Emerg Infect Dis 20091514711473 6 Demma LJ Traeger M Blau D Gordon R Johnson B Dickson J Ethelbah R Piontkowski S Levy C Nicholson WL Duncan C Heath K Cheek J Swerdlow DL McQuiston JH Serologic evidence for exposure to Rickettsia rickettsii in eastern Arizona and recent emergence of Rocky Mountain spotted fever in this region Vector Borne Zoonotic Dis 20066423429 7 Fritz CL Kriner P Garcia D Padgett KA Espinosa A Chase R Hu R Messenger SL Tick infestation and spottedfever group Rickettsia in shelter dogs California 2009 Zoonoses Public Health 2009594 7 8 Fritzen CM Huang J Westby K Freye JD Dunlap B Yabsley MJ Schardein M Dunn JR Jones TF American Association of Zoo Veterinarians Infectious Disease Manual RICKETTSIOSIS Moncayo AC Infection prevalences of common tickborne pathogens in adult lone star ticks Amblyomma americanum and American dog ticks Dermacentor variabilis in Kentucky Am J Trop Med Hyg 201185718723 9 Grasperge BJ Wolfson W Macaluso KR Rickettsia parkeri infection in domestic dogs Southern Louisiana USA 2011 Emerg Infect Dis 201218995997 10 Labruna MB Kamakura O MoraesFilho J Horta MC Pacheco RC Rocky Mountain spotted fever in dogs Brazil Emerg Infect Dis 200915458460 11 McQuiston JH Guerra MA Watts MR Lawaczeck E Levy C Nicholson WL Adjemian J Swerdlow DL Evidence of exposure to spotted fever group rickettsiae among Arizona dogs outside a previously documented outbreak area Zoonoses Public Health 2011588592 12 Moraru GM Goddard J Paddock CD VarelaStokes A Experimental infection of cotton rats and bobwhite quail with Rickettsia parkeri Parasit Vectors 2013670 13 Moraru GM Goddard J Murphy A Link D Belant JL VarelaStokes A Evidence of antibodies to spotted fever group rickettsiae in small mammals and quail from Mississippi Vector Borne Zoonotic Dis 20131315 14 Nicholson WL Allen KE McQuiston JH Breitschwerdt EB Little SE The increasing recognition of rickettsial pathogens in dogs and people Trends Parasitol 201026205212 15 Paddock CD Finley RW Wright CS Robinson HN Schrodt BJ Lane CC Ekenna O Blass MA Tamminga CL Ohl CA McLellan SL Goddard J Holman RC Openshaw JJ Sumner JW Zaki SR Eremeeva ME Rickettsia parkeri rickettsiosis and its clinical distinction from Rocky Mountain spotted fever Clin Infect Dis 20084711881196 16 Padgett KA Bonilla D Eremeeva ME Glaser C Lane RS Porse CC Castro MB Messenger S Espinosa A Hacker J Kjemtrup A Ryan B Scott JJ Hu R Yoshimizu MH Dasch GA Kramer V The ecoepidemiology of Pacific Coast Tick Fever in California PLoS Negl Trop Dis 201610e0005020 17 Parola P Labruna MB Raoult D Tickborne rickettsioses in America unanswered questions and emerging diseases Curr Infect Dis Rep 2009114050 18 Piranda EM Faccini JL Pinter A Saito TB Pacheco RC Hagiwara MK Labruna MB Experimental infection of dogs with a Brazilian strain of Rickettsia rickettsii clinical and laboratory findings Mem Inst Oswaldo Cruz 2008103696701 19 Purcell K Fergie J Richman K Rocha L Murine typhus in children South Texas Emerg Infect Dis 200713926927 20 Starkey LA West MD Barrett AW Saucier JM OConnor TP Paras KL Reiskind MH Reichard MV Little SE Prevalence of antibodies to spotted fever group Rickettsia spp and Ehrlichia spp in coyotes Canis latrans in Oklahoma and Texas USA J Wildl Dis 201349670673 21 Stromdahl EY Jiang J Vince M Richards AL Infrequency of Rickettsia rickettsii in Dermacentor variabilis removed from humans with comments on the role of other humanbiting ticks associated with spotted fever group Rickettsiae in the United States Vector Borne Zoonotic Dis 201111969977 22 TerVartanov VN Gusev VM Reznik PA Guseva AA Mirzoeva MN Bocharnikov ON Bakeev NN Transport of ticks and fleas by birds Zoologicheskiy Zhurnal 195635173189 In Russian American Association of Zoo Veterinarians Infectious Disease Manual RIFT VALLEY FEVER Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Domestic ruminants some wild ruminants humans some primates gray squirrels some rodents newborn cats and dogs Vectorborne direct contamination in humans Virus harbored in mosquito eggs remains dormant Periodic heavy rains and flooding cause mosquito hatching and virus transmission and amplification in mammalian hosts Epizootic abortion storms in pregnant ewes high fever weakness gastro intestinal signs mortality May be inapparent mild or fatal Abortions may reach 100 High mortality in susceptible young and pregnant animals None supportive care Animal movement remove infected animals and vector control Vaccination in endemic areas Barrier protocols for exposed humans Yes Fact Sheet compiled by Thomas W deMaar updated by Mark W Atkinson Sheet completed on 21 January 2011 updated 26 August 2013 Fact Sheet Reviewed by John C Morrill Pierre Rollin Susceptible animal groups Sheep cattle goats African buffalo water buffalo Asian monkeys and humans can be infected Susceptibility of cervids is not known Death in wild African ruminants is rare but there are recent reports of abortion andor deaths with virus isolation in African buffalo wildebeest waterbuck giraffe sable springbok and impala Camels African monkeys baboons equids pigs and domestic carnivores are considered resistant experiencing only asymptomatic viremia Gray squirrels mice hamsters and newborn dogs and cats can be experimentaly infected but dont usually play a role in the transmission Causative organism RVF virus is an RNA Phlebovirus of the family Bunyaviridae Only one serotype is recognized but strains of variable virulence exist Virus circulates in endemic areas among wild ruminants and hematophagus mosquitoes certain Aedes species act as reservoirs during interepizootic periods and increased precipitation in dry areas leads to an explosive hatching of eggs Precipitation cycles of 525 years produce RVFimmuno naïve animal populations and introduction of virus can lead to explosive outbreaks Virus can be transmitted by many species of mosquitoes and other biting insects during viremic phase in mammalian hosts Zoonotic potential Humans infected via contact with nasal discharge and blood from viremic animals as well as aborted fetuses and vaginal secretions following abortion in animals mosquitoes and by aerosols and possibly though unproven by consumption of raw milk It is possible that humans can act as amplifying hosts Generally raw meat is not a source although it can contain viremic blood and for humans it is usually cooked Distribution Serologic or virologic evidence over most of Africa Considered endemic in subSaharan Africa but recently it has made incursions into some Middle Eastern countries and Madagascar Incubation period 16 days 1236 hrs in lambs Clinical signs Abortion storms occur in domestic livestock at any stage of pregnancy Biphasic fever up to 106 F up to 104 F in humans to 107 F in sheep Young animals more severely affected showing high fever listlessness and unwillingness to move up to 90 mortality in newborn and young animals after very short incubation period Affected animals die within 2436 hours and are often just found dead without exhibiting clinical signs Older susceptible animals 2 weeks of age show high fever American Association of Zoo Veterinarians Infectious Disease Manual RIFT VALLEY FEVER listlessness anorexia and weakness and often develop a high titered viremia Gastrointestinal signs are common abdominal pain regurgitation foul smelling bloody diarrhea and icterus Abortion maybe the only sign 40100 in sheep Adults may have inapparent infections with abortion being the only sign Mortality in adult sheep ranges from 20 to 70 and approximately 10 in adult cattle Camels present either hyperacute form with sudden death in 24 hours or and an acute form with fever ataxia dyspnea bloodtinged nasal discharge icterus severe conjunctivitis hemorrhages of gums and tongue foot lesions nervous symptoms and abortions Humans experience a febrile disease that is usually mild and transient but in rare cases can be fatal with hemorrhagic fever ocular disease retinal vasculitis liver disease and meningoencephalitis Post mortem gross or histologic findings Focal or generalized hepatic necrosis enlarged discolored soft friable liver with irregular congestion and white necrotic foci 1 mm diameter Lesions are most severe in aborted fetus and young animals Widespread cutaneous hemorrhages petechiae and ecchymoses on serosal membranes Gall bladder wall edematous with possible hemorrhage Spleen and lymph nodes are edematous enlarged and may show petechiae Hemorrhagic enteritis intestinal contents dark chocolatebrown Diagnosis It is suspected in endemic areas when presented with abortions and relevant signs combined with febrile disease in humans after heavy rains andor flooding Histopathology of liver is relevant Most tissues will contain virus and can be used for detection virus isolation PCR ELISA antigen detection and numerous serologic tests exist VN ELISA IgG and IgM Material required for laboratory analysis Blood liver spleen brain and aborted fetuses are tissues of choice Relevant diagnostic laboratories Centers for Disease Control and Prevention Viral Special Pathogens Branch 1600 Clifton Road NE Atlanta GA 30333 Phone 404 6391115 or 404 6391510 Contact prior to specimen submission Treatment No specific treatment is available but supportive care can be provided Prevention and control Vector control and prevent movement of livestock are important measures for managing this disease General barrier measures gloves masks goggles etc should be used when handling suspected materials Attenuated Smithburn strain and inactivated virus vaccines available for use in Africa No licensed vaccine for use in US but several liveattenuated mutant vaccines are undergoing experimental analysis The Smithburn vaccine strain is known to cause abortion and birth defects so immunization of pregnant animals is not advised Suggested disinfectant for housing facilities While this is not usually performed virus is susceptible to acidic solutions lipid solvents and hypochlorite solutions Notification Reportable to USDA National Animal Health Reporting System A080 Measures required under the Animal Disease Surveillance Plan None described but response would be massive Measures required for introducing animals to infected animal Unadvised Conditions for restoring diseasefree status after an outbreak A disease free period with active surveillance longer than 4 years Recovery probably confers lifelong immunity Experts who may be consulted John C Morrill DVM PhD Dept of Microbiology Immunology American Association of Zoo Veterinarians Infectious Disease Manual RIFT VALLEY FEVER University of Texas Medical Branch 301 University Blvd Rm 4142B MRB Galveston TX 775551070 409 7724908 Cell 254 2232868 jcmorrilutmbedu CDC Viral Special Pathogens Branch 1600 Clifton Rd Atlanta GA 30333 4046391115 or 4046391510 Dvd1spathcdcgov Amy L Hartman PhD University of Pittsburgh Graduate School of Public Health Regional Biocontainment Laboratory 8038 BST 3 3501 Fifth Avenue Pittsburgh PA 15261 4126488765 Fax 4126488917 hartman2pittedu References 1 httpwwwcdcgovncidoddvrdspbmnpagesdispagesrvfhtm Accessed 25 September 2013 2 httpwwwcfsphiastateeduDiseaseInfodiseasephpnameqfever Accessed 26 August 2013 3 httpwwwoieintindexphpid169L0htmfilechapitre1812htm Accessed 26 August 2013 4 El Mamy ABO MO Baba Y Barry K Isselmou ML Dia B Hampate MOB El Kory M Diop MM Lo Y Thiongane M Bengoumi L Puech L Plee F Claes S de La Rocque and B Doumbia 2011 Unexpected Rift Valley Fever outbreak northern Mauritania Emerg Infect Dis 1710 18941896 5 Kasari T DA Carr TV Lynn and JT Weaver 2008 Evaluation of pathways for release of Rift Valley fever virus into domestic ruminant livestock ruminant wildlife and human populations in the continental United States J Am Vet Med Assoc 232451429 American Association of Zoo Veterinarians Infectious Disease Manual ROTAVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals including humans and certain avian species Fecaloral Diarrhea and other signs of enteritis including inappetence and lethargy Self limiting to severe Supportive correcting dehydration acid base imbalance antibiotics to prevent secondary infection Vaccines available for humans cattle horses and pigs poultry Yes potentially Fact Sheet compiled by Meredith M Clancy Sheet completed on 15 October 2018 Fact Sheet Reviewed by Cara Field Susceptible animal groups Ruminants including nondomestic bovids antilocaprids pronghorn cervids and giraffids Rotaviral enteritis also documented in poultry and wild birds ferrets rabbits guinea pigs felids canids camelids equids and domestic pigs Rotaviruses especially of Group A are the most common cause of severe diarrhea in children under 5 years of age Rotavirus infections are considered speciesspecific but reassortment of the virus between species may occur Causative organism Rotaviruses family Reoviridae are generally named after the species where it was first found Bovine Rotavirus Porcine Rotavirus Feline Rotavirus Canine Rotavirus etc Much diversity exists in these viruses due to their genomes ability to mutate reassert and rearrange In human medicine and virology rotaviral isolates are grouped according to antigens present using A E with Group A being the most prevalent cause of illness in humans but Group C can also cause outbreaks Zoonotic potential Animal rotaviruses are reservoirs for genetic exchange with human rotaviruses and animal rotaviruses can infect humans both naturally and experimentally Distribution Worldwide Incubation period Variable from 15h to 5d Clinical signs Enteritis resulting in diarrhea is nearly always the presenting sign sometimes pale yellow or mucoid in character Lactoseintolerance may be present due to the lack of lactase secretion by enterocytes an important sign in nursing animals Other clinical signs may include fever inappetance dullness and progressive dehydration causing metabolic acidosis which if severe enough can lead to death Post mortem gross or histologic findings Gross lesions include thinning of the intestinal walls with sequestration of fluid into the small intestine leading to marked distention of the intestines and abdomen In young animals nondigested milk may be present in the intestine Depending on the strains virulence lesions may present in only localized areas of the jejunum or may be throughout the small intestine and into the large intestine Rotaviruses infect mature enterocytes on the villi surface in the small intestine leading to villous atrophy and blunting with clubshaped stumpy villi that are often fused Crypt epithelium is often hyperplastic while trying to recover the lost villous enterocytes Columnar epithelium is lost and replaced with cuboidal or squamous epithelium Diagnosis Electron microscopy EM can be used as a screening tool to identify virus in the feces EM alone is not sufficient to diagnose rotavirus as the cause of diarrhea comparative levels with nonclinical animals are used in cattle to support diagnosis Antigen detection can be performed via enzymelinked immunosorbent assay ELISA commonly used to diagnose rotavirus Enzyme immunoassays EIA pointofcare tests exist for human medicine that have been validated in detecting bovine rotavirus Latex agglutination testing can also be used to detect Group A rotavirus antigen Polymerase chain reaction PCR including reversetranscriptase qPCR can both detect rotavirus and differentiate between species Indirect fluorescent assay IFA can detect antigen in tissue generally using American Association of Zoo Veterinarians Infectious Disease Manual ROTAVIRUS postmortem samples Serology is generally noncontributory as rotavirus exposure is often widespread and results are nonspecific Material required for laboratory analysis PCR has become the most widely available test Feces for ELISA EIA latex agglutination PCR Fresh tissue small intestine for IFA Relevant diagnostic laboratories Michigan State University Diagnostic Center for Population and Animal Health PCR Bovine Equine Ferret Porcine Clinical Pathology Laboratory A215 Veterinary Medical Center Michigan State University East Lansing MI 488241314 517 3531683 httpswwwanimalhealthmsuedu Texas AM Veterinary Diagnostic Laboratory Electron microscopy PCR bovine College Station Laboratory PO Box Drawer 3040 College Station TX 778413040 Phone 979 8453414 Fax 979 8451794 httptvmdltamuedu Point of care testing ImmunoCard STAT Rotavirus test is available through numerous suppliers produced by Meridian Bioscience httpwwwmeridianbiosciencecomdiagnosticproductsrotovirusand adenovirusimmunocardimmunocardstatrotavirusaspx Treatment Treatment relies on correction of dehydration and metabolic acidosis using IV fluid resuscitation or oral rehydration solutions and bicarbonate given orally or IV to address acidosis Antibiotics are often used to prevent secondary bacterial infections via the compromised gastrointestinal tract Zinc is used adjunctively in management of human rotavirus Prevention and control In ruminants colostrum often contains antibodies IgA to rotavirus in herds where rotavirus is naturally circulating but the calfs antibody concentrations decline sharply after one week Vaccination of the dam 13m prior to calving increases circulating antibodies in the milk and helps reduce rotavirus in calves Vaccination strategies differ among practitioners for nondomestic hoofstock In species without viable vaccine prevention and control are best achieved by reducing fecal contamination of the environment through routine cleaning and removal of feces disinfection of enclosures and all material the animal contacts Isolation of sick individuals and quarantine of new animals is important to reduce exposure of naïve animals to shed virus In production animals the allinallout technique is used to reduce exposure and contamination Suggested disinfectant for housing facilities Rotaviruses are hardier than coronaviruses and other diarrheal viruses Disinfectants that are reported to be effective include formaldehyde 025 phenol 2 sodium hypochlorite 1 quaternary ammonium compounds and iodophores Cleaning steaming and disinfecting of housing facilities is recommended Notification Not reportable to USDA or OIE Measures required under the Animal Disease Surveillance Plan NA American Association of Zoo Veterinarians Infectious Disease Manual ROTAVIRUS Measures required for introducing animals to infected animal Not recommended Animals that have been naturally infected may have shortlived immunity via mucosal and cellmediated immunity however so can be reintroduced once convalesced Conditions for restoring diseasefree status after an outbreak NA Experts who may be consulted Roger K Maes DVM MS PhD Michigan State University Section Head Virology 4125 Beaumont Road Bldg 0215 Ste 161 Lansing MI 48910 5164325811 maesdcpahmsuedu Delbert Hank L Harris DVM PhD Iowa State University Professor Emeritus of Animal Science 11 Kildee Hall Ames Iowa 50011 5152941664 hharrisiastateedu K Gary Magdesian DVM DACVIM DACVECC DACVCP University of California Davis Professor of Medicine Epidemiology 3202 Tupper Hall Davis CA 95616 kgmagdesianvmthucdavisedu References 1 American Association of Swine Veterinarians Swine Disease Manual Neumann EJ Ramirex A Schwartz KJ eds Perry IA American Association of Swine Veterinarians 2010 Available from httpsvetmediastateeduvdpamFSVDswineindexdiseases 2 Baumeister BM Castro AE McGuireRodgers SJ Ramsay EC Detection and control of rotavirus infections in zoo animals J Am Vet Med Assoc 198318312521254 3 Citino SB Rotavirus and coronavirus infections in nondomestic ruminants In Fowler ME Miller RE eds Zoo and wild animal medicine Volume 4 Current therapy Philadelphia PA WB Saunders Co 1999 p 605612 4 Cook N Bridger J Kendall K Gomara MI ElAttar L Gray J The zoonotic potential of rotavirus J Infect 200448289302 5 Eugster AK Strother J Hartfield DA Rotavirus reoviruslike infection of neonatal ruminants in a zoo nursery J Wildl Dis 197814351354 6 Izzo M Gunn AA House JK Neonatal diarrhea In Smith BP ed Large animal internal medicine 5th edition St Louis MO Elsevier 2015 p 317 7 Maes RK Grooms DL Wise AG Han C Ciesicki V Hanson L Vickers ML Kanitz C Holland R Evaluation of a human Group A rotavirus assay for onsite detection of bovine rotavirus J Clin Microbiol 200341290294 8 Martella V Banyai K Matthijnssens J Buonavoglia C Ciarlet M Zoonotic aspects of rotaviruses Vet Microbiol 2010140 246255 9 Mulherin E Bryan J Beltman M OGrady L Pidgeon E Garon L Lloyd A Bainbridge J OShea H Whyte P Fanning S Molecular characterisation of a bovinelike rotavirus detected from a giraffe BMC Vet Res 2008446 10 Raphael BL Sneed L OttJoslin J Rotaviruslike infection associated with diarrhea in okapi J Am Vet Med Assoc 198618911831184 American Association of Zoo Veterinarians Infectious Disease Manual SALMONELLOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Most vertebrates Fecaloral Mild gastroenteritis with vomiting diarrhea Severe additionally anorexia lethargy pyrexia dehydration Severe acute septicemia systemic infection possible Varies from subclinical carriage to septicemia and death Septicemic form often is fatal without prior or unobserved clinical signs Antibiotics essential for septic salmonellosis controversial for enteric infection Biosecurity essential Pest control Sanitation Vaccination with autogenous bacterin available Yes Fact Sheet compiled by Cornelia J KetzRiley updated by Meredith M Clancy Sheet completed on 18 December 2018 Fact Sheet Reviewed by Lana Krol Susceptible animal groups Nontyphoidal salmonellosis causes natural infection in all taxa of vertebrates Reptiles are important carriers but multiple exotic pet species have been implicated in human disease outbreaks Only humans are susceptible to S typhi the causative agent of typhoid Causative organism Family Enterobacteriaceae Genus Salmonella Salmonella enterica has 6 subspecies but common language can abbreviate the serotype Salmonella enterica subsp enterica serotype Typhimurium can be abbreviated to Salmonella Typhimurium S enterica subspecies enterica I with common serovars S enteritidis S paratyphi S typhimurium S typhi S pullorum S gallinarum S enterica subspecies salamae II S enterica subspecies arizonae IIIa S enterica subspecies diarizonae IIIb S enterica subspecies houtenae IV S enterica subspecies indica VI There are over 2600 extant serovars recognized determined by phenotyping of the O somatic and H flagellar antigens Nomenclature for this genus has constantly evolved leading to some inconsistences in the literature particularly for serovars from subspecies arizonae IIIa and diarizonae IIIb which were once listed in their own genus Arizona or species Salmonella arizona and some laboratories fail to differentiate between these 2 during initial biochemical testing S bongori formerly S enterica subspecies V is of less veterinary importance For nomenclature clarify WHO CDC and Institut Pasteur use the KauffmanWhite scheme for naming serovars the most recent of which is found at httpswwwpasteurfrsitesdefaultfilesveng0pdf Zoonotic potential High Distribution Worldwide Incubation period Generally 14 days American Association of Zoo Veterinarians Infectious Disease Manual SALMONELLOSIS Clinical signs Acute gastroenteritis including vomiting and diarrhea pyrexia and anorexia Severesepticemic lethargy polydipsia dehydration petechial hemorrhages on cutaneous and mucosal surfaces joint pain polyarthritis abdominal pain respiratory signs neurological signs possibly death Chronic reduced productivity such as egg and milk production suppressed growth decreased fertility decreased hatchability and abortion Post mortem gross or histologic findings Most common findings during gross necropsy include signs of dehydration gastroenteritis hepatomegaly with or without miliary white foci splenomegaly and mesenteric lymphadenopathy Pneumonia can be observed more often in birds and calves In cases of septicemia petechial hemorrhages can occur in multiple organs with muscular necrosis typically involving myocardial and gizzard in avian species muscle nephropathy polyserositis and synovitis commonly found Histopathological findings include multifocal necrotic hepatitis necrosis of cryptic or surface enterocytes in lower small intestines cecum and colon Diagnosis Culture of fresh fecal material is still the most commonly used diagnostic tool to detect Salmonella shedding PCR can be used to evaluate shedding with a quicker turnaround time than culture Historically serotyping was performed on isolates to elucidate course of disease in individuals and epidemiology in populations Molecular techniques such as pulsedfield gel electrophoresis now allow for more exact epidemiologic tracing Serological examinations can be used to establish presence of Salmonella on herd basis but are not reliable for individual animal status identification although have been used to evaluate vaccination response and flock exposure Material required for laboratory analysis For culture or PCR feces organ tissue whole blood milk or other environmental material are recommended Serum is best used for serology such as ELISA Relevant diagnostic laboratories Any laboratory that is set up for culture methods can be used for first screening for Salmonella Serotyping is most commonly sent to the National Veterinary Services Laboratories Treatment Mild infections are selflimiting and are only treated with supportive care such as rehydration electrolytes and analgesics Antibiotic therapy is controversial as elimination is rare reinfection common and creation of a carrier state a likely outcome Animals treated with antibiotics have shown prolonged bacterial shedding post treatment Antibiotics are generally used for suspected sepsis or in immunocompromised or young animals where sepsis is likely While ideally antibiotics are based on antimicrobial resistance patterns commonly used antibiotics include trimethoprimsulfonamide combinations ampicillin fluoroquinolones and thirdgeneration cephalosporins although resistance to nearly all classes have been reported in some isolates Prevention and control Eradication is difficult due to asymptomatic carriers Preventive control programs should consist of a good biosecurity protocols Multiple nonpharmaceutical therapeutic measures including food and water additives such as probiotics have been tried to increase intestinal immunity Vaccination is not possible for most taxa of animals although vaccines exist for production animals poultry cattle and swine and autogenous vaccines may be produced for local use Suggested disinfectant for housing facilities Most commonly used disinfectants such as diluted hypochlorite quaternary ammonium based products are effective against Salmonella sp Notification Fowl Typhoid Salmonella enterica subsp enterica Gallinarum and serovar Pullorum Salmonella Pullorum reportable to USDA and OIE Salmonella Abortusovis reportable to USDA and OIE Positive laboratory tests are often reportable and various serovars may be reportable in particular states or jurisdictions Measures required under the Animal Disease Surveillance Plan Salmonellosis is part of the National Animal Disease Surveillance Plan due to its importance as a foodborne bacterial illness Specific measures required depend on the animal species and nature of the outbreak American Association of Zoo Veterinarians Infectious Disease Manual SALMONELLOSIS Measures required for introducing animals to infected animal Regular quarantine in a clean environment reduce access to host animals separate tools and personnel for quarantined animals Conditions for restoring diseasefree status after an outbreak Quarantine of whole collection isolation of sick and potentially infected animals testing of any potentially contaminated feed water surface and also healthy animals as well as personnel before giving access to previously contaminated area Multiple cultures of potentially infected animals necessary due to inconsistent shedding of bacteria Experts who may be consulted Centers for Disease Control and Prevention Division of Foodborne Waterborne and Environmental Diseases 1600 Clifton Rd Atlanta GA 30333 800CDCINFO USDAAPHISVSCenter for Epidemiology and Animal Health NRRC Building B MS 2E7 2150 Centre Avenue Fort Collins CO 805268117 9704947000 Email NAHMSaphisusdagov httpnahmsaphisusdagov References 1 CDC Internet Salmonella cited 16 Dec 2018 Available from httpswwwcdcgovsalmonellaindexhtml 2 Clancy MM Davis M Valitutto MT Nelson K Sykes IV JM Salmonella infection and carriage in reptiles in a zoological collection J Am Vet Med Assoc 201624810501059 3 Desin TS Köster W Potter AA Salmonella vaccines in poultry past present and future Expert Rev Vaccines 2013128796 4 Grimont PAD Weill FX Internet Antigenic formulae of the Salmonella serovars In WHO Collaborating Centre for Reference and Research on Salmonella 2007 2007 cited 2019 March 19 Available from httphemltdrupublicationssectionsbakterioziSalmonellamedicinesalm4articlepdf 5 Kirkwood JK Salmonellosis in songbirds order Passeriformes In Fowler ME Miller RE eds Zoo and wild animal medicine volume 6 St Louise MO Elsevier 2008 p 166169 6 National Association of State Public Health Veterinarians Animal Contact Compendium Committee Compedium of measures to prevent disease associated with animals in public settings J Am Vet Med Assoc 20132431701288 7 Spickler AR Internet Salmonella Nontyphoidal 2013 cited 16 Dec 2018 Available from httpwwwcfsphiastateeduDiseaseInfofactsheetsphp 8 Wattiau P Bolan C Bertrand S Methodologies for Salmonella enterica subsp enterica subtyping gold standards and alternatives Appl Environ Mirobiol 20117778777885 9 Wolfenden RE Layton SL Wolfenden AD Khatiwara A GaonaRamirez G Pumford NR Cole K Kwon YM Tellez G Bergman LR Hargis BM Development and evaluation of candidate recombinant Salmonellavectored Salmonella vaccines Poult Sci 20108923702379 American Association of Zoo Veterinarians Infectious Disease Manual SCHISTOSOMIASIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Old World monkeys great apes humans dogs cows rats water buffaloes pigs Percutaneous in contaminated water S mansoni S japonicum fever nausea cough diarrhea abdominal pain gastroesophageal bleeding CNS signs S haematobium hematuria dysuria SCC of the bladder Sometimes fatal more often a chronic disease Praziquantel Snail control good sanitation access to clean water Yes via snail vector Fact Sheet compiled by Christine Fiorello Sheet completed on January 25 2011 updated 1 November 2012 Fact Sheet Reviewed by Sara Childs Sanford Walter Boyce Susceptible animal groups Natural infections of S japonicum have been reported in nearly 50 mammalian species including humans rhesus macaques dogs cats rats pigs water buffalo cows horses donkeys goats rabbits wild carnivores wild pigs wild rodents shrews hedgehogs Many more primates and other species have been experimentally infected The most important species thought to maintain the disease in natural transmission cycles include humans dogs cows and pigs S haematobium infects humans and hybridizes with S bovis to infect cattle Causative organism Schistosoma japonicum S mansoni S haematobium Zoonotic potential Yes via a snail vector Humans are the most common host for S mansoni and S haematobium but S japonicum infects many domestic and wild mammals that can serve as reservoirs of the fluke Old World monkeys including baboons and vervet monkeys are hosts for S mansoni These host species are commonly found around human settlements and share water sources with humans Distribution S mansoni Africa Arabian peninsula South America S japonicum China Phillipines Indonesia S haematobium African Arabian peninsula Incubation period 46 weeks although signs due to the acute phase of infection may be immediate Clinical symptoms S japonicum and S mansoni acute phase fever nausea cough diarrhea chronic phase anemia bloody diarrhea gastroesophageal bleeding hepatomegaly splenomegaly cirrhosis cachexia ascites portal hypertension pulmonary hypertension S haematobium hematuria dysuria ureteral obstruction hydronephrosis squamous cell carcinoma of the bladder Post mortem gross or histologic findings Portal and periportal hepatic fibrosis hepatosplenomegaly gastroesophageal varices granulomatous hepatic inflammation mesenteric lymphadenopathy colonic ulceration urinary bladder and ureteral fibrosis hydronephrosis Diagnosis Fecal sedimentation or centrifugation Falcon assay screening test FAST ELISA IgGELISA PCR Urine centrifugation S haematobium Material required for laboratory analysis Feces serum urine Relevant diagnostic laboratories Any commercial lab should be able to find ova in feces or urine ARUP Laboratories in Salt Lake City UT can perform antibody testing 800 5222787 aruplabcom Treatment Praziquantel is the treatment of choice it should be repeated in 46 weeks Recently resistance to praziquantel is being recognized in some areas American Association of Zoo Veterinarians Infectious Disease Manual SCHISTOSOMIASIS Prevention and control Snail control improved sanitation access to clean water Suggested disinfectant for housing facilities Niclosamide 10 mgl to kill snails Notification none Measures required under the Animal Disease Surveillance Plan none Measures required for introducing animals to infected animal NA requires vector for transmission Conditions for restoring diseasefree status after an outbreak NA not in USA Experts who may be consulted Dr Patrick Skelly Molecular Helminthology Lab Cummings School of Veterinary Medicine Tufts University httpvettuftsedumhl Phone 5088874348 Fax 5088397911 Email PatrickSkellytuftsedu References 1 Brack M 2003 Schistosomiasis EAZWV Transmissible Disease Fact Sheet No 120 2 Fernandez Jr TJ MR Tarafder E Balolong Jr L Joseph AL Willingham 3rd P Bélisle JP Webster RM Olveda ST McGarvey and H Carabin 2007 Prevalence of Schistosoma japonicum infection among animals in fifty villages of Samar province the Phillipines Vector Borne and Zoonotic diseases 7214755 3 Gryseels B K Polman J Clerinx and L Kestens 2006 Human schistosomiasis Lancet 3689541 110618 4 Hardin BM WM White CT Clark and GT Maclennan Urinary tract schistosomiasis Journal of Urology 1845 213637 5 He YiXun B Salafsky and K Ramaswamy 2001 Hostparasite relationships of S japonicum in mammalian hosts Trends in Parasitology 177 32024 6 Kassa L A Omer W Tafesse T Taye F Kebebew and A Beker 2005 Schistosomiasis Ethiopian Public Health Training Initiative httpwwwcartercenterorgresourcespdfshealthephtilibrarymodulesDegreeModSchistoDegfina lpdf Accessed 10 July 2013 7 Legesse M and B Erko 2004 Zoonotic intestinal parasites in Papio anubis baboon and Cercopithecus aethiops vervet from four localities in Ethiopia Acta Tropica 90 3 23136 8 MüllerGraf CDM DA Collins C Packer and ME Woolhouse 1997 Schistosoma mansoni infection in a natural population of olive baboons in Gombe Stream National Park Tanzania Parasitology 115 621627 9 Oliveira LMA HLC Santos MML Goncalves MG Barreto and JM Peralta 2010 Evaluation of PCR as an additional tool for the diagnosis of lowintensity S mansoni infection Diagnostic Microbiology and Infectious Disease 68 4 41621 10 Standley CJ L Mugisha JJ Verweij M Adriko M Arinaitwe C Rowell A Atuhaire M Betson E Hobbs CR van Tulleken RA Kane L van Lieshout L Ajarova NB Kabatereine and JR Stothard 2011 Confirmed infection with intestinal schistosomiasis in semicaptive wildborn chimpanzees on Ngamba Island Uganda VectorBorne and Zoonotic Diseases epub doi101089vbz20100156 11 Vale TC SR de SousaPereira JG Ribas et al 2012 Neuroschistosomiasis mansoni literature review and guidelines Neurologist 18 6 333342 American Association of Zoo Veterinarians Infectious Disease Manual SCHISTOSOMIASIS 12 Wang W L Wang and YS Liang 2012 Susceptibility or resistance of praziquantel in human schistosomiasis a review Parasitological Research 111 5 187177 American Association of Zoo Veterinarians Infectious Disease Manual NEW WORLD SCREWWORM Cochliomyia hominivorax Fact Sheet compiled by Carlos R Sanchez Sheet completed on updated December 2017 Fact Sheet Reviewed by Heather Robertson Susceptible animal groups Mammals with most cases occurring in cattle goats sheep and wildlife however dogs and cats may be affected Birds are rarely affected Causative organism Cochliomyia hominivorax Zoonotic potential Yes with the young elderly or infirm higher risk of infection Distribution Current distribution includes Caribbean islands eradicated in Curacao Virgin Islands and Puerto Rico and northern countries of South America to Uruguay northern Chile and northern Argentina Panama was recognized free of NWS in 2006 and a permanent barrier zone was established in the Darien province of Eastern Panama New World screwworm had been eradicated from the United States more than three decades ago On October 3 2016 USDA declared the confirmation of New World screwworm Cochliomyia hominivorax in Key deer from the National Key Deer Refuge in Big Pine Key Florida In March 2017 the USDAs APHIS announced the successful eradication of the New World Screwworm from Florida Incubation period After 1224 hrs eggs are deposited in wounds or mucous membranes have larvae emerge which burrow into the wound After 7 days the larvae exit from the wound and fall to the ground Pupal period ranges from 7d2mo depending on temperatures Complete cycle takes between 3 weeks and 3 months Clinical signs Animals with screwworm infestation often display discomfort and appear unthrifty and depressed Other nonspecific clinical signs include separation from group anorexia and reduced milk production in dairy cattle Typically an open wound is present with malodorous reddishbrown fluid that has either eggs or larvae Egg masses are found around the wound as shinglelike raft of whitish or cream colored egg The larvae can be visible or deep inside the wound closed wounds may have slight movement inside Larvae can also be observed on intact mucous membranes of body orifices nose anus vaginal area The wound can enlarge due to multiple infestations and if not treated animal could die within 2 weeks Post mortem gross or histologic findings Screwworms do not feed on dead tissue or carrion so larvae are unlikely to be found on postmortem examination unless the animal died recently Larvae of different ages are normally found on wounds or natural opening mucous membranes Other fly larvae may be present in lesion making gross diagnostic difficult Microscopic lesions are not useful for the definitive diagnosis of screwworm Diagnosis Screwworm is a reportable disease in US Before collecting or sending any samples from animals with suspected screwworm federal and state authorities should be contacted Identification of the eggs and flies Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All warm blooded animals but most cases occur in cattle goats and sheep In Oct 2016 cases were confirmed in Key deer O virginianus clavium in Florida USA Gravid female flies deposit eggs either in wounds or directly onto intact mucous membranes Discomfort decreased appetite wounds with malodorous reddishbrown fluid with larvae slight movement inside a closed wound Upon closer observation of wound a mass of clearcolored eggs can be observed Untreated animals could die Mortality rates in Texas when disease was endemic in the USA was 20 80 in fawns However no cases of myiasis in newborn Key deer fawns were observed in 2016 Mortality in the 2016 outbreak varied between 7 98 animalsmonth Treatment of wounds with organo phosphates spray foam dip dust eg coumaphos ronnel or lindane Carbamate and pyrethroid compounds are also effective vs larvae immature forms and flies Monitoring wounds and treating infested wounds with insecticides Doramectin injection Yes American Association of Zoo Veterinarians Infectious Disease Manual NEW WORLD SCREWWORM Cochliomyia hominivorax are best to left to an entomologist However specifically for larvae they should be removed from the deepest part of the wound and examined grossly by dissecting microscope Larvae grow from 2mm to fully grown larvae that can reach 15cm in length Larvae are identified by their wood screw shape Screwworm larvae have whitish bodies and can be differentiated from other larvae by the darkly pigmented tracheal tubes on the dorsal aspect of the posterior end of 3rd stage larvae Material required for laboratory analysis Larvae eggs or flies can be conserved in vials containing 80 ethanol or isopropyl alcohol formalin should not be used Larvae should be removed from the deepest part of the wound to reduce the possibility of collecting nonscrewworm species optimal preservation of larvae in their natural extended state can be made by killing them in boiling water 1530 seconds immersion before storage in 80 ethanol Suspected screwworm eggs or flies may also be submitted for diagnosis eggs may be collected using a scalpel as scraper Before collecting or sending any samples from animals with suspected screwworm infections federal and state authorities should be contacted In the US screwworm is a reportable disease and should be reported within 24 hours Samples should only be sent under secure conditions and to authorized laboratories to prevent the spread of the disease Screwworms can infest humans samples should be collected and handled with all appropriate precautions Relevant diagnostic laboratories USDAAPHISVSNVSL 1920 Dayton Ave for parasite specimen submission Use VS Form 538 available on the APHIS website httpwwwaphisusdagovlibraryformspdfVSForm538pdf PO Box 844 for letters Ames IA 50010 515 3377266 Fax 515 3377397 For detailed information concerning the handling and shipping of diagnostic specimens as well as overall guidance on FAD investigations please see APHIS Veterinary Services VS Guidance Document 12001 previously VS Memorandum 5804 and the FAD Investigation Manual Manual 40 available at httpwwwaphisusdagovfadprep Treatment Before any treatment is implemented federal and local authorities must be notified Organophosphate insecticides coumaphos ronnel and lindane are effective against newly hatched larvae immature forms and adult flies Carbamates and pyrethroids may also be used as are effective against larvae and adult flies In a recent study nitenpyram showed 100 efficacy on the treatment of myiasis by C hominivorax in naturally infested dogs Screwworms in wounds are killed by direct application of aerosol dust or foam that contain any of these products Removal of necrotic tissue may be necessary and antibiotics may be given when secondary bacterial contamination is present Prevention and control In areas where NWS is found measures should be implemented to prevent wounds and avoid myiasis For example eliminate wounding procedures handle livestock with care and inspect pens for sharp objects In 1966 US was declared officially free of indigenous screwworms therefore any presumptive case must be reported The OIE International Animal Health Code stipulates that is necessary to follow strict observation of the requirements for international trade When importing domestic and wild mammals from countries considered infested with New World or Old World screwworm veterinary administrations should require the presentation of an international veterinary certificate attesting that 1 Immediately prior to loading the animals have been inspected on the premises by an official veterinarian and that any infested animal has been rejected for export 2 Immediately prior to entering the quarantine pens in the exporting country American Association of Zoo Veterinarians Infectious Disease Manual NEW WORLD SCREWWORM Cochliomyia hominivorax a each animal has been thoroughly examined for infested wounds by an official veterinarian and that no infestation has been found in any animal and b any wounds have been treated prophylactically with an officially approved only larvicide at the recommended dose and c all animals have been dipped sprayed or otherwise treated immediately after inspection with a product officially approved by the importing and exporting countries for the control of New World or Old World screwworm under the supervision of an official veterinarian and in conformity with the manufacturers recommendations 3 at the end of the quarantine and immediately prior to shipment for export a all animals have been reexamined for the presence of infestation and all animals have been found free of infestation b all wounds have been prophylactically treated with an approved only larvicide under the supervision of an Official Veterinarian c all animals have been prophylactically treated again by dipping or spraying as in point 2 above The floor of the quarantine area and transport vehicles must be thoroughly sprayed with an officially approved larvicide before and after each use The transit route must be the most direct with no stopover without prior permission of the importing country On arrival at the importation point all animals must be thoroughly inspected for wounds and possible new world or old world screwworm infestation under the supervision of an Official Veterinarian The bedding material of the vehicle and the quarantine area should immediately be gathered and burned following each consignment In addition any imported animals from areas where screwworms are endemic must be thoroughly inspected for wound and infestations before they are allowed to enter premises Wounds that do not appear to be infested are treated with an insecticide as preventative measure Any infestations that become apparent after an animal enters the country must be treated promptly APHIS began releasing sterile flies in October 2016 as part of aggressive eradication effort undertaken in collaboration with the US Fish and Wildlife Service Florida Department of Agriculture and Consumer Services and local partners Suggested disinfectant for housing facilities Facilities where screwworm was diagnosed and vehicles that may contain adults or immature screwworms should be sprayed with insecticides any bedding material used in the area where animal was quarantined should immediately be gathered and burned Notification Any presumptive screwworm infestation must be reported to both state and federal Area Veterinarian In Charge AVIC authorities Residents who have warmblooded animals pets livestock etc should watch their animals carefully Florida residents should report any potential cases to 1800HELPFLA 18004357352 or nonFlorida residents should call 850 4103800 Measures required under the Animal Disease Surveillance Plan Because New World screwworm has been recently eradicated from the US the National Animal Health Surveillance System NAHSS does not have a program for active surveillance at this time However APHIS and Florida Department of Agriculture and Consumer Services FDACS will continue passive surveillance to ensure any new findings are quickly identified This surveillance includes veterinarians reporting any suspicious cases wildlife surveillance concerned citizens that see suspicious wounds on animals or even on a person and continued communication with the parks and the National Key Deer Refuge Because this is a reportable disease state and federal AVIC authorities should be notified of any presumptive screwworm infestation Measures required for introducing animals to infected animal In nonendemic regions any infected animal is quarantined until treatment is complete and the wounds have healed Treatment of the environment as explained above may also be necessary Conditions for restoring diseasefree status after an outbreak Areas must be sprayed with approved larvicide the disease has been eradicated in the US by the Sterile Male Release Technique SMRT program and therefore if there is indication of infection in the USA the USDAAPHIS must be involved on any discussion about freestatus of a premise American Association of Zoo Veterinarians Infectious Disease Manual NEW WORLD SCREWWORM Cochliomyia hominivorax Experts who may be consulted Steven R Skoda Research entomologist USDAAgricultural Research Service 2700 Fredericksburg Road Kerrville TX 78028 Telephone 830 7920334 Fax 830 7920314 steveskodaarsusdagov National Preparedness and Incident Coordination Veterinary Services Animal and Plant Health Inspection Service US Department of Agriculture 4700 River Road Unit 41 Riverdale MD 207371231 Telephone 301 8513595 Fax 301 7347817 FADPRePCommentsaphisusdagov References 1 Anziani OS Flores SG Moltedo H Derozier C Guglielmone AA Zimmermann GA Wanker O Persistent activity of doramectin and ivermectin in the prevention of cutaneous myiasis in cattle experimentally infested with Cochliomyia hominivorax Vet Parasitol 200087243247 2 The Center for Food Security and Public Health Iowa State University Internet Screwworm myiasis 2016 cited 2019 March 11 Available from httpwwwcfsphiastateeduFactsheetspdfsscrewwormmyiasispdf 3 Correia TR Scott FB Verocai GG Souza CP Fernandes JI Melo RM Vieira VP Ribeiro FA Larvicidal efficacy of nitenpyram on the treatment of myiasis caused by Cochliomyia hominivorax Diptera Calliphoridae in dogs Vet Parasitol 20101731216972 4 Disease Response Strategy New World Screwworm Myiasis Foreign Animal Disease Preparedness Response Plan USDA APHIS Veterinary Services 2014 5 Robbins K Khachemoune A Cutaneous myiasis a review of the common types of myiasis Int J Dermatol 2010491010921098 6 United States Department of Agriculture Internet 2016 Investigation into Introduction of New World Screwworm into Florida Keys 2016 cited 2019 March 5 Available from httpswwwaphisusdagovstakeholdersdownloads2017nwsepireportpdf 7 United States Department of Agriculture Animal and Plant Health Inspection Service Internet Status of Reportable Diseases in the United States 2015 cited 2013 June 21 Available from httpswwwaphisusdagovaphisourfocusanimalhealthmonitoringand surveillanceSANAHSSCTDiseasestatus2015 8 United States Department of Agriculture National Agriculture Library Internet Selections from the Screwworm Eradication Collection 2000 cited 2019 March 11 Available from httpswwwnalusdagovexhibitsspeccollexhibitsshowstopscrewwormsselectionsfr 9 World Organization for Animal Health Internet OIE Technical disease cards Screwworm Old World and New World 2013 cited 2019 March 11 Available from httpwwwoieintfileadminhomeenganimalhealthintheworlddocspdfdiseasecardsscrewwor mpdf 10 World Organization for Animal Health Internet Terrestrial Animal Health Code Volume 1 Section 8 Chapter 812 New World Screwworm Cochliomyia homnivorax and Old World Screwworm Chrysomya bezziana c19922018 cited 2019 March 11 Available from Available at httpwwwoieintindexphpid169L0htmfilechapitrecochliomyiachrysomyahtm American Association of Zoo Veterinarians Infectious Disease Manual OLD WORLD SCREWWORM Chrysomya bezziana Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All warm blooded animals including birds Flies are attracted to open superficial wounds as small as a tick bite Occasionally Old World screwworms also lay their eggs on unbroken soft skin particularly if it has blood or mucous on its surface Gravid female flies deposit eggs either into wounds or directly onto intact mucous membranes Severe myiasis in open wounds associated discomfort and decreased appetite Severe infestations that remain untreated may result in the death of the host in a short time 714 days Removal and killing of the larvae in lesion Treatment of the wound with approved insecticide Treatment is normally repeated until the wound has healed Removal of necrotic tissue is necessary Ivermectin 200300 mcgkg Monitoring wounds and treating infested wounds with insecticides Yes Fact Sheet compiled by Carlos R Sanchez Sheet completed on last update December 2017 Fact Sheet Reviewed by Sarrah Kaye Susceptible animal groups All mammals domestic and many species of wildlife are affected potentially problem is rare in birds Causative organism Chrysomya bezziana Zoonotic potential Yes humans can be hosts for screwworm larvae but it is primarily a veterinary pest Distribution The distribution of Old World screwworm is confined to the Old World Chrysomya bezziana is widely distributed throughout tropical areas It is most prevalent in Southeast Asia and throughout much of Africa from Ethiopia and subSaharan countries to northern South Africa some countries in the Middle East reports confirmed from Iran Iraq and recently Yemen India the Malay Peninsula the Indonesian and Philippine Islands and Papua New Guinea C bezziana has never become established in Europe Australia New Zealand or the Western Hemisphere Because of its distribution the most likely potential port of entry into the US is Hawaii Incubation period Eggs hatch within 824 hrs after being laid Once the larvae emerge they immediately begin to feed on the wound fluids and underlying tissues burrowing as a group headdownwards into the wound The entire larval stage lasts 58 days followed by larvae leaving the wound and pupating in the soil Maturation of pupae to adult is temperature dependent and ranges from 7 days at 28C to 60 days at temperatures of 1015C Female flies mate usually only once but can lay more than one batch of eggs at intervals of a few days Clinical signs Animals with screwworm infestations often display discomfort and appear unthrifty and depressed other nonspecific clinical signs include separation from group and anorexia Screwworms can infest a wide variety of wounds from tick bites to cuts and dehorning or branding wounds Infestations are very common in the navels of newborns fawns with screwworms in their navels may stand in water up to their abdomen and the perivulvar and perineal regions of their dams If a screwworm deposits its eggs on mucous membranes the larvae may enter any orifice including the nostrils sinuses mouth orbits of the eye ears or genitalia Infested wounds often have a serosanguineous discharge and sometimes a distinctive odor By the third day the larvae may be easily found secondary bacterial contamination is also common The wound can enlarge due to multiple infestations and if not treated animal could die within 2 weeks Post mortem gross or histologic findings The larvae of C bezziana are obligatory wound parasites that never develop in carcasses or decomposing organic material Larvae are unlikely to be found on postmortem American Association of Zoo Veterinarians Infectious Disease Manual OLD WORLD SCREWWORM Chrysomya bezziana examination unless the animal died recently Larvae of different ages are normally found on wounds or natural openings and mucous membranes in live animals Other fly larvae may be present in lesions making gross diagnosis difficult Microscopic lesions are not useful for the diagnosis of screwworm Diagnosis Diagnosis is by identification of the parasite under the microscope however before collecting or sending any samples from animals with suspected screwworm infections federal and state authorities should be contacted Clinical presentation of screwworm is always associated with a variety of preestablished wounds and should be considered in the event of any myiasis Definitive diagnosis can be made after observation extraction and identification of typical larvae along with history of travel to an area endemic for C bezziana Larvae must be removed from the deeper areas as well as superficial regions to be sure all species present are examined Larva should be placed in 70 alcohol and not in formalin for future identification Fully mature larvae develop a reddishpink tinge over the creamy white color of younger larvae Screwworm species have prominent rings of spines around the body and these spines appear large and conspicuous under a microscope when compared with most nonscrewworm species If a wound is considered to be infested with Old World screwworms samples should be collected and sent to eradication officials Adult screwworms are uncommonly seen They are also difficult to distinguish from other flies Other techniques used mostly in research laboratories include cuticular hydrocarbon analysis analysis of mitochondrial DNA and random amplified polymorphic DNA polymerase chain reaction RAPDPCR assays Material required for laboratory analysis Before collecting or sending any samples from animals with suspected screwworm infections federal and state authorities should be contacted Screwworms can infest humans samples should be collected and handled with all appropriate precautions Larvae eggs or flies can be conserved in vials containing 7080 ethanol or isopropyl alcohol formalin should not be used Different larval stages should be collected larvae should be removed from the deepest part of the wound to reduce the possibility of collecting nonscrewworm species Optimal preservation of larvae in their natural extended state can be made by killing them in boiling water 1530 seconds immersion before storage in 80 ethanol Suspect screwworm eggs or flies may also be submitted for diagnosis eggs are best collected using a scalpel as a scraper Relevant diagnostic laboratories USDAAPHISVSNVSL 1920 Dayton Ave for packages PO Box 844 for letters Ames IA 50010 515 3377266 Fax 515 3377397 httpwwwaphisusdagovservicesreportpestdiseasereportpestdiseaseshtml USDAAPHISVSNVSLFADDL 40550 Route 25 for packages Orient Point NY 11957 PO Box 848 for letters Greenport NY 119440848 631 3233256 Fax 631 3233366 Treatment Removal and killing of the larvae present in any wound or lesion Immediate treatment of all detected wounds with an approved insecticide organophosphate insecticides carbamates and pyrethroids should be followed by a precautionary spraying or dipping of the animals before transport For residual protection against reinfestation insecticides must be applied at 23day intervals until the wound has healed animals with screwwormsuspect wounds should be quarantined until treated and wounds have clearly healed American Association of Zoo Veterinarians Infectious Disease Manual OLD WORLD SCREWWORM Chrysomya bezziana A single subcutaneous injection of ivermectin 200 mcgkg has been effective against OWS in preventing navel strike of newborn calves and scrotal strike of castrated calves and also prevented restrike of treated wounds of adult cattle Prevention and control The OIE International Animal Health Code stipulates that is necessary to follow strict observation of the requirements for international trade When importing domestic and wild mammals from countries considered infested with New World or Old World screwworm veterinary administrations should require presentation of an international veterinary certificate attesting that 1 Immediately prior to loading the animals have been inspected on the premises by an official veterinarian and that any infested animal has been rejected for export 2 Immediately prior to entering the quarantine pens in the exporting country a each animal has been thoroughly examined for infested wounds by an official veterinarian and that no infestation has been found in any animal and b any wounds have been treated prophylactically with an officially approved larvicide at the recommended dose and c all animals have been dipped sprayed or otherwise treated immediately after inspection with a product officially approved by the importing and exporting countries for the control of New World or Old World screwworm under the supervision of an official veterinarian and in conformity with the manufacturers recommendations 3 At the end of the quarantine and immediately prior to shipment for export a all animals have been reexamined for the presence of infestation and all animals have been found free of infestation b all wounds have been prophylactically treated with an approved larvicide under the supervision of an official veterinarian c all animals have been prophylactically treated again by dipping or spraying as in point 2 above The floor of the quarantine area and transport vehicles must be thoroughly sprayed with an officially approved larvicide before and after each use The transit route must be the most direct with no stopover without prior permission of the importing country On arrival at the importation point all animals must be thoroughly inspected for wounds and possible New World or Old World screwworm infestation under the supervision of an official veterinarian The bedding material of the vehicle and the quarantine area should immediately be gathered and burned following each consignment In addition any imported animals from areas where screwworms are endemic must be thoroughly inspected for wounds and infestations before they are allowed to enter premises Wounds that do not appear to be infested are treated with an insecticide as preventative measure Any infestations that become apparent after an animal enters the country must be treated promptly Suggested disinfectant for housing facilities Facilities where screwworm was diagnosed and vehicles that may contain adults or immature screwworms should be sprayed with insecticides any bedding material used in the area where the animal was quarantined should immediately be gathered and burned Notification Any presumptive screwworm infestation must be reported to both state and federal Area Veterinarian In Charge AVIC authorities Measures required under the Animal Disease Surveillance Plan Because Old World screwworm has never been reported in the US the National Animal Health Surveillance System NAHSS does not have a program for active surveillance However as this a reportable disease state and federal AVIC authorities should be notified of any presumptive screwworm infestation Measures required for introducing animals to infected animal In nonendemic regions any infected animal is quarantined until treatment is complete and the wounds have healed Treatment of the environment as explained above may also be necessary American Association of Zoo Veterinarians Infectious Disease Manual OLD WORLD SCREWWORM Chrysomya bezziana Conditions for restoring diseasefree status after an outbreak Old World screwworm has never been reported in the US and therefore if there is any indication of any screwworm infection in the US the USDA APHIS must be notified immediately Experts who may be consulted Steven R Skoda Research entomologist USDAAgricultural Research Service 2700 Fredericksburg Road Kerrville TX 78028 830 7920334 Fax 830 7920314 steveskodaarsusdagov Project Manager Old World screwworm fly Animal Health Australia 02 6203 3912 ahaanimalhealthaustraliacomau or call or call the Emergency Animal Disease Watch Hotline 1800 675 888 References 1 The Center for Food Security and Public Health Iowa State University Internet Screwworm myiasis 2016 cited 2019 March 11 Available from httpwwwcfsphiastateeduFactsheetspdfsscrewwormmyiasispdf 2 Spradbery JP Tozer RS Pound AA The efficacy of insecticides against the screwworm fly Chrysomya bezziana Aust Vet J 19916810 338342 3 United States Department of Agriculture Animal and Plant Health Inspection Service Internet Status of Reportable Diseases in the United States 2015 cited 2013 June 21 Available from httpswwwaphisusdagovaphisourfocusanimalhealthmonitoringand surveillanceSANAHSSCTDiseasestatus2015 4 World Organization for Animal Health Internet OIE Technical disease cards Screwworm Old World and New World 2013 cited 2019 March 11 Available from httpwwwoieintfileadminhomeenganimalhealthintheworlddocspdfdiseasecardsscrewworm pdf 5 World Organization for Animal Health Internet Terrestrial Animal Health Code Volume 1 Section 8 Chapter 812 New World Screwworm Cochliomyia homnivorax and Old World Screwworm Chrysomya bezziana c19922018 cited 2019 March 11 Available from Available at httpwwwoieintindexphpid169L0htmfilechapitrecochliomyiachrysomyahtm American Association of Zoo Veterinarians Infectious Disease Manual SEALPOX VIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Many pinniped species especially seals and sea lions Direct contact ie rubbing bites scratches saliva bodily fluids and fomites ie rubber gavage tubing feeding apparatus gloves needle puncture Most often seen in juveniles animals in distress or newly housed Firm skin nodules 13cm will appear on head neck and thorax and can spread to abdomen flippers and mucosa Infected area can become inflamed or necrotic Often mild severity with low mortal ity Those individuals with immune suppressive conditions are at risk for a more severe infection Lesions usually heal within a few weeks without treatment and leave a slightly raised gray scar without fur Restrict movement of animals between enclosures replace or disinfect gloves when handling animals drain and scrub pens with 10 bleach solution regularly wear proper personal protective equipment Yes Fact Sheet compiled by Nadia F GallardoRomero Benjamin P Monroe Sheet updated on 20 August 2013 Fact Sheet Reviewed by William Van Bonn Ginny Emerson Susceptible animal groups Harbor seals grey seals Northern fur seals Northern elephant seals California sea lions Stellers sea lions and South American sea lions Causative organism Sealpox virus a member of the Parapoxvirus genus Zoonotic potential Yes Distribution The geographic range of sealpox virus is considered worldwide and infection has been confirmed in freeranging pinnipeds in the Atlantic and Pacific Oceans including America Europe and Siberia and Antarctica Sealpox infection has been identified in captive pinnipeds and humans at marine rehabilitation centers in North America and Europe Incubation period Clinical signs can appear within 15 weeks post exposure in captive animals Human clinical signs have reportedly developed one week after exposure Clinical signs Animals Sealpox infection is highly contagious in confined spaces with low mortality rates but very high morbidity Juveniles distressed and newlyhoused animals are the most likely to have active disease The skin will present 13 cm firm skin nodules or lumps on head neck and thorax and may spread to abdomen flippers and mucosa Lesions can present as solitary in clusters or generalized and progress from inflamed skin to necrotic Humans Persons who handle sick animals may come into contact with the virus and may get infected if they have small open cuts or breaks in the skin Rare casesdevelop painful swollen sores that may evolve into a bullous lesion Infection may be more severe in persons with skin or immunedeficient medical conditions American Association of Zoo Veterinarians Infectious Disease Manual SEALPOX VIRUS Post mortem gross or histologic findings Firm cutaneous nodules 13 cm diameter are the characteristic lesions of the disease They can be congested and focally ulcerated solitary in clusters or generalized along the animal body Histologically the lesions are characterized by epithelial hyperplasia and acanthosis The dermis may present intense inflammatory infiltrate and necrosis the epidermis may demonstrate edema vacuolization and ballooning degeneration of keratinocytes Eosinophilic cytoplasmic inclusions are also typical findings Diagnosis Classic clinical presentation is used predominantly especially in rehabilitation settings where it is observed seasonally Molecular assays for viral DNA detection are most commonly used including PCR RFLPs and sequencing Observation of typical cytoplasmic effect CPE in cell culture histology viral isolation and virion visualization by electron microscopy also are used as confirmation of findings Differential diagnosis with seal finger caused by a Mycoplasma anthrax and fungal infections should be performed Material required for laboratory analysis Swabs of swelling mucosal or other lesions are the preferred sample Place swab in a dry sterile micro tube store at 20ºC Skin biopsies containing a margin of normal tissue around the affected area Place the half of the sample in 10 formalin and the other half in a dry sterile micro tube store at 20ºC CDC laboratories can provide specimen collection guidance Contact the reference laboratory prior to shipping to inquire about necessary permits Relevant diagnostic laboratories Centers for Disease Control and Prevention Poxvirus and Rabies Branch CDC Poxvirus Inquiry line 4046394129 1600 Clifton Rd NE Atlanta GA 30333 Nzr6cdcgov University of Florida College of Veterinary Medicine Marine Mammal Health Program Fax 352 3925464 PO Box 100126 Gainesville FL 32610 NollensHmailvetmedufledu Treatment Lesions usually resolve within a few weeks without treatment and may leave a scar Palliative treatment is recommended for human infection to control secondary infections inflammation and pain However the literature has previously reported in vitro susceptibility of sealpox virus to cidofovir Prevention and control Quarantine newly admitted animals restrict movement of animals between enclosures and decrease the number of animals per pen Replace or disinfect gloves and equipment when handling sick animals and between enclosures drain and scrub pens with 10 bleach solution or other disinfectant regularly Wear proper personal protective equipment PPE including rubber or latex gloves rain pants overalls or suits goggles andor masks Frequent hand washing is encouraged after handling animals enclosures or equipment Suggested disinfectant for housing facilities 10 bleach solution chlorhexidine gluconate based solutions and other antiviral solutions Notifications Sealpox virus infection is not a reportable disease However state or local health departments should be notified of suspected human infections Measures required under the Animal Disease Surveillance Plan The disease is not currently listed under the USDA National Animal Health Surveillance andor Reporting systems Measures required for introducing animals to an infected animals Sealpox is highly contagious among pinnipeds and will spread easily between animals in direct contact Introduction of healthy animals American Association of Zoo Veterinarians Infectious Disease Manual SEALPOX VIRUS to sick animals is not recommended until skin lesions have completely healed Conditions for restoring diseasefree status after an outbreak No specific standards exist at this time However it is recommended to test the animals for viral DNA presence once the lesions are completely healed If all animals from the center are negative diseasefree status can be restored and recommendation of quarantine and testing of new individuals should be applied Experts who may be consulted Mary Reynolds PhD MPH Poxvirus and Rabies Branch CDC Poxvirus Inquiry line 4046394129 1600 Clifton Rd NE Atlanta GA 30333 Nzr6cdcgov References 1 Becher P M König G Müller U Siebert and HJ Thiel 2002 Characterization of sealpox virus a separate member of the parapoxviruses Arch Virol 1476 11331140 2 Clark C PG McIntyre A Evans CJ McInnes and S LewisJones 2005 Human sealpox resulting from a seal bite confirmation that sealpox virus is zoonotic Br J Dermatol 1524 791 793 3 Hicks BD and GA Worthy 1987 Sealpox in captive grey seals Halichoerus grypus and their handlers J Wildl Dis 231 16 4 Müller G S Gröters U Siebert T Rosenberger J Driver M König P Becher U Hetzel and W Baumgärtner 2003 Parapoxvirus infection in harbor seals Phoca vitulina from the German North Sea Vet Pathol 404 445454 5 Nollens HH FM Gulland ER Jacobson JA Hernandez PA Klein MT Walsh and RC Condit 2008 In vitro susceptibility of sea lion poxvirus to cidofovir Antiviral Res 801 7780 6 Nollens HH ER Jacobson FM Gulland DO Beusse GD Bossart JA Hernandez PA Klein and RC Condit 2006 Pathology and preliminary characterization of a parapoxvirus isolated from a California sea lion Zalophus californianus J Wildl Dis 421 2332 7 Roess AA RS Levine L Barth BP Monroe DS Carroll IK Damon and MG Reynolds 2011 Sealpox virus in marine mammal rehabilitation facilities North America 20072009 Emerg Infect Dis 1712 22032208 American Association of Zoo Veterinarians Infectious Disease Manual SHEEP AND GOAT POX Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Sheep and goats Airborne direct contact with infected animals and fomites biting insects are possible source Inappetence fever skin lesions of maculae papules and scabs dyspnea nasal discharge conjunctivitis Mild to severe depending on age breed and immunity None although can administer antibiotics to prevent secondary bacterial infections Quarantine incoming and cull infected animals isolate recovering animals properly clean infected area and utensils Outside US prophylactic vaccination is used commonly No Fact Sheet compiled by Kevin Leiske revised by Alfonso Torres Sheet completed on 20 January 2011 updated 2 August 2013 Fact Sheet Reviewed by James Rasmussen Charles Lamien Susceptible animal groups All breeds of domestic and wild sheep and goats Causative organism Sheep pox and Goat pox viruses Family Poxviridae Genus Capripoxvirus While it is recognized that sheep pox virus and goat pox virus are different but related viruses both agents have the ability to infect either sheep or goats causing a disease that is clinically and pathologically identical Zoonotic potential None Distribution Africa north of Equator Middle East Turkey Greece Central Asia South East Asia several countries in East Asia including parts of China Russia and Mongolia This disease is one of the most actively spreading diseases affecting small ruminants during the last 510 years Incubation period 421 days but usually 12 weeks Clinical signs Fever usually precedes the skin lesions that start as erythematous macules and progress to hard papules The center of the papules become depressed and turns a whitish grey color The area then becomes necrotic and is surrounded by an area of hyperemia Necrotic skin lesions culminate in scabs that leave a scar after scab loss Lesions are usually easier to find in areas of the body that have sparse hair ie axillary and inguinal areas and under the tail Mucous membranes can develop similar lesions that may become necrotic Dyspnea nasal discharge and conjunctivitis also can occur In endemic areas the disease can be mild or the infection inapparent Post mortem gross or histologic findings Typical pox skin lesions ulceration of the mucous membranes firm nodules in the lungs grey or white papules and ulcerations can also be seen in the abomasal mucosa as well as the rumen large intestines pharynx trachea and esophagus Lymph nodes are enlarged and edematous and the liver and kidney may have pale discrete subcapsular foci on the surface Diagnosis Virus detection by electron microscopy on dry skin scabs Nucleic acid detection by PCR in tissue samples or virus isolation on cell culture AGIDs or ELISAs can detect viral antigens Serology AGID IFA ELISA VN Western blotting is available but is not that reliable given that capripoxvirus immunity is mostly cellassociated Nasal swab can be sampled for molecular diagnostics American Association of Zoo Veterinarians Infectious Disease Manual SHEEP AND GOAT POX Material required for laboratory analysis In live animals biopsies of skin lesions scraping of skin lesions as well as lymph node aspirates and blood Nasal swabs can be utilized for PCR At necropsy samples from skin lesions lymph nodes and lung lesions should be collected Lesions in other organs can also be submitted based on postmortem findings Relevant diagnostic laboratories Foreign Animal Disease Diagnostic Laboratory USDAAPHISVSNVSLFADDL 40550 Route 25 for packages Orient Point NY 11957 PO Box 848 for letters Greenport NY 119440848 Director Dr Fernando TorresVelez Phone 631 3233256 Fax 631 3233366 Email FernandoJTorresVelezaphisusdagov Treatment None although antibiotics could be used to prevent secondary bacterial infections Prevention and control Quarantine incoming and cull infected animals Recovering animals should be isolated for 45 days after clinical signs are no longer present Infected areas and utensils should be cleaned properly Viable virus may be found in shaded areas of the environment for up to 6 months after an outbreak Vaccination after 6 months of age has helped decrease morbidity and control spread in other countries MLV products tend to provide best protection but they are not 100 protective These MLV products are not allowed for use in the US Suggested disinfectant for housing facilities Approved disinfectants for sheepgoat pox include 4 sodium carbonate solutions 2 sodium hydroxide solution or up to 125 sodium hypochorite Notification Any suspected case should be notified to State and federal authorities within 24 hours for proper investigation and diagnosis by trained State or Federal Foreign Animal Disease Diagnosticians Measures required under the Animal Disease Surveillance Plan Early stages of sheepgoat pox can be similar to some cases of Contagious Ectyma orf Measures required for introducing animals to infected animal Animals that are infected and survive have very good immunity However they should be isolated for 45 days after clinical signs are no longer present Conditions for restoring diseasefree status after an outbreak Culling infected herd may be required Isolation for 45 days after no more clinical signs seen and properly disinfected However since this disease has never been reported in the Western Hemisphere diseasefree status after a confirmed outbreak will require a comprehensive surveillance program conducted by state and federal authorities Experts who may be consulted Foreign Animal Disease Diagnostic Laboratory USDAAPHISVSNVSLFADDL 40550 Route 25 for packages Orient Point NY 11957 PO Box 848 for letters Greenport NY 119440848 Director Dr Fernando TorresVelez Phone 631 3233256 Fax 631 3233366 Email FernandoJTorresVelezaphisusdagov American Association of Zoo Veterinarians Infectious Disease Manual SHEEP AND GOAT POX References 1 Diallo A and G Viljoen 2007 Genus Capripoxvirus In Mercer AA A Schmidt and O Weber eds Poxviruses Birkhäuser Verlag Basel Switzerland Pp 167181 2 Kitching P 2008 Capripoxvirus In Committee on Foreign and Emerging Diseases of the United States Animal Health Association ed Foreign Animal Diseases 7th edition Revised 2008 Boca Publishing Group Inc Boca Raton Florida Pp 189 196 httpwwwaphisusdagovemergencyresponsedownloadsnahemsfadpdf Accessed 10 September 2013 3 Lamien CE C Le Goff R Silber DB Wallace V Gulyaz E Tuppurainen H Madani P Caufour T Adam M El Harrak AG Luckins E Albina and A Diallo 2011 Use of the Capripoxvirus homologue of Vaccinia virus 30 kDa RNA polymerase subunit RPO30 gene as a novel diagnostic and genotyping target development of a classical PCR method to differentiate Goat poxvirus from Sheep poxvirus Vet Microbiol 149 3039 4 NAHEMS USDA Guidelines Cleaning and Disinfection httpwwwaphisusdagovanimalhealthemergencymanagementdownloadsnahemsguidelinesc leaningdisfectionpdf Accessed 10 September 2013 5 OIE 2013 Manual of diagnostic tests and vaccines for terrestrial animals sheep and goat pox httpwwwoieintfileadminHomeengHealthstandardstahm20714SPOXGPOXpdf Accessed 10 September 2013 6 Spickler AR 2008 Sheep and goat pox httpwwwcfsphiastateeduFactsheetspdfssheepandgoatpoxpdf Accessed 10 September 2013 American Association of Zoo Veterinarians Infectious Disease Manual SHIGELLOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Humans and non human primates ruminants occasionally dogs Fecaloral via direct contact with infected animals or indirectly via food water flies or inanimate objects contaminated and contact with shedding animals Food borne disease sexual contact Diarrhea or dysentery with potentially blood andor mucus abdominal cramps tenesmus and pyrexia Asymptomati c carriers are possible Generally self limiting disease Complication due to bacteremia is possible mainly in immuno compromised individuals that result in arthritis neuritis vulvo vaginitis chronic colitis conjunctivitis eventually death Oral rehydration and antibiotics Proper sanitation reduction of stress and isolation of potential carriers fly control High zoonotic potential Fact Sheet compiled by Cornelia J KetzRiley Sheet completed on updated 8 February 2018 Fact Sheet Reviewed by David Miller Susceptible animal groups Primates humans and nonhuman are natural hosts Reports of infection in cattle and dogs have been made Causative organism Family Enterobacteriaceae genus Shigella four species Shigella dysenteriae serogroup A Shigella flexneri serogroup B Shigella boydii serogroup C Shigella sonnei serogroup D Infection and transmission occurs mainly via fecaloral route through contaminated food water or direct contact in humans persontoperson transmission is the most common route Arthropods such as houseflies can function as mechanical vectors Serovars are of antigenetic difference serotyping and subtyping via pulsedfield gel electrophoresis is important in epidemiogic investigations Shigella bacteria are able to invade intestinal mucosa cells but this varies by strain cytotoxins Shiga toxin may also be produced While Shigella dysenteriae is mostly responsible to larger outbreaks in humans mainly children there seems to be an epidemiological shift towards other serogroups mainly Shigella sonnei This will have additional consequences for treatment and vaccine production Zoonotic potential High Distribution Worldwide Originally a common problem encountered mostly in underdeveloped regions but with higher tourist travel activity and movements of refugees in more recent times infections more often seen in other parts of the worlds Incubation period 16 days Clinical signs Pyrexia headache abdominal cramps and severe painful diarrhea that is watery and potentially with mucus pus or blood The presentation is usually selflimiting within 10 days However in its more severe form other signs can present such as dehydration and neurological signs Bacteremia has potential complications of arthritis neuritis vulvovaginitis chronic colitis conjunctivitis iritis hemolytic uremic syndrome or death Shigella infection is affecting Tlymphocyte activity and therefore alters immune response It also stimulates protective local IgA secretion supporting the integrity of intestinal epithelial cells Gingivitis has been reported in macaques Post mortem gross or histologic findings Most common findings during gross necropsy signs of dehydration gastroenteritis enteritis hepatomegaly splenomegaly military white foci in the liver and mesenteric lymphadenopathy After development of septicemia submucosal and subserosal petechial American Association of Zoo Veterinarians Infectious Disease Manual SHIGELLOSIS hemorrhages in multiple organs muscular necrosis typically involving myocardial and gizzard muscle nephropathy polyserositis synovitis are commonly found Histopathologic findings include multifocal necrotic hepatitis necrosis of cryptic or surface enterocytes in lower small intestines sometimes in cecum and colon depending on bacterial species involved Diagnosis Culture of fresh fecal material or use of a transport medium due to limited viability is still the most commonly used diagnostic tool Selective media are used for identification of Shigella sp Such media are MacConkey SalmonellaShigella Agar SS XyloseLysinDesoxycholate XLD Lysine iron agar In cases of small samples and bacterial overgrowth transfer of cultured sample to enrichment media such as Gramnegative broth is recommended Serological and immunohistochemical methods can be used to identify Shigella species and serotypes involved in disease process These methods are essential when a Shigella infection is suspected and when isolation of live organisms by culturing is not possible ELISA and similar modified assays for antibody reactions against Shigella types in individuals Serological examinations valid for identification of acute or subacute infected individuals but chronic carriers are often seronegative A variety of PCR assays is researched and used to recover Shigella DNA in live material or dead surfaces PCR is also used for further classification of Shigella serovars A multiplex PCR assay was recently optimized for simultaneous detection and differentiation of three pathogenic Shigella species by using amplified target genes of the bacteria Also a flow cytometry method and other molecular methods have been investigated as rapid methods for detection of Shigella bacteria Material required for laboratory analysis For culture feces organ tissue and whole blood are recommended For ELISA and other serologic assays feces organ tissue serum food milk and water may be used Tissue feces whole blood soil or processed food can be used for PCR testing Relevant diagnostic laboratories Any laboratory that is set up for culture methods can be used for first screening for Shigella Treatment Mild infections are selflimiting and are only treated with supportive care such as rehydration electrolyte and analgesic treatment Antibiotics should be used only in cases of severe acute and life threatening infection when a subsequent bacteremia is anticipated mainly in immunocompromised and young individuals The choice of antibiotics should be based on an antibiogram of the culture however recommended antibiotics are quinolones nalidixic acid norfloxacin enrofloxacin ciprofloxacin danofloxacin betalactams ampicillin amoxicillin 1st 2nd cephalosporin macrolids azithromycin erythromycin clindamycin aminoglycosides gentamicin streptomycin others tetracyclines sulfonamides cotrimoxazole and furazolidon Antibiotic and chemotherapeutic use can reduce severity of the disease as well as the period of convalescent carriage of Shigella organisms Multidrug resistance against the commonly recommended antibiotics and chemotherapeutics including the more recently advocated drugs like azithromycin ciprofloxacin marbofloxacin is developing rapidly worldwide Therefore newer drugs and alternative treatment methods are constantly researched for their efficacy and safety in the treatment of shigellosis Prevention and control Asymptomatic carriers make eradication and control of shigellosis difficult Preventative control programs should include a good sanitation protocol and animal collection management Feeding additives to introduce competitive bacteria through food or to influence the local pH values and mucosal integrity such as probiotics plant extracts and essential oils with antimicrobial activity seems to be beneficial in controlling Shigella infections Bacteria and yeast found in kefir yogurt have shown to effectively inhibit the invasion of intestinal tissue by Shigella bacteria and the subsequent local inflammation The existence of multiple Shigella serotypes and their growing resistance to antibiotics stress the urgent need for the development of a lowcost vaccine that is protective across all serotypes No vaccine is yet officially available but human and animal challengerechallenge trials with virulent Shigella as well as observational studies in Shigellaendemic areas have shown that the incidence of disease decreases following Shigella infection pointing to biological feasibility of a vaccine A variety of Shigella vaccine constructs are under development including live attenuated formalinkilled wholecell glycoconjugate subunit and novel antigen vaccines eg Type III secretion system and outer membrane proteins All persons involved in American Association of Zoo Veterinarians Infectious Disease Manual SHIGELLOSIS animal care dealing with and processing and preparing food and feed need to be properly educated in sanitation and potential risks of contamination of the animal collection or the food chain with Shigella High sanitation standards and lowstress impact to the animals are key elements in the control of Shigella infections Suggested disinfectant for housing facilities Most commonly used disinfectants such as diluted hydrochlorite quaternary ammoniumbased products are effective against Shigella Notification Reportable disease Most states require that local health departments report outbreaks to their state health department States report voluntarily to CDC Measures required under the Animal Disease Surveillance Plan Culture and serotyping of Shigella of any animals potentially in contact with infected animals and asymptomatic carrier in a collection with shigellosis outbreak Any potential sources such as introduced animals care personnel feed and water sources and any potentially contaminated dead surfaces need to be cultured and potentially serologically and immunohistochemically investigated Measures required for introducing animals to infected animal Regular quarantine in a clean environment reduce access to potential vectors and host animals separate tools and personnel for quarantined animals fecal examination and culture as preshipment evaluation and quarantine examination before introduction Conditions for restoring diseasefree status after an outbreak Quarantine of whole collection Isolation of sick and potentially infected animals Testing of any potentially contaminated feed water surface and also healthy animals before giving access to previously contaminated area Multiple cultures of potentially infected animals necessary due to inconsistent shedding of bacteria Experts who may be consulted Centers for Disease Control and Prevention Division of Foodborne Waterborne and Environmental Diseases 1600 Clifton Rd Atlanta GA 30333 800CDCINFO Cornelia J KetzRiley DMV DVM DACZM Exotic and Zoo Veterinary Specialist Neel Veterinary Hospital 2700 N MacArthur Blvd Oklahoma City OK 73127 Phone 405 9478387 Emailzoodoc12gmailcom References 1 Acha PN Szyfres B Shigellosis In Zoonoses and Communicable Diseases Common to Man and Animals 3rd ed vol I Bacterioses and Mycoses Washington DC Pan American Health Organization 2001 p 247251 2 Centers for Disease Control and Prevention Internet Shigella Shigellosis 2018 cited 2019 March 15 Available from httpswwwcdcgovshigellaindexhtml 3 Allam NG Eldrieny EA Mohamed AZ Effect of Combination Therapy Between Thyme oil and ciprofloxacin on ulcerforming Shigella flexneri J Infect Dev Ctries 2015 9548695 4 Allen GP Harris KA In vitro resistance selection in Shigella flexneri by azithromycin ceftriaxone ciprofloxacin levofloxacin and moxifloxacinagents Chemother 2017617pii e0008617 5 Bolla PA Abraham AG Pérez PF de Los Angeles Serradell M Kefirisolated bacteria and yeasts inhibit Shigella flexneri invasion and modulate proinflammatory response on intestinal epithelial cells Benef Microbes 201671103110 American Association of Zoo Veterinarians Infectious Disease Manual SHIGELLOSIS 6 Brown JD Willcox SJ Franklin N Hazelton B Howard P Reinten T Sheppeard V OSullivan M Shigella species epidemiology and antimicrobial susceptibility The implications of emerging azithromycin resistance for guiding treatment guidelines and breakpoints J Antimicrob Chemother 2017721131813186 Available from doi 101093jacdkx268 7 Butler T Haemolytic uraemic syndrome during shigellosis Trans R Soc Trop Med Hyg 20121067 395399 8 Cantlay JC Ingram DJ Meredith AL A Review of Zoonotic Infection Risks Associated with the Wild Meat Trade in Malaysia EcoHealth 201714361388 9 Chakraborty S Harro C DeNearing B Bream J Bauers N Dally L Flores J Van de Verg L Sack DA Walker R Evaluation of the safety tolerability and immunogenicity of an oral Inactivated wholecell Shigella flexneri 2a vaccine in healthy adult subjects Clin Vaccine Immunol 201623431525 10 Chitradevi STS Kaur G Sivaramakrishna U Singh D Bansal A Development of recombinant vaccine candidate molecule against Shigella infection Vaccine 2016344453765383 11 Chowdhury FM Rahman MZ Sarkar MMH Rabbi F Khan SI Ahsan CR Birkeland NK Protection against shigellosis caused by Shigella dysenteriae serotype 4 in Guinea pigs using Escherichia albertii DM104 as a live vaccine candidate strain Acta Microbiol Immunol Hung 2017642151164 12 DeLaine BC Wu T Grassel CL Shimanovich A Pasetti MF Levine MM Barry EM Characterization of a multicomponent live attenuated Shigella flexneri vaccine Pathog Dis 2016745 13 Deldar A Yakhchali B The influence of riboflavin and nicotinic acid on Shigella sonnei colony conversion Iran J Microbiol 2011311320 14 Farag TH Faruque AS Wu Y Das SK Hossain A Ahmed S Ahmed D Nasrin D Kotloff KL Panchilangam S Nataro JP Cohen D Blackwelder WC Levine MM Housefly population density correlates with shigellosis among children in Mirzapur Bangladesh a time series analysis PLoS Negl Trop Dis 201376e2280 15 Gu B Cao Y Pan S Zhuang L Yu R Peng Z Qian H Wei Y Zhao L Liu G Tong M Comparison of the prevalence and changing resistance to nalidixic acid and ciprofloxacin of Shigella between EuropeAmerica and AsiaAfrica from 1998 to 2009 Int J Antimicrob Agents 2012401917 16 Gu B Ke X Pan S Cao Y Zhuang L Yu R Qian H Liu G Tong M Prevalence and trends of aminoglycoside resistance in Shigella worldwide 19992010 J Biomed Res 2013272103115 17 Haddar C Begaud E Maslin J Germani Y Pointofcare tests for the rapid diagnosis of shigellosis Bull Soc Pathol Exot 2017110118 Article in French 18 Hoffmann C Sahly H Jessen A Ingiliz P Stellbrink HJ Neifer S Schewe K Dupke S Baumgarten A Kuschel A Krznaric I High rates of quinoloneresistant strains of Shigella sonnei in HIVinfected MSM Infection 2013 cited 2013 September 114159991003Available from httpwwwncbinlmnihgovpubmed23852945 19 Hussain SA Patil GR Reddi S Yadav V Pothuraju R Singh RRB Kapila S Aloe vera Aloe barbadensis Miller supplemented probiotic lassi prevents Shigella infiltration from epithelial barrier into systemic blood flow in mice model Microb Pathog 2017102143147 20 Jeong KI Venkatesan MM Barnoy S Tzipori S Evaluation of virulent and live Shigella sonnei vaccine candidates in a gnotobiotic piglet model Vaccine 2013313740394046 21 Joshi RK Volatile composition and antimicrobial activity of the essential oil of Artemisia absinthium growing in Western Ghats region of North West Karnataka India Pharm Biol 2013517888892 22 Kaminski RW Clarkson K Kordis AA Oaks EV Multiplexed immunoassay to assess Shigella specific antibody responses J Immunol Meth 2013393121829 23 Khan WA Griffiths JK Bennish ML Gastrointestinal and extraintestinal manifestations of childhood shigellosis in a region where all four species of Shigella are endemic PLoS One 201385e64097 American Association of Zoo Veterinarians Infectious Disease Manual SHIGELLOSIS 24 Khiveh A Hashempur MH Shakiba M Lotfi MH Shakeri A Kazemeini S Mousavi Z Jabbari M Kamalinejad M Emtiazy M Effects of rhubarb Rheum ribes L syrup on dysenteric diarrhea in children a randomized doubleblind placebocontrolled trial J Integr Med 20175365372 25 Kim J Coble DJ Salyards GW Bower JK Rinaldi WJ Plauche GB Having GG Antimicrobial Use for and Resistance of Zoonotic Bacteria Recovered from Nonhuman Primates Comp Med 20176717986 26 Klontz KC Singh N Treatment of drugresistant Shigella infections Expert Rev Anti Infect Ther 20151316980 27 Kotloff KL Riddle MS PlattsMills JA Pavlinac P Zaidi AKM Shigellosis The Lancet 201839110122801812 28 Li YL Tewari D Yealy CC Fardig D Mikanatha NM 2016 Surveillance for travel and domestically acquired multidrugresistant human Shigella infectionsPennsylvania 20062014 Health Secur 2016314351 Available from doi 101089hs20160026 29 Lindsay B Ochieng JB Ikumapayi UN Toure A Ahmed D Li S Panchalingam S Levine MM Kotloff K Rasko DA Morris CR Juma J Fields BS Dione M Malle D Becker SM Houpt ER Nataro JP Sommerfelt H Pop M Oundo J Antonio M Hossain A Tamboura B Stine OC Quantitative PCR for detection of Shigella improves ascertainment of Shigella burden in children with moderatetosevere diarrhea in lowincome countries J Clin Microbiol 201351617401746 30 Lowenstine L A primer of primate pathology lesions and nonlesions Tox Pathol 200331S92102 31 Martin DJ White BK Rossman MG 2012 Reactive arthritis after Shigella gastroenteritis in American military in Afghanistan J Clin Rheumatol 2012185257258 32 Mani S Wierzba T Walker RI Status of vaccine research and development for Shigella vaccine 2016342628872894 33 Mathias A Longet S Corthésy B Agglutinating secretory IgA preserves intestinal epithelial cell integrity during apical infection by Shigella flexneri Infect Immun 201381830273034 34 Mirnejad R Vahdati AR Rashidiani J Erfani M Piranfar V The antimicrobial effect of Lactobacillus casei culture supernatant against multiple drug resistant clinical isolates of Shigella sonnei and Shigella flexneri in vitro Iran Red Crescent Med J 2013152122126 35 Mitobe J Sinha R Mitra S Nag D Saito N Shimuta K Koizumi N Koley H An attenuated Shigella mutant lacking the RNAbinding protein Hfq provides crossprotection against Shigella strains of broad serotype PLoS Negl Trop Dis 2017117e0005728 Available from doi101371journalpntd0005728 36 Mokhtari W Nsaibia S Gharbi A Aouni M Realtime PCR using SYBR Green for the detection of Shigella spp in food and stool samples Mol Cell Probes 20132715359 37 Nag D Sinha R Mitra S Barman S Takeda Y Shinoda S Chakrabarti MK Koley H Heat killed multiserotype Shigella immunogens induced humoral immunity and protection against heterologous challenge in rabbit model Immunobiology 201522011127583 38 NüeschInderbinen M Heini N Zurfluh K Althaus D Hächler H Stephan R Shigella antimicrobial drug resistance mechanisms 20042014 Emerg Infect Dis 201622610835 39 Ojha SC Yean Yean C Ismail A Singh KK 2013 A pentaplex PCR assay for the detection and differentiation of Shigella species Biomed Res Int 2013412370 40 Olajuyigbe OO Afolayan AJ In vitro antibacterial and timekill assessment of crude methanolic stem bark extract of Acacia mearnsii de wild against bacteria in shigellosis Molecules 20121722103 2118 41 Onyango DM Wandili S Kakai R Waindi EN Isolation of Salmonella and Shigella from fish harvested from the Winam Gulf of Lake Victoria Kenya J Infect Dev Countries 200932 99104 42 Ottosson H Nylén F Sarker P Miraglia E Bergman P Gudmundsson GH Raqib R Agerberth B Strömberg R Potent inducers of endogenous antimicrobial peptides for host directed therapy of infections Sci Rep 2016636692 Available from doi 101038srep36692 American Association of Zoo Veterinarians Infectious Disease Manual SHIGELLOSIS 43 Overbeck S Rink L Haase H Modulating the immune response by oral zinc supplementation a single approach for multiple diseases Arch Immunol Ther Exp Warsz 20085611530 44 Pichel M Brengi SP Cooper KL Ribot EM AlBusaidy S Araya P Fernández J Vaz TI Kam KM Morcos M Nielsen EM Nadon C Pimentel G PérezGutiérrez E GernerSmidt P Binsztein N Shigella flexneri PulseNet PFGE Protocol Working Group Standardization and international multicenter validation of a PulseNet pulsedfield gel electrophoresis protocol for subtyping Shigella flexneri isolates Foodborne Pathog Dis 201295418424 45 Pons MJ Gomes C MartínezPuchol S Ruiz L Mensa L Vila J Gascón J Ruiz J Antimicrobial resistance in Shigella spp causing travellers diarrhea 19952010 a retrospective analysis Travel Med Infect Dis 2013 cited 2013 September 101153159 Available from httpwwwncbinlmnihgovpubmed23886737 46 Ranallo RT Fonseka S Boren TL Bedford LA Kaminski RW Thakkar S Venkatesan MM Two live attenuated Shigella flexneri 2a strains WRSf2G12 and WRSf2G15 a new combination of gene deletions for 2nd generation live attenuated vaccine candidates Vaccine 2012303451595171 47 Ranjbar R Afshar D Mehrabi Tavana A Najafi A Pourali F Safiri Z Sorouri Zanjani R Jonaidi Jafari N Development of Multiplex PCR for simultaneous detection of three pathogenic Shigella species Iran J Public Health 20144312165763 48 SalgadoPabón W Celli S Arena ET Nothelfer K Roux P Sellge G Frigimelica E Bousso P Sansonetti PJ Phalipon A Shigella impairs T lymphocyte dynamics in vivo Proc Natl Acad Sci USA 20131101244584463 49 Shiferaw B Solghan Palmer A Joyce K Barzilay EJ Krueger A Cieslak P Antimicrobial susceptibility patterns of Shigella isolates in Foodborne Diseases Active Surveillance Network FoodNet sites 20002010 Clin Infect Dis 201254Suppl 5S458S463 50 Shipley ST Panda A Khan AQ Kriel EH Maciel Jr M Livio S Nataro JP Levine MM Sztein MB DeTolla LJ A challenge model for Shigella dysenteriae 1 in cynomolgus monkeys Macaca fascicularis Comp Med 20106015461 51 Sperandio B Fischer N Joncquel ChevalierCurt M Rossez Y Roux P Robbe Masselot C Sansonetti PJ 2013 Virulent Shigella flexneri affects the secretion expression and glycosylation of gelforming mucins in mucusproducing cells Infect Immun 20138110363243 Available from httpwwwncbinlmnihgovpubmed23876800 Accessed 10 September 2013 52 Thompson CN Duy PT Baker S The Rising Dominance of Shigella sonnei An intercontinental shift in the etiology of bacillary dysentery Negl Trop Dis 201596e0003708 53 Wang Y Wang Y Xu J Ye C Development of multiple cross displacement amplification labelbased gold nanoparticles lateral flow biosensor for detection of Shigella spp Front Microbiol 201671834 54 Wu Y Chakravarty S Li M Wai TT Hoffman SL Sim BK Development of a live attenuated bivalent oral vaccine against Shigella sonnei shigellosis and typhoid fever J Infect Dis 20172152259268 55 Xue Y Wilkes JG Moskal TJ Williams AJ Cooper WM Nayak R Rafii F Buzatu DA Development of a flow cytometrybased method for rapid detection of Escherichia coli and Shigella spp using an oligonucleotide probe PLoS One 2016112e0150038 Available from doi 101371journalpone0150038 American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN FOAMY VIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Found in most non human primates Horizontal through contact with saliva Not known to cause disease Not known to cause disease None Lifelong infection Yes Fact Sheet compiled by Natalie Mylniczenko Sheet completed on Jan2019 Fact Sheet Reviewed by Donna Ialeggio Susceptible animal groups All species of nonhuman primates are susceptible Causative organism Simian foamy virus SFV in Genus Spumavirus Zoonotic potential Yes Distribution Worldwide distribution in wild and captive nonhuman primate populations Incubation period Unknown Clinical signs None reported considered to be medically insignificant Post mortem gross or histologic findings No known pathology is associated with SFV infection Co infection with SIV may increase SIVrelated disease progression At least in NHP coinfection with species specific SFV eg chimp colobus see ref 14 below is documented Diagnosis Serology ELISA and WB for confirmation PCR and virus isolation can be used Material required for laboratory analysis Whole blood serumplasma body fluids and tissues Relevant diagnostic laboratories Primate Assay Laboratory PAL Formerly PDL California National Primate Research Center University of California Davis Phone 5307528242 Email cnprcpdlucdavisedu httpwwwcnprcucdaviseduprimateassaylaboratorycore Virus Reference Laboratories Inc VRLSan Antonio USA PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 Office 8776157275 Fax 2106157771 httpwwwvrlsatcom Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 913113800 8187178880 Fax 8187178881 Email infozoologixcom httpwwwzoologixcom accessed 15Jan19 Treatment None is reported Prevention and control Infection is ubiquitous in nonhuman primates Suggested disinfectant for housing facilities 70 ethanol formalin 10 household bleach sodium hypochlorite Lysol and most lipophylic detergents Notification None at this time American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN FOAMY VIRUS Measures required under the Animal Disease Surveillance Plan None at this time Measures required for introducing animals to infected animal Seroconversion of naïve animals is possible with exposure Conditions for restoring diseasefree status after an outbreak Lifelong infection so no changes can be made to restore diseasefree status Experts who may be consulted William M Switzer MPH Retrovirus Surveillance Activity Leader Laboratory Branch Division of HIVAIDS Prevention NCHSTP Centers for Disease Control and Prevention 1600 Clifton Rd Atlanta Georgia 30333 bis3cdcgov References 1 Calattini S Betsem EBA Froment A Mauclère P Tortevoye P Schmitt C Njouom R Saib A Gessain A Simian foamy virus transmission from apes to humans rural Cameroon Emerg Infect Dis 20071313141320 2 Choudhary A Galvin TA Williams DK Beren J Bryant MA Khan AS Influence of naturally occurring simian foamy viruses SFVs on SIV disease progression in the rhesus macaque Macaca mulatta model Viruses 2013514141430 3 Craig KL PintoSantini DM Linial ML Simian Foamy Virus SFV In Fuentes A ed The International Encyclopedia of Primatology Chester UK John Wiley Sons Ltd 2017 4 Khan AS Simian foamy virus infection in humans prevalence and management Expert Rev Anti infective Ther 20097569580 5 Meiering CD Linial ML Historical perspective of foamy virus epidemiology and infection Clin Microbiol 2001141165176 6 MouingaOndémé A Kazanji M Simian foamy virus in nonhuman primates and crossspecies transmission to humans in Gabon an emerging zoonotic disease in central Africa Viruses 20135615361552 7 Muniz CP Cavalcante LT Jia H Zheng H Tang S Augusto AM Pissinatti A Fedullo LP Santos AF Soares MA Switzer WM Zoonotic infection of Brazilian primate workers with New World simian foamy virus PLoS One 2017129e0184502 8 Sandstrom PA Phan KO Switzer WM Fredeking T Chapman L Heneine W Folks TM Simian foamy virus infection among zoo keepers The Lancet 20003559203551552 9 Switzer WM Bhullar V Shanmugam V Cong M Parekh B Lerche NW Yee JL Ely JJ Boneva R Chapman LE Folks TM Heneine W Frequent simian foamy virus infection in persons occupationally exposed to nonhuman primates J Virol 20047827802789 10 Switzer WM Heneine W Foamy virus infection of humans In Liu D ed Molecular Detection of Viral Pathogens Boca Raton FL CRC Press 2011 p 131146 11 Voevodin AF Marx PA Simian Virology Ames IA Wiley Blackwell 2009 p 217236 12 WestonMurphy H Switzer WM Occupational exposure to zoonotic simian retroviruses health and safety implications for persons working with nonhuman primates In Fowler ME Miller RE eds Zoo Wild Animal Medicine Current Therapy 6 St Louis MO SaundersElsevier 2008 p 251264 13 PintoSantini DM Stenbak CR Linial ML Foamy virus zoonotic infections Retrovirology 201714155 Leendertz FH Zirkel F CouacyHymann E Ellerbrok H Morozov VA Pauli G Hedemann C Formenty P Jensen SA Boesch C Junglen S Interspecies transmission of simian foamy virus in a natural predatorprey system J Virol 2008821577414 American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN HEMORRHAGIC FEVER Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Natural host Patas monkey Erythrocebus patas and other African primates Aberrant host Asian macaques Direct and indirect contact with infected animals secretions or fomites Iatrogenic transmission Anorexia lethargy fever diarrhea or melena with frank blood facial edema petechia DIC Fatal in macaques but no clinical disease in natural hosts Isolation of unaffected animals No successful clinical treatment Testing of African primates Separation of African primates and macaques in captivity No Fact Sheet compiled by Thomas P Meehan updated by Dawn Zimmerman Sheet completed on 30 June 2011 updated 15 August 2013 updated 27 December 2017 Fact Sheet Reviewed by Kimberlee B Wojick Meredith M Clancy Susceptible animal groups Captive rhesus macaques Macaca mulatta were affected during an explosive outbreak in the index case in 1964 This and subsequent outbreaks in macaques have apparently resulted from contact with or iatrogenic transmission from asymptomatic captive African monkeys African monkey species including Patas monkey Erythrocebus patas vervet monkeys Cercopithecus aethiops and baboons Papio spp are suspected to be the natural reservoirs Red colobus monkeys and redtailed guenons also have been identified as natural hosts for SHFV variants Currently SHFV is thought only to affect Asian macaques of diverse species including rhesus macaque Macaca mulatta bonnet macaque M radiata cynomolgus macaque M fasicularis stumptailed macaque M arctoides Assam macaque M assamensis and Southern pigtailed macaque M nemestrina Causative organism SHF is caused by at least three Arteriviruses family Arteriviridae simian hemorrhagic fever virus SHFV simian hemorrhagic encephalitis virus SHEV and Pebjah virus PBJV Since 2011 nine additional distant relatives of these three viruses were discovered in apparently healthy African cercopithecid primates and are thought to also be potential causes of SHF Zoonotic potential None however the virus is being researched for species jump potential due to the presence of highly divergent SHFV variants Distribution Natural hosts in Africa but consideration for captive animals worldwide Incubation period 29 days Clinical signs Natural hosts asymptomatic Macaques Although these aberrant hosts can be asymptomatic in clinical animals fever depression facial edema anorexia adipsia dehydration proteinuria cyanosis skin petechiae melena epistaxis DIC and retrobulbar hemorrhages can present Mortality ranges widely at 11100 64 in recent study but death occurs in 1015 days Post mortem gross or histologic findingsPetechial hemorrhages on mucosal and serosal surfaces hemorrhage of proximal duodenum splenomegaly splenic lymphoid follicles ringed with zone of hemorrhage multiorgan necrosis vasculitis and hemorrhage intravascular fibrin fibrin in spleen lymphohistiocytic meningoencephalitis Diagnosis Real time RT PCR ELISA DIA Material required for laboratory analysis blood serum Relevant diagnostic laboratories Zoologix 9811 Owensmouth Ave Suite 4 Chatsworth CA 91311 8187178880 American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN HEMORRHAGIC FEVER BioReliance Corp 14920 Broschart Rd Rockville MD 208503349 3017381000 VRLSan Antonio USA PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 8776157275 httpwwwvrlsatcomcatalogspecimen45 Treatment None Prevention and control Separation of African primates and macaques in captive settings Testing of African primate species for antibodies Due to the indication that SHF may be caused by a number of distinct simian arteriviruses screening procedures for SHFV in primateholding facilities should allow for detection of all known simian arteriviruses Suggested disinfectant for housing facilities Disinfectants effective against Arteriviridae quaternary ammonium and glutaraldehyde mixture Synergize Preserve International 08 potassium monopersulfate VirkonS TM DuPont Animal Health 10 Notification None Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Depopulation of affected macaque group and premise disinfection Experts who may be consulted While this disease is not zoonotic similarities to other hemorrhagic diseases of primates should indicate consultation with Centers for Disease Control and Prevention CDC Division of Global Migration and Quarantine May be contacted 24 hoursday through the CDC emergency operations center 7704887100 References 1 Dalgard DW Hardy RJ Pearson SL Pucak GJ Quander RV Zack PM Peters CJ Jahrling PB Combined simian hemorrhagic fever and Ebola virus infection in cynomolgus monkeys Lab Anim Sci 199242152157 2 Godeny EK Enzymelinked immunosorbent assay for detection of antibodies against simian hemorrhagic fever virus Comp Med 200252229232 3 Gravell M London WT Leon ME Palmer AE Hamilton RS Differences among isolates of simian hemorrhagic fever SHF virus Proc Soc Exp Biol Med 1986181112119 4 Johnson RF Dodd LE Yellayi S Gu W Cann JA Jett C Bernbaum JG Ragland DR St Claire M Byrum R Paragas J Blaney JE Jahrling PB Simian hemorrhagic fever virus infection of rhesus macaques as a model of viral hemorrhagic fever clinical characterization and risk factors for severe disease Virol 20114212129140 5 Lauck M Hyeroba D Tumukunde A Weny G Lank SM Chapman CA OConnor DH FriedrichTC Goldberg TL Novel divergent simian hemorrhagic fever viruses in a wild Ugandan red colobus monkey discovered using direct pyrosequencing PLoS One 201164e19056 6 Lauck M Sibley SD Hyeroba D Tumukunde A Weny G Chapman CA Ting N Switzer WM Kuhn JH Friedrich TC OConnor DH Goldberg TL Exceptional simian hemorrhagic fever virus diversity in a wild African primate community J Virol 2013871688691 7 London WT Epizootiology transmission and approach to prevention of fatal simian haemorrhagic fever in rhesus monkeys Nature 1977268344345 American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN HEMORRHAGIC FEVER 8 Palmer AE Allen AM Tauraso NM Shelokov A Simian hemorrhagic fever I Clinical and epizootiologic aspects of an outbreak among quarantined monkeys Am J Trop Med Hyg 196817404 412 9 WahlJensen V Johnson JC Lauck M Weinfurter JT Moncla LH Weiler AM Charlier O Rojas O Byrum R Ragland DR Huzella L Divergent Simian Arteriviruses Cause Simian Hemorrhagic Fever of Differing Severities in MacaquesMBio 201671 e0200915 American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN IMMUNODEFICIENCY VIRUSES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Found in many African nonhuman primates Macaques susceptible Mainly horizontal through sexual contact and bite wounds Vertical transmission reported by virus infected milk Clinical disease occurs in only a minority of infected individuals When pathogenic disease depends on the nature of the organ and opportunistic infections Severe and fatal in non natural host None specific although same treatment options for HIV could be used Test collect ion and determine risk to benefit of introductions to naïve animals Infection should be considered a zoonotic disease since many SIV species can grow in human cell lines in vitro Fact Sheet compiled by Sam Rivera updated by Natalie Mylniczenko Sheet completed on 1 June 2011 updated 10 September 2013 April 2018 Fact Sheet Reviewed by Lana Krol Susceptible animal groups Natural host can be susceptible to disease and older animals may succumb to AIDSrelated disease Nonnatural host infections can be fatal Asian macaques are highly susceptible to fatal infection Causative organism Identified in 45 species including SIVagm SIVasc SIV bkm SIVblu SIVcol SIVcpz SIVdeb SIVden SIVdrl SIVgor SIVgsn SIV lhoest SIVmnd 1 and 2 possibly 3 SIVmon SIVmus SIV olc SIVrcm SIVschm SIVsmm SIVstm SIVsun SIVsyk SIVtal SIVwrc Zoonotic potential The virus should be considered a zoonotic disease Many SIV species can grow in human cell lines in vitro HIV1 originated from SIVcpz and SIVgor HIV2 from SIVsmm Distribution Natural infections occur in Africa Infection in captive nonhuman primates occurs worldwide Cross species viral jumping has been reported but appears relatively rare Incubation period Strain and host dependent Can be as short as a few weeks in nonnatural host or as long as several decades in natural host Clinical signs Clinical disease does not usually present in natural hosts However when disease occurs common findings are lymphadenopathy and diarrhea Other signs may include wasting malabsorption and weight loss Cardiac disease arteriopathies transient cutaneous erythematous maculopapular rash and CNS involvement can be observed Secondary infections can be due to immunodeficiency and hypergammaglobulinemia can be observed Post mortem gross or histologic findings Lymphoid organs may be hypertrophied Other findings depend on affected organ systems encephalitis cardiac necrosis myocarditis coronary or systemic arteriopathy glomurulosclerosis pneumonia follicular hyperplasia and fragmentation in lymphoid tissues extramedullary hematopoiesis in lymph nodes and follicular and paracortical hyperplasia epididymitis prostatitis urethritis malignant lymphomas Diagnosis Serology ELISA Western blot PCR virus isolation If positive on serology SIV genotyping is recommended to identify natural reservoirs that are often African nonhuman primates Screening is typical with ELISA testing but confirmation should be completed with Western blot or PCR It should be noted that highly divergent SIVs may not react completely with HIV and SIVmac antigens used in commercial assays Viral isolation efficiency is highly variable Material required for laboratory analysis Whole blood serumplasma body fluids tissues Relevant diagnostic laboratories Primate Assay Laboratory PAL Formerly PDL California National Primate Research Center University of California Davis Phone 5307528242 Email cnprcpdlucdavisedu httpwwwcnprcucdaviseduprimateassaylaboratorycore American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN IMMUNODEFICIENCY VIRUSES Virus Reference Laboratories Inc VRLSan Antonio USA PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 Office 8776157275 Fax 2106157771 httpwwwvrlsatcom Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 913113800 8187178880 Fax 8187178881 infozoologixcom httpwwwzoologixcom Treatment None Prevention and control Identify status of animals in collection Determine risk to benefit of maintaining a closed population in the face of population needs Suggested disinfectant for housing facilities 70 ethanol formalin 10 household bleach sodium hypochlorite most lipophilic detergents quaternary ammonium chloride bezalkonium chloride Notification None at this time Measures required under the Animal Disease Surveillance Plan None at this time Measures required for introducing animals to infected animal Determine current status of both groups of these animals then determine risk to benefit of introducing negative individuals to positive individuals It is important to remember that natural reservoirs of particular SIV variants exist Conditions for restoring diseasefree status after an outbreak Lifelong infection results in inability to restore disease free status Experts who may be consulted William M Switzer MPH Retrovirus Surveillance Activity Leader Laboratory Branch Division of HIVAIDS Prevention NCHSTP Centers for Disease Control and Prevention 1600 Clifton Rd Atlanta Georgia 30333 bis3cdcgov References 1 Cohen J AIDS virus traced to chimp subspecies Sci 1999283772773 2 Essex M Simian immunodeficiency virus in people N Engl J Med 1994330 209 210 3 Etienne L Nerrienet E LeBreton M Bibila GT Foupouapouognigni Y Rousset D Nana A Djoko CF Tamoufe U Aghokeng AF MpoudiNgole E Characterization of a new simian immunodeficiency virus strain in a naturally infected Pan troglodytes troglodytes chimpanzee with AIDS related symptoms Retrovirol 201184 4 Etienne L Nerrienet E LeBreton M Bibila GT Foupouapouognigni Y Rousset D Nana A Djoko CF Tamoufe U Aghokeng AF MpoudiNgole E Delaporte E Peeters M Wolfe ND Ayouba A Characterization of a new simian immunodeficiency virus strain in a naturally infected Pan troglodytes troglodytes chimpanzee with AIDS related symptoms Retrovirol 201184 American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN IMMUNODEFICIENCY VIRUSES 5 Filippone C De Oliveira F Betsem E Schaeffer L Fontanet A Lemée V Gessain A Plantier JC Simian Immunodeficiency Virus seroreactivity in inhabitants from rural Cameroon frequently in contact with nonhuman primates Virology 20175037682 6 Keele BF Jones JH Terio KA Estes JD Rudicell RS Wilson ML Li Y Learn GH Beasley TM SchumacherStankey J Wroblewski E Mosser A Raphael J Kamenya S Lonsdorf EV Travis DA Mlengeya T Kinsel MJ Else JG Silvestri G Goodall J Sharp PM Shaw GM Pusey AE Hahn BH Increased mortality and AIDSlike immunopathology in wild chimpanzees infected with SIVcpz Nature 20094607254515519 7 Lerche NW Common viral infections of laboratory primates In WolfeCoote S ed The Handbook of Experimental Animals The Laboratory Primate San Diego CA Elsevier Academic Press 2005 p 7589 8 Lowestine LJ Lerche NW Nonhuman primate retroviruses and simian acquired immunodeficiency syndrome In Fowler ME ed Zoo Wild Animal Medicine Current Therapy 3 Philadelphia PA WB Saunders Co 2003 p 373378 9 Sharp PM Hahn BH The evolution of HIV1 and the origin of AIDS Philos Trans R Soc Lond B Biol Sci 2010365155224872494 10 Tebit DM Arts EJ From Simian to Human Immunodeficiency Viruses SIV to HIV Emergence from Nonhuman Primates and Transmission to Humans In Johnson N ed The Role of Animals in Emerging Viral Diseases San Diego CA Elsevier 2014p 201234 11 Terio KA Kinsel MJ Raphael J Mlengeya T Lipende I Kirchhoff CA Gilagiza B Wilson ML Kamenya S Estes JD Keele BF Rudicell RS Liu W Patton S Collins A Hahn BH Travis DA Lonsdorf EV Pathologic lesions in chimpanzees Pan trogylodytes schweinfurthii from Gombe National Park Tanzania 20042010 J Zoo Wildl Med 201142597607 12 Voevodin AF Marx PA Apetrei C Simian Virology Ames IA WilleyBlackwell 2009 p 77118 13 WestonMurphy H Switzer WM Occupational exposure to zoonotic simian retroviruses health and safety implications for persons working with nonhuman primates In Fowler ME Miller RE eds Zoo Wild Animal Medicine Current Therapy 6 St Louis MO SaundersElsevier 2008 p 251264 14 Whetter LE Ojukwu IC Novembre FJ Dewhurst S Pathogenesis of simian immunodeficiency virus infection J Gen Vir 19998015571568 American Association of Zoo Veterinarians Infectious Disease Manual Type D SIMIAN RETROVIRUSES SRV Animal Groups Affected Transmission Clinical Signs Severity Treatmen t Prevention and Control Zoonotic Macaques are natural host langurs squirrel monkeys baboons talapoins Direct contact transplacentally Diarrhea weight loss fever splenomegaly lymphadenopathy anemia neutropenia lymphopenia cutaneous fibrosarcoma and malignant lymphomas Fatal disease None Test and remove isolate positive animals Yes Fact Sheet compiled by Sam Rivera updated by Natalie Mylniczenko Sheet completed on 1 June 2011 updated September 2013 April 2018 Fact Sheet Reviewed by Sam Rivera Susceptible animal groups Macaques are natural hosts langurs squirrel monkeys baboons and talapoins also susceptible Largely this disease is one of laboratory colonies Causative organism Simian type D retroviruses SRV seven genotypes recognized SRV1 SRV7 Genus Betaretroviruses Zoonotic potential Zoonotic infection serologic evidence of human infection in one study Distribution Mostly in Asian macaques and langurs Incubation period Unknown lifelong infection Clinical signs Immunosuppressive disease neutropenia and lymphopenia generalized lymphadenopathy diarrhea weight loss anemia opportunistic infections SRV1 causes malignant lymphomas and SRV2 abdominal fibromatosis and subcutaneous fibrosarcomas Post mortem gross or histologic findings Splenomegaly hyperplastic lymphoid follicles follicular atrophy fibrosarcomas polymyositis nonsuppurative enteritis sialoadenitis bone marrow hyperplasia SRV2 retroperiotoneal fibromatosis subcutaneous fibrosarcomas Diagnosis Serology ELISA Western blot for confirmation PCR virus isolation Some animals can have latent infection and be antibody negative High false positive rate with standard ELISA but newer microbead based immunoassays have improved specificity Material required for laboratory analysis Whole blood serumplasma saliva urine tissues Relevant diagnostic laboratories Primate Assay Laboratory PAL Formerly PDL California National Primate Research Center University of California Davis Phone 5307528242 Email cnprcpdlucdavisedu httpwwwcnprcucdaviseduprimateassaylaboratorycore Virus Reference Laboratories Inc VRLSan Antonio USA PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 Office 8776157275 Fax 2106157771 httpwwwvrlsatcom Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 913113800 8187178880 Fax 8187178881 Email infozoologixcom httpwwwzoologixcom American Association of Zoo Veterinarians Infectious Disease Manual Type D SIMIAN RETROVIRUSES SRV Treatment None Prevention and control Test and removeisolate positive animals Suggested disinfectant for housing facilities 70 ethanol formalin 10 household bleach sodium hypochlorite Lysol and most lipophylic detergents can be used Notification None at this time Measures required under the Animal Disease Surveillance Plan None at this time Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Lifelong infection so diseasefree status cannot be restored Experts who may be consulted William M Switzer MPH Retrovirus Surveillance Activity Leader Laboratory Branch Division of HIVAIDS Prevention NCHSTP Centers for Disease Control and Prevention 1600 Clifton Rd Atlanta Georgia 30333 bis3cdcgov References 1 Engel GA Besnard F HumanNonhuman Primate Disease Transmission In Fuentes A ed The International Encyclopedia of Primatology Chester UK John Wiley Sons Ltd 2017 1 Lerche NW Common viral infections of laboratory primates In WolfeCoote S ed The Handbook of Experimental Animals The Laboratory Primate San Diego CA Elsevier Academic Press 2005 p 7589 2 Lerche NW Cotterman RF Dobson MD Yee JL Rosenthal AN Heneine WM Screening for simian type D retrovirus infection in macaques using nested polymerase chain reaction Lab Anim Sci 199747263 268 3 Lerche NW Emerging viral diseases of nonhuman primates in the wild In Fowler ME ed Zoo Wild Animal Medicine Current Therapy 3 Philadelphia PA WB Saunders Co 1993 p 340344 4 Lerche NW Switzer WM Yee JL Shanmugam V Rosenthal AN Chapman LE Folks TM Heneine W Evidence of infection with simian Type D retrovirus in persons occupationally exposed to nonhuman primates J Virol 20017517831789 5 Liao Q Guo H Tang M Touzjian N Lerche NW Lu Y Yee JL Simultaneous detection of antibodies to five simian viruses in nonhuman primates using recombinant viral protein based multiplex microbead immunoassays J Virol Meth 201117814352 6 Lowestine LJ Lerche NW 2003 Nonhuman primate retroviruses and simian acquired immunodeficiency syndrome In Fowler ME ed Zoo Wild Animal Medicine Current Therapy 3 Philadelphia PA WB Saunders Co 2003 p 373 378 7 Montiel NA An updated review of simian betaretrovirus SRV in macaque hosts J Med Primatol 2010395303314 8 Voevodin AF Marx PA Simian Virology Ames IA Wiley Blackwell 2009 P 163181 9 WestonMurphy H Switzer WM Occupational exposure to zoonotic simian retroviruses health and safety implications for persons working with nonhuman primates In Fowler ME Miller RE eds Zoo Wild Animal Medicine Current Therapy 6 St Louis MO SaundersElsevier 2008 p 251 264 American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN TLYMPHOTROPIC VIRUSES Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Old World non human primates Direct contact bite wounds sexual contact sharps puncture IV or transdermal Transmission rate is low STLV1 has been associated with lymphoma leukemia and wasting disease in several nonhuman primates non Hodgkins lymphomas and lymphosarcomas Can be fatal affects a small percentage of the population None reported Test collection and determine risk to benefit of introductions to naïve animals Yes it can infect humans Fact Sheet compiled by Sam Rivera updated by Natalie Mylniczenko Sheet completed on 1 June 2011 10 September 2013 19 April 2018 Fact Sheet Reviewed by Sam Rivera Susceptible animal groups Bonobo Cercocebus sp Cercopithecus sp Erthrocebus patas Gorilla gorilla macaques Mandrillus sp Pan troglodytes Pan paniscus Papio sp Pongo pygmaeus Symphalangus syndactylus colobines and others Causative organism STLV1 most likely STLV2 STLV3 STLV4 that are in genus Deltaretrovirus Zoonotic potential STLV can infect humans and causes disease in up to 5 of infected persons HTLV1 2 3 and 4 originated from STLV1 2 3 and 4 respectively Distribution Africa and Asia naturally and captive nonhuman primates worldwide Incubation period Long incubation period has been reported of at least four years however it can be shorter in persons receiving blood transfusions from persons with HTLV1induced leukemia Cases are generally spontaneous Clinical signs Mostly reported in laboratory animals in isolated outbreaks where the virus jumped species Most immunocompetent infected animals are healthy Disease occurs in a few percent of the positive carriers Leukemia lymphoma syndrome enlarged lymph nodes persistent lymphocytosis and abnormal Tcells T cell lymphomas and leukemia lymphadenopathy and splenomegaly and nonHodgkins lymphomas Lymphoma without presence of virus is more common in NHPs and in humans disease includes leukemia lymphoma inflammatory disorders and neurologic disease STLV4 recently described in wild gorillas Post mortem gross or histologic findings Generalized enlarged neoplastic lymph nodes are seen in affected animals Malignant lymphomas sometimes metastasize with pale foci or larger nodules found in various organs such as spleen kidney and liver In some individuals lymph nodes are depleted Other findings are more variable Diagnosis Serology IFA and EIA and WB for confirmation and PCR Rarely virus isolation is performed Care must be taken in interpreting seropositive animals with associated disease manifestations Lymph node and bone marrow PCR are used to determine disease presence Dual STLV1 and STLV3 infections have been reported in naturally infected simians Material required for laboratory analysis Whole blood serumplasma lymph nodes bone marrow and urine Relevant diagnostic laboratories Primate Assay Laboratory PAL Formerly PDL California National Primate Research Center University of California Davis 5307528242 cnprcpdlucdavisedu httpwwwcnprcucdaviseduprimateassaylaboratorycore American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN TLYMPHOTROPIC VIRUSES Virus Reference Laboratories Inc VRLSan Antonio USA PO Box 40100 7540 Louis Pasteur Suite 200 San Antonio Texas 78229 Office 8776157275 Fax 2106157771 httpwwwvrlsatcom Zoologix Inc 9811 Owensmouth Avenue Suite 4 Chatsworth California 913113800 8187178880 Fax 8187178881 infozoologixcom httpwwwzoologixcom Treatment None Prevention and control Identify status of animals in collection Determine risk to benefit of maintaining a closed population in the face of population needs Suggested disinfectant for housing facilities 70 ethanol formalin 10 household bleach sodium hypochlorite benzalkonium chloride and most lipophylic detergents Notification None Measures required under the Animal Disease Surveillance Plan None at this time Measures required for introducing animals to infected animal Determine current status of both animal sets determine risk to benefit of introducing negative individuals to positive individuals Conditions for restoring diseasefree status after an outbreak Lifelong infection so diseasefree status cannot be restored Experts who may be consulted William M Switzer MPH Retrovirus Surveillance Activity Leader Laboratory Branch Division of HIVAIDS Prevention NCHSTP Centers for Disease Control and Prevention 1600 Clifton Rd Atlanta Georgia 30333 bis3cdcgov References 1 Courgnaud V Van Dooren S Liegeois F Pourrut X Abela B Loul S MpoudiNgole E Vandamme A Delaporte E Peeters M Simian Tcell leukemia virus STLV infection in wild primate populations in Cameroon evidence for dual STLV type 1 and type 3 infection in agile mangabeys Cercocebus agilis J Virol 20047847004709 2 Lerche NW Common viral infections of laboratory primates In WolfeCoote S ed The Handbook of Experimental Animals The Laboratory Primate San Diego CA Elsevier Academic Press 2005 p 7589 3 Lowestine LJ Lerche NW Nonhuman primate retroviruses and simian acquired immunodeficiency syndrome In Fowler ME ed Zoo Wild Animal Medicine Current Therapy 3 Philadelphia PA WB Saunders Co 2003 p 373378 4 Masters N Niphuis H Verschoor E Breuer J Quinlivan M Wawrzynczyk T Stidworthy M Debilitating clinical disease in a wildborn captive western lowland gorilla Gorilla gorilla gorilla coinfected with varicella zoster virus VZV and simian Tlymphotropic virus STLV J Zoo Wildl Med 201041713716 American Association of Zoo Veterinarians Infectious Disease Manual SIMIAN TLYMPHOTROPIC VIRUSES 5 Richard L Betsem E Filippone C Nerrienet E Gessain A Search for primate Tlymphotropic virus type 4 in highly exposed human populations and gorillas from Central Africa Retrovirology 2015121P83 6 Sintasath DM Wolfe ND LeBreton M Jia H Garcia AD Diffo JL Tamoufe U Carr JK Folks TM MpoudiNgole E Burke DS Heneine W Switzer WM Simian Tlymphotropic virus diversity among nonhuman primates Cameroon Emerg Infect Dis 200915175184 7 Voevodin AF Marx PAeds 2009 Deltaretroviruses In Simian Virology WilleyBlackwell Ames Iowa Pp 193215 8 Voevodin AF Marx PA Simian Virology Ch 8 Deltaretroviruses Ames IA WilleyBlackwell 2009 p 193212 9 WestonMurphy H Switzer WM Occupational exposure to zoonotic simian retroviruses health and safety implications for persons working with nonhuman primates In Fowler ME Miller RE eds Zoo Wild Animal Medicine Current Therapy 6 St Louis MO SaundersElsevier 2008 p 251 264 American Association of Zoo Veterinarians Infectious Disease Manual SPIRURIDOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Nonhuman primates equids cervids bovids camelids canids felids insectivores birds and reptiles Ingestion of intermediate invertebrate or verte brate or paratenic host Variable but may include chronic gastritis vomiting hemoptysis anemia anorexia weight loss conjunctivitis keratitis and sudden death Inapparent to severe many are subclinical Levamisole albendazole mebendazole ivermectin and other anthelminthics Control of arthropod intermediate and paratenic hosts quarantine of shedding animals Rare although foodborne infection or vector borne can occur Fact Sheet compiled by Inga F Sidor updated by Christopher S Hanley Sheet completed on 31 January 2011 updated 24 August 2013 Fact Sheet Reviewed by Guilherme G Verocai Inga Sidor Susceptible animal groups Many vertebrates are susceptible to members of this order of nematode parasites including wild and captive primates equids cervids bovids camelids suids canids felids insectivores marsupials rodents birds amphibians and reptiles Causative organism Commonly encountered pathogenic spirurids of zoo and wildlife species include nematodes of the genera Habronema Draschia equids camelids Parabronema primates Thelazia mammals birds Spirocerca canids felids ruminants Gongylonema primates ruminants equids suids birds Trichospirura primates reptiles amphibians Tetrameres Oxyspirura birds Physaloptera small carnivores primates insectivores rodents and Gnathostoma carnivores suids primates marsupials Zoonotic potential Most species are not known to cause human disease although some zoonotic spirurids exist Gnathostoma spp may be acquired by ingestion of uncooked infected paratenic hosts fishfrogs crustaceans and cause cutaneous visceral or ocular larva migrans Thelazia spp Also can affect human eyes and it is transmitted by flies directly into the eyes Distribution Global more common in warm climates Incubation period Variable typically weeks to months the life cycle includes an obligate arthropod intermediate host including house or stable flies cockroaches coprophagous beetles and crickets Paratenic hosts rodents and other small mammals amphibians reptiles small birds may also be involved Gnathostoma are aquatic with a secondary fish or amphibian intermediate host Clinical signs Most species of spirurids live in the lumen or walls of the upper gastrointestinal tract oral cavity esophagus stomach proventriculus or ventriculus cutaneous or conjunctival infections are also seen Habronema and Thelazia respectively Signs vary according to site of parasitism and infections are often inapparent but signs can include esophagitis with aneurysms chronic gastritis vomiting hemoptysis anemia anorexia weight loss aortic stenosis or aneurysm or may induce tumors such as sarcoma Spirocerca acute or chronic pancreatitis Trichospirura cutaneous ulceration or nodules ocular discharge keratitisconjunctivitis andor sudden death Post mortem gross or histologic findings Superficial epithelial infections Gongylonema may result in esophageal epithelial hypertrophy and cornification With more invasive infections Spirocerca Habronema and Tetrameres granulomatous or ulcerative lesions of organs develop surrounding necrotic nematodes and caseous debris including gastritis esophagitis and aortitis Granulomas may be large and American Association of Zoo Veterinarians Infectious Disease Manual SPIRURIDOSIS coalescent appearing neoplastic Larval migration may cause focal tissue hemorrhage and necrosis Nodular granulomatous dermatitis can be seen with cutaneous infections due to erratic larval migration when lifecycle is not completed Conjunctivitis and progressive keratitis are typical of Thelazia Diagnosis Morphological identification of larvae eggs or adult nematodes Adults may be recovered from ocular conjunctiva eg Thelazia Oxyspirura including surgical removal or during necropsy Because of encysting or encapsulation for some species of the adult nematodes in granulomas fecal shedding of eggs may be intermittent Imaging techniques such as endoscopy may assist in some cases eg granulomas by Spirocerca Eggs of different species may be difficult to separate morphologically eg Spirocerca and Physaloptera and may require larvae to make a definitively identification Confirmation of infection in biopsies or necropsy tissues may be desired by histopathology Oral and lingual scraping has been used to identify Gongylonema in callitrichids but results are inconsistent Molecular techniques including EM are available for identification of some parasites Material required for laboratory analysis Feces vomitus surgicalpostmortem lesions Relevant diagnostic laboratories Any diagnostic laboratory with routine parasitologic capabilities should be able to diagnose this infection Treatment A variety of anthelminthics have been used to treat these infections with variable efficacy including mebendazole albendazole levamisole fenbendazole ivermectin doramectin moxidectin and milbemycin oxime but controlled studies are uncommon Surgical removal of nematodes Thelazia or granulomas eg Spirocerca may apply Prevention and control Removal of arthropod intermediate hosts terrestrial and aquatic or paratenic hosts from enclosures is key to controlling infections Prophylactic treatment of animals with endectocides or insecticides may prevent contact of arthropod intermediate hosts In endemic regions preventative treatment may be possible for some spirurid species Animals with active fecal shedding or vomiting should be separated from uninfected animals Quarantine routine parasitological diagnostics and prophylactic treatment of new arrivals Suggested disinfectant for housing facilities General measures for cleaning and disinfection should reduce environmental parasite contamination Bleach or ethanol treatment may reduce viability of spirurid eggs which are believed not to be very resistant in the environment Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Direct infection is not observed the indirect life cycle of these parasites makes control of intermediate hosts the most important measure Conditions for restoring diseasefree status after an outbreak Undefined as ante mortem testing may be unreliable due to the low sensitivity of certain techniques and return to diseasefree status may be difficult to ascertain Experts who may be consulted Guilherme G Verocai DVM MSc Department of Ecosystem and Public Health University of Calgary 3330 Hospital Drive NW HSC 2531 Calgary AB Canada T2N 4N1 Phone 4032107869 Fax 4032107869 guiverocaiucalgaryca References 1 Adkesson M J J N Langan and A Paul 2007 Evaluation of control and treatment of American Association of Zoo Veterinarians Infectious Disease Manual SPIRURIDOSIS Gongylonema spp infections in callitrichids J Zoo Wildl Med 381 2731 2 Otranto D and M L Eberhard 2011 Zoonotic helminths affecting the human eye Parasit Vectors 441 3 Hawkins J V N K Clapp R L Carson M A Henke M D McCracken C T Faulkner and S Patton 1997 Diagnosis and Treatment of Trichospirura leptostoma infection in common marmosets Callithrix jacchus Contemp Top Lab Anim Sci 36 5255 4 Hodgkinson J E 2006 Molecular diagnosis and equine parasitology Vet Parasitol 136 109116 5 Kelly P J M Fisher H Lucas and R C Krecek 2008 Treatment of esophageal spirocercosis with milbemycin oxime Vet Parasitol 156 358360 6 Kudo N H Kubota H Gotoh H Ishida H Ikadai and T Oyamada 2008 Efficacy of thiabendazole mebendazole levamisole and ivermectin against gullet worm Gongylonema pulchrum in vitro and in vivo studies Vet Parasitol 151 4652 7 Myers DA C D Smith E C Greiner E Wiedner J Abbott R Marsella and C Nunnery 2010 Cutaneous periocular Habronema infection in a dromedary camel Camelus dromedarius Vet Dermatol 21 527530 8 Rossi L C Rigano E Tomio D Frassetto and E Ferroglio 2007 Use of sustainedrelease moxidectin to prevent eyeworm Thelazia callipaeda infection in dogs Vet Rec 161 820821 9 Soulsby E J L ed 1982 Helminths Arthropods and Protozoa of Domestic Animals Lea and Febiger Philadelphia Pennsylvania Pp 285306 10 Van der Merwe L L R M Kirberger S Clift M Williams N Keller and V Naidoo 2008 Spirocerca lupi infection in the dog a review Vet J 176 294309 11 Vicente J J H O Rodrigues D C Gomes and R MagalhãesPinto 1997 Nematóides do Brasil Parte V Nematóides de mamíferos Rev Bras Zool 141 1452 12 Walker M L and W W Becklund 1971 Occurrence of a cattle eyeworm Thelazia gulosa Nematoda Thelaziidae in an imported giraffe in California and T lacrymalis in a native horse in Maryland J Parasitol 57 13621363 American Association of Zoo Veterinarians Infectious Disease Manual SPRING VIREMIA OF CARP Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Fishes specifically members of the Family Cyprinidae Salmonids and a percid have been experimentally infected Horizontal transmission direct vectors fomites Most cases occur in the spring or early summer when the water begins to warm but remains below 150C One report of virus isolation from ovarian fluid in carp Multiple and varied including lethargy pale gills fecal cast and branchial hemorrhage Mortality with SVCv in carp may reach 100 but is frequently much less None Strict biosecurity and quarantine protocols should be followed based on information available through the OIE and USDA A DNA vaccine has potential as a method of prevention and control No Fact Sheet compiled by Gregory A Lewbart Sheet completed on updated 20 May 2018 updated 12 January 2019 Fact Sheet Reviewed by Kathryn Tuxbury and Elsburgh Tres Clarke Susceptible animal groups Fishes of the family Cyprinidae Some notable examples include arpkoi Cyprinus carpio golden orfe Leuciscus idus goldfish Carassius auratus tench Tinca tinca Percocypris pingi and sheatfish Silurus glanis Documented in Chinese firebelly newts Cynops orientalis in 2016 Causative organism Spring Viremia of Carp Virus SVCv Rhabdovirus carpio Zoonotic potential None Distribution Global especially in temperate geographical areas Incubation period Varies depending on water temperature Latent infections can likely persist for months or even years Arthropods such as the fish louse Argulus sp are likely vectors Clinical signs Infected fish may present with a variety of clinical signs including but not limited to abdominal distention exophthalmia lethargy pale gills darkening of the body surface fecal casts skin and branchial hemorrhage and distention or protrusion of the vent Post mortem gross or histologic findings On necropsy affected fish may have generalized edema which may be sanguineous organ hemorrhage intestinal inflammation and the gastrointestinal tract may contain mucus and no ingesta Histopathologic examination may reveal multifocal necrosis in liver and pancreas pericarditis and renal tubular degeneration Diagnosis Diagnosis is usually made with viral isolation from spleen andor caudal kidney andor serum antibody titers and confirmed with virus neutralization It is important to note that SVCv infected fish also may present with opportunistic Gramnegative bacterial infections Material required for laboratory analysis A minimum of 10 moribund fish or 10 fish exhibiting clinical signs of SVCv must be collected Fish should be sent live to the laboratory or sacrificed and packed separately in sealed aseptic refrigerated containers or on ice Depending on the size of fish whole fish body length 04 cm or the entire viscera including kidney and encephalon body length 46 cm should be collected If the fish is larger liver kidney spleen and encephalon should be collected aseptically Samples should be combined to form pools of a maximum of five fish per pool that should not exceed 15g Tissues should be placed in sterile vials and stored at 4C until virus extraction is performed at the laboratory which is recommended to begin within 24 hours of sample collection For detecting asymptomatic carriers tissue samples of kidney spleen gill and encephalon should be collected Depending on the population size fish collection must encompass a statistically significant number of specimens The sampling should be designed in order to enable detection at a 95 confidence level of infected animals Ultrafiltration using large volumes of water can be used to concentrate and isolate the virus American Association of Zoo Veterinarians Infectious Disease Manual SPRING VIREMIA OF CARP Relevant diagnostic laboratories Various approved state and federal laboratories Information is available through the USDA web site Treatment None Prevention and control Facilities holding and importing high risk cyprinid fishes should be diligent in following standard quarantine protocols and adhere to appropriate and periodic screening as prescribed by the OIE and USDA A DNA vaccine utilizing the SVCv glycoprotein gene has proved promising in challenge trials using koi USDA placing restrictions on import of SVCv susceptible species gametes fertilized eggs and live fish Suggested disinfectant for housing facilities The disinfection protocol depends on the size type and nature of the materials and sites to be disinfected When an active outbreak of SVCv has occurred the infected stocks should be depopulated and all areas that held the infected fish must be disinfected The virus may be inactivated by formalin ozone sodium hypochlorite organic iodophors gamma and ultraviolet radiation pH extremes of 40 or 1000 and heating at 600 C for 15 minutes All equipment and tanks raceways and ponds should be disinfected The USDA APHIS also recommends if surface water rather than municipal water source is used as incoming water to the farms it be treated with sand filtration and UV Notification All suspect cases should be necropsied and the United States Department of Agriculture USDA contacted for proper routing of diagnostic samples Confirmed cases must be reported to the USDA and state veterinarian Measures required under the Animal Disease Surveillance Plan Once an infection is reported a facility has to follow the recommendations described in the International Aquatic Animal Health Code and the Diagnostic Manual for Aquatic Animal Diseases by OIE to be declared free of SVCv In the United States the USDA recommendations must be followed Measures required for introducing animals to infected animal Not applicable Conditions for restoring diseasefree status after an outbreak See the OIE web site for most current information Facilities must be disease free for at least 2 years before diseasefree status can be granted Periodic testing with negative results is required to maintain this status Experts who may be consulted A complete summary of the disease and diagnostic procedures are available through the Office International des Epizooties OIE httpwwwoieint References 1 Ahne W Argulus foliaceus L and Philometra geometra L as mechanical vectors of spring viraemia of carp virus SVCV J Fish Dis 19858241242 2 Ahne W Bjorklund HV Essbauer S Fijan N Kurath G Winton JR Spring viremia of carp SVC Dis Aquat Org 200252261272 3 World Organisation for Animal Health Internet Aquatic Animal Health Code 2010 cited 2018 May 19 Available from httpswwwoieintdocgedD7821PDF 4 World Organisation for Animal Health Internet Manual of Diagnostic Tests for Aquatic Animals 2018 2018 cited 2018 May 19 Available from httpwwwoieintstandardsettingaquatic manualaccessonline 5 Emmenegger EJ Kurath G DNA vaccine protects ornamental koi Cyprinus carpio against North American spring viremia of carp virus Vaccine 20082664156421 6 Emmenegger EJ Sanders GE Conway CM Binkowski FP Winton JR Kurath G Experimental infection of six North American fish species with the North Carolina strain of spring viremia of carp virus Aquaculture 2016450273282 7 Fijan N Petrince Z Sulimanovic D Zwillenberg L Isolation of the viral causative agent from the acute form of infectious dropsy of carp Veterinarski Arhiv 197141125138 8 Goodwin AE First report of spring viremia of carp virus SVCV in North America J Aquatic Anim Health 200214161164 9 Grant AA Jakob E Richard J Garver KA Concentration of infectious aquatic rhabdoviruses from American Association of Zoo Veterinarians Infectious Disease Manual SPRING VIREMIA OF CARP freshwater and seawater using ultrafiltration J Aquatic Anim Health 2011 23218223 10 Lewbart GA Shivappa R Spring Viremia of Carp Virus In Fowler ME Miller RE eds Zoo and Wild Animal Medicine Current Therapy vol 6 St Louis MO Saunders Elsevier 2007 p 121125 11 Overstreet RM Jovonovich J Ma H Parasitic crustaceans as vectors of viruses with an emphasis on three penaeid viruses Integ Comp Biol 2009492127141 12 Petty PD Riggs AC Klinger R Yanong RPE FrancisFloyd R Internet University of Florida IFAS Extension Spring viremia of carp c20022016 cited 2018 May 19 Available from httpedisifasufleduvm106 American Association of Zoo Veterinarians Infectious Disease Manual ST LOUIS ENCEPHALITIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Humans clinical disease Other mammals inapparent infection or clinical illness may be possible Birds usually subclinical reservoirs amplifying hosts possible illness Bite of infected mosquito theoretical risk of direct contact with infected tissues at necropsy Fever stiff neck seizures coma In people mild to severe can be fatal although most infections are asymptomatic Illness in animals is not completely understood Supportive care fluids anticonvulsants anti inflammatories Prevention of mosquito exposure and bites Yes primarily via mosquito vector Fact Sheet compiled by Rose Borkowski Sheet completed on 2 February 2011 updated 13 August 2013 August 1 2018 Fact Sheet Reviewed by Michael McBride Susceptible animal groups This disease is primarily a concern for humans especially the elderly but it may be a concern for other mammals including nonhuman primates and birds SLE was isolated from a domestic horse with neurologic disease raising concern for other equid species Several zoo animal taxa mammals and birds were found to have positive serologic tests for St Louis encephalitis virus SLEV during arbovirus surveillance studies The relationship of positive SLEV serology to clinical disease in these species was not completely understood Usually wild birds are subclinical reservoirs Causative organism A single stranded RNA virus in the genus Flavivirus family Flaviviridae it is closely related to West Nile virus Zoonotic potential Yes Primarily via mosquito vector usually Culex sp Distribution Human SLEV infections are known from Canada to Argentina The illness occurs throughout the US particularly eastern and central states and an SLE outbreak recently occurred in Arizona Incubation period 515 days in people Clinical signs Wild birds serving as viral reservoirs and amplifying hosts generally do not show signs of illness Signs of SLE illness in other animal species are incompletely understood yet the virus was isolated from a horse that succumbed to neurologic disease In humans fever headache and fatigue are common clinical signs More serious clinical signs including stiff neck altered mental status seizures and coma or death are more likely to occur in the elderly The casefatality ratio in humans has been reported as 515 May be a concern for nonhuman primates Post mortem gross or histologic findings In humans evidence of meningitis andor encephalitis may be found Diffuse inflammation of the brain and edema of the substantia nigra have been described Diagnosis Care must be taken to perform virusspecific testing as SLEV crossreacts with West Nile virus on many diagnostic tests Animals Serology Plaque Reduction Neutralization Test PRNT or virus isolation from various tissues Humans Isolation of virus from or demonstration of specific SLEV antigen or nucleic acid in tissue blood CSF or other body fluid fourfold or greater change in SLEVspecific quantitative antibody titers in paired sera SLEVspecific IgM antibodies in serum with confirmatory PRNT antibodies in the same or a later specimen SLEVspecific IgM antibodies in CSF and a negative result for other IgM antibodies in CSF for arboviruses endemic to the region where exposure occurred Material required for laboratory analysis Serum cerebrospinal fluid and tissues American Association of Zoo Veterinarians Infectious Disease Manual ST LOUIS ENCEPHALITIS Relevant diagnostic laboratories Veterinary samples New York State Veterinary Diagnostic Lab Serology Plaque Reduction Neutralization Test Cornell University PO Box 5786 for letters 240 Farrier Rd for packages Ithaca NY 148525786 Phone 6072533900 Fax 6072533943 diagcentercornelledu httpahdcvetcornelledu Louisiana Animal Disease Diagnostic Laboratory Virus Isolation from Tissues School of Veterinary Medicine 1909 Skip Bertman Drive Room 1519 Baton Rouge LA 70803 laddlinfovetmedlsuedu Human Samples Contact CDC state or county public health departments for appropriate laboratories Treatment Supportive care is based on clinical signs at presentation No specific treatment regime is available for SLEV infection and illness Prevention and control No vaccine is available Prevention of mosquito bites is important by use of repellants protective clothing screens and fans Reduction in mosquito presence includes elimination of standing water in containers that can support mosquito breeding and modification of animal enclosures to reduce areas for mosquito access and breeding Efforts to limit exposure of animals and humans to insect vector should be taken eg indoors housing at night to avoid exposure during times of peak mosquito feeding activity or repellent application Use personal protective equipment and proper sharps handling when working with infected animals or their tissues Prevent aerosolization of virus and contact of infected tissues and fluids with skin and mucous membranes Do not use mechanical saws to obtain spinal cord samples due to risk of aerosolization Additional recommendations for handling of potentially infected tissues include use of 3 pairs of gloves inner layer disposable middle layer waterproof and outer layer of metal or Kevlar gloves face shield or goggles plus a disposable half mask high efficiency particle arresting HEPA respirator Suggested disinfectant for housing facilities Sodium hypochlorite 500 5000 ppm 2 glutaraldehyde 2 3 hydrogen peroxide 1 iodine and ethanol can be used The virus may be inactivated by UV light Notification SLE in humans is notifiable to State Public Health Departments If the disease occurs in an animal state veterinary regulations should be queried for requirements to report the disease Measures required under the Animal Disease Surveillance Plan None at this time Measures required for introducing animals to infected animal SLE is not known to be transmissible between mammals birds reptiles or people except via the bite of an infected mosquito A newly diagnosed SLEVpositive animal indicates that SLEVinfected mosquitoes have been active in the area In people infection with SLE is believed to confer lifelong immunity to subsequent SLE infection Conditions for restoring diseasefree status after an outbreak If an outbreak of SLE among zoo animals is verified informationgathering regarding SLEV serologic status of sentinel animals managed by public health officials may be prudent Thorough evaluation and enhancement of mosquito control efforts would also contribute to restoration of diseasefree status American Association of Zoo Veterinarians Infectious Disease Manual ST LOUIS ENCEPHALITIS Experts who may be consulted Division of VectorBorne Diseases Centers for Disease Control and Prevention 3156 Rampart Road Ft Collins Colorado 80521 800CDCINFO References 1 Centers for Disease Control and Prevention Internet Saint Louis Encephalitis 2018 cited 2018 July 31 Available from httpswwwcdcgovsleindexhtml 2 Blackmore C West Nile Virus and other arboviral infections In Rabinowitz PM Conti L eds HumanAnimal Medicine Clinical Approaches to Zoonoses Toxicants and Other Shared Risks Maryland Heights MO Saunders Elsevier 2010 p 294 298 3 De Thoisy B Dussart P Kazanji M Wild terrestrial rainforest mammals as potential reservoirs for flaviviruses yellow fever dengue 2 and St Louis encephalitis viruses in French Guiana Trans of Royal Society of Trop Med and Hygiene 2004987409412 Available from httpsdoiorg101016jtrstmh200312003 4 Hukkanen RR Liggitt HD Kelley ST Grant R Anderson DM Hall RA Tesh RB DaRosa AP BielefeldtOhmann H West Nile virus and St Louis encephalitis virus antibody seroconversion prevalence and persistence in naturally infected pigtailed macaques Macaca nemstrina Clin Vaccine Immunol 200613711714 5 Maharaj PD BoscoLauth AM Langevin SA Anishchenko M Bowen RA Reisen WK Brault AC 2018 West Nile and St Louis encephalitis viral genetic determinants of avian host competence PLoS Negl Trop Dis 2018 cited 2018 August 1122e0006302 Available from httpsdoiorg101371journalpntd0006302 Accessed August 1 2018 6 Reimann CA Hayes EB DiGuiseppi C Hoffman R Lehman JA Lindsey NP Campbell GL Fischer M Epidemiology of neuroinvasive arboviral disease in the United States Am J Trop Med Hyg 20087969749 7 Rosa R Costa EA Marques RE Oliveira TS Furtini R Bomfim MR Teixeira MM Paixão TA Santos RL Isolation of St Louis Encephalitis Virus from a Horse with Neurologic Disease in Brazil Negl Trop Dis 2013711 e2737 8 Siirin MT Duan T Lei H Guzman H da Rosa A Watts DM Xiao SY Tesh RB Chronic SLE virus infection in the golden hamster Merocricetus auratus Am J Trop Med Hyg 200776299306 9 White GS Symmes K Sun P Fang Y Garcia S Steiner C Smith K Reisen WK Coffey LL Reemergence of St Louis Encephalitis Virus California 2015 Emerg Infect Dis 2016 cited 2018 August 1221221852188 Available from httpswwwnccdcgoveidarticle2212160805article American Association of Zoo Veterinarians Infectious Disease Manual STAPHYLOCOCCUS SPP INFECTIONS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals including humans birds reptiles Opportunistic pathogens often involving breaks in the skin Ubiquitous and live free in the environment and commensal parasites of skin and upper respiratory tract Droplet directindirect contact transmission can occur Can affect every organ system and clinical signs depend upon organ affected Common cause of dermatitis Fever anorexia pain abscesses and infections of the skin eyes ears respiratory system mammary glands genitourinary tract skeleton joints Toxins may produce signs of food poisoning Depends upon organs affected and immune status of host Antibiotics Firstchoice antibiotics pending culture and sensitivity testing include cephalosporins and fluoroquinolones Antibiotic resistance is common so sensitivity testing is recommended Appropriate wound care Frequent hand washing Sanitation of environment Avoid abrasions or injury to skin Isolate animals under treatment Appropriate PPE for animal care takers Yes Fact Sheet compiled by June Olds Sheet completed on 5 April 2011 updated 7 March 2013 updated February 21 2018 Fact Sheet Reviewed by Leah Greer Susceptible animal groups All mammals including humans birds reptiles Causative organism Staphylococcus spp of various species but not MRSA Staphylococcus spp are Gram positive facultative anaerobic cocci occurring typically in clusters although pairs and short chains do occur Zoonotic potential Yes Distribution Worldwide ubiquitous Staphylococcal species have been identified as part of the normal microflora in the nasal mucosa and intestinal tract of wild freshly shot agouti from various areas of Trinidad and are expected to be part of the normal flora of most mammals humans birds and reptiles Incubation period Interval of 210 days although signs of poisoning from food contaminated with toxins may occur within 30 minutes and up to 6 hours following ingestion Clinical signs Members of the genus Staphylococcus are among the most common pyogenic or pusinducing bacteria causing local abscesses and generalized infections in a wide variety of species Depending upon organ system affected and if bacteremia and septicemia occur clinical signs may include pneumonia endocarditis meningitis metritis peritonitis osteomyelitis all organs are susceptible Dermatitis and local abscesses are common The organisms are opportunistic pathogens that require some damage to skin or mucous membranes to become established in underlying tissues Staphyococcal infections in wild rabbits may result in severe and sometimes fatal disease Clinical signs of the disease are nonspecific Infected lagomorphs may be listless emaciated and lame if joints or tendons are involved Large subcutaneous abscesses may be visible externally as well as swelling and draining tracts resulting in crusting of the hair Infected areas of the skin are usually crusted with exudate Staphylococcal organisms have also been identified as part of mixed infections with fusobacterium spp and actinomyces spp in mandibular osteomyelitis in wallabies and kangaroos Post mortem gross or histologic findings Purulent inflammation of any organ can be produced Skin Staph pyoderma abscesses cellulitis necrotizing dermatitis It is also a common cause of pneumonia endocarditis osteomyelitis urinary tract infection septicemia mastitis and meningitis Diagnosis Clinical picture andor gross presentation of skin lesions pyoderma observed Inflammatory leukogram is often present Large Grampositive cocci arranged in clusters are readily found in smears of exudate from lesions Culture and sensitivity testing of affected tissues should be performed for definitive diagnosis American Association of Zoo Veterinarians Infectious Disease Manual STAPHYLOCOCCUS SPP INFECTIONS Material required for laboratory analysis Culture aerobic of affected tissues with media designed for facultative anaerobe The organism grows well on 5 blood agar media Relevant diagnostic laboratories Any lab capable to perform microbiology culturesensitivity testing should be able to identify this organism Treatment Appropriate antibiotics can be guided by culture and sensitivity testing Prevention and control Appropriate antibacterial disinfectants that list efficacy against Staphylococcus should be used Clean environments reduce skin contamination and decreasing risk of skin trauma reduces entry point Clean environment with dilute bleach solution to the extent possible Suggested disinfectant for housing facilities Use disinfectants that list efficacy against Staphyloccoccus Clean environment with dilute bleach solution to the extent possible Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Clear infection and sanitize environment to the extent possible prior to introductions Conditions for restoring diseasefree status after an outbreak Resolution of infection in affected animals sanitation of environment Experts who may be consulted These are common bacterial pathogens most diagnostic laboratories and bacteriologists should be familiar with the diseases associated with these bacteria References 1 Andreasen CB Internet Overview of Staphylococcosis in Poultry In The Merck Veterinary Manual 2019 cited 2019 March 19 Available from httpswwwmerckvetmanualcompoultrystaphylococcosisoverviewofstaphylococcosisinpoultry 2 Beehler BA Sauro AM Aerobic bacterial isolates and antibiotic sensitivities in a captive reptile population In Proc Am Assoc Zoo Vet 1983 p 198201 3 Centers for Disease Control and Prevention Internet Staphylococcal Staph Food Poisoning 2018 cited 2019 March 19 Available from httpswwwcdcgovfoodsafetydiseasesstaphylococcalhtml 4 Kiel JP Pagets disease in snakes 1983 In Proc Am Assoc Zoo Vet 1983p 201207 5 Suepaul R Charles RC Dziva F Aerobic microflora and endoparasites of freshly shot wild agouti Dasyprocta leporina in Trinidad West Indies J Zoo Wildl Med 201647410441048 6 Tilly LP Smith FWK The 5minute veterinary consult canine feline 2nd Edition Philadelphia PA Lippincott Williams Wilkins 2000 p 12221223 7 Wobeser G Staphylococcus Infection In Williams ES Barker IK eds Infectious Diseases of Wild Mammals Ames IA Iowa State University Press 2001 p 509 American Association of Zoo Veterinarians Infectious Disease Manual STREPTOCOCCUS GROUP C Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Equines as Strangles pneumonias or reproductive disease Swine as pneumonias and polyarthritis Ruminants as mastitis and polyarthritis Marine mammals birds and salmon as septicemias Fish as ulcers Inhalation ingestion during breeding transplacental Indirectly via hands andor fomites Direct contact with infectious exudates Undercooked horsemeat Variable based on organ system affected Abscesses pharyngitis cellulitis septicemias rhinitis ocular discharge coughing sneezing draining tracts Abortions Mastitis Severity can range from mild to severe or fatal depending on age species and immune status of the individual 1st choice Procaine penicillin and Ampicillin 2nd choice Cephalosporins Chloramphenicol macrolides Rifampin and Trimethoprim sulfas Vaccination and isolation Yes although rarely and mostly in immuno compromised individuals Death has occurred Strep zooepidemicus has been the main isolate in those cases Strep dysgalactiae is also zoonotic Fact Sheet compiled by Christie Hicks Sheet completed on 30 April 2011 updated 7 August 2013 updated 14 February 2018 Fact Sheet Reviewed by Ryan Colburn Susceptible animal groups Virtually all mammals including humans can be susceptible Equine swine ruminants and marine mammals are at risk and published reports include pyometra in a spotted seal Birds salmon and other fish species also can be affected 3 separate outbreaks in shelters have led to the death of many dogs with Streptococcus zooepidemicus as the cause Causative organism Streptococcus species classified into Lancefield Group C which are Gram positive cocci occurring in pairs and chains Zoonotic potential Streptococcus zooepidemicus has been reported as the cause of zoonosis in several individuals with some cases leading to death Possible routes of zoonotic infection are consumption of infected milk and milk products exposure to bodily fluids or contaminated fomites or occupationally during the care of infected individuals Streptococcus dysgalactiae is now being seen more frequently in people Distribution Widely distributed worldwide Incubation period Streptococcus equi subsp equi 3 to 14 days In humans it can be significantly shorter Clinical signs An abscess filled with purulent material especially around the head and neck Fever nasal discharge pharyngitis rhinitis ocular discharge coughing sneezing draining tracts and more rarely cellulitis and septicemia can be seen Streptococcus equi subsp equi is highly infectious Retropharyngeal and submandibular lymph node swelling and abscesses can progress to affect other organs such as the mesentery liver spleen kidney brain and less commonly the thorax Classic Strangles is typically limited to the head and neck regions But when the disease progresses past these areas it is known as metastatic strangles or Bastard Strangles and can result in colic like symptoms fever andor weight loss Purpura hemorrhagica can develop secondary a Type III hypersensitivity presenting with ventral and limb edema petechia and ecchymoses and result in renal and muscle disease This infection has been considered a possible link in Idiopathic Hemorrhagic Vasculopathy Syndrome in black rhinos Streptococcus equi subsp zooepidemicus causes mastitis abortions and infertility in adults and pneumonias in adults and foals Purulent rhinitis and bronchitis in weanling foals Cases of fibrinous pleuritis and pneumonia in sheep mastitis in goats and hemorrhagic pneumonia in dogs have been reported Streptococcus dysgalactiae is seen in cattle as mastitis Piglets lambs goats and calves as polyarthritis Acute death in puppies And recently it has been stated to cause ulcers in fish American Association of Zoo Veterinarians Infectious Disease Committee Manual 2018 STREPTOCOCCUS GROUP C Post mortem gross or histologic findings Abscesses tend to be fluid filled with Streptococcus equi subsp equi Empyema with or without chondroids may be found in the guttural pouches Metastasis is most commonly to the mesenteric lymph nodes Streptococcocus equi subsp zooepidemicus is associated with consolidation and adhesions of the lungs with debris in the airways Reproductive disease is associated with placentitis especially around the cervical star S dysgalactiae causes endocarditis with yellow or white vegetations of varying sizes fibrous and multifocal abscesses of tissues and hypertrophy of synovial villi Diagnosis On CBC anemia neutrophilic leukocytosis and hyperfibrinogenemia are present while the chemistry panel remains unremarkable Polymerase chain reaction is the most sensitive and efficient Growth of the organism on cow or sheep blood agar at 37oC in 3 5 CO2 or using the CAMP phenomenon Ultrasound endoscopy particularly of the guttural pouches andor radiographs may be helpful to determine the extent of the abscesses and infection Material required for laboratory analysis Aspirates from unopened abscesses collected in a sterile manner andor milk collected under sterile conditions can be cultured Aspirates and washes from the nasopharyngeal and guttural pouches can be submitted for Streptococcocus equi subsp equi PCR and culture Relevant diagnostic laboratories Any laboratory that performs cultures and sensitivities on a routine basis can complete testing for this organism Streptococcocus equi subsp equi PCR can be found at many major commercial and veterinary diagnostic laboratories Treatment Antibiotics that are found to be effective against Streptococcus Group C on culture penicillins cephalosporins macrolides Chloramphenicol Rifampin and Trimethoprimsulfonamides have proven to be effective Procaine Penicillin is the antibiotic of choice However the use of antibiotics is controversial in Streptococcocus equi subsp equi unless given in the early stages of disease because many clinicians feel that treatment at later stages only prolongs the course of disease Antibiotic use should therefore be dependent on the severity of disease and can help limit shedding The use of antibiotics may prevent the development of natural immunity therefore reinfection is possible Encouraging assessable lymph nodes and abscesses to drain via warm compresses aspiration andor lancing may help to speed up the recovery process Guttural pouch flushes with a gelatinbenzyl penicillin mixture may also help Administer NSAIDS or corticosteroids to help decrease fever and provide analgesia Prevention and control Streptococcocus equi subsp equi Intramuscular vaccination has proven to not be completely protective but can help decrease the severity of disease Injection site reactions are possible An intranasal product with a live attenuated strain of Streptococcus equi subsp equi is available and used commonly except in Europe It is recommended to vaccinate with 2 initial boosters separated by 2 weeks and then annually Vaccination of any kind is not recommended for exposed horses at a facility with an ongoing outbreak and for 2 years afterwards due to the increased risk of purpura hemorrhagica Vaccine titers can be performed It is important to monitor temperatures and isolate febrile animals as minimal to no shedding occurs within the first 48 hours Isolate the infected individuals as recovered individuals because they can still shed the bacteria for months Examination of guttural pouches can identify carriers Prophylactic treatment of exposed animals may be considered Foals should be appropriately vaccinated for respiratory viruses to help prevent secondary bacterial infections Limit crowding when housing foals Suggested disinfectant for housing facilities Clean with detergents and then disinfect either with chlorhexidine gluconate or glutaraldehyde Notification Not federally reportable but Streptococcocus equi subsp equi is reportable in some states Measures required under the Animal Disease Surveillance Plan Currently none American Association of Zoo Veterinarians Infectious Disease Manual STREPTOCOCCUS GROUP C Measures required for introducing animals to infected animal Streptococcus equi subsp equi can live outside the host for several weeks and can be shed for at least 4 weeks so all facilities should not accept any new individuals for at least 1 month after an outbreak has resolved Specifically for S equi subsp equi all new animals should observe a 21day quarantine period with three negative nasopharyngeal wash PCRs or one guttural pouch wash PCR obtained before entry into the group Conditions for restoring diseasefree status after an outbreak Careful monitoring of those that are infected for a resolution of clinical signs and all blood parameters returning to normal Following clinical resolution three negative nasopharyngeal PCRs separated by 4 to 7 days should be performed before recovered individuals are allowed back into the group with a minimum of 1 month of isolation It should be noted that some individuals can become prolonged shedders for months with the source being within the guttural pouch therefore PCR of the guttural pouch may prove beneficial Experts who may be consulted Any laboratory that routinely tests for this bacterium as well as large animal internists and equine veterinarians References 1 Boyle AG Streptococcus equi subspecies equi infection Strangles in horses Compend Contin Educ Vet 201133E18 2 Clancy MM WocColburn M Viner T Sanchez C Murray S Retrospective analysis of mortalities in elephant shrews Macroscelididae and tree shrews Tupaiidae at the Smithsonian National Zoological Park USA J Zoo Wild Med 201344302309 3 DVM360 Internet Deadly Bacterium Strikes Shelter Dogs 2008 cited 2018 March 3 Available from httpwwwveterinarynewsdvm360com 4 Hirsh D Biberstein E eds Streptococcus and Enterococcus In Hirsh D MacLachlan NJ Walker RL eds Veterinary Microbiology 2nd Edition Ames IA Blackwell Publishing Professional 2004 p 159165 5 Hueffer K Lieske CL McGilvary LM Hare RF Miller DL OHara TM Streptococcus phocae isolated from a spotted seal Phoca largha with pyometra in Alaska J Zoo Wildl Med 201142108112 6 Kahn C Line S eds The Merck Veterinary Manual 9th Edition Whitehouse Station NJ Merck Co Inc 2005 p 587 1130 and 12121213 7 Kahn C Line S eds The Merck Veterinary Manual 10th Edition Whitehouse Station NJ Merck Co Inc 2010 p 665 13391341 and 2468 8 Medscape Internet Emergence of Streptococcus Equi Subspecies Zooepidemicus Infections in Humans by Zoonotic Transmission from Horses 2013 cited 2018 March 3 Available from httpwwwmedscapeorg 9 Murray S Lung NP Alvarado TP Gamble KC Miller MA Paglia DE Montali RJ Idiopathic hemorrhagic vasculopathy syndrome in seven black rhinoceros J Am Vet Med Assoc 20002162230233 10 Pasquini C Pasquini S eds Guide to Bovine Clinics 3rd Ed Pilot Point TX Sudz Publishing 1996 p 195 11 Pasquini C Pasquini S Woods P eds Guide to Equine Clinics 3rd Edition Pilot Point TX Sudz Publishing 1998 p 96 114115 180 and 217 12 Sweeny CR Streptococcus equi infection Strangles In Smith BP ed Large Animal Internal Medicine 4th edition St Louis MO Mosby Elsevier 2009 p 533536 13 Vet Folio Internet Streptococcus equi subspecies equi Infection Strangles in Horses 2011 cited 2018 March 3 Available from httpwwwvetfoliocom 14 Vet Specialists Internet Horse StranglesStreptococcus equi subsp equi infection in horses 2015 cited 2018 March 3 Available from httpwwwvetspecialistscom 15 Wikipedia Internet Streptococcus dysgalactiae 2017 cited 2018 March 3 Available from httpenwikipediaorg American Association of Zoo Veterinarians Infectious Disease Manual STRONGYLOIDIASIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primates especially young captive orangutan Various Strongyloides spp can affect humans canids felids suids equids ruminants rodents birds Larvae or ova shed in feces develop into freeliving adults or infectious larvae that can penetrate skin They then migrate to intestines many species go through lungs on the way to gut also some species are transmitted transmammary Some species can autoinfect within intestines and produce pulmonary hyperinfection Often insidious acute lethargy or sudden death diarrhea abdominal distension and discomfort nausea anorexia cough shortness of breath Can cause severe disease and death from hyper infection in young animals typically subclinical in immune competent adults Usually unsuccessful in severe symptomatic cases However can attempt to treat with ivermectin andor benzimidazoles Ivermectin also benz imidazoles improve hygiene to reduce fecal contamination Yes Fact Sheet compiled by Ellen Bronson med vet DACZM Sheet completed on 31 January 2011 updated 12 March 2013 updated 24 December 2017 Fact Sheet Reviewed by Tom Nolan PhD Christy Rettenmund DVM DACZM Susceptible animal groups All vertebrates Primates especially captive orangutans 5 yr also canids felids suids ruminants equids rodents Causative organism Strongyloides stercoralis in primates domestic dog S fuelleborni in Old World primates S cebus in New World primates Other Strongyloides spp reported in other primates suids felids equids ruminants rodents birds and reptiles Zoonotic potential Yes S stercoralis and S fuelleborni infective larvae can penetrate intact skin also fecal oral transmission possible Common parasite of humans in subtropical and tropical climates Reported in human caretakers in orangutan rehabilitation facilities Distribution Worldwide with different geographic strains and species It is most prevalent in tropics and subtropics also endemic in Southeastern US Incubation period 12 weeks in most species individuals can be chronically affected Clinical signs Strongyloides spp infections are usually subclinical in adult immunocompetent animals In young or immunocomprimised primates with disseminated hyperinfestations due to autoinfection sudden death without premonitory signs is seen Other clinical signs include abdominal pain diarrhea paralytic ileus constipation cough shortness of breath urticaria and rash Post mortem gross or histologic findings Petechiae and ecchymoses in lungs pulmonary hemorrhage erosive or ulcerative enterocolitis Adult parasites larvae and eggs in pulmonary very rare and intestinal mucosal tissue on histologic examination and can also be found in other tissues lymph nodes liver etc in disseminated infections In hyperinfections secondary bacterial septicemia pneumonia and meningitis are common Diagnosis With S stercoralis infection rhabditiform or less frequently filariform larvae can be seen in feces with Baermann fecal exam or direct wet mount or with charcoal or HoradiMori fecal culture but diagnosis often challenging due to infrequent shedding in feces In infants severe tissue destruction and death can occur before fecal shedding begins Eggs can be seen in feces with S fuelleborni infections In hyperinfections may be able to detect larvae in sputum or respiratory tract mucus Eosinophilia possible during acute and chronic stages S stercoralis ELISA and other serology available for humans levels shown to decrease after treatment in humans ELISA has been used in orangutans but has not been validated and usefulness in nonhumans is unknown Material required for laboratory analysis Fresh feces for fecal exam serum for ELISA antibody testing American Association of Zoo Veterinarians Infectious Disease Manual STRONGYLOIDIASIS Relevant diagnostic laboratories Most reference laboratories can perform Baermann fecal exams ELISA antibody test available through CDC for human cases but not currently commercially available for non human primates or other species Treatment Difficult in symptomatic or chronically infected animals but can reduce burdens with ivermectin albendazole other benzimidazoles Ivermectin treatment is the preferred treatment and is usually 2 doses one week apart resulting in rapid amelioration of clinical signs Treatment with benzimidazoles usually is daily for two weeks with no change in clinical signs expected before 3 to 7 days Aggressive combination treatment recommended for hyperinfection cases A second dosing of antiparasitic a week after the end of the first treatment is usually needed to kill adults developing from larvae that were migrating in the tissues during the first treatment Treatments should always be performed in combination with control measures to prevent reinfection during treatment since the larvae are not killed by the same dosages as the adults Prevention and control Daily removal of feces to break cycle if animals on soil will not be able to break cycle Can keep burdens low with regular anthelmintics Due to high morbiditymortality in captive orangutans monthly anthelmintic strongly recommended for all members of orangutan groups with infants juveniles or pregnant adults Monthly ivermectin is the most commonly used preventative regimen for orangutans Suggested disinfectant for housing facilities Mechanical removal of feces most important cleaning with soap and water and complete drying is recommended Quaternary ammonium products containing Nalkyl dimethyl benzyl ammonium chloride or didecyl dimethyl ammonium chloride will kill infective larvae very rapidly and are suitable for hard solid surfaces Steam cleaning also effective for disinfecting housing areas Notification None Measures required under the Animal Disease Surveillance Plan NA Measures required for introducing animals to infected animal Consider prophylactic deworming regimen during introduction phase and frequent fecal examinations but transmission likely difficult to avoid goal should be to avoid clinical signs especially in groups with young primates Conditions for restoring diseasefree status after an outbreak If animals have access to soil it will be impossible to eliminate parasite If area can be completely disinfected can attempt daily complete removal of feces cleaningdrying area but if chronically infected animal is present will be unlikely to eliminate infection Experts who may be consulted Thomas J Nolan PhD Director of the Clinical Parasitology Laboratory University of Pennsylvania School of Veterinary Medicine Phone 2158987895 Email parasitvetupennedu References 1 Bowman DD Helminths In Bowman DD ed Georgis Parasitology for Veterinarians 10th Ed St Louis MO Elsevier Saunders 2014 p 192194 2 Centers for Disease Control and Prevention Internet Strongyloidiasis 2016 cited 2017 November 17 Available from httpswwwcdcgovparasitesstrongyloideshealthprofessionalsindexhtml 3 Murphy HW Great Apes In Fowler ME Miller RE eds Zoo and Wild Animal Medicine Volume 8 St Louis MO Elsevier Saunders 2015 p 336354 4 Nurcahyo W Konstanzová V Foitová I Parasites of orangutans primates ponginae An overview Am J Primatol 201679e22650 5 Swenson B Great Ape Neonatology In Fowler ME Miller RE eds Zoo and Wild Animal Medicine Current Therapy Volume 4 Philadelphia PA WB Saunders 1999 p 385386 6 Toft JE Eberhard ML Parasitic Diseases In Bennett BT Abee CR Herickson R eds Nonhuman Primates in Biomedical Research Diseases San Diego CA Academic Press 1998 p 133140 American Association of Zoo Veterinarians Infectious Disease Manual SWINE VESICULAR DISEASE Fact Sheet compiled by Cora Singleton Sheet completed on 8 August 2018 Fact Sheet Reviewed by Marjorie Bercier Susceptible animal groups Domestic pigs wild boar Causative organism An enterovirus of the Picornaviridae family Zoonotic potential Possible More recent studies suggest that the virus has adapted to swine and has lost its ability to infect humans SVDV is closely related to human coxsackievirus B5 Distribution Europe some parts of Asia Exotic to the United States Incubation period 27 days Clinical signs Pyrexia anorexia lameness vesicles progressing to erosions coronary bands snout lips oral cavity and teats horn of hoof occasionally shed May present with unsteady gait with jerky leg movements due to encephalitis Young animals are usually more severely affected Clinically indistinguishable from foot and mouth disease vesicular exanthema of swine Seneca virus A and vesicular stomatitis Recovery within 2 3 weeks presence of a dark horizontal line on the hoof where growth had stopped Post mortem gross or histologic findings Vesicles on coronary bands snout lips oral cavity Hydropic degeneration and edema of stratum spinosum of the affected epidermis followed by ballooning degeneration of keratinocytes that then float into the vesicular fluid Stratum basale remains intact A nonsuppurative meningoencephalitis and necrotizing myocarditis and endocarditis have been reported Diagnosis Agent identification virus culture along with electron microscopy ELISA method of choice complement fixation RTPCR Serology ELISA virus neutralization also double immunodiffusion radial immunodiffusion counter immunoelectrophoresis Material required for laboratory analysis Vesicular fluid epithelium covering a vesicle heparinized whole blood serum feces tissues in formalin Relevant diagnostic laboratories Foreign Animal Disease Diagnostic Laboratory Plum Island 40550 Route 25 for packages Orient Point NY 11957 PO Box 848 for letters Greenport NY 119440848 631 3233256 Fax 631 3233366 Since vesicular diseases cannot be distinguished clinically contact the proper authorities prior to sample collection and shipment Treatment No effective treatment Supportive care and treatment of secondary problems Prevention and control Prevention should include no feeding of uncooked pork products regulation of movement of animals and animal products and serologic monitoring to detect infections No vaccine is available Control measures include notification of authorities quarantine or depopulation of infected animals Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Domestic pigs wild boar Direct not common contact with infected pig fecal transmission Indirect feeding uncooked infected pork products fomites Pyrexia anorexia lameness vesicles progression to erosions coronary bands snout lips oral cavity teats Moderately contagious Moderate to high morbidity Very low mortality None Rare persistent carriers Test and quarantine animals disinfect environment do not feed uncooked pork products Possibly American Association of Zoo Veterinarians Infectious Disease Manual SWINE VESICULAR DISEASE and disinfection of the environment Suggested disinfectant for housing facilities Phenols sodium hydroxide formalin sodium carbonate ionic and nonionic detergents strong iodophors in phosphoric acid chloroform The virus is extremely persistent in the environment thus difficult to eradicate Notification Reportable to the USDAAPHIS through the State Veterinarian or the federal Area Veterinarian in Charge The disease is also reportable to the World Organization for Animal Health OIE Measures required under the Animal Disease Surveillance Plan Reportable disease Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Infections must be reported to USDAAPHIS for management Experts who may be consulted USDA State Veterinarians or federal Area Veterinarians in Charge References 1 Alexandersen S Knowles NJ Belsham GJ Dekker A Nfon C Zhang Z Koenen F Picornaviruses In Zimmerman JJ Karriker LA Ramirez A Schwartz KJ Stevenson GW Zhang J eds Diseases of Swine 11th ed Ames IA WileyBlackwell 2018 in press 2 Jackson PGG Cockcroft PD Handbook of Pig Medicine London England Saunders Elsevier 2007 p 186187 3 Knowles NJ McCauley JW Coxsackievirus B5 and the relationship to swine vesicular disease virus Curr Top Microbiol Immunol 1997223153167 4 Spickler AR Internet Swine vesicular disease 2015 cited 2018 August 08 Available from httpwwwcfsphiastateeduFactsheetspdfsswinevesiculardiseasepdf 5 United States Department of Agriculture Animal Plant and Health Inspection Services Internet All National Animal Health Laboratories Network NAHLN Laboratory List 2018 cited 2018 August 08 Available from httpwwwaphisusdagovanimalhealthnahlndownloadsallnahlnlablistpdf 6 United States Department of Agriculture Animal Plant and Health Inspection Services Internet Diagnostic Testing at the National Veterinary Services Laboratories 2015 cited 2018 August 08 Available from httpwwwaphisusdagovaphisourfocusanimalhealthlabinfo servicessadiagnostictestsctdiagnostictests 7 World Organization for Animal Health OIE Internet Swine vesicular disease In Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2018 2018 cited 2018 August 08 Available from httpwwwoieintfileadminHomeengHealthstandardstahm20808SVDpdf 8 Fernandez PJ and White WR Swine vesicular disease In Atlas of Transboundary Animal Diseases World Organization for Animal Health OIE 2010 237242 American Association of Zoo Veterinarians Infectious Disease Manual TANAPOXVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primates including humans African species are usually source for Asian species Humans infected via skin wounds Erythematous 2 3cm raised thickened skin lesions with umbilicated centers that developing within days to weeks of contact Lesions often on face Mild to moderate severity Increased severity with immuno compromise conditions Supportive as lesions usually have spontaneous regression Avoid cohabitation of African and Asian non human primate species Disinfection of fomites and vector control Yes Fact Sheet compiled by E Marie Rush Sheet completed on 3 December 2010 updated 15 July 2013 May 1 2018 Fact Sheet Reviewed by Marc Valitutto Susceptible animal groups Primates human and nonhuman Causative organism Tanapoxvirus genus Yatapoxviridae Principle reservoir is unknown thought to be a nonhuman primate Zoonotic potential Yes Distribution SubSaharan Africa originated in Tana River Valley of Kenya Cases have been reported from travelers in Tanzania and during WHO smallpox eradication in Central Africa Incubation period Unknown but clinical signs can appear within days of inoculation Replication has been shown in owl monkey renal cells Clinical signs In nonhuman primates vesicles may be numerous are often around the upper body and head region and appear within 23 weeks of inoculation In humans often a single occasional clusters of 10 lesions erythematous thickwalled dermatologic vesicle papule is noted often on the extremities or lower body regions and the patient may have prostration general body ache or headache tender regional adenopathy and prodromal 24 days pyrexia prior to lesion onset Lesions may reach maxmal size by two weeks then typically regress spontaneously within 46 weeks Pruritus may accompany lesions This disease is clinically virtually indistinguishable from Yabalike disease virus which is in the same genus Yatapoxviridae but is different from Yaba Monkey tumor virus also in the same genus In humans risk for secondary bacterial infections in humans Post mortem gross or histologic findings Grossly apparently epidermal lesions that when biopsied show marked thickening and ballooning degeneration of prickle cell layer and eosinophilic viral inclusion bodies characteristic of poxviruses on histopathology and enveloped forms seen on EM Diagnosis History of direct or indirect contact with nonhuman primates or transport from or travel to Africa complement fixation serum neutralization and precipitation tests ELISA and PCR Material required for laboratory analysis Serum tissue for histopathology or EM Relevant diagnostic laboratories This is an uncommon disease but has been noted in North American collections Most laboratories that process nonhuman primate samples can either run the PCR for this virus or can direct personnel accordingly to an appropriate laboratory facility for testing of samples Histopathology or EM can be done at most laboratories that normally process tissues and have the capabilities for these procedures Treatment Supportive spontaneous resolution usually in 6 weeks in humans Prevention and control Avoid contact with primates that have had potential exposure Proper quarantine and testing of animals with history of exposure or recent shipment from Africa Humans should keep all skin wounds cleaned bandaged and covered when working with nonhuman primates Thorough American Association of Zoo Veterinarians Infectious Disease Manual TANAPOXVIRUS disinfection of all potential fomites in housing areas for primates in collections and protection of animal care staff through education and proper clothing and protective wear gloves long sleeves Vector control Previous exposureimmune reaction to Yabalike disease virus may provide immunity for tanapox but not visaversa Suggested disinfectant for housing facilities Detergents hypochlorite alkalis Virkon and glutaraldehyde Notification Public health officials may need to be notified if zoonotic transmission occurs depending on the state Measures required under the Animal Disease Surveillance Plan Currently none Measures required for introducing animals to infected animal Do not introduce animals with clinical disease active or resolving pustuleslesions to noninfected or new animals Allow resolution of all lesions completely prior to introduction and follow proper quarantine measures for individual facility Conditions for restoring diseasefree status after an outbreak Condition typically spontaneously resolves within weeks with supportive care Treatment of any secondary infections should assist in wound healing Immunosuppressed animals may be more susceptible to infection and secondary diseasecomplications Proper disinfection of animal area and fomites should be done following an outbreak or care of an infected animal prior to housing new animals in the area Experts who may be consulted Centers for Disease Control and Prevention Poxvirus and Rabies Branch Division of HighConsequence Pathogens and Pathology 1600 Clifton Rd Atlanta GA 30333 800CDCINFO References 1 USAF Internet Zoonotic Diseases Viral Diseases Yabapox 2006 cited 2013 July 18 Available from httpwwwphsourceusPHZDVDYabapoxhtm 2 International Veterinary Information Service Internet Contageous Ecthyma cited 2013 July 18 Available from httpwwwivisorgadvancesDiseaseFactsheetscontagiousecthymapdf 3 Berger S Infectious diseases of the Democratic Republic of Congo Los Angeles CA Gideon Informatics Inc 2018 p 286 4 Brunetti CR Amano H Ueda Y Qin J Miyamura T Suzuki T Li X Barrett JW McFadden G Complete genomic sequence and comparative analysis of the tumorigenic poxvirus Yaba monkey tumor virus J Virol 2003771333513347 5 Dhar AD Werchniak AE Li Y Brennick JB Goldsmith CS Kline R Damon I Klaus SN Tanapox infection in a college student N Engl J Med 2004350361366 6 Downie AW Espana C A Comparative Study of Tanapox and Yaba Viruses J Gen Virol 1973193749 7 Downie AW Espana C Comparison of Tanapox virus and Yabalike viruses causing epidemic disease in monkeysEpidemiol Infect 1972 702332 8 Jezek Z Arita I Szceniowski M Paluku KM Ruit K Nakano JH Human Tanapox in Zaire clinical and epidemiological observations on cases confirmed by laboratory studies Bull World Health Org 19856310271035 9 Joslin J Other primates excluding great apes In Fowler ME Miller RE eds Zoo and Wild Animal Medicine 5th ed St Louis MO Elsevier 2003 p346381 10 Knight JC Novembre FJ Brown DR Goldsmith CS Esposito JJ Studies on Tanapox virus Virol 1989172116124 11 Mediratta S Essani K The replication cycle of tanapox virus in owl monkey kidney cells Can J Microbiol 19994519296 American Association of Zoo Veterinarians Infectious Disease Manual TANAPOXVIRUS 12 Monroe BP Nakazawa YJ Reynolds MG Carroll DS Estimating the geographic distribution of human Tanapox and potential reservoirs using ecological niche modeling Int J Health Geogr 2014151334 13 Schielke JE Kalishman J Liggitt D BielefeldtOhmann H What is your diagnosis multifocal subcutaneous tumors in a young male baboon Contemp Top Lab Anim Sci 2002412729 14 Stich A Meyer H Köhler B Fleischer K Tanapox first report in a European traveler and identification by PCR Trans R Soc Trop Med Hyg 200296178179 15 Zimmermann P Thordsen I Frangoulidis D Meyer H Realtime PCR assay for the detection of Tanapox virus and Yabalike disease virus J Virol Meth 2005130149153 American Association of Zoo Veterinarians Infectious Disease Manual TOXOPLASMOSIS Fact Sheet compiled by Joseph A Smith Sheet completed on 30 June 2011 updated 15 July 2013 Fact Sheet Reviewed by Charles Faulkner Jitender P Dubey Susceptible animal groups Felids are the only definitive host for Toxoplasma gondii Australian marsupials lemurs New World primates brown hares southern sea otters and pronghorn antelope are reported to be highly susceptible Cattle rats horses Old World monkeys and turkeys are reported as relatively resistant to clinical disease Pallas cats are an exception to most felids in that a positive queens immune response does not prevent congenital transmission Causative organism Toxoplasmosis is caused by the obligate intracellular coccidian Toxoplasma gondii Felids are the definitive host and are the only taxa known to transmit infective oocysts in feces Other species are most frequently infected by ingestion of oocysts from felid feces which may survive for months to years in the environment Once ingested by an intermediate host the organism forms tachyzoites that rapidly reproduce in host tissues Tachyzoites are the cause of most clinical signs Tachyzoites can then transform into thinwalled tissue cysts containing bradyzoites The life cycle is completed when felids ingest the tissue cysts from prey species Other nonfelid carnivorous species may also become infected from ingestion of tissue cysts but are unable to complete the life cycle and do not produce infective oocysts in feces however they as prey species can become carrier hosts which are infective and usually termed intermediate hosts in the literature although they are not required to complete the life cycle Zoonotic potential In the US it is estimated that 225 of the population has been infected with toxoplasmosis with this number approaching 95 in some other parts of the world Transmission can occur from ingestion of oocysts passed in cat feces eg cleaning pet litter boxes gardeningcontact with contaminated soil contaminated produce ingestion of undercooked meat transplacentally or rarely through blood transfusions and organ transplants Most infections are asymptomatic or cause mild self limiting flulike symptoms Infections acquired during pregnancy can cause abortion congenital defects or more severe disease in the child Clinical signs in the child including ocular disease seizures and mental disability may not be present until later in life Infections in immunocompromised persons may be severe Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All vertebrates primarily birds and mammals Ingestion of oocysts from felid feces ingestion of tissue cysts transplacental transmammary Variable depending on species and organs affected Can range from asymptomatic to sudden death Variable depending on species Causes severe disease in Australian marsupials New World primates and lemurs Usually asymptomati c in most felids Atovaquone clindamycin sulfonamide Prevent exposure to felid feces Control intermediate hosts in environment Yes American Association of Zoo Veterinarians Infectious Disease Manual TOXOPLASMOSIS Immunosuppression may also cause a recrudescence of an infection that was acquired earlier in life Distribution Worldwide anywhere felids are present or have been introduced Runoff water infected with oocysts can introduce the organism to ocean environments Incubation period Infections acquired from ingestion of tissue cysts have a 310 day prepatent period in felids Infections acquired from ingestion of oocysts have a 1948 day prepatent period in felids Oocysts passed in feces become infective after 15 days in the environment Felids can shed millions of oocyts over 13 weeks Tissue cysts can remain present for years Clinical signs Infections in felids are usually subclinical although a transient mild diarrhea may occur In species sensitive to the disease animals are often found dead with no clinical signs observed prior to death If present clinical signs may vary depending on the organs affected Reported clinical signs include respiratory signs dyspnea tachypnea coughing gastrointestinal signs diarrhea general signs depression anorexia behavioral changes lymphadenopathy muscle weakness neurologic signs blindness ataxia dysphagia ocular disease keratitis uveitis chorioretinitis endophthalmitis cataracts and abortion Serum biochemical abnormalities may include elevated muscle and liver enzymes Post mortem gross or histologic findings GrossAffected animals may have no gross lesions If present gross lesions may include congestion hemorrhage organomegaly or necrosis of any affected organs HistologicMultifocal multiorgan necrosis is often associated with acute toxoplasmosis Focal necrosis of affected organs may be associated with free and intracellular tachyzoites 2µm x 6µm crescentshaped structures with pointed anterior and rounded posterior Brain encephalitis with microglial nodules and perivascular cuffing myocardium myocarditis and lung interstitial pneumonia are frequently affected Tissue cysts measuring 5100µm in diameter can be found in any tissue but frequently occur in the brain eye and muscle Cysts have thin 05µm elastic walls and contain up to hundreds of 7µm x 15µm crescentshaped bradyzoites Diagnosis Definitive diagnosis can be achieved by observation of tachyzoites or bradyzoites in affected tissues with cytology or histopathology Multiple serologic testing modalities capable of detecting IgG and IgM antibodies are available including ELISA Western blot direct agglutination test DAT modified agglutination test MAT latex agglutination test LAT and indirect hemagglutination test IHAT A single positive serologic test indicates exposure to the organism In young animals transfer of maternal antibodies can produce positive serology results Active infections are generally characterized by a high positive IgM titer with subsequent seroconversion and development of an IgG antibody titer 32 or by a 4 fold increase in paired IgG titers taken 24 weeks apart PCR and immunohistochemical staining can also be used to detect Toxoplasma antigen in tissues Material required for laboratory analysis Formalinfixed affected tissues can be used for histopathology and immunohistochemical staining Fresh and frozen tissue can be used for PCR DNA denatures in formalin so PCR becomes less accurate in tissues that have been fixated in formalin for long periods Serum is needed for the serologic tests Aqueous humour cerebrospinal fluid and plasma can also be assayed for IgG antibodies by the MAT Relevant diagnostic laboratories Clinical Parasitology Diagnostic Service Laboratory immunoassay by MAT Room A233 University of Tennessee College of Veterinary Medicine 2407 River Drive Knoxville TN 379964500 8659745645 parasitologyutkedu American Association of Zoo Veterinarians Infectious Disease Manual TOXOPLASMOSIS Colorado State University Veterinary Diagnostic Laboratory 300 West Drake Road Ft Collins CO 80526 9702971281 dlabcolostateedu Treatment Atovaquone has shown the most promise in treating toxoplasmosis in multiple species Administration with a high fat meal eg canola oil has been suggested to increase absorption of the drug However the efficacy of this practice is unknown for foregut fermenters Other drugs including sulfa drugs clindamycin spiramycin ponazuril and pyrimethamine have also been used alone or in combination with variable success General supportive care is also usually needed for active cases of toxoplasmosis Prevention and control Controlling exposure to cat feces is an important part of toxoplasmosis prevention Feral cats are a common source of infective oocysts in the environment Contamination of food and bedding materials with cat feces may be a source of infection in situations where felids are not known to be present near the affected animal A live attenuated vaccine has been developed for livestock but efficacy is variable in other species Meat containing tissue cysts can be rendered noninfective by cooking to 67 ºC or freezing to 12 ºC for at least 24 hours Control of intermediate hosts eg rodents in the environment can help prevent transmission to carnivores Prophylactic treatment of queens or kittens has been recommended to reduce morbidity and mortality in Pallas cats Suggested disinfectant for housing facilities Toxoplasma is resistant to most disinfectants but is usually susceptible to boiling water formalin and iodine Notification Not a reportable disease Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Animals introduced to the environment of an infected felid are at risk of contracting toxoplasmosis Nonfelid species that are infected with toxoplasmosis do not pose a risk to other individuals in the environment unless their tissue is ingested Vertical transmission between females and their offspring is possible in all mammalian species when the infection occurs during gestation Conditions for restoring diseasefree status after an outbreak Once an individual becomes infected with toxoplasmosis it can remain infected for life Toxoplasma organisms can remain dormant in tissue cysts where they are protected from the hosts immune response Episodes of immunosuppression can result in a recrudescence of clinical disease Serologic testing and removal of positive individuals is a possible way of reaching diseasefree status provided that there is not continued exposure to infective oocysts in the environment Experts who may be consulted Joseph A Smith DVM Fort Wayne Childrens Zoo 3411 Sherman Blvd Fort Wayne IN 46808 2604276815 voice 2604276859 fax vetkidszooorg Jitender P Dubey USDA ARS ANRI APDL BARCEast Bldg 1001 American Association of Zoo Veterinarians Infectious Disease Manual TOXOPLASMOSIS 10300 Baltimore Avenue Beltsville MD 20705 3015048128 voice 3015049222 fax JitenderDubeyarsusdagov Sharon Patton MS PhD University of Tennessee College of Veterinary Medicine 2407 River Drive Knoxville TN 37996 8659745654 voice spattonutkedu Michael R Lappin DVM PhD ACVIM Colorado State University Veterinary Teaching Hospital and Diagnostic Laboratory 300 West Drake Road Ft Collins CO 80526 9702970313 michaellappincolostateedu References 1 De Camps S JP Dubey and WJA Saville 2008 Seroepidemiology of Toxoplasma gondii in zoo animals in selected zoos in the Midwestern United States J Parasitol 943 648653 2 Dubey JP and K Odening 2001 Toxoplasmosis and related infections In Samuel WM MJ Pybus and AA Kocan eds Parasitic Diseases of Wild Mammals 2nd ed Iowa State Press Ames Iowa Pp 478519 3 Dubey JP 2008 Toxoplasma In Atkinson CT NJ Thomas and DB Hunter eds Parasitic Diseases of Wild Birds WileyBlackwell Ames Iowa Pp 204222 4 Miller MA 2008 Tissue cystforming coccidia of marine mammals In Fowler ME and RE Miller eds Zoo and Wild Animal Medicine Current Therapy 6 Saunders St Louis Missouri Pp 319340 5 Portas TJ 2010 Toxoplasmosis in macropodids a review J Zoo Wild Med 41 16 6 Wolfe BA 2003 Toxoplasmosis In Fowler ME and RE Miller eds Zoo and Wild Animal Medicine 5th ed Saunders Elsevier Science St Louis Missouri Pp 745749 American Association of Zoo Veterinarians Infectious Disease Manual TRICHOSTRONGYLOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Birds bovids camels cervids equids giraffe suidae rabbits rodents primates Fecaloral with a direct life cycle Heavy burdens cause weight loss lethargy anorexia watery diarrhea weakness anemia and death Lowlevel infections are usually asymptomatic Young animals more severely affected Benzimidazoles or macrocyclic lactones Alternatives to anthelminthics have been investigated in artiodactylids including cooper oxide wire particles and nemato phagous fungus environmental control Pasture rotation Consider strategic and evidencebased treatment using in vitro sensitivity testing with anthelmintic usage Immunity develops as animals age Some species are zoonotic Fact Sheet compiled by Christopher S Hanley Sheet completed on 29 December 2010 updated 1 April 2013 updated 8 February 2018 Fact Sheet Reviewed by Deidre Fontenot Susceptible animal groups Birds bovids camelids cervids equids giraffe suidae rabbits rodents and as accidental hosts primates Causative organism Any of the 35 species of nematodes of the genus Trichostrongylus Zoonotic potential Yes although not all species are zoonotic Most human infections are asymptomatic or associated with mild clinical signs as all primates are accidental hosts Abdominal pain rashes nausea diarrhea anorexia flatulence dizziness generalized fatigue and malaise all possible Distribution Worldwide Incubation period Under ideal conditions the third stage infective larvae develop within 510 days Depending on the species of Trichostrongylus prepatency is generally 1525 days but can be delayed for prolonged periods Some species of Trichostrongylus T colubriformis T tenuis can undergo winter arrest in certain geographic areas Soil moisture climate warming and pasture loads can all play a role in the incubation and infectivity Clinical signs Most infections are asymptomatic or only have mild signs Weakness and death can occur with heavy worm burdens especially in young animals Wasting black or watery diarrhea depression anorexia swollen mucosa eosinophilia and anemia can all occur especially in chronic infections Birds may have the above as well as decreased egg production Because of the great variability in host and organ invaded each species of Trichostrongylus must be evaluated in the specific circumstance of presentation Post mortem gross or histologic findings Depending on the species of Trichostrongylus adult worms may be seen in the small intestine abomasum of ruminants stomach of monogastrics or ceca of birds They are very fine parasites and if they are removed from the organs and placed against a dark background they look like small hairs Mucosal congestion inflammation and thickening may be present Gastric infection may produce an edematous stomach or abomasum Histologically villus atrophy enterocyte destruction mucosal ulceration capillary erosion blood loss mucosal edema fibrinonecrotic membranes and secondary bacterial infection may be seen Gastric infection may produce gastric edema and hyperplasia Diagnosis Eggs can be found on fecal parasite evaluation or parasites can be identified on histologic evaluation of the gastrointestinal tract Material required for laboratory analysis Feces or adult worms American Association of Zoo Veterinarians Infectious Disease Manual TRICHOSTRONGYLOSIS Relevant diagnostic laboratories Any laboratory that can provide endoparasite identification and quantification Eggs of Trichostrongylus spp cannot be reliably differentiated from those of most other Trichostrongyloidea or Strongyloidea Egg quantification fecal egg count via McMasters technique is recommended in hoofstock species to determine whether treatment is warranted Treatment Benzimidazoles or macrocyclic lactones Alternatives to anthelminthics have been investigated in artiodactylids including cooper oxide wire particles and nematophagous fungus environmental control Prevention and control Proper sanitation pasture rotation strategic and evidence based anthelmintic treatment using in vitro sensitivity testing Immunity with age develops in some species although this has not been proven in hoofstock species Suggested disinfectant for housing facilities None Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal In artiodactylids fecal egg counts are recommended before releasing new animals on pasture to determine current level of infection prior to introduction Pasture infection levels can also be considered pasture larval counts as well as current infection levels in animals to make risk benefit assessment for treatment prior to pasture introduction In vitro sensitivities can be performed to determine level of resistance to classes of anthelminthics prior to treatment If in vitro sensitivity testing cannot be performed then treatment of newly infected animals with a cocktail of anthelminthics with at least two drugs in different families at full dose using accurate animal body weights may eliminate previously acquired anthelmintic resistant worms Conditions for restoring diseasefree status after an outbreak Directed treatment at clinically affected animals by employing quantitative fecal parasitology McMasters counts Low levels of parasitism are common and may aid in the development of immunity Experts who may be consulted Thomas Craig DVM MS PhD Department of Veterinary Pathobiology Texas AM University 4467 TAMU College Station TX 778434467 979 8459191 tcraigcvmtamuedu James E Miller DVM MPVM PhD Department of Pathobiological Sciences School of Veterinary Medicine Louisiana State University Baton Rouge LA 70803 2255789652 Fax 2265789701 jmille1lsuedu Ray M Kaplan DVM PhD Associate Professor Department of Infectious Diseases College of Veterinary Medicine University of Georgia Athens GA 30602 7065425670 Fax 7065425771 rkaplanvetugaedu American Association of Zoo Veterinarians Infectious Disease Manual TRICHOSTRONGYLOSIS References 1 Roberts LS Janovy J Nematodes Strongyloidia Bursate Rhabditians In Roberts LS Janovy J eds Foundations of parasitology 8th ed St Louis MO McGraw Hill 2009 p 419432 2 Bowman DD Helminths In Bowman DD ed Georgis parasitology for veterinarians 10th ed St Louis MO Elsevier 2014 p 122240 3 Hoberg EP Kocan AA Rickard LG Gastrointestinal strongyles in wild ruminants In Samuel WM Pybus MJ Kocan AA eds Parasitic diseases of wild mammals 2nd ed Ames IA Iowa State Press 2001 p 193227 American Association of Zoo Veterinarians Infectious Disease Manual CAPILLARIASISTRICURIASIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Wide range of vertebrates Fecaloral transmission via transmission of eggs with infective L2 Some capillarids use earthworms or fish as intermediate hosts Weight loss diarrhea High morbidity but low mortality Fenbendazole and other benzimidazoles milbemycin oxime Sanitation eggs are very resistant Do not consume undercooked fish Yes some species of Trichuris Capillaria hepaticum and C philippinensis Fact sheet compiled by Janna Wynne Sheet completed on 15 March 2018 Fact Sheet Reviewed by Michael McBride Susceptible animal groups Mammals birds and reptiles Causative organism Capillarids of many genera eg Capillaria Eucleus Calodium Pearsonema occur in mammals birds reptiles amphibians and fish Trichuris spp occurs in mammals primates ruminants carnivores suids and rodents Zoonotic potential Yes some species of Trichuris Capillaria hepatica and C philippinensis Distribution Worldwide although parasites of concern will vary by location and species Incubation period Variable but tends to be longer than many other parasites Prepatent period is three months in many intestinal Trichuris Clinical signs Clinical cases and fatal disease are rare Many low parasite burdens can be asymptomatic and infections are frequently asymptomatic in hoofed stock In clinical animals weight loss colitis diarrhea hematochezia or melena can be present Capillaria tend to infect airways nasal cavity or the urinary bladder such as air sacculitis or pneumonia from Eucolies spp Or Pearsonema spp In the urinary system Capillaria hepaticum causes hepatic cirrhosis and C philippenensis is found in the tissues of fish causing an intestinal infection when affected raw fish are consumed Post Mortem gross or histologic findings Trichuris spp Can be observed embedded in the wall of the colon of carnivores and ungulates and found in the neutral pH forestomach of some leafeating monkeys eg Colobus Capillaria hepatica induces cirrhosis of the liver It is usually identified on post mortem Other capillarids can cause nasal bronchial intestinal hepatic and urinary infections and findings will vary according to parasitic and host species and site of parasitism Diagnosis Centrifugation fecal floatation can be performed for identification of infection However The eggs bipolar plugs are very dense and require correct floatation solution good choice is Sheathers with specific gravity of 127 and centrifugation to recover them Eggs are shed intermittently so repeated fecals may be necessary For pulmonary species BAL and for urinary tract infections urine sedimentation Ova of different capillarids that infect the same host eg carnivores can be distinguished by structure of patterns of egg case Biopsies of affected areas gastrointestinal tract or liver can be used Material required for laboratory analysis Fecal sample colon or gastric biopsy hepatic biopsy BAL Relevant diagnostic laboratories These diagnostics are readily available as inhouse fecal floatation or any laboratory performing fecal exams or histopathology Treatment Fenbendazole and other benzimidazoles milbemycin oxime and pyrantel pamoate can be used Variable sensitivity to ivermectin has been noted Due to its long prepatent period it is appropriate to treat monthly for 3 treatments Prevention and control Quarantine measure and treatment before introduction is best Chronic treatment may be required Environmental control and preventing recontamination are critical Suggested disinfectant for housing facilities Eggs are very resistant to destruction and may remain infective in the soil for long periods of time Remove fecal material promptly from enclosures Dirt floored American Association of Zoo Veterinarians Infectious Disease Manual CAPILLARIASISTRICURIASIS enclosures are almost impossible to disinfect Dig out dirt or use fire to sterilize Notifications None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Many facilities manage chronically infected groups with varying levels of problems Many use chronic anthelmintic treatment Conditions for restoring diseasefree status after an outbreak Treat for a minimum of 34 months Clear animals while held in cement floored facility before introducing to a clean group in a clean environment Continue long term monthly fecal screening and environmental sanitation Experts who may be consulted References 1 Centers for Disease Control and Prevention Internet Parasites Capillariasis also known as Capillaria Infection 2018 cited on 2018 March 15 Available from httpwwwcdcgovparasitescapillaria 2 Centers for Disease Control and Prevention Internet Parasites Trichuriasis also known as Whipworm Infection 2013 cited on 2018 March 15 Available from httpwwwcdcgovparasiteswhipworm 3 Bowman DD Helminths In Bowman DD Lynn RC Eberhard ML eds Georgis Parasitology for Veterinarians 8th de St Louis MO WB Saunders 2003 p 228231 4 Fuehrer H Igel P Auer H Capillaria hepatica in man and an overview of hepatic capillariosis and spurious infections Parasitol Res 20111094969979 5 Goncalves AQ Ascaso C Santos I Calodium hepaticum Household Clustering Transmission and the Finding of a Source of Human Spurious infection in a Community of the Amazon Region PLoS Negl Trop Dis 2012612e1943 6 Limsrivilai J Pongprasobchai S Apisarnthanarak P Intestinal capillariasis in the 21st century clinical presentations and the role of endoscopy and imaging BMC Gastroenterol 201412207 7 Liu GH Gasser RB Nejsum P Wang Y Chen Q Song HQ Zhu XQ Mitochondrial and nuclear ribosomal DNA evidence supports the existence of a new Trichuris species in the endangered Francois leafmonkey PLoS One201386e66249 8 Ravasi DF ORiain M Davids F Illing N Phylogenetic evidence that two distinct Trichuris genotypes infect both humans and nonhuman primates PLoS one 201278e44187 9 Stephenson LS Holland CV Cooper ES 2000 The public health significance of Trichuris trichiura Parasitol 2000121S1S73S95 10 Stidworthy MF Lewis JC Masters NJ Boardman S Capillaria hepatica in primates in zoological collections in the British Isles Vet Rec 2009164266 11 Wynne J Garner M Elimination of trichuriasis in a group of colobus monkeys Colobus quereza In Proc Am Assoc Zoo Vet 2004 p 202203 American Association of Zoo Veterinarians Infectious Disease Manual TRYPANOSOMA CRUZI CHAGAS DISEASE Fact Sheet compiled by Sarah A Hamer Sheet completed on 4 September 2013 Fact Sheet Reviewed by Tom Sidwa Susan Montgomery Susceptible animal groups All mammal species are considered to be susceptible to Trypanosoma cruzi including more than 150 species of 24 families that have been reported to be infected Disease is best described from humans and dogs the degree to which other domestic or wild animals present disease upon infection is unknown Causative organism Trypanosoma cruzi is a flagellated protozoan parasite that maintains many life stages The parasite is spread by triatomine bugs Triatomines are bloodsucking vectors commonly referred to as kissing bugs or conenosed bugs After ingesting trypomastigotes from the blood of a vertebrate host the bugs hindgut contains epimastigotes which also can multiply in the vector Metacyclic trypomastigotes appear in the insects rectum 810 days after infection These metacyclic forms pass in the feces and can enter the body of a vertebrate host through the bite scratched skin or mucous membranes Trypomastigotes are the abundant blood form that circulates in the mammalian host after infection Amastigotes develop in muscle and other tissue cells and multiply by binary fission Amastigotes differentiate into to trypomastigotes which lyse the host cell and burst free and this stage can then attack other host cells Pseudocysts of parasites may form in muscle cells Zoonotic potential Many kinds of wild and domestic mammals serve as reservoirs for T cruzi This parasite can be bridged to humans from mammalian reservoirs through kissing bug vectors Zoonotic potential is high in areas of Mexico and South and Central America where kissing bugs maintain peridomestic cycles and colonize human dwellings In contrast the housing structures in US are generally less able to be colonized by bugs and therefore zoonotic potential is reduced relative to areas with peridomestic cycles Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All mammals are susceptible to infection Wildlife reservoirs include woodrats opossums armadillos and raccoons Disease is reported in dogs humans and nonhuman primates Contamination of blood feeding lesion or mucous membrane by feces of insect vector ingestion of infected vector or food or water contaminated with bug feces transplacental or trans mammary blood transfusion Dogs and humans range from asymptomatic to acute myocarditis and sudden death Chronic disease signs are related to cardio myopathy and in humans mega esophagus andor megacolon can be seen Dogs and humans variable can cause severe disease or death The degree to which wildlife reservoirs present disease is unknown No FDA approved treatment is available Prevent exposure to vectors control vector populations minimize wildlife reservoir access blood donor screening prevent seropositive female dogs from breeding Yes American Association of Zoo Veterinarians Infectious Disease Manual TRYPANOSOMA CRUZI CHAGAS DISEASE Distribution Chagas disease in humans or animals can occur wherever there is overlap among kissing bug vectors the T cruzi parasite and vertebrate reservoir hosts The disease is endemic in many areas of Mexico South and Central America and is increasingly recognized across the southern US In the US 11 species of kissing bugs occur and are distributed across the southern half of the country and range as far north as the CaliforniaOregon border and New Jersey In Latin America an estimated 1219 million people were infected in the early 1990s with an annual incidence exceeding 500000 Since then control campaigns have assisted in reducing the disease burden The disease burden in the US is largely unknown due to lack of awareness testing and reporting However CDC has estimated that more than 300000 cases of Chagas disease are found in US among immigrants from endemic countries of Latin America The American Association of Blood Banks maintains The Chagas Biovigilance Network for reporting of screening and confirmatory results from the testing of US blood donors for antibodies to T cruzi Incubation period Once the metacyclic trypomastigotes enter the host an acute local inflammatory reaction may occur In humans within 12 weeks of infection the parasites spread to lymph nodes and multiply within phagocytic cells The intracellular amastigotes multiply and pseudocysts may form Within days some organisms may transform to trypomastigotes and burst free from the pseudocyst A generalized parasitemia can occur followed by parasite invasion of many tissues within body The incubation period may be up to several months if contaminated blood from transfusion is the source of infection Clinical signs Chagas disease manifests as acute and chronic phases in the absence of treatment the host is infected for life The chronic phase of infection has two forms an indeterminate form during which the host is asymptomatic followed by development of clinical disease years to decades later In humans and dogs the initial acute phase of infection is usually asymptomatic or undetected regional or generalized lymphadenopathy fever myalgia headache hepatosplenomegaly edema rash vomiting diarrhea or anorexia may occur Humans may note a lesion chagoma where the parasite enters the body Severe manifestations such as acute myocarditis or meningoencephalitis are rare Chronic phase of disease may develop in a subset of human patients who survive the acute phase of infection In chronic disease cardiac abnormalities may be noted including right bundle branch block and left anterior hemiblock atrioventricular conduction abnormalities and arrhythmias Megacardia may be noted on radiographs In humans and dogs systolic dysfunction is indistinguishable from dilated cardiomyopathy Weakness and exercise intolerance may be noted Humans with Chagas disease may also have complications of the digestive system including megaesophagus and megacolon with or without cardiac manifestations Post mortem gross or histologic findings Gross cardiac changes may include megacardia and focal thinning of the myocardium including apical aneurysm Dilatation and thinning of the wall of the esophagus and colon may occur Histologically in canines examination of the heart may reveal unruptured pseudocysts with no inflammatory response or ruptured pseudocysts with characteristic infiltration of lymphocytes monocytes andor polymorphonuclear leukocytes Diagnosis During acute infections the trypomastigotes blood stage of the parasite may be identified by microscopy of a peripheral blood sample or through culture techniques the organism has a single flagellum and a large kinetoplast at the posterior end of the cell and appears as a characteristic C shape in Giemsa stains of bloodsmears Additionally PCR can be used to amplify the DNA of the parasite from a blood sample Serologic tests may be of limited utility during acute infections Because the level of circulating parasites decreases within months parasites are undetectable in blood by most methods during the chronic phase of disease During chronic disease serologic tests are used to detect antibodies to the parasite To increase sensitivity and specificity a standard serodiagnostic approach is to apply two or more tests that use different techniques or different antigens Two commonly used techniques are enzymelinked immunosorbent assay ELISA and immunofluorescent antibody test IFA Some serological tests are crossreactive and will also detect American Association of Zoo Veterinarians Infectious Disease Manual TRYPANOSOMA CRUZI CHAGAS DISEASE antibodies to Leishmania species Rapid immunochromatographic dipstick assays have been developed for the detection of antibodies to T cruzi in humans and dogs While sensitivity and specificity meet or exceed the characteristics of other available tests their use for Chagas disease diagnosis is considered experimental Two tests are FDA approved for use as screening tests for human blood donations most samples that screen positive are then subjected to a supplemental test with greater specificity Blood donors who screen positive are notified of results are urged to contact their physician and are no longer able to donate blood In chronic disease particular ECG abnormalities combined with positive serology results can be highly indicative The only parasitological techniques currently considered useful in the chronic phase of disease would be xenodiagnoses and hemoculture although it is no longer used in human diagnostics In humans PCR and IHC also are used and PCR would be considered more sensitive Postmortem heart or other tissues may be examined using histopathology for the amastigotes tissue stage of the parasite and associated inflammation Material required for laboratory analysis Whole blood plasma serum andor cardiac tissue Relevant diagnostic laboratories Texas AM Veterinary Medical Diagnostic Laboratory PO Box Drawer 3040 College Station TX 778413040 979 8453414 888 6465623 httptvmdltamuedu T cruzi rapid immunoblot assay Primate Diagnostic Services Laboratory PDSL Washington National Primate Research Center University of Washington Seattle Washington 981957330 diagnosticwanprcorg httpwwwwanprcorgpdsl Treatment Although two antiparasitics can be used to treat human patients with Chagas disease nifurtimox and benznidazole these drugs are not approved by FDA so in the US they are available only from CDC under investigational protocols For both drugs side effects are fairly common and contraindications for treatment include severe hepatic disease and renal disease However antiparasitic treatment is indicated for all cases of congenital acute or reactivated Chagas disease and for chronic T cruzi infection in children Treatment is recommended for adults up to 50 years old with chronic infection who do not already have advanced Chagas cardiomyopathy For adults older than 50 years with chronic T cruzi infection the decision to treat with antiparasitic drugs should be individualized Prevention and control In the absence of a human or veterinary vaccine and given the limited treatment options prevention and control of Chagas disease across the Americas relies heavily on vector control and community education Improvement of housing structures combined with insecticide treatment inside homes has significantly reduced peridomestic transmission of the T cruzi parasite in Central and South America To reduce the attraction of kissing bugs to homes or kennels outdoor lights should be eliminated and rodent habitat immediately surrounding the home or kennel should be removed Screening of blood donations is an important public health tool for prevention of disease transmission through blood transfusion Early detection and treatment of acute disease including congenital cases can reduce the burden of disease Suggested disinfectant for housing facilities The duration of time the parasite can live outside a vector or host on environmental surfaces contaminated by bug feces is unknown but the parasite will be destroyed by direct exposure to sunlight and other harsh environments Surfaces that have come in contact with bugs or American Association of Zoo Veterinarians Infectious Disease Manual TRYPANOSOMA CRUZI CHAGAS DISEASE bug feces should be disinfected using 10 bleach or 70 ethanol Notification States are not required by federal law to report cases of Chagas disease However Chagas disease in humans is reportable in 4 states Arizona Massachusetts Tennessee and Texas Chagas disease in animals is reportable in Texas Measures required under the Animal Disease Surveillance Plan NA Measures required for introducing animals to infected animal The risk of animal to animal direct transmission in the absence of the kissing bug vector is minimal However infected animals may increase the infection prevalence in vectors in a local environment Efforts should be made to prevent seropositive female dogs from breeding due to congenital transmission Conditions for restoring diseasefree status after an outbreak NA Experts who may be consulted Sarah A Hamer MS PhD DVM Department of Veterinary Integrative Biosciences Texas AM University TAMU 4458 College Station TX 77443 shamercvmtamuedu Tom J Sidwa DVM MPH Manager Zoonosis Control Branch Texas Department of State Health Services 1100 W 49Th St 5127766628 TomSidwadshsstatetxus References 1 Brown EL DM Roellig ME Gompper RJ Monell KM Wenning MW Gabriel and MJYabsley MJ 2010 Seroprevalence of Trypanosoma cruzi among eleven potential reservoir species from six states across the southern United States Vectorborne Zoonotic Dis 108 757763 2 American Association of Blood Banks Chagas Biovigilance Network httpswwwaabborgprogramsbiovigilancePageschagasaspx Accessed 9 September 2013 3 Bern C S Kjos MJ Yabsley and SP Montgomery 2012 Trypanosoma cruzi and Chagas disease in the United States Clin Microbiol Rev 24 655681 4 Centers for Disease Control and Prevention Chagas disease antiparasitic treatment httpwwwcdcgovparasiteschagashealthprofessionalstxhtml Accessed 9 September 2013 5 Miles MA 2009 American trypanosomiasis Chagas disease In Cook GC and AI Zumla eds Mansons Tropical Disease Elsevier St Louis Missouri Pp 13271340 6 Roberts LS and J Janovy 2005 Kinetoplasta trypanosomes and their kin In Roberts L and Janovy Jr J eds Foundations of Parasitology 7th ed McGraw Hill New York New York Pp 61 88 American Association of Zoo Veterinarians Infectious Disease Manual TULAREMIA Fact Sheet compiled by Cornelia J KetzRiley Sheet Revised on 2 February 2018 Fact Sheet Reviewed by David Miller Susceptible animal groups Natural infection in mammals and birds Causative organism Francisella tularensis four subspecies most commonly associated with disease outbreaks are F tularensis subsp tularensis type Aassociated with cottontail rabbit ticks biting flies and F tularensis subsp holarctica type Bassociated with muskrat and beaver while F tularensis subsp mediasiatica and novicida are rarely associated with severe infections Type A is regarded as a category A biowarfarebioterrorism agent 3 because of the diversity of its route of transmission ease of dissemination especially the aerosol route high infectivity and potentially high mortality rate Type A and B can be distinguished by the ability of type A to ferment glycerol and polymerase chain reaction test PCR Zoonotic potential The zoonotic potential is very high with inhalation of only 1050 organisms needed to cause severe infection Distribution Throughout the Northern hemisphere this disease represents one of the largest host distributions of any zoonotic disease Type A only occurs in North America whereas type B found throughout Northern hemisphere In North America geographic overlap of both subspecies is present although type A associated with highest disease incidence and mortality rate Changes involving climate and animal as well as vector distribution seem to cause emergence or re emergence in areas considered noncritical for appearance of Francisella tularensis Flooding may be associated with increased transmission Arthropods such as ticks mosquitoes and biting flies are common vectors associated with transmission of F tularensis While ticks are believed to be the primary biological vectors transmission by mosquitoes and biting flies is believed to be mostly mechanical through their Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic All warm blooded animals Arthropod vectors such as ticks biting flies and in some areas mosquitoes Inhalation of aerosolized infectious material Ingestion of contaminated food or water Direct transmission Skinning dead infected animals contaminated water Depends on route of infection general lethargy anorexia pyrexia Transdermal exposure ulcer at site of inoculation and swollen glands or rarely swollen glands without ulcer lymphadenopathy Oculoglandular conjunctivitis and lymphadenopathy Oral exposure lymphadenopathy Inhalation pneumonia coughing Clinical signs vary from mild to severe depending on route of exposure and death can result if untreated Pneumonic form severe Septicemia often death occurs without prior signs Antibiotics streptomycin gentamicin tetracyclines ciprofloxacin Rodent lagomorph mosquito biting fly and tick control Sanitation including use of gloves and masks avoid ingestion and contact with untreated water avoid ingestion of uncooked meat and rodent carcasses High zoonotic potential American Association of Zoo Veterinarians Infectious Disease Manual TULAREMIA mouthparts Infection of a patient through a ringtail possum in Tasmania Australia indicated the emergence of F tularensis type B in the Southern hemisphere Incubation period generally 35 days but 114 days possible Clinical signs Clinical presentation of tularemia varies with the route of infection First development non specific signs such as depression lethargy anorexia vomiting diarrhea marked pyrexia or peracute death without prior clinical signs Clinical disease in humans includes forms of ulceroglandular glandular oculoglandular oropharyngeal pneumonic and typhoidal disease First three forms occur via local infection through arthropod bites injuries or mechanical transfer involving skin and lymphoid tissue and result in local or even generalized lymphadenopathy Skin ulcers may form at the site of dermal infection Oropharyngeal form ingestion of contaminated food or water involving the tonsils and retropharyngeal lymph nodes Pneumonic form as most severe clinical form of tularemia leading to mortality if untreated that results from direct inhalation of organisms from infected tissue Typhoidal form systemic disease high fever but without lymphadenitis or cutaneous lesions All forms can develop into secondary septicemia pleuropneumonia and meningitis F tularensis is usually invading and replicating in vectorderived cells and hemolymph and in macrophages within the host Cytokines such as intereferongamma and tumor necrosis factor produced by Tcells are critical for activation of macrophages and cellmediated and protective immunity Yet F tularensis is able to proliferate in macrophages without destroying the host cell It also has developed good survival and adaptation strategies using surface proteins to suppress innate immune response which makes it harder to diagnose and control it within the host New research has discovered that F tularensis is also able to invade erythrocytes The high hemoglobin and iron content in erythrocytes could influence the virulence gene expression in F tularensis Yet erythrocytes do not support replication of the pathogen and therefore do not seem to be a major contributor to the pathogenesis of tularemia Post mortem gross or histologic findings Gross congested organs mostly lungs lymph nodes spleen liver with multiple light tan miliary foci on the surface as well as in the parenchyma Histopathology pyogranulomatous lymphadenitis tonsillitis splenitis hepatitis and pneumonia with necrotic foci Diagnosis Although culture is considered the gold standard diagnostic tool to confirm tularemia recovery of live organisms of F tularensis from carcasses can pose a challenge The bacterium is very slow growing and has special biochemical needs so poor competitive characteristics in the presence of other bacterial pathogens Selective antibiotic media CHABA are needed for isolating the bacteria from contaminating environmental flora in carcasses Western blot and microagglutination assay demonstrate the highest level of sensitivity and specificity for F tularensis higher than enzymelinked immunosorbent assay ELISA or indirect immunofluorescence IFA A combination of at least two serological tests such as ELISA and Western blot was demonstrated to be a suitable diagnostic tool for laboratory confirmation of both individual cases and larger epidemiological studies Immunohistochemistry IHC has been successfully used for post mortem diagnosis in formalinfixed tissue To detect serologic titers in live animals or humans besides microagglutination latex or tube agglutination a novel competitive ELISA test can be recommended Realtime PCR Multiplex qPCR 16S rDNA sequencing and molecular subtyping using differential insertion sequence amplification and regions of differences RD can be especially useful for samples where organisms are nonculturable or nonviable Serology is often difficult as shortterm diagnosis due to low antigenicity of the organism Repeated serology is necessary for evaluation of titer development Although some commercially available serologic tests are available showing good results these should be interpreted cautiously because of the quick onset of clinical signs as compared to the development of humoral response clinically silent cases have been reported and antibodies in humans can persist for years A recombinase PCR amplification assay has been developed for rapid detection of F tularensis Molecular tests provide a safer diagnostic tool while avoiding hazardous multiplying of the pathogen However cultivation of F tularensis will still be required for evaluation of antibiotic resistance patterns molecular epidemiological and pathological analysis of the pathogen Investigation into molecular level of host macrophage survival and innate immune response to American Association of Zoo Veterinarians Infectious Disease Manual TULAREMIA infection with F tularensis enabled the identification of newer tools for diagnosis of and immunologic prevention of tularemia in laboratory animals and humans Material required for laboratory analysis The best result is achieved by immediate culturing of fresh tissue or by immediate freezing of tissue specimens from carcasses for subsequent culture Blood samples are often used to confirm serologic titers in live animals or humans Molecular tests can nowadays be used for testing of any type of tissue Relevant diagnostic laboratories The contagious nature of F tularensis poses an additional challenge to laboratory personnel high biohazardous risk of infection via inhalation of aerosolized bacteria Testing for tularemia demands a laboratory setting with a minimum biological safety level 2 BSL2 and testing procedures performed according to BSL3 regulations Confirmation of results are suggested in Centers for Disease Control and Prevention National Center for Zoonotic VectorBorne and Enteric Diseases Division of VectorBorne Infectious Diseases Bacterial Diseases Branch Foothills Campus Fort Collins Colorado 80522 USA Treatment Streptomycin is considered the treatment of choice in humans with tularemia Other chemotherapeutics such as gentamicin tetracyclines chloramphenicol and fluoroquinolones have been used successfully Tetracyclines and chloramphenicol are bacteriostatic and require a longer treatment period of at least 1421 days Due to frequent treatment relapses or failure combined with increase in resistance against commonly used products alternative chemotherapeutics and newer chemotherapeutic generations such as glycocyclines ketolides and new generation fluoroquinolones are currently investigated and show promising results Cystatin 9 a type 2 cystein protease inhibitor with immunomodulatory properties has shown to help develop effective protection against F tularensis in vitro and in vivo and may become a future treatment tool against tularemia Prevention and control There are still no approved vaccine products available in the USA A live attenuated vaccine strain of F tularensis type B was developed in the Soviet Union for immunization of humans Although this live vaccine serum LVS strain was also shown to be effective against the type A strain and oral infection this vaccine was not fully effective against infection acquired by inhalation Currently newer LVS vaccine affords no better efficient protection against an aerosolization challenge by F tularensis Subunit or recombinant vaccines have been more recently researched but any results did not show better prevention efficacy than the LVS DNA Gold Micronanoplex used for genetic immunization seems to produce efficient levels of antibodies against F tularensis Ongoing trials were completed to develop vaccine using mutant strains or nonpathogenic F novicida strain but they have not shown improved protection efficacy over the LVS either Some research is concentrating on virusvectored vaccine for better stimulation of immunity in presence of F tularensis Newest research is focusing on adding epitope to the immunogenic products to atimulate high avidity of CD4 and CD8 Tcells as well as using adjuvants to help stimulate higher antibody titers against F tularensis to increase efficacy of any existing LVS Monophosphoryl Lipid A has already been approved by the FDA as adjuvants for other vaccine One study identified nitric oxide as a predictor of vaccine efficacy which also has already been used in connection with other diseases Good pest control is the best defense against development of F tularensis carrying population on zoo grounds Suggested disinfectant for housing facilities Diluted hypochlorite quaternary ammonium disinfectants or any other ordinary medical disinfectants are useful F tularensis can be inactivated by heat at least at 60 C for 20 min Notification Reportable disease at a variety of levels city county state and federal as F tularensis is considered a Category A Bioterrorism agent Measures required under the Animal Disease Surveillance Plan Continuous surveillance of wildlife and vector populations as well as firstlevel emergency response plan after detection of tularemia cases are important to prevent or minimize outbreaks in animals and humans American Association of Zoo Veterinarians Infectious Disease Manual TULAREMIA Measures required for introducing animals to infected animal Regular quarantine in a clean environment reduce access to potential vectors and host animals Conditions for restoring diseasefree status after an outbreak Pest and vector control are necessary to minimize exposure Constant pathogen surveillance of wildlife populations is strongly recommended Experts who may be consulted Jeannine M Petersen PhD Nordin S Zeidner DVM PhD Centers for Disease Control and Prevention National Center for Zoonotic VectorBorne and Enteric Diseases Division of VectorBorne Infectious Diseases Bacterial Diseases Branch Foothills Campus Fort Collins Colorado 80522 Cornelia J KetzRiley Drmedvet DVM DACZM Exotic and Zoo Veterinary Specialist Neel Veterinary Hospital 2700 N MacArthur Blvd Oklahoma City OK 73127 Phone 405 9478387 zoodoc12gmailcom References 1 Akimana C Kwaik YA Francisellaarthropod vector interaction and its role in pathoadaptation to infect mammals Front Microbiol 2011234 2 Anderson PD Bokor G Bioterrorism pathogens as weapons J Pharm Pract 2012255512529 3 ArizaMiguel J Johansson A FernándezNatal MI MartínezNistal C Orduña A RodríguezFerri EF Hernández M RodríguezLázaro D Molecular investigation of tularemia outbreaks Spain 19972008 Emerg Infect Dis 201420575461 4 Boisset S Caspar Y Sutera V Maurin M New therapeutic approaches for treatment of tularaemia a review Front Cell Infect Microbiol 201428440 5 Brown VR Adney DR OleaPopelka F Bowen RA 2015 Prior Inoculation with Type B Strains of Francisella tularensis Provides Partial Protection against Virulent Type A Strains in Cottontail Rabbits PloS one 20151010e0140723 6 Carvalho CL Lopes de Carvalho I ZéZé L Núncio MS Duarte EL Tularaemia a challenging zoonosis Comp Immunol Microbiol Infect Dis 20143728596 7 Celebi B Kılıç S Yeşilyurt M Acar B Evaluation of a newlydeveloped readytouse commercial PCR kit for the molecular diagnosis of Francisella tularensis Mikrobiyol Bul 201448113542 8 Celebi B Kilic S Development of a novel Francisella tularensis antigen stained with tetrazolium blue for tularemia microagglutination test Mikrobiyol Bul 201347351422 9 Celli J and TC Zahrt TC Mechanisms of Francisella tularensis intracellular pathogenesis Cold Spring Harbor Perspect Med 201334a010314 10 Centers for Disease Control and Prevention Internet Tularemia 2018 cited 2019 February 20 Available from httpswwwcdcgovtularemiaindexhtml 11 Chaignat V DjordjevicSpasic M Ruettger A Otto P Klimpel D Müller W Sachse K Araj G Diller R Tomaso H Performance of seven serological assays for diagnosing tularemia BMC Infect Dis 2014514234 12 Christian MD Biowarfare and bioterrorism Crit Care Clin 201329371756 13 Dauphin LA Walker RE Petersen JM Bowen MD Comparative evaluation of automated and manual commercial DNA extraction methods for detection of Francisella tularensis DNA from American Association of Zoo Veterinarians Infectious Disease Manual TULAREMIA suspensions and spiked swabs by realtime polymerase chain reaction Diagn Microbiol Infect Dis 2011703299306 14 EavesPyles T Patel J Arigi E Cong Y Cao A Garg N Dhiman M Pyles RB Arulanandam B Miller AL Popov VL Soong L Carlsen ED Coletta C Szabo C Almeida IC Immunomodulatory and antibacterial effects of cystatin 9 against Francisella tularensis Mol Med 2013281926375 15 Euler M Wang Y Otto P Tomaso H Escudero R Anda P Hufert FT Weidmann M 2012 Recombinase polymerase amplification assay for rapid detection of Francisella tularensis J Clin Microbiol 201250722342238 16 Golovliov I Lindgren H Eneslätt K Conlan W Mosnier A Henry T Sjöstedt A An InVitro Co culture Mouse Model Demonstrates Efficient VaccineMediated Control of Francisella tularensis SCHUS4 and Identifies Nitric Oxide as a Predictor of Efficacy Front Cell Infect Microbiol 20166152 17 Hansen DT Robida MD Craciunescu FM Loskutov AV Dörner K Rodenberry JC Wang X Olson TL Patel H Fromme P Sykes KF Polyclonal Antibody Production for Membrane Proteins via Genetic Immunization Scientific Reports 2016621925 18 Hong KJ Park PG Seo SH Rhie GE Hwang KJ 2013 Current status of vaccine development for tularemia preparedness Clin Exp Vacc Res 213439 19 Horzempa J ODee DM Stolz DB Franks JM Clay D Nau GJ Invasion of erythrocytes by Francisella tularensis J Inf Dis 201120415159 20 Isherwood KE Titball RW Davies DH Felgner PL Morrow WJW Vaccination strategies for Francisella tularensis Adv Drug Del Rev 20055714031414 21 Jackson J McGregor A Cooley L Ng J Brown M Ong CW Darcy C Sintchenko V Francisella tularensis subspecies holarctica Tasmania Australia 2011 Emerg Infect Dis 201218 91484 1486 22 Jacob D Wahab T Edvinsson B Peterzon A Boskani T Farhadi L Barduhn A Grunow R Sandström G Identification and subtyping of Francisella by pyrosequencing and signature matching of 16S rDNA fragments Lett Appl Microbiol 201153 6592595 23 Janse I Hamidjaja RA Bok JM van Rotterdam BJ Reliable detection of Bacillus anthracis Francisella tularensis and Yersinia pestis by using multiplex qPCR including internal controls for nucleic acid extraction and amplification BMC Microbiol 201010314 24 Jia Q Lee BY Bowen R Dillon BJ Som SM Horwitz MA A Francisella tularensis live vaccine strain LVS mutant with a deletion in capB encoding a putative capsular biosynthesis protein is significantly more attenuated than LVS yet induces potent protective immunity in mice against F tularensis challenge Infect Immun 201078 1043414355 25 Kaur R Chen S Arevalo MT Xu Q Chen Y Zeng M Protective immunity against tularemia provided by an adenovirusvectored vaccine expressing Tul4 of Francisella tularensis Clin Vacc Immunol 201219 3359364 26 KetzRiley CJ Kennedy GA Carpenter JW Zeidner NS Petersen JM 2009 Outbreak of tularemia type A in captive Bornean orangutans Pongo pygmaeus pygmaeus J Zoo Wildl Med 2009402257262 27 Kiliç S Celebi B Yeṣilyurt M Evaluation of a commercial immunochromatographic assay for the serologic diagnosis of tularemia Diagn Microbiol Infect Dis 201274115 28 Kingry LC Petersen JM Comparative review of Francisella tularensis and Francisella novicida Front Cell Infect Microbiol 201413435 29 Kuehn A Schulze C Kutzer P Probst C Hlinak A Ochs A Grunow R Tularemia seroprevalence of captured and wild animals in Germany the fox Vulpes vulpes as a biological indicator Epidemiol Infect 2013141 94833840 30 Lang S Kleines M Harik NS 2013 Two at one blow reemergence of tularemia in Upper Austria Pediatr Ann 2013427288292 American Association of Zoo Veterinarians Infectious Disease Manual TULAREMIA 31 Larson MA Fey PD Bartling AM Iwen PC Dempsey MP Francesconi SC Hinrichs SH Francisella tularensis molecular typing using differential insertion sequence amplification J Clin Microbiol 201149 827862797 32 Lõhmus M Janse I van de Goot F van Rotterdam BJ Rodents as potential couriers for bioterrorism agents Biosecur Bioterror 201311 Suppl 1S24757 33 Lyko C Chuard C Tularemia an emerging disease in Switzerland Rev Med Suisse 2013940118168 1820 34 MaetzRensing K Floto A Schrod A Becker T E J Finke EJ Seibold E Splettstoesser WD Kaup FJ Epizootic of tularemia in an outdoor housed group of cynomolgus monkeys Macaca fascicularis Vet Pathol 200744 327334 35 Mahawar M Atianand MK Dotson RJ Mora V Rabadi SM Metzger DW Huntley JF Harton JA Malik M Bakshi CS Identification of a novel Francisella tularensis factor required for intramacrophage survival and subversion of innate immune response J Biol Chem 201228730 2521625229 36 Marohn ME Barry EM 2013 Live attenuated tularemia vaccines recent developments and future goals Vaccine 2013313534853491 37 MätzRensing K Floto A Schrod A Becker T Finke EJ Seibold E Splettstoesser WD Kaup FJ Epizootic of tularemia in an outdoor housed group of cynomolgus monkeys Macaca fascicularis Vet Pathol2007443327334 38 Meinkoth KR Morton RJ Meinkoth JH Naturally occurring tularemia in a dog J Am Vet Med Assoc 2004225545547 39 Pennisi MG Egbering H Hartmann K Lloret A Addie D Belák S BoucrautBaralon C Frymus T GruffyddJones T Hosie MJ Lutz H Marsilio F Möstl K Radford AD Thiry E Truyen U Horzinek MC Francisella tularensis infection in cats ABCD guidelines on prevention and management J Feline Med Surg 201315 7585587 40 Origgi FC Frey J Pilo P Characterisation of a new group of Francisella tularensis subsp holarctica in Switzerland with altered antimicrobial susceptibilities 1996 to 2013 Euro Surveill 20141929 pii 20858 41 Origgi FC Wu N Pilo P Francisella tularensis infection in a stone marten Martes foina without classic pathological lesions consistent with tularemia J Vet Diagn Invest 2013254 519521 42 Petersen JM Schriefer ME Tularemia emergencereemergence Vet Res 200536 455467 43 Petersen JM Schriefer ME Gage KL Montenieri JA Carter LG Stanley M Chu MC Methods of enhanced culture recovery of Francisella tularensis Appl Environ Microbiol 20047037333735 44 Petersen JM Schriefer ME Carter LG Zhou Y Sealy T Bawiec D Yockey B Urich S Zeidner NS Avashia S Kool JL Buck J Lindley CM Celeda L Montenieri JA Gage KL Chu MC Laboratory analysis of tularemia in wildtrapped commercially traded prairie dogs Texas 2002 Emerg Inf Dis 200510419425 45 Ramond E Gesbert G Barel M Charbit A Proteins involved in Francisella tularensis survival and replication inside macrophages Future Microbiol 201271112551268 46 Richard K Mann BJ Qin A Barry EM Ernst RK Vogel SN Monophosphoryl Lipid A Enhances Efficacy of a Francisella tularensis LVS Catanionic Nanoparticle Subunit Vaccine against F tularensis Schu S4 Challenge by Augmenting both Humoral and Cellular Immunity Clin and Vacc Immunol 201724 3115 47 Richard K Vogel SN Perkins DJ Type I interferon Licenses Enhanced Innate Recognition and Transcriptional Responses to Franciscella tularensis LVS Innate Immun 2016225363372 48 Revich B Tokarevich N Parkinson AJ Climate change and zoonotic infections in the Russian Arctic Int J Circumpolar Health 20127118792 49 Rijks JM Kik M Koene MG Engelsma MY van Tulden P Montizaan MG Oomen T Spierenburg MA Ijzer J van der Giessen JW Gröne A Roest HJ Tularaemia in a brown hare American Association of Zoo Veterinarians Infectious Disease Manual TULAREMIA Lepus europaeus in 2013 first case in the Netherlands in 60 years Euro Surveill 20131849pii 20655 50 Roberts LM Crane DD Wehrly TD Fletcher JR Jones BD Bosio CM Inclusion of epitopes that expand high avidity CD4 T cells transforms subprotective vaccines to efficacious immunogens against virulent Francisella tularensis J Immunol 2016197727382747 51 Ryden P Björk R Schäfer ML Lundström JO Petersén B Lindblom A Forsman M Sjörstedt A Johansson A Outbreaks of tularemia in a boreal forest region depend on mosquito prevalence J Inf Dis 20112052 297304 52 Sharma N Hotta A Yamamoto Y Fujita O Uda A Morikawa S Yamada A Tanabayashi K Detection of Francisella tularensisspecific antibodies in patients with tularemia by a novel competitive enzymelinked immunosorbent assay Clin Vaccine Immunol 201320 1 916 53 Shen H Harris G Chen W Sjostedt A Ryden P Conlan W Molecular immune responses to aerosol challenge with Francisella tularensis in mice inoculated with live vaccine candidates of varying efficacy PLoS One 2010510e13349 54 Sjoestedt AB Francisella In BrennerDJ Krieg NR Staley JT Garrity GM eds The Proteobacteria part B Bergeys Manual of Systematic Bacteriology 2nd ed New York NY Springer Verlag 2005 p 200210 55 Sting R Runge M Eisenberg T Braune S Müller W Otto P Comparison of bacterial culture and polymerase chain reaction PCR for the detection of F tularensis subsp holarctica in wild animals Berl Munch Tierarztl Wochenschr20131267828590 56 Walker RE Petersen JM Stephens KW Dauphin LA Optimal swab processing recovery method for detection of bioterrorismrelated Francisella tularensis by realtime PCR J Microbiol Methods 201083 1 4247 57 Wolfe DN Florence W Bryant P Current biodefense vaccine programs and challenges Hum Vaccin Immunother 201397 American Association of Zoo Veterinarians Infectious Disease Manual ULCERATIVE STOMATITIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Reptiles Opportunistic normal flora of the oral cavity or present in the environment but also seen with some primary pathogens such as herpesvirus Anorexia dysphagia ptyalism periodontal disease ulceration of mucous membranes with caseous exudate pneumonia osteomyelitis Severe cases can result in septicemia and death Debridement irrigation with antimicrobial solution topical ointment analgesia and long term antibiotics or antifungal based on culture and sensitivity testing Appropriate nutrition hygiene and temperature minimize stress prevent trauma to oral cavity Some associated agents can be human pathogens Fact Sheet compiled by Genevieve Vega Weaver Sheet completed on 27 January 2011 updated 1 October 2012 15 December 2017 Fact Sheet Reviewed by Charles Innis Susceptible animal groups Mostly reptiles especially snakes chelonians and some groups of lizards such as chameleons bearded dragons and monitors Causative organisms Gramnegative bacteria are most commonly implicated but there are multiple possible causative agents including various aerobic and anaerobic bacteria viruses and fungi Bacteria Aeromonas Pseudomonas Escherichia coli Morganella Proteus Vibrio alginolyticus Providencia Salmonella Corynebacterium Flavobacterium Citrobacter freundii Acinetobacter Micrococcus Aureobacterium Beta hemolytic Staphylococcus Streptococcus group C Enterobacter Klebsiella Pasteurella Bacteroides Clostridium Fusobacterium Peptostreptococcus Mycoplasma and Mycobacterium Virus herpesvirus ranavirus adenovirus Fungi Candida albicans Aspergillus Sporothrix schenkii and Paecilomyces Zoonotic potential Yes Immunocompromised individuals and young children are most at risk Aeromonas can cause enteric disease in humans Pseudomonas can cause urinary tract respiratory tract soft tissue bone joint and gastrointestinal disease Salmonella E coli Klebsiella Enterobacter Pasteurella Corynebacterium Mycobacterium Vibrio Staphylococcus and Streptococcus also can cause disease in humans Distribution Worldwide in both captive reptiles and injured and immunosuppressed freeliving animals Incubation period Weeks to months Clinical signs Anorexia dysphagia ptyalism tongue paralysis gingivitis ecchymosis petechiation loss of teeth tongue sheath abscesses ulceration of mucous membranes with caseous material accumulation and osteomyelitis In lizards with acrodont dentition eg bearded dragons water dragons periodontal disease may be seen more frequently Infection can spread from the nasolacrimal duct and involve the eyes or can descend the trachea and cause pneumonia Septicemia and death can result in complicated and untreated cases An ulcerative stomatitisobstructive rhinitispneumonia disease complex has been reported in sea turtles and tortoises Differential diagnoses include exposure gingivitis due to nutritional secondary hyperparathyroidism and neoplasia Post mortem gross or histologic findings Gross findings Yellow plaques with a diphtheritic membrane and caseous exudate covering eroded oral mucosa and surrounded by inflamed tissue that bleeds easily Histologic findings Plaques consist of serofibrinous material pyknotic nuclei and cellular debris above an ulcerated degenerated epithelium layer with lymphocytic infiltration and hyperplastic epithelium along the periphery of the ulcer American Association of Zoo Veterinarians Infectious Disease Manual ULCERATIVE STOMATITIS Diagnosis Aerobic and anaerobic bacterial culture and sensitivity fungal culture and sensitivity cytology showing increased heterophils and large numbers of Gramnegative bacteria acidfast stain for Mycobacterium radiographs to determine bone involvement chemistry profile to detect underlying renal disease Material required for laboratory analysis Culture swab or tissue sample of the affected area A stab incision culture protocol may be necessary Histopathology and molecular methods useful for viral identification Relevant diagnostic laboratories Laboratories should be experienced with reptilian tissue and culturing from ectotherms Samples should be incubated at the standard 37 C and also at 25 C Treatment Periodic debridement possibly under anesthesia irrigation with dilute antimicrobial solution eg povidoneiodine chlorhexidine etc topical ointment eg silver sulfadiazine triple antibiotic gentamicinbetamethasone etc analgesia and long term antibiotics at least 4 weeks or antifungal therapy at minimum 46 weeks based on culture and sensitivity testing Antimicrobials should be given for both aerobic and anaerobic bacteria using doses established by speciesspecific pharmacokinetic testing when available Ensure proper husbandry and a low stress environment Maintain animals at the high end of their optimal temperature range and also provide heat at night Address any systemic or metabolic illness Euthanasia should be considered for animals with nonhealing lesions due to Mycobacterium spp Commonly used drugs include tetracyclines cephalosporins trimethoprimsulfa aminoglycosides fluoroquinolones clindamycin metronidazole and chloramphenicol Oral acyclovir for viral stomatitis at 4080 mgkg every 824 hours has been used Laser therapy reduces inflammation and provides pain relief Nonsteroidal antiinflammatories can be used if animal is well hydrated and does not have underlying renal disease Supportive therapy with Vitamins A Bcomplex and C can be given to boost the immune system For anorexic animals avoid forced feeding of whole prey and instead administer a puree or slurry via a gastric tube Prevention and control Proper nutrition including adequate vitamin especially Vitamin A and mineral supplementation appropriate temperatures good hygiene preventing oral trauma from food or habitat minimizing stress clearing mite infestations and avoiding hibernating recently fed animals Suggested disinfectant for housing facilities 1 sodium hypochlorite for most microbes vinegar or 2 glutaraldehyde for mycobacteria Notification None Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Isolate infected animal until lesions are healed Ensure good hygiene and appropriate husbandry practices Do not introduce infected animal to immunocompromised animals Avoid all stress or continued suppression of immune system Conditions for restoring diseasefree status after an outbreak Properly disinfect habitat Experts who may be consulted Rob Coke DVM DACZM DABVP Reptile and Amphibian PracticeSenior Staff Veterinarian San Antonio Zoo 210 7347184 x1320 zoosrvetsazooaqorg Dr Jörg Mayer Associate Professor of Zoological Medicine College of Veterinary Medicine University of Georgia mayerjugaedu References 1 Melissa Kaplans Herp Care Collection Ulcerative Stomatitis Mouthrot in Reptiles cited 2017 December 15 Available from httpwwwanapsidorgstomatitishtml 2 Hedley J Anatomy and disorders of the oral cavity of reptiles and amphibians Vet Clin Exot Anim 201619689706 American Association of Zoo Veterinarians Infectious Disease Manual ULCERATIVE STOMATITIS 3 Jacobson ER Bacterial diseases of reptiles In Jacobson ER ed Infectious diseases and pathology of reptiles Boca Raton FL CRC Press Taylor and Francis Group 2007 p 476477 4 Mehler SJ Bennett RA Upper alimentary tract disease In Mader D ed Reptile medicine and surgery 2nd edition St Louis MO Elsevier 2006 p 926928 5 ORourke DP Lertpiriyapong K Chapter 19 Biology and diseases of reptiles In Anderson LC Otto G PritchettCorning KR Whary MT Fox JG Laboratory animal medicine 3rd edition Amsterdam NL Elsevier 2015 p 9671013 6 Reavill DR Griffin C Chapter 2 Common pathology and diseases seen in pet store reptiles In Mader D Divers SJ eds Current therapy in reptile medicine and surgery Philadelphia PA Saunders 2014 p 1319 American Association of Zoo Veterinarians Infectious Disease Manual VESICULAR EXANTHEMA OF SWINESAN MIGUEL SEA LION VIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Preventio n and Control Zoonotic Swine various marine mammals Direct contact with infected animal Indirect feeding uncooked infected products fomites Pyrexia anorexia lameness vesicles progression to erosions coronary bands snout lips oral cavity teats Moderately contagious Moderate to high morbidity Very low mortality None Do not feed uncooked fish to swine No Fact Sheet compiled by Cora Singleton Sheet completed on 1 January 2011 updated 31 October 2012 updated 8 August 2018 Fact Sheet Reviewed by Ryan Colburn Susceptible animal groups Swine cattle horses skunk primates reptiles fish and various marine mammals Causative organism Vesicular exanthema of swine VES and San Miguel sea lion virus SMSV are caliciviruses in the Caliciviridae family Zoonotic potential VES has occasionally been isolated from humans with blisters however the virus is not considered to be a serious public health threat Distribution VES has been eradicated worldwide SMSV is found on Pacific coast of North America The Opaleye fish is considered the primary host of SMSV Incubation period 15 days Clinical signs Swine Pyrexia anorexia lameness vesicles progressing to erosions coronary bands snout lips oral cavity teats Clinically indistinguishable from foot and mouth disease vesicular stomatitis Seneca virus A and swine vesicular disease Pinnipeds Abortion vesicles progressing to erosions on flippers Post mortem gross or histologic findings Vesicles on coronary bands snout lips oral cavity teats Hydropic degeneration and edema of stratum spinosum of the affected epidermis followed by ballooning degeneration of keratinocytes that then float into the vesicular fluid Stratum basale may be disrupted Diagnosis Virus culture antigen detection or serology Material required for laboratory analysis Vesicular fluid epithelium covering a vesicle heparinized whole blood serum tissues in formalin Relevant diagnostic laboratories Foreign Animal Disease Diagnostic Laboratory Plum Island 40550 Route 25 for packages Orient Point NY 11957 PO Box 848 for letters Greenport NY 119440848 631 3233256 Fax 631 3233366 Since vesicular diseases cannot be distinguished clinically contact the proper authorities prior to sample collection and shipment Treatment No effective treatment Supportive care and treatment of secondary problems Prevention and control VES is thought to have emerged from feeding uncooked fish and marine mammal tissues containing SMSV to pigs Strict enforcement of cooking of feed in conjunction with a slaughter program lead to eradication of the disease in swine in 1959 Early diagnosis and eradication by test and slaughter are important if VES were to recur SMSV is endemic in pinnipeds along the western coast of the United States Suggested disinfectant for housing facilities Phenols sodium hydroxide formalin sodium carbonate ionic and nonionic detergents strong iodophors in phosphoric acid chloroform Sodium hypochlorite 01 solution or a 132 dilution are effective in the absence of organic material American Association of Zoo Veterinarians Infectious Disease Manual VESICULAR EXANTHEMA OF SWINESAN MIGUEL SEA LION VIRUS Notification VES is not reportable to USDAAPHIS or OIE However this disease is considered eradicated and is clinically indistinguishable from other vesicular diseases that are reportable Measures required under the Animal Disease Surveillance Plan None specifically but due to similar appearance to other reportable vesicular diseases Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Consult USDAAPHIS Experts who may be consulted USDA State Veterinarians or federal Area Veterinarians in Charge References 1 Davies PR Internet Overview of Vesicular Exanthema of Swine San Miguel sea lion virus disease 2019 cited 2019 January 17 Available from httpswwwmerckvetmanualcomgeneralized conditionsvesicularexanthemaofswineoverviewofvesicularexanthemaofswine 2 Iowa State University College of Veterinary Medicine Veterinary Diagnostic and Production Animal Medicine Internet Vesicular Exanthema of Swine San Miguel Sea Lion Viral Disease 2019 cited 2019 January 17 Available from httpsvetmediastateeduvdpamFSVDswineindex diseasesvesicularexanthema 3 Knowles NJ Reuter G Porcine Caliciviruses In Zimmerman JJ Karriker LA Ramirez A Schwartz KJ Stevenson GW Zhang J eds Diseases of Swine 11th ed Ames IA WileyBlackwell 2018 in press 4 Smith AW Skilling DE Cherry N Mead JH Matson DO Calicivirus Emergence from Ocean Reservoirs Zoonotic and interspecies movements Emerg Infect Dis 1998 41 1320 5 Smith AW Iversen PL Skilling DE Stein DA Bok K Matson DO Vesivirus viremia and seroprevalence in humans J Med Virol 2006785693701 6 Swine Health Information Center Internet Vesicular Exanthema of Swine Virus 2015 cited 2019 January 17 Available from httpwwwcfsphiastateedupdfshicfactsheetvesicularexanthema swinevirus 7 Thorne ET San Miguel sea lion virus and vesicular exanthema of swine virus In Williams ES Barker IK eds Infectious Diseases of Wild Mammals 3rd ed Ames IA Iowa State University Press 2001 p 286288 8 United States Department of Agriculture Animal Plant and Health Inspection Services Internet All National Animal Health Laboratories Network NAHLN Laboratory List 2018 cited 2018 August 08 Available from httpwwwaphisusdagovanimalhealthnahlndownloadsallnahlnlablistpdf 9 United States Department of Agriculture Animal Plant and Health Inspection Services Internet Diagnostic Testing at the National Veterinary Services Laboratories 2015 cited 2018 August 08 Available from httpwwwaphisusdagovaphisourfocusanimalhealthlabinfo servicessadiagnostictestsctdiagnostictests American Association of Zoo Veterinarians Infectious Disease Manual VESICULAR STOMATITIS Fact Sheet compiled by Cora Singleton Sheet completed on updated 8 August 2018 Fact Sheet Reviewed by Kristi Delaski Susceptible animal groups Swine horses cattle Tapirs serologically positive but no clinical disease reported Causative organism A vesiculovirus in the Rhabdoviridae family Zoonotic potential Yes Vesicular stomatitis virus causes pyrexia headache myalgia and occasional blisters in the oral cavity of humans Distribution Enzootic in the US and present in North Central and South America Incubation period 15 days Clinical signs Pyrexia anorexia lameness vesicles progressing to erosions coronary bands oral cavity teats Clinically indistinguishable from foot and mouth disease vesicular exanthema of swine Seneca virus A and swine vesicular disease Epizootics in the United States occur about every 1013 years starting in early summer and ending with the onset of freezing weather Post mortem gross or histologic findings Vesicles on coronary bands snout lips oral cavity Hydropic degeneration and edema of stratum spinosum of the affected epidermis followed by ballooning degeneration of keratinocytes that then float into the vesicular fluid Stratum basale remains intact Diagnosis Agent identification virus culture with electron microscopy ELISA complement fixation PCR Serology ELISA virus neutralization often preferred may need to test for Indiana and New Jersey strains complement fixation Material required for laboratory analysis Vesicular fluid epithelium covering a vesicle serum tissues in formalin Relevant diagnostic laboratories Foreign Animal Disease Diagnostic Laboratory Plum Island 40550 Route 25 for packages Orient Point NY 11957 PO Box 848 for letters Greenport NY 119440848 631 3233256 Fax 631 3233366 Since vesicular diseases cannot be distinguished clinically contact the proper authorities prior to sample collection and shipment Treatment No effective treatment Supportive care and treatment of secondary problems Prevention and control Prevention should include no feeding of uncooked pork products regulation of movement of animals and animal products and control of insect vectors Vaccination has not been used routinely in the United States but might be useful during an epizootic Control measures include notification of authorities quarantine or depopulation of infected animals and disinfection of the environment Suggested disinfectant for housing facilities Phenols sodium hydroxide formalin sodium carbonate ionic and nonionic detergents strong iodophors in phosphoric acid chloroform ethanol glutaraldehyde Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Swine equids bovids South American camelids Biting insects transovarial transmission in sandflies and blackflies direct contact fomites Pyrexia anorexia lameness vesicles progression to erosions coronary bands oral cavity teats Low to moderately contagious Low to moderate morbidity None No carrier state Test and quarantine animals disinfect environment control insect vectors do not feed uncooked pork products Yes American Association of Zoo Veterinarians Infectious Disease Manual VESICULAR STOMATITIS Notification Reportable to the USDAAPHIS through the State Veterinarian or the federal Area Veterinarian in Charge The disease is also reportable to the World Organization for Animal Health OIE Measures required under the Animal Disease Surveillance Plan Reportable Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Infections must be reported to USDAAPHIS for management Experts who may be consulted USDA State Veterinarians or federal Area Veterinarians in Charge References 1 HernandezDivers SM Aguilar R LeandroLoria D Foerster CR Health Evaluation of a radiocollared population of freeranging Bairds tapirs Tapirus bairdii in Costa Rica J Zoo Wild Med 362 2005 P 176187 2 Spickler AR Internet Vesicular stomatitis 2016 cited 2018 August 08 Available from httpwwwcfsphiastateeduFactsheetspdfsvesicularstomatitispdf 3 Swenson SL Mead DG Kinker DR Rhabdoviruses In Zimmerman JJ Karriker LA Ramirez A Schwartz KJ Stevenson GW Zhang J eds Diseases of Swine 11th ed Ames IA Wiley Blackwell 2018 in press 4 United States Department of Agriculture Animal Plant and Health Inspection Services Internet National Animal Health Laboratories Network NAHLN Laboratories approved for VSV Preparedness and Surge Testing 2018 cited 2018 August 08 Available from httpwwwaphisusdagovanimalhealthnahlndownloadsvsvlablistpdf 5 United States Department of Agriculture Animal Plant and Health Inspection Services Internet Diagnostic Testing at the National Veterinary Services Laboratories 2015 cited 2018 August 08 Available from httpwwwaphisusdagovaphisourfocusanimalhealthlabinfo servicessadiagnostictestsctdiagnostictests 6 World Organization for Animal Health OIE Internet Vesicular stomatitis In Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2018 2015 cited 2018 August 08 Available from httpwwwoieintfileadminHomeengHealthstandardstahm20123VESICULAR STOMATITISpdf American Association of Zoo Veterinarians Infectious Disease Manual VIBRIOSIS Fact Sheet compiled by Catherine A Hadfield Sheet completed on 28 November 2010 updated 5 July 2013 Fact Sheet Reviewed by Brent R Whitaker E Scott Weber III Susceptible animal groups Over 50 species of marine and brackish fish including elasmobranchs are susceptible and disease is occasionally reported in freshwater fish Causative organism Vibrio spp are pleomorphic Gram negative rods Some can be primary pathogens but most are ubiquitous in the environment and cause secondary disease More than 20 serovars may cause disease Vibrio anguillarum salt water furunculosis V salmonicida hitra or cold water vibriosis V alginolyticus V cholerae V fischeri V harveyi carchariae V ichthyoenteri V logei V ordalli V parahaemolyticus V pelagius V splendidus V tapetis V vulnificus Moritella viscosa M marina Photobacterium damselae damselae P damselae piscicida Zoonotic potential Many species have zoonotic potential through skin wounds or ingestion of infected shellfish Distribution Worldwide first reported in North America in 1953 Incubation period Variable Clinical signs Acute or chronic presentation occurs with nonspecific clinical signs eg lethargy inappetance skin darkening scale loss ulcers hyperemia petechiation erythema coelomic distension from ascites or organomegaly corneal edema or ulceration and exophthalmia Neurologic or respiratory signs may be observed Many fish die acutely without external signs and mortalities may be 50 High index of suspicion in a zooaquarium setting after shipping or other stressors Post mortem gross or histologic findings Visceral petechiation congestion andor necrosis of organs especially kidney organomegaly especially spleen and fibrinous adhesions can be observed Weakly motile pleomorphic Gram negative rods may be present Inflammation which may be granulomatous can be observed histologically Diagnosis Pure bacterial culture from lesions blood or organs especially kidney and spleen with consistent Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Marine and brackish fish Occasionall y reported in freshwater fish Commonly found in mollusks and crustaceans Unknown in many cases Fish to fish contact and oral transmission is suspected Some species may use invertebrate vector Acute or chronic forms Nonspecific eg lethargy darkening ulcers petechial hemorrhages erythema coelomic distension ocular neurologic or respiratory signs Significant mortalities possible in outbreaks 50 Systemic antibiotics based on culture and sensitivity and regulations Appropriate water quality and reduction of other stressors eg over crowding elevated temperature Effective vaccines available for V anguillarum Many strains are zoonotic American Association of Zoo Veterinarians Infectious Disease Manual VIBRIOSIS clinical signs is supportive for diagnosis although the organism may be commensal in elasmobranch tissues Selective media available eg TCBS but these organisms can grow well on blood agar and other nutrientrich media Incubation temperature needs to be lower for Vibrio salmonicida Serology not available Material required for laboratory analysis Aerobic culturette andor blood culture vials Tissue swabs or preferably tissue samples for culture Transport at 4C Relevant diagnostic laboratories Laboratories specializing in fish pathogens although regular laboratories may be able to culture and identify Vibrio spp Treatment Systemic antibiotics eg trimethoprim sulfa tetracyclines florenfenicol aminoglycosides are needed but treatment should be adjusted as indicated by culture and sensitivity results and should follow all relevant legislation For foodfish follow guidelines for FDAapproved antibiotics eg oxtetracycline Nutritional support and supportive care can assist treatment Immunostimulants eg glucans alginate or ascorbic acid Prevention and control For outbreaks in aquaculture stocks regulations may require movement restrictions depopulation and disinfection of premises Most serovars however are ubiquitous secondary pathogens Control of stressors eg temperature water quality stocking density organic load nutrition is sometimes enough to control infection Selective breeding has been used in salmonids to develop resistance to V anguillarum Immersion vaccine for V anguillarum in salmonids Novartis is available and autogenous vaccines may be considered Suggested disinfectant for housing facilities Susceptible to most common disinfectants eg sodium hypochlorite and other chlorinebased disinfectants ethanol iodophors quaternary ammonium compounds and peroxygen compounds Notification None required Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal To be avoided with V anguillarum Other Vibrio spp are ubiquitous but avoid introducing animals if clinical signs are present Conditions for restoring diseasefree status after an outbreak Not applicable in most settings Experts who may be consulted Most fish clinicians will be familiar with vibriosis and can be consulted if an outbreak is encountered References 1 Actis LA ME Tolmasky and JH Crosa 2010 Vibriosis In Woo PTK ed 2nd ed Fish Diseases and Disorders Volume 3 Viral Bacterial and Fungal Infections CABI Publishing Wallingford UK Pp 570605 2 Austin B and DA Austin 2007 Bacterial Fish Pathogens Disease in Farmed and Wild Fish 4th ed Springer Praxis New York 552p 3 Chang CS HL Huang S Chen and SN Chen 2013 Innate immune responses and efficacy of using mushroom betaglucan mixture MBG on orangespotted grouper Epinephelus coioides aquaculture Fish Shellfish Immunol 35 115125 4 Ferguson HW 2006 Systemic Pathology 2nd ed Scotian Press London 366p 5 Grimes DJ P Brayton RR Colwell and SH Gruber 1985 Vibrios as autochthonous flora of neritic sharks System Appl Microbiol 6 221226 6 Inglis V RJ Roberts and NR Bromage 1993 Bacterial Diseases of Fish Halsted Press New York pp107166 7 Noga EJ 2010 Fish Disease Diagnosis and Treatment 2nd ed WileyBlackwell Ames Iowa Pp 193197 8 Plumb JA 1999 Salmonid bacterial diseases In Plumb JA ed Health Maintenance and Principal Microbial Diseases of Cultured Fishes Iowa State University Press Ames Iowa Pp 230 American Association of Zoo Veterinarians Infectious Disease Manual VIBRIOSIS 296 9 Ringo E RE Olsen JLG Vecino S Wadsworth and SK Song 2012 Immunostimulants and nucleotides in aquaculture a review J Marine Sci Res Devel 2 122 10 Roberts RJ 2001 The bacteriology of teleosts In Roberts RJ ed 3rd ed Fish Pathology WB Saunders Philadelphia Pennsylvania Pp 297331 11 Stoskopf MK 1993 Bacterial diseases of marine tropical fish In Stoskopf MK ed Fish Medicine WB Saunders Philadelphia Pennsylvania Pp 635646 12 Zhou Q L Wang H Wang F Xie and T Wang 2012 Effect of dietary vitamin C on growth performance and innate immunity of juvenile cobia Rachycentron canadum Fish Shellfish Immunol 32 969975 American Association of Zoo Veterinarians Infectious Disease Manual VIRAL HEMORRHAGIC SEPTICEMIA Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Fish more than 80 susceptible marine and freshwater species Horizontal transmission via fish waste water fomites etc Clinical presentation varies by host species and strain ranging from severe dermal muscle and organ hemorrhage to lethargy to no significant lesions Dependent on species from mild to lethal No effective treatment is available for freeranging or captive fish Limit the spread through the movement of infected fish water and fomites No Fact Sheet compiled by Nicholas Phelps Sheet updated on 17 January 2018 Fact Sheet Reviewed by James G Johnson III Elsburgh Tres Clarke Susceptible animal groups Fish 80 susceptible marine and freshwater species The virus has also been detected in amphipods leeches and turtles It is not known what role these nonfish species play in the ecology of the virus Causative organism Viral hemorrhagic septicemia virus previously known as Egtved virus in the Family Rhabdoviridae Zoonotic potential No Distribution Viral hemorrhagic septicemia virus has a broad distribution in the northern hemisphere Four primary strains of VHSV are known to exist distributed in Europe VHSVI II III East Asia VHSVI III IV and North America VHSVIV VHSVIV is further divided into marine VHSVIVa and freshwater VHSVIVb In North America VHSVIV has been detected off the Northern Pacific and Atlantic coasts as well as in the Great Lakes region Incubation period An inverse correlation has been recorded between virus stability and water temperatures ranging from 1C to 20C Transmission occurs at cooler temperatures 112C with an incubation time of 12 weeks at high temperature and 34 weeks at low temperatures Clinical signs Acute Results in rapid destruction of endothelial cells and extravasation of the blood supply which may ultimately result in diffuse or petechial hemorrhage ascites exophthalmia organ failure anemia pale gills and high mortality Chronic Results in prolonged disease with neurologictype behavior characterized by anorexia erratic swimming or lethargy Clinical presentation is dependent on a variety of factors including host pathogen or environmental variables Some species exhibit no clinical lesions while infected with high levels of VHSV while others develop severe lesions with low levels of VHSV Presumptive diagnosis can be difficult and secondary testing is recommended Post mortem gross or histologic findings VHSV has a predilection for endothelial cells and will often induce hemorrhagic lesions throughout the body visible by gross and histologic examination The virus will also cause necrosis and degeneration of hematopoietic tissues macrophage proliferation within renal tissue and degeneration and vacuolization of hepatic tissue Diagnosis The gold standard for VHSV detection is virus isolation by cell culture Suitable cell lines include Epithelioma Papulosum Cyprini EPC Rainbow Trout Gonad RTG2 Bluegill fry BF2 Chinook salmon embryo CHSE214 and the Fathead minnow FHM cell lines incubated at 15C Cytopathic effects are typically observed within 46 days but may take up to four weeks and two passages to appear Secondary testing by RTPCR or IFA are recommended Realtime RTPCR is becoming widely used for preliminary diagnosis and surveillance testing and can be performed on nonlethal samples ie fin or gill biopsy American Association of Zoo Veterinarians Infectious Disease Manual VIRAL HEMORRHAGIC SEPTICEMIA Material required for laboratory analysis Virology Fresh tissue homogenate of the kidney and spleen should be placed in plastic tubes or whirlpack bags with 1g tissue to 10mL dilution with virus transport media ie Hanks Balanced Salt Solution Ship samples overnight on frozen gel packs RTPCR Tissue should be placed in tubes with RNAlater or immediately frozen Tissue storage in 70 ethanol is an option but freezing is necessary for long term storage Contact the diagnostic lab where tissues will be sent to determine the types of tissues they will accept for nonregulatory testing and their recommended method of preservation Relevant diagnostic laboratories Please see the list of experts below all of whom will accept diagnostic samples for preliminary testing Additionally USDAAPHIS approved labs for export certification of aquacultured species can be found at httpwwwaphisusdagovanimalhealthanimaldisspecaquaculture Virus Reference Laboratory Diagnostic Virology Laboratory USDAAPHIS National Veterinary Service Laboratory 1920 Dayton Avenue Ames Iowa 50010 janetvwargaphisusdagov Treatment Therapeutics are not widely used to control VHS infection General supportive care and stress reduction are recommended Prevention and control Given the lack of available therapeutics preventing the introduction of VHSV is the primary method of control In addition early detection of the virus by proactive surveillance programs provides value in determining areas or activities of risk Strict biosecurity protocols should be implemented in areas of risk Prevention can be achieved by eliminating the transfer of the virus via contaminated fomites eggs fish and water Typical antiviral disinfectants such as chlorine sodium hypochlorite and UV irradiation are effective Iodophor treatment of eggs is not always effective at removing the virus from the eggs surface However at this time no evidence for true vertical transmission of VHSV has been recorded viral adherence to the egg surface and presence in ovarian fluid has been documented Suggested disinfectant for housing facilities If captive fish test positive the population should be isolated or euthanized Housing facilities should be cleaned and disinfected with standard products such as chlorine and sodium hypochlorite Facility effluent should also be disinfected with similar chemicals For recirculating facilities inline UV sterilization should be incorporated to prevent the transmission of the virus via contaminated water Notification VHSV is a reportable pathogen to the OIE and USDA Upon suspicion or preliminary diagnosis the area veterinarian in charge should be notified Measures required under the Animal Disease Surveillance Plan The National Aquatic Animal Health Plan provides some guidelines for surveillance of aquatic animals There is no coordinated surveillance plan for this disease in wild populations however regulatory and research surveys do occur Any suspect case in a new species or geographic region needs to be reported to AVIC USDA APHIS Measures required for introducing animals to an infected animals Susceptible species of naïve fish should not be introduced to a previously infected population It may be possible to cohabitat non susceptible species with a previously infected population however this approach is risky because the host range is broad and rapidly expanding Conditions for restoring diseasefree status after an outbreak No specific standards exist at this time however nonlethal antibody and quantitative RTPCR methods are available to monitor a population over time American Association of Zoo Veterinarians Infectious Disease Manual VIRAL HEMORRHAGIC SEPTICEMIA Experts who may be consulted Nicolas Phelps University of Minnesota 1333 Gortner Ave St Paul Minnesota 55108 6126247450 phelp083umnedu Rod Getchell Aquatic Animal Health Program Department of Microbiology and Immunology College of Veterinary Medicine Cornell University Upper Tower Road Ithaca NY 14853 6072534028 prb4cornelledy rgg4cornelledu erc58cornelledu Mohammed Faisal Michigan State University 174 Food Safety and Toxicology Building East Lansing MI 48823 5178842019 faisalmsuedu Gael Kurath and Jim Winton Western Fisheries Research Center 6505 NE 65th St Seattle WA 981155016 2065266282 gkurathusgsgov jwintonusgsgov References 1 Cornwell ER Bellmund CA Groocock GH Wong P Hambury KL Getchell RG Bowser PR Fin and gill biopsies are effective nonlethal samples for detection of Viral hemorrhagic septicemia virus genotype IVb J Vet Diag Invest 201324203209 2 Faisal M Shavalier M Kim RK Millard EV Gunn MR Winters AD Schulz CA Eissa A Thomas MA Wolgamood M Whelan GE Winton J Spread of the emerging viral hemorrhagic septicemia virus strain genotype IVb in Michigan USA Viruses 20124734760 3 Goodwin AE Merry GE Replication and persistence of VHSV IVb in freshwater turtles Dis Aq Org 201194173177 4 Groocock GH Getchell RG Cornwell ER Frattini SA Wooster GA Bowser PR LaPan SR Iodophor disinfection of walleye eggs exposed to viral hemorrhagic septicemia virus type IVb N Am J Aquacult 2012752533 5 Kim R Faisal M Emergence and resurgence of viral hemorrhagic septicemia virus Novirhabdovirus Rhabdovirus Mononegavirales J Adv Res 20112923 6 Phelps NBD Craft ME Travis D Pelican K Goyal SM Riskbased management of viral hemorrhagic septicemia virus VHSVIVb in Minnesota N Am J Fish Manag 201434373379 American Association of Zoo Veterinarians Infectious Disease Manual VIRAL HEMORRHAGIC SEPTICEMIA 7 OIE World Organization for Animal Health Aquatic Health Standards Commission 2016 Manual of diagnostic tests for aquatic animals Office international des epizooties Paris France 8 USFWS and AFSFHS US Fish and Wildlife Service and American Fisheries Society Fish Health Section 2016 AFSFHS Blue Book Suggested procedures for the detection and identification of certain finfish and shellfish pathogens American Fisheries Society Bethesda Maryland 9 VHSV Expert Panel Working Group Viral hemorrhagic septicemia virus VHSVIVb risk factors and association measure derived by expert panel Prev Vet Med 201094128139 10 Warg JV Clement T Cornwell ER Cruz A Getchell RG Giray C Goodwin AE Groocock GH Faisal M Kim R Merry GE Phelps NBD Reising MM Standish I Zhang Y TooheyKurth K Detection and surveillance of viral hemorrhagic septicemia virus using realtime RTPCR II Diagnostic evaluation of two protocols Dis Aq Org 20141111522 American Association of Zoo Veterinarians Infectious Disease Manual VIRULENT NEWCASTLE DISEASE Formerly Exotic Newcastle Disease Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Birds Highly contagious Avian Paramyxovirus 1 APMV1 Aerosol and ingestion are the primary routes Inadvertent comingling asymptomatic with nonexposed birds Death gastro intestinal and respiratory signs Severe typically fatal Not usually performed In zoo specimens treatment is supportive care with consideration of vaccination Strict biohazard containment Vaccination program may be considered Depopulation and disinfection of premises then no new birds for 30 days Rarely humans exposed may develop self limiting infections Cooked poultry products are safe to eat Fact Sheet compiled by Nancy Carpenter Sheet completed on 1 January 2011 updated 18 March 2013 updated 2018 Fact Sheet Reviewed by Erika TravisCrook Donald L Janssen Susceptible animal groups Numerous species of birds 250 species to date have been affected Primary concerns are domestic poultry operations chickens turkey and freeranging doublecrested cormorants are particularly susceptible Penguins are highly susceptible and often die acutely psittacines show varying susceptibility and prolonged shedding of virus It has not been reported in mammals except humans when they are exposed to a highly infected environment or during the vaccination process Causative organism RNA virus within avian paramyxovirus1 group APMV1 Genus Avulavirus Family Paramyxoviridae It should be noted that the mild strains are endemic to the US with the most virulent strains being in other countries Zoonotic potential Yes Humans who have exposure to infected birds may get conjunctivitis or mild flulike symptoms No human cases of Newcastle Disease have ever occurred from eating poultry products Distribution Worldwide but endemic in the Middle East Asia Africa Central and South America Incubation period 215 days and depends upon the virulence of the strain the susceptibility of the population and the species affected Clinical signs In rare human infections clinical signs include selflimiting conjunctivitis and flulike symptoms In animals clinical signs vary by pathotype Asymptomatic enteric generally subclinical Lentogenic or respiratory mild or subclinical respiratory signs Mesogenic respiratory and occasional neurologic signs with low mortality Velogenic most virulent with high mortality rates a neurotropic respiratory coughing gasping and neurologic signs muscle tremors circling paralysis green watery diarrhea decreased egg production NVND b viscerotropic hemorrhagic gastrointestinal disease and lesions VVND In domestic laying hen operations initially a drop in egg production occurs and then numerous deaths within 2448 hours which will continue for 710 days Birds that survive for 1214 days may live but may have permanent neurologic damage Post mortem gross or histologic findings No specific post mortem lesions are present However relevant gross lesions are usually found only in birds infected with velogenic strains include hemorrhage ulcers edema andor necrosis often occur in the cecal tonsils and lymphoid tissues of the intestinal wall including Peyers patches this lesion is particularly suggestive of Newcastle disease In chickens infected with less virulent strains the lesions may be limited to congestion and mucoid exudates in the respiratory tract and opacity and thickening of the air sacs American Association of Zoo Veterinarians Infectious Disease Manual VIRULENT NEWCASTLE DISEASE Formerly Exotic Newcastle Disease Diagnosis Virus isolation and microscopic lesions identified in tissues Differential diagnosis list for infectious diseases includes avian cholera Pasteurella multocida highly pathogenic avian influenza HPAI infectious aryngotracheitis herpesvirus infectious coryza Hemophilus paragallinarium diphtheritic avianpoxvirus psittacosis chlamydophylosis Chlamydophila psittaci mycoplasmosis infectious bronchitis coronavirus and in psittacines only Pachecos disease Material required for laboratory analysis Contact laboratory in advance of collections to ensure proper collection storage and shipping methods Brain and Heart infusion broth BHI with high concentrations of antibiotics should be used for transport Freeze if samples will not be received by the laboratory within 24 hours Swabs of trachea oropharynx and cloaca can be collected from live birds Tissue samples from dead birds include trachea lung spleen cloaca intestines cecal tonsils brain Feces for culture can be collected from either live or dead birds Serum for ELISA can be used but previous exposure and vaccination may affect results Reverse Transcriptase PCR is also available However results returning before that particular animal might die may be problematic Relevant diagnostic laboratories Testing is performed at numerous state labs Treatment It is not recommended to pursue treatment and typically flock depopulation is performed in domestic poultry operations However in a zoo situation the benefit of treatment should outweigh the risk of transmission to other birds Prevention and control There is no effective cure for virulent Newcastle Disease Once identified strict biohazard control methods should be immediately implemented Slaughter and disposal of all infected and exposed birds is recommended No new birds in for 30 days Pests must be controlled to minimize mechanical transfer of the virus Suggested disinfectant for housing facilities cresylics and phenolics Notification State and Federal veterinarians should be notified Federal httpwwwaphisusdagovanimalhealthareaoffices use map for regional instructions State httpwwwusahaorgPortals6StateAnimalHealthOfficialspdf Measures required under the Animal Disease Surveillance Plan This is a reportable disease and control must be managed with regional veterinary authorities Once the disease is confirmed strict biosecurity measures should be taken Depopulation to prevent spread must be considered Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak Do not repopulate infected areas for at least 30 days from final disinfection Experts who may be consulted Donald Janssen DVM Dipl ACZM San Diego Zoo donjanssengmailcom Nadine Lamberski DVM Dipl ACZM San Diego Zoo NLamberskisandiegozooorg References 1 The Center for Food Security and Public Health Internet Newcastle Disease 2016 cited 2018 February 2 Available from httpwwwcfsphiastateeduFactsheetspdfsnewcastlediseasepdf 2 Dvorak G USDA Division of Animal Industry The Center for Food Security and Public Health Chart Additional High Consequence Livestock Pathogens Vers 154 3 Janssen D SutherlandSmith M Papendick R Lamberski N Lewins E Mace M Edwards M Exotic Newcastle Disease outbreak in Southern California biosecurity measures for prevention in zoo American Association of Zoo Veterinarians Infectious Disease Manual VIRULENT NEWCASTLE DISEASE Formerly Exotic Newcastle Disease collections In Proc Am Assoc Zoo Vet 2003 p 107110 4 King DJ Newcastle Disease In Committee on Foreign and Emerging Diseases of the United States Animal Health Association eds Foreign Animal Diseases 7th Ed Boca Raton FL Boca Publishing Group 2008 p 343349 5 Newcastle Disease In Friend M Franson JC Ciganovich EA eds Field Manual of Wildlife Diseases US Dept of the Interior US Geological Survey 1999 p 175179 6 Spicker AR Newcastle Disease In Spickler AR Roth J eds Emerging and Exotic Diseases of Animals 3rd ed Center for Food Security and Public Health Ames IA Iowa State University 2008 p 203206 American Association of Zoo Veterinarians Infectious Disease Manual VISCERAL LEISHMANIASIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Canids Humans Phlebotomine sand flies Lutzomyia spp transplacental sexual and via blood transfusion also reported in dogs Lymphadenopathy onychogryphosis weight loss alopecia conjunctivitis Dogs Fever weakness lethargy weight loss hepatosplenomegaly lymphadenopathy Humans Fatal if not treated Allopurinol meglumine antimoniate liposomal amphotericin B Insecticides for sandfly control Yes but requires vector Fact Sheet compiled by Christine Fiorello Sheet completed on 20 January 2011 updated 1 November 2012 Fact Sheet Reviewed by Sara Childs Sanford Walter Boyce Susceptible animal groups Domestic and wild canids are the main host species Humans are commonly infected and the infection is becoming more commonly recognized in domestic cats Opossums and some rodents are also commonly infected although usually asymptomatic However the domestic dog is the only epidemiologically important reservoir Causative organism Protozoal organisms Leishmania donovani Asia Middle East Africa and L infantum Asia Middle East Europe South America Zoonotic potential Transmission occurs via sandfly bites dogs are the reservoir host Humans are accidental hosts and not considered important in the epidemiology of the disease Dog to human and human to human transmission does not seem to occur Distribution Europe South America Africa Middle East Asia Dogs in North America are occasionally infected Incubation period Weeks to months Clinical symptoms Humans Fever weakness lethargy weight loss muscle wasting hepatosplenomegaly lymphadenopathy pallor anemia thrombocytopenia are common Dogs lymphadenopathy onychogryphosis weight loss conjunctivitis alopecia Post mortem gross or histologic findings Inflammation and parasites found in macrophages of infected organs specific findings vary with parasite and host species chronicity of disease and immune status of host Diagnosis Gold standard demonstration of parasites amastigote form in splenic or bone marrow aspirates Serologic tests include an IFAT ELISA rK39 antigen most promising DAT and immunochromagraphic test strip Numerous blood and bone marrow PCR protocols are also often used Material required for laboratory analysis Depends on diagnostic method could include bone marrow lymph node or splenic aspirates or blood Relevant diagnostic laboratories In the US Cornell University Animal Health Diagnostic Lab Michigan State Diagnostic Center for Population and Animal Health National Bio Vet Lab are some of the many labs that have commercial tests available Treatment Humans Liposomal amphotericin B is first choice Meglumine antimoniate is less expensive but has more adverse effects Miltefosine is a newer oral drug that has shown good efficacy in India Dogs Allopurinol meglumine antimoniate and liposomal amphotericin B have all been used a complete cure is American Association of Zoo Veterinarians Infectious Disease Manual VISCERAL LEISHMANIASIS usually impossible and euthanasia is often recommended Prevention and control Culling of dogs does not seem to be effective Insecticide spraying around human settlements to control sandflies has been effective is some areas but not in others Insecticideimpregnated nets can provide protection for individuals Deltamethrinimpregnated collars and various insecticide pourons for dogs provide limited efficacy in decreasing transmission Suggested disinfectant for housing facilities Control of the disease is based on control of the insect vector Notification Not a nationally notifiable disease in the US it is notifiable in a few states such as Texas Measures required under the Animal Disease Surveillance Plan Measures required for introducing animals to infected animal Not relevant vectorborne disease Conditions for restoring diseasefree status after an outbreak Not relevant vectorborne disease Experts who may be consulted Dr Edward Breitschwerdt North Carolina State University College of Veterinary Medicine CVM Main Building 454 Box 8401 NCSU Campus Raleigh NC 27695 Phone 9195138277 Fax 9195136336 Email edbreitschwerdtncsuedu References 1 Cruz I L Acosta MN Gutierrez J Nieto C Cañavate J Deschutter FJ BornayLlinares 2010 A canine leishmaniasis pilot survey in an emerging focus of visceral leishmanisis Posadas Misiones Argentina BMC Infectious Diseases 10 34249 2 Maroli M L Gradoni G Oliva M Castagnaro A Crotti G Lubas S Paltrinieri X Roura E Zini and A Zatelli 2010 Guidelines for prevention of leishmaniasis in dogs Journal of the American Veterinary Medical Association 236 11 1201206 3 Patra P SK Guha AK Maji P Saha S Ganguly A Chakraborty P Kundu S Sarker and K Ray 2012 Efficacy of oral miltefosine in visceral leishmaniasis in rural West Bengal India Indian Journal of Pharmacology 44 4 500503 4 Pavli A and HC Maltezou 2010 Leishmaniasis an emerging infection in travelers International Journal of Infectious Diseases 14 10321039 5 Quinnell RJ and O Courtenay 2009 Transmission reservoir hosts and control of zoonotic visceral leishmaniasis Parasitology 136 191534 6 Savani ESMM MCGO Camargo MR de Carvalho RA Zampieri MG dos Santos SRN DAuria JJ Shaw LM FloeterWinter 2004 The first record in the Americas of an autochthonus case of Leishmania Leishmania infantum chagasi in a domestic cat from Cotia County São Paulo State Brazil Veterinary Parasitology 120 22933 7 Schantz PM FJ Steurer ZH Duprey KP Kurpel SC Barr JE Jackson EB Breitschwerdt MG Levy and JC Fox 2005 Autochthonous visceral leishmaniasis in dogs in North America Journal of the American Veterinary Medical Association 226 8 13161322 8 Srivastava P A Dayama S Mehrotra S Sundar 2011 Diagnosis of visceral leishmaniasis Transactions of the Royal Society of Tropical Medicine and Hygiene 105 16 9 Vercammen F 2009 Visceral leishmaniasis EAZWV Transmissible Disease Fact Sheet No 113 American Association of Zoo Veterinarians Infectious Disease Manual WEST NILE VIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Avian Equids Squirrels Other mammals Alligators Primarily via mosquito bite possibly ticks less efficient means include ingestion of virus via infected carcasses or contaminated tissues or fluids feces urine oral or cloacal secretions occupational exposure blood transfusion organ transplant and maternal transmission Range asymptomatic to nonspecific eg anorexia weight loss dehydration to neurologic eg ataxia lethargy paresis paralysis convulsions seizures death High fatality in some avian species especially corvids and some raptors 1030 of equine clinical cases are fatal 1 of human cases are severe ie West Nile neuroinvasive disease Supportive care immuno globulin therapy Mosquito control avoiding mosquito bites repellant screens clothing staying indoors at dawn and dusk vaccination licensed for horses also used extralabel in some birds primarily captive Yes Fact Sheet compiled by Genevieve Vega Weaver Sheet completed on 15 January 2018 Fact Sheet Reviewed by Heather Robertson Susceptible animal groups Changes in global climate landuse and biodiversity as well as potential virus evolution will continue to increase exposure as well as increasing the potential for disease in vulnerable naïve species Many avian species serve as amplifying hosts for WNV American robins house finches house sparrows and other species are considered high amplification hosts due to high proportions of WNVpositive mosquito blood meals Several species of mammals squirrels chipmunks and rabbits a reptile alligators and an amphibian lake frogs are unlikely to serve as amplifying hosts for West Nile virus WNV as viremia titers are relatively low in these species as compared to birds and the duration of infectious viremia is short eg approximately 1 day Most mammals are incidental ie deadend hosts Very young and old animals are likely most susceptible to adverse effects of infection Birds WNV has been reported in at least 326 species of birds in North America and over 1300 avian species worldwide All bird species are likely susceptible to WNV infection although most infections in most species are likely subclinical North American birds that are of particularly high susceptibility to WNVassociated morbidity and mortality are the American crow as well as other corvids eg blue jays black and yellow billed magpies fish crows and others and to a lesser extent other passerine species eg common grackles house sparrows house finches Some competent mosquito vector species are ornithophilic and at least one study has shown that Culex pipiens preferentially feeds on raptor species in some situations owls eagles falcons hawks Species of special concern due to apparently high rates of susceptibility and conservation status include California condors Florida scrub jays greater sage grouse ruffed grouse loggerhead shrike and native Hawaiian birds High rates of death were observed in freeranging juvenile American white pelicans in nesting colonies captive lesser scaup ducklings experimentallyinfected and freeranging greater sage grouse and experimentallyinfected ruffed grouse There is also concern over numerous raptor species such as great horned owls and northern owl species most observations come from rehabilitation facilities Other birds have been documented with WNV infection including flamingos penguins emus wild turkeys cormorants bronze winged ducks sandhill cranes common coots redlegged partridges and others A variety of psittacine species housed in outdoor aviaries many of which were of Australian origin had clinical WNV disease Reports of WNV disease and death in New World psittacines are relatively rare Antibodies to WNV have been detected in a vast array of avian species sometimes at high prevalences Mammal WNVassociated disease in mammals is most severe in equids and can also be significant in squirrels It has rarely been reported in alpacas sheep reindeer harbor seals Indian rhinoceroses a polar bear American Association of Zoo Veterinarians Infectious Disease Manual WEST NILE VIRUS a wolf and several domestic canids a Barbary macaque whitetailed deer and a killer whale Antibodies to WNV have been detected in a variety of mammals including cattle dogs cats goats rabbits raccoons Virginia opossums coyotes striped skunks bats black bears wild boar red foxes and killer whales indicating prior infection Reptile and amphibian Some reptiles and amphibians are susceptible to experimental infection including the American alligator Nile crocodile green iguana crocodile monitor garter snake various chelonians lake frog and North American bullfrog Among these alligators had clinical neurologic signs Causative organism West Nile virus is a singlestranded enveloped RNA virus of the Japanese encephalitis antigenic group genus Flavivirus and Family Flaviviridae It is an arthropodborne virus arbovirus transmitted by mosquitoes Culex spp and Aedes spp are primary vector species Culex pipiens in particular is an important bridge vector from avian hosts to humans There is one published study that suggests that WNV may be waterborne with at least one major outbreak in bald eagles and eared grebes in Utah caused by contaminated water and invertebrate prey Zoonotic potential Yes Transmission to humans is predominantly via mosquito bite but risk is also present during handling tissues and fluids as transmission can occur via inhalation mucous membrane contact open cuts and puncture wounds from a needle stick or contaminated equipment Mask with face shield and gloves should be worn when handling suspect animals and bedding Distribution Worldwide Incubation period Approximately 315 days in horses 214 days in humans and 414 days in birds Some birds become detectably viremic by 1 day postinoculation Clinical signs People The fatality rate is approximately 4 The majority of infected people are asymptomatic although some have mild nonspecific symptoms West Nile fever involving fever headache fatigue andor myalgiaarthralgia skin rash is also possible and rarely 1 of those diagnosed with WNV experience severe neurological symptoms West Nile neuroinvasive disease involving encephalitis meningitis andor paralysis leading to death in geriatric patients There is evidence that the human fatality rate may actually be higher than what is currently reported especially in people less than 60 years old Complications such as cognitive dysfunction can develop many years later related to the initial WNV infection Birds Clinical signs vary and can include depression ruffled feathers anorexia dehydration rapid weight loss decreased activity to lethargy torticollis opisthotonos nystagmus ataxia diarrhea nasal discharge drooping wings labored breathing and sudden death Most affected birds deteriorate rapidly following the onset of clinical signs however there are several reports of captive birds exhibiting clinical signs for weeks or months In some cases WNVinfected raptors have had feather abnormalities including stunted growth and pinchedoff feathers at the quill Equids About 10 of infected horses develop clinical disease that may include anorexia depression ataxia paresis paralysis teeth grinding aimless wandering convulsions circling tremors of facial and neck muscles cranial nerve deficits difficulty swallowing hyperesthesia apprehension hyperexcitability facial edema coma impaired vision conjunctivitis abdominal pain colic urinary dysfunction fever and head pressing Injuries and secondary pulmonary infections due to prolonged recumbency can also occur Horses that recover usually show improvement within 7 days of onset of signs About 1020 of recovered horses have residual effects such as neurologic deficits Squirrels Head tilt tremors paralysis and ataxia Reptiles alligators Anorexia weakness tremors slow reflexes heat tilt anisocoria opisthotonos circling and lymphohistiocytic proliferative cutaneous lesions Postmortem gross or histologic findings Lesions are variable among species and there or no pathognomonic findings Birds Gross lesions are often absent but can be nonspecific including whitetan mottling or streaking of the myocardium splenomegaly congested cerebral vessels and poor nutritional condition Histologic lesions can American Association of Zoo Veterinarians Infectious Disease Manual WEST NILE VIRUS be minimal to severe and can include lymphoplasmacytic myocarditis encephalitis ganglionitis hepatitis and nephritis and occasional adrenal gland and pancreatic necrosis Vasculitis can also occur Equids Gross lesions are usually absent When gross lesions are present they are most often in the CNS submeningeal edema and hemorrhage of spinal cord brain stem and midbrain Histologic findings nonsuppurative encephalitis or encephalomyelitis Squirrels No gross lesions are evident Histologic findings may include lymphoplasmacytic encephalitis or meningoencephalitis with multifocal microglial nodules perivascular and meningeal infiltrates of neutrophils neuronal necrosis and neuronophagia Other mammals Few reports of gross lesions Histologic lesions are similar to equids Reptiles Fluid in coelomic cavity mottled enlarged liver spleen and myocardium Intracellular heterophilic infiltrates in epithelial cells and cellular necrosis Diagnosis Serology Increase in WNVspecific antibodies in acute and convalescent sera IgM in CSF or IgM in serum suggestive ELISA with confirmation of results by plaque reduction neutralization test Virus isolation or antigen or RNA detection Infectious virus virus isolation or viral components RTPCR can be detected in serum CSF homogenized tissues brain heart kidneys and spleen oralcloacal swabs andor urine of some animals The period in which virus can be detected in live animals is limited and can be especially difficult in animals with low viremia titers eg horses RTPCR can be more sensitive than virus isolation Immunohistochemistry is most useful during active infection and in birds viral antigen may be evident in kidney heart spleen and to a lesser extent in other tissues such as brain pancreas liver and intestine and others Material required for laboratory analysis Bodily fluids such as blood centrifuged for separation of serum or plasma CSF urine saliva or swabs of body cavities oropharyngeal or cloacal cavities rectum or tissues heart kidney and spleen have been consistently useful for virus isolation and PCR testing in birds and can also be useful for immunohistochemistry IHC in birds feather pulp nonvascular feathers brain eye spinal cord liver and others tissues can be pooled to possibly increase sensitivity Testing maggots from carcasses for RNA may be useful in decomposed birds Relevant diagnostic laboratories Most state public health laboratories conduct WNV testing however virus isolation and plaque reduction neutralization tests are time and labor intensive and require BSL3 laboratory conditions Arbovirus Diagnostic Laboratory DRA CDCDVBIDADB 3150 Rampart Road Fort Collins C0 80521 Phone 970 2216445 httpwwwcdcgovncidoddvbidmiscarboviralshippinghtm Formalinfixed specimens for immunohistochemistry Infectious Disease Pathology Activity CDC MSG32 1600 Clifton Rd NE Atlanta GA 30333 Phone 18002324636 National Wildlife Health Center USGS 6006 Schroeder Road Madison Wisconsin 53711 Phone 608 2702400 Fax 608 2702415 American Association of Zoo Veterinarians Infectious Disease Manual WEST NILE VIRUS Treatment Supportive care ie fluids nutrition heat or cold can be provided with the goal of reducing CNS inflammation preventing injuries minimizing the effects of prolonged recumbency and nursing the animal beyond the severe morbidity that can occur Morbid birds and horses can have neurologic deficits that range from ataxia to paralysis and seizures and therefore padded caging may be necessary to prevent further injury Longterm ie up to several years neurologic defects have been observed in some raptors following WNV infection Immunoglobulin therapy has been used in horses serum based Novartis Animal Health and a plasma based product Lake Immunogenics Inc Llysine supplement and homeopathic treatments have been used with some success in raptors Mild cases may resolve without treatment Prevention and control Mosquito control measures should be implemented screened housing fans repellants 10 DEET avoiding stagnant water larvicides and stocking mosquito fish in ponds Insect repellants listed by the CDC as being EPAregistered and providing longlasting protection include DEET picaridin natural or synthetic oil of lemon eucalyptus and IR3535 3NButylNacetylaminopropionic acid ethyl ester Isolation of infected individuals and quarantine of new animals is recommended Avoid feeding potentially contaminated meatcarcasses Four vaccines were developed for use in horses a killed vaccine West NileInnovator DNA vaccine Fort Dodge Animal Health a recombinant vaccine in a canarypox vector Recombitek Merial Animal Health a flavivirus chimera vaccine EquiNile Intervet and a recombinant DNA plasmidpCBWN CDCFort Dodge Animal Healthnot yet licensed Many zoological facilities vaccinate equids and sensitive avian species with available vaccines A hydrogen peroxideinactivated whole virion WNV vaccine HydroVax001 for use in humans is currently in development Extralabel use of vaccines or use of vaccines that have not been adequately assessed in the target animal ie controlled challenge studies should be used with caution and not assumed to be protective Numerous vaccines have been tested to various degrees in birds some without challenge with varied responses Flamingoes failed to seroconvert after a single vaccination with the killed product This vaccine provided some level of protection at a small dose in ruffed grouse vaccinated grouse had no clinical disease lower viremia titers and milder microscopic lesions than nonvaccinated grouse A modified live vaccine was tested in domestic geese in Israel with 7594 protection The killed equine vaccine DNA plasmid vaccine and recombinant equine vaccine provided partial protection in island scrub jays Some redtailed hawks vaccinated with a DNAplasmid vaccine had partial protection while American robins and California condors vaccinated with the same vaccine seroconverted Results were variable among adult and juvenile thickbilled parrots vaccinated with the killed equine vaccine Seroconversion occurred in some penguins following administration of DNA plasmid and killed vaccines A DNA plasmid vaccine failed to protect greater sage grouse from mortality Oral vaccines in fish crows were ineffective The Recombitek vaccine was immunogenic in rhinos Suggested disinfectant for housing facilities As an enveloped virus WNV does not persist for long periods in the environment 70 ethanol and bleach are sufficient for general cleaning Viricides such as Virkon are highly effective when concern is high but can be damaging to skin and mucus membranes Notification Certain states require veterinary cases to be reported to the state animal health authority Measures required under the Animal Disease Surveillance Plan Laboratoryconfirmed positive cases in humans horses other mammals birds and mosquitoes from across the United States are collected by ArboNET Centers for Disease Control and Prevention httpwwwcdcgovncidoddvbidwestnileusgsframehtml Equine cases are usually determined from passive reporting from private practitioners and diagnostic submissions Measures required for introducing virus to infected animals WNV has been spread horizontally shortly after experimental inoculation in some birds that were housed in close captive quarters as well as in the American alligator Infected individuals should be isolated Viremia usually wanes 510 days in birds and up to 14 days in alligators However experimental infection in hamsters resulted in urine viral shedding for over 300 days and infectious virus persisted in tissues of house sparrows for up to 43 days Antibodies persist in some previously infected birds for years to lifelong American Association of Zoo Veterinarians Infectious Disease Manual WEST NILE VIRUS Conditions for restoring diseasefree status after an outbreak WNV is firmly established in avian and mosquito populations worldwide The virus is endemic and transmission is reinitiated annually in the summer within temperate areas of North America and Europe Therefore animals housed outdoors in endemic or atrisk areas will be at a continual risk Seasonal and climatic factors may precipitate outbreaks of disease in wildlife ie wild birds that may spillover into captive populations and humans Proper disinfection of housing facilities and equipment after an outbreak is necessary Experts who may be consulted Nicole M Nemeth DVM PhD Dipl ACVP Assistant Professor and Wildlife Pathologist Southeastern Cooperative Wildlife Disease Study Departments of Population Health and Pathology University of Georgia Athens GA 30602 References 1 Center for Disease Control and Prevention Internet West Nile Virus cited 2017 December 15 Available from httpswwwcdcgovwestnileindexhtml 2 Center for Food Security Public Health Internet West Nile Virus Infection cited 2017 December 15 Available from httpwwwcfsphiastateeduFactsheetspdfswestnilefeverpdf 3 Nemeth NM West Nile virus in raptors In Fowler ME Miller RE eds Fowlers Zoo and wild animal medicine Current Therapy Volume 7 St Louis MO Elsevier Saunders 2012 p 329335 4 Nemeth NM Oesterle PT West Nile virus from an avian conservation perspective Int Zoo Yb 201448101115 5 Travis D West Nile virus in birds and mammals In Fowler ME Miller RE eds Zoo and wild animal medicine Current Therapy Volume 6 St Louis MO Saunders 2008 p 29 American Association of Zoo Veterinarians Infectious Disease Manual WESTERN EQUINE ENCEPHALITIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals Equids may show mild to severe clinical illness Other mammals may be inapparently infected or show clinical illness Humans may experience mild to severe disease Birds Emus chukar partridges pheasants turkeys and some other avian species may show clinical illness Native birds generally serve as viral reservoirs without clinical illness Reptiles Inapparent infection noted for snakes tortoises as well as amphibians frogs Bite of WEE infected mosquito may also be transmitted by ticks Possibly from direct contact with infected tissues at necropsy ie through broken skin or mucous membranes Equids Fever anorexia lethargy impaired vision dysphagia circling head pressing paresis paralysis seizures Emus asymptomatic infections are common anorexia watery diarrhea weight loss abnormal neck movements neurologic signs Mild to severe may be fatal No specific treatment but supportive care hydration and nutritional support are important Anticonvulsant and anti inflammatory treatment may be used Vaccination mosquito control is important for routine exposure Personal protective equipment when handling tissues and performing necropsies Yes primarily by mosquito less frequently via tick Fact Sheet compiled by Rose Borkowski Sheet completed on updated 2 August 2018 Fact Sheet Reviewed by Danelle Okeson Sarah Cannizzo Susceptible animal groups Mammals Equids Birds emus other exotics turkeys pheasants Causative organism Western Equine Encephalitis Virus an Alphavirus Family Togaviridae Zoonotic potential Yes primarily via mosquito bite Primary mosquito vector is Culex tarsalis although Aedes sp may also transmit ticks Dermacentor andersoni can serve as vectors as well Distribution Argentina to Canada In the US it generally occurs west of Mississippi River Currently a rare disease of humans and horses in the US Incubation period 514 days Clinical signs Animals Equids Fever anorexia lethargy impaired vision difficulty swallowing circling head pressing paresis paralysis and seizures may be seen and disease is potentially fatal Clinical signs may be similar to other neurologic disease including rabies necessitating cautious examination and appropriate protective equipment Birds Emus have demonstrated watery diarrhea weight loss neurologic signs and fatalities A drop in egg production may occur in poultry The potential for WEE to cause disease in other avian species particularly nonnative birds exists WEE generally causes inapparent infection in native birds as virus naturally cycles between mosquitoes and several passerine species Reptiles Positive serologic tests indicating exposure have been demonstrated in reptiles The ability of the virus to cause clinical disease in captive or wild reptiles is incompletely understood American Association of Zoo Veterinarians Infectious Disease Manual WESTERN EQUINE ENCEPHALITIS Humans Fever headache stiff neck disorientation altered consciousness coma convulsions and paralysis can be present and death may occur Infection is of particular concern for infants elderly Can have asymptomatic infections Primates Theoretic concern for nonhuman primates as fatal human illness has occurred Post mortem gross or histologic findings Gross lesions are usually nonspecific Congestion of brain and meninges may be seen as well as ecchymotic hemorrhages due to antemortem trauma Severe inflammation of gray matter neuronal degeneration gliosis perivascular cuffing and hemorrhage Diagnosis Serology is from paired samples for virus neutralization Plaque Reduction Neutralization Test and IgM determination Complement fixation CF and hemagglutination inhibition HI can be used for identification as well Vaccination history is essential for accurate interpretation of serologic tests Molecular Diagnostics PCR and virus isolation on brain and other tissues are available brain preferred in equids although many tissues may demonstrate virus in emus Diagnostic testing to exclude rabies virus infection is required for submitted brain tissue Material required for laboratory analysis Serum Tissues particularly brain Note rabies testing must be performed on brain tissue prior to submission of any additional brain samples from the same animal for WEE testing at National Veterinary Services Laboratory Relevant diagnostic laboratories National Veterinary Services Laboratory 1920 Dayton Ave Ames IA 50010 Phone 515 3377266 Fax 515 3377397 Will test serum for Eastern Equine Encephalitis as well as WEE If submitting brain cerebrospinal fluid or whole blood for virus isolation the brain must be tested for rabies prior to submission httpswwwaphisusdagovanimalhealthlabinfoservicesdownloadsAmesDiagnosticTestingCatalogpdf Treatment No specific treatment is available for this disease Identification of neutralizing antibodies that may have therapeutic value has been recently investigated Patient management includes hydration nutritional support anticonvulsant and antiinflammatory treatment Prevention and control Vaccination of equids is an important means of prevention Extralabel use of vaccination for emus and potentially other ratites has been implemented Prevention of mosquito and tick bites via use of repellants protective clothing screens and fans Enclosure modification to reduce areas for mosquito access and breeding Avoidance of outdoor exposure during times of day when mosquitoes are most active As viral neurologic diseases such as arboviral encephalitides and rabies cannot be distinguished from one another clinically and may cause death it is imperative that proper sharps handling and use of personal protective equipment occur when working with infected animals or their tissues Although WEE is not believed to be directly transmissible from horses to humans under usual circumstances performance of necropsies on infected animals of any species and handling of their tissues blood and cerebrospinal fluid may pose risk Prevent aerosolization of virus and contact of infected tissues and fluids with skin and mucous membranes Do not use mechanical saws to obtain spinal cord samples due to risk of aerosolization Additional recommendations for handling of potentially infected tissues include use of 3 pairs of gloves inner layer disposable middle layer waterproof and outer layer of metal or Kevlar gloves face shield or goggles plus a disposable half mask high efficiency particle arresting HEPA respirator Suggested disinfectant for housing facilities The virus cannot survive outside of the host It is susceptible to bleach most disinfectants aldehydes ethanol moist and dry heat as well as drying Notification A reportable animal disease in some states refer to individual state veterinary regulations It also is a notifiable disease in humans wwwcdcorg Measures required under the Animal Disease Surveillance Plan Currently none American Association of Zoo Veterinarians Infectious Disease Manual WESTERN EQUINE ENCEPHALITIS Measures required for introducing animals to infected animal WEE is not known to be transmissible between mammals birds reptiles or people Vaccination against WEE is prudent for equids ratites and potentially other mammalian and avian species in endemic areas Conditions for restoring diseasefree status after an outbreak Susceptible animals should be vaccinated Ensure that veterinary equipment used with infected animals is discarded or disinfected prior to use with diseasefree animals Continue preventive measures against mosquito breeding and biting If mosquito numbers are excessive reduction in mosquito population via aerial spraying of pesticides can be discussed with public health officials and state or county mosquito control agents Experts who may be consulted CDCDivision of Vector Borne Diseases Arboviral Diseases Branch 3150 Rampart Road Foothills Campus Fort Collins CO 80521 970 2216400 References 1 Ayers JR Lester TL Angulo AB An epizootic attributable to Western equine encephalitis in emus in Texas J Am Vet Med Assoc 199420504600601 2 Blackmore C West Nile Virus and other arboviral infections In Rabinowitz PM Conti LA eds HumanAnimal Medicine Clinical Approaches to Zoonoses Toxicants and Other Shared Risks Maryland Heights MO Saunders 2010 p 294 298 3 The Center for Food Security Public Health Internet Eastern Western and Venezuelan Equine Encephalomyelitis 20152017 cited 2018 August 2 Available from httpwwwcfsphiastateeduFactsheetspdfseasterwestervenezuelanequineencephalomyelitispdf 4 Chapman GE Baylis M Archer D Daly JM The challenges posed by equine arboviruses Equine Vet J 2018504 436445 5 Delfraro A Burgueño A Morel N Gonzalez G Garcia A Morelli J Perez W Chiparelli H Arbiza J Fatal Human Case of Western Equine Encephalitis Uruguay Emerg Infect Dis 2011175952954 6 Hülseweh B Rülker T Pelat T Langermann C Frenzel A Schirrmann T Dübel S Thullier P Hust M Humanlike antibodies neutralizing Western equine encephalitis virus MAbs 201463717726 7 Medici EP Mangini PR FernandesSantos RC Health assessment of wild lowland tapir Tapirus terrestris populations in the Atlantic forest and Pantanal biomes Brazil 19962012 J Wild Dis 2014504817828 8 Randolph KD Vanhooser SL Hoffman M Western equine encephalitis virus in emus in Oklahoma J Vet Diagn Invest 19946492493 9 USDAAPHISVSCEAH National Surveillance Unit Internet Case Definition for Wester Equine Encephalitis 2010 cited 2018 August 2 Available from httpwwwaphisusdagovvsnahssequineeecasedefinitionwesternequineencephalitis011811 pdf American Association of Zoo Veterinarians Infectious Disease Manual WHITE NOSE SYNDROME Cutaneous Invasive Ascomycosis in Hybernating Bats Fact Sheet compiled by Michelle L Verant and Carol U Meteyer Sheet completed on 3 August 2011 updated 10 July 2013 updated 15 February 2018 Fact Sheet Reviewed by David Blehert Anne Ballmann Susceptible animal groups Microchiropteran bats and primarily hibernating species In North America species confirmed with WNS include little brown bat Myotis lucifugus tricolored bat Perimyotis subflavus northern longeared bat Myotis septentrionalis big brown bat Eptesicus fuscus eastern small footed bat Myotis leibii Indiana bat Myotis sodalis gray bat Myotis grisescens southeastern bat Myotis austroriparius yuma bat Myotis yumanensis western longlegged bat Myotis volans and cave bat Myotis velifer Species or subspecies that have been detected with Pd but no diagnostic signs of WNS include eastern red bat Lasiurus borealis silverhaired bat Lasionycteris noctivagans cave bat Myotis velifer Rafinesques bigeared bat Corynorhinus rafinesquii Virginia bigeared bat Corynorhinus townsendii virginianus Townsends bigeared bat Corynorhinus townsendii western smallfooted bat Myotis ciliolabrum and Mexican freetailed bat Tadarida brasiliensis In Europe and Asia Russia Mongolia and China 14 species of bats have been confirmed with WNS and an additional seven species have been detected with Pd but no diagnostic signs of WNS For updates on affected species see wwwwhitenosesyndromeorg Causative organism Pseudogymnoascus formerly Geomyces destructans Zoonotic potential Not likely psychrophilic character of fungus makes warm hosts unsuitable although related Geomyces species have been known to rarely induce superficial infection of the skin and nails in humans Distribution Since its first diagnosis in a New York cave in early 2007 WNS has continued its spread across eastern North America with newly affected sites identified annually At this sheet completion WNS has been Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Any hibernating bat in a WNS affected area is considered at risk for the disease Microscopic lesions visible in hibernating bats in Europe and China without mass mortality Aerosol direct contact environmental exposure Abnormal hibernation activity more frequent arousal daytime flights during winter congregating at or near cave openings White mold fungal hyphae on muzzle wings or both may be present but is neither necessary nor specific for WNS North America 90100 mortality in some hibernacula Populationwide losses of some species in the northeastern US are 80 since emergence of WNS Recovery has been documented experimentally and multiyear survival has been documented in wild banded bats Europe Asia Disease present with little noted morbidity or mortality Supportive care warmth fluid food supplement ation Natural recovery has been documented experimentall y and in wild banded bats upon emergence from hibernation Biosecurity limit human access to affected areas decontaminate clothing and equipment after entering hibernacula or trapping bats in affected areas biosecurity practices for handling Pseudogymnoas cus destructans Pd in laboratory eg BSL2 Reduce disturbance of hibernating bats restrict human access to hibernacula Not likely Pd is a psychrophill ic fungus body temperature of humans is above that conducive to growth of Pd American Association of Zoo Veterinarians Infectious Disease Manual WHITE NOSE SYNDROME Cutaneous Invasive Ascomycosis in Hybernating Bats confirmed in hibernating bats in 32 states and 7 Canadian provinces Additionally Pseudogymnoascus destructans has been found in Mississippi Texas and Wyoming without confirmation of disease todate The fungus remains viable in suitable underground environments yearround even in the absence of bats Upto date distribution maps for North America can be found at httpwhitenosesyndromeorgresourcesmap The Pd fungus has also been found on bats or in caves across Europe and in Russia Mongolia and China but without mass morbidity or mortality Incubation period In the wild WNS occurs seasonally with the earliest confirmed case in late September and peak infections and mortality occurring about 120 days after bats enter hibernation Experimentally induced infections result in epidermal pathology and mortality as early as 88 days postinfection Clinical signs Whitenose syndrome was named for the characteristic white fungal growth on the muzzles pinnae and wings of hibernating bats However this sign is not always apparent in bats with WNS nor is it specific for the disease as other nonpathologic dermatophytes may have a similar appearance Epidermal erosions and destruction of wing tissue by Pd cause disruptions in homeostasis resulting in dehydration electrolyte imbalances and acidbase disturbances Abnormal behaviors associated with WNS include increased frequency of arousal from torpor movement to roosting areas near cave entrances or other exposed sites and increased day flights from hibernacula during midwinter This increased activity likely contributes to premature depletion of fat reserves seen in infected individuals Bats with WNS may present with obvious damage to wing membranes increased fragility decreased elasticity irregular pigmentation and tears or holes in the patagium as they emerge from hibernation and become euthermic Wing damage may increase over the first few weeks postemergence due to an excessive inflammatory response but these lesions can heal completely by midsummer Post mortem gross or histologic findings Visible white fungal material on the muzzle and wings often disappears when a bat is removed from the hibernaculum Infected wings typically look normal during hibernation but areas of contraction or tears can be present and wing membrane may stick together when the wing is extended Bats that die from WNS during hibernation often have reduced subcutaneous fat and when touched with a gloved finger during necropsy exposed pectoral muscle may be tacky suggesting antemortem dehydration Microscopic findings are characterized by dense aggregations of Periodic acidSchiff PAS positive hyphae eroding through epidermis forming distinctive cups filled with fungus Invasion may extend into the deeper connective tissue Hyphae are often seen replacing adnexal structures filling skin glands and follicles Curved conidia may be present on the surface of infected skin Cellular inflammation is usually not present during hibernation but can become intense following emergence from hibernation as the bat becomes active and euthermic Diagnosis Although gross lesions can be suggestive of WNS confirmation of WNS requires histopathologic visualization of lesions cupping erosion of dermis with PAS stain and confirmation of presence of Pd by realtime polymerase chain reaction PCR analysis of wing tissue or a swab sample from the wing Molecular detection of Pd has also been demonstrated in guano collected from bats Alternatively Pd may be cultured from samples using fungal media Sabouraud dextrose agar or dextrosepeptoneyeast extract agar and incubated at cold temperatures approximately 5 10 C for six weeks until calling the culture negative Curved conidia produced by Pd are morphologically distinct from other fungi generally found on bats but molecular identification of the isolate by PCR is necessary for definitive confirmation Biopsies of wing tissue can be taken as nonlethal samples vide infra for histological examination but should be guided by visible signs to increase sensitivity Ultraviolet light can be used as a screening tool to assist with targeted specimen selection in the field the cupping dermal erosions have been associated with fluorescence under longwave 368385 nm UVA light The unknown specificity of UV fluorescence precludes this technique from being diagnostic Material required for laboratory analysis Nonlethal swab samples of the wing skin surface can be collected to test for the presence of Pd However confirmation of WNS requires histopathological examination of skin Skin tissue from the wing andor muzzle American Association of Zoo Veterinarians Infectious Disease Manual WHITE NOSE SYNDROME Cutaneous Invasive Ascomycosis in Hybernating Bats can be submitted for PCR analysis fungal culture and histopathology PAS stain Areas submitted should preferably demonstrate white fungal growth or abnormal appearance The use of longwave UVA light can aid in identifying areas likely to be affected particularly when nonlethal sampling is desired A 35 mm biopsy of wing tissue may be submitted for histopathology if analysis of a whole carcass is not available or otherwise not an option Although tape impressions of fungal growth on bats can be mounted on glass slides to search for conidia characteristic of Pd suggestive samples should be confirmed by PCR and histopathology Relevant diagnostic laboratories Samples known or suspected to harbor viable Pd should at minimum be handled in a biosafety cabinet in a Biosafety Level2 laboratory Guidelines for decontamination of personal and equipment should be followed httpwhitenosesyndromeorgtopicsdecontamination Treatment and Management At this time the only effective treatment for WNS is supportive care of homeothermic bats Natural recovery of freeranging bats that survive infection during hibernation and subsequently clear all signs of disease has been documented However in wild freeflying bats wing damage may prevent successful foraging causing additional mortality Disease management options are still in the discovery phase including use of vaccination antifungal compounds ultraviolet light and biologic control Although there has been some demonstration of effectiveness against Pd in the laboratory safety efficacy and transferability of this research to wild bats as well as potential ecological impacts of these management actions have not been determined At this time improving survival of bats outside of hibernation is a management action directed at population recovery in the face of WNS Prevention and control Current prevention and control strategies focus on biosecurity and restricting access to hibernacula primarily caves and mines to limit movement of people and contaminated equipment between hibernacula and other sites used by bats To support this effort a national cave access advisory and standardized decontamination protocols have been developed see wwwwhitenosesyndromeorg Other studies assessing the utility of artificial hibernacula chemical and biocontrol agents and vaccination are currently in progress Suggested disinfectant for housing facilities To minimize the spread of Pd decontamination protocols should be followed whenever moving bats or equipment that may have been exposed to Pd or contaminated environments see httpwhitenosesyndromeorgtopicsdecontamination Biosecurity and decontamination procedures should also be implemented for rehabilitation facilities to limit spread of Pd between individuals and geographic areas following release of bats back into the wild To date there are no disinfection methods that are considered safe and effective for natural hibernacula Notification At this time notification of WNS or detection of the Pd fungus is voluntary Reports of WNS observations can be sent to the state wildlife resources agency the US Fish and Wildlife Service or the USGS National Wildlife Health Center Instructions for reporting mortality events to the USGS can be found here httpwwwnwhcusgsgovmortalityeventsreportingjsp For inclusion of information on the WNS Occurrence Map httpswwwwhitenosesyndromeorgresourcesmap report updates to GSwnsmapusgsgov Measures required under the Animal Disease Surveillance Plan There are no national requirements See section above Notification for recommendations for reporting pathogen detections and disease observations see Bat Submission Guidelines httpwwwnwhcusgsgovdiseaseinformationwhitenosesyndrome Measures required for introducing animals to infected animal Not recommended Conditions for restoring diseasefree status after an outbreak None Underground sites where Pd has been detected are considered permanently contaminated until an effective environmental treatment method is identified American Association of Zoo Veterinarians Infectious Disease Manual WHITE NOSE SYNDROME Cutaneous Invasive Ascomycosis in Hybernating Bats Experts who may be consulted Jeremy Coleman National WNS Coordinator USFWS Phone 4132538223 JeremyColemanfwsgov USGS National Wildlife Health Center 6006 Schroeder Road Madison WI 537116223 Phone 6082702400 Fax 6082702415 Anne Ballmann aballmannusgsgov David Blehert dblehertusgsgov References An updated full WNS bibliography can be found at httpswwwwhitenosesyndromeorgwnsbibliography 1 Ballmann AE Torkelson MR Bohuski EA Russell RE Blehert DS Dispersal hazards of Pseudogymnoascus destructans by bats and human activity at hibernacula in summer J Wildl Dis 201753 725735 2 Blehert DS Hicks AC Behr MJ Meteyer CU BerlowskiZier BM Buckles EL Coleman JTH Darling SR Gargas A Niver R Okoniewski JC Rudd RJ Stone WB Bat whitenose syndrome an emerging fungal pathogen Science 2009323 227 3 Cheng TL Mayberry H McGuire LP JR Hoyt Langwig KE Nguyen H Parise KL Foster JT Willis CKR Kilpatrick AM Frick WF Efficacy of a probiotic bacterium to treat bats affected by the disease white nose syndrome J Appl Ecol 201654701708 4 Cornelison C Keel M Gabriel K Barlament C Tucker T Pierce G Crow Jr A A preliminary report on the contactindependent antagonism of Pseudogymnoascus destructans by Rhodococcus rhodochrous strain DAP96253 BMC Microbiol 20141417 5 Cryan PM Meteyer CU Boyles JG Blehert DS Wing pathology of whitenose syndrome in bats suggests lifethreatening disruption of physiology BMC Biology 20108135 6 Drees KP Lorch JM Puechmaille SJ Parise KL Wibbelt G Hoyt JR Sun K Jargalsaikhan A Dalannast M Palmer JM Lindner DL Kilpatrick AM Pearson T Keim PS Blehert DS Foster JT 2017 Phylogenetics of a fungal invasion Origins and widespread dispersal of whitenose syndrome mBio 20178e0194117 Available from doi101128mBio0194117 7 Frick WF Puechmaille SJ Hoyt JR Nicke BA Langwig KE Foster JT Disease alters macroecological patterns of North American bats Glob Ecol Biogeogr 20152477419 8 Fuller NW Reichard JD Nabhan ML Fellows SR Pepin LC Kunz TH Freeranging little brown myotis Myotis lucifugus heal from wing damage associated with whitenose syndrome EcoHealth 20118154162 9 Gargas A Trest MT Christensen M Volk TJ and Blehert DS Geomyces destructans sp nov asssociated with bat whitenose syndrome Mycotaxon 2009108147154 10 Hoyt JR Sun K Parise KL Lu G Langwig KE Jiang T Yang S Frick WF Kilpatrick AM Foster JT Feng J Widespread bat whitenose syndrome fungus northeastern China Emerg Infect Dis 2016221402 11 Langwig KE Frick WF Hoyt JR Parise KL Drees KP Kunz TH Foster JT Kilpatrick AM Drivers of variation in species impacts for a multihost fungal disease of bats Phil Trans R Soc B 2016371170920150456 12 Langwig KE Frick WF Reynolds R Parise KL Drees KP Hoyt JR Cheng TL Kunz TH Foster JT Kilpatrick AM Host and pathogen ecology drive the seasonal dynamics of a fungal disease whitenose American Association of Zoo Veterinarians Infectious Disease Manual WHITE NOSE SYNDROME Cutaneous Invasive Ascomycosis in Hybernating Bats syndrome Proc Biol Sci 2015282 20142335 13 Lorch JM Lindner DL Gargas A Muller LK Minnis AM Blehert DS A culturebased survey of fungi in soil from bat hibernacula in the eastern United States and its implications for detection of Geomyces destructans the causal agent of bat whitenose syndrome Mycologia 201310523752 14 Lorch JM Meteyer CU Behr MJ Boyles JG Cryan PM Hicks AC Ballmann AE Coleman JTH Redell D Reeder DM Blehert DS Experimental infection of bats with Geomyces destructans causes whitenose syndrome Nature 20114803768 15 Lorch JM Minnis AM Meteyer CU Redell JA White JP Kaarakka HM Muller LK Lindner DL Verant ML ShearnBochsler V Blehert DS The fungus Trichophyton redellii sp nov causes skin infections that resemble whitenose syndrome of hibernating bats J Wildl Dis 2015513647 16 Lorch JM Muller LK Russell RE OConnor M Lindner DL Blehert DS Distribution and environmental persistence of the causative agent of whitenose syndrome Geomyces destructans in bat hibernacula of the Eastern United States Appl Environ Microbiol 2013791293301 17 Maslo B Valent M Gumbs JF Frick WF Conservation implications of ameliorating survival of little brown bats with whitenose syndrome Ecol Appl 201525183240 18 Meteyer CU Barber D Mandl JN Pathology in euthermic bats with whitenose syndrome suggests a natural manifestation of immune reconstitution inflammatory syndrome Virulence 2012 375838 19 Meteyer CU Buckles EL Blehert DS Hicks AC Green DE ShearnBochsler V Thomas NJ Gargas A Behr MJ Histopathologic criteria to confirm whitenose syndrome in bats J Vet Diagn Invest 2009214114 20 Meteyer CU Valent M Kashmer J Buckles EL Lorch JM Blehert DS Lollar A Berndt D Wheeler E White CL Ballmann AE 2011 Recovery of little brown bats Myotis lucifugus from natural infection with Geomyces destructans whitenose syndrome J Wildl Dis 20114761826 21 Minnis AM Lindner DL Phylogenetic evaluation of Geomyces and allies reveals no close relatives of Pseudogymnoascus destructans comb nov in bat hibernacula of eastern North America Fungal Biology 2013117638649 22 OShea TJ Cryan PM Hayman DTS Plowright RK Streicker DG Multiple mortality events in bats a global review Mammal Rev 201646175190 23 Palmer JM Drees KP Foster JT Lindner DL Extreme sensitivity to ultraviolet light in the fungal pathogen causing whitenose syndrome of bats Nat Commun 2018935 24 Puechmaille SJ Wibbelt G Korn V Fuller H Forget F Muehldorfer K Kurth A Bogdanowicz W Borel C Bosch T Cherezy T Drebet M Goerfoel T Haarsma AJ Herhaus F Hallart G Hammer M Jungmann C Le Bris Y Lutsar L Masing M Mulkens B Passior K Starrach M Wojtaszewski A Zoephel U Teeling EC PanEuropean distribution of whitenose syndrome fungus Geomyces destructans not associated with mass mortality PLoS One 201164e19167 25 Reeder DM Frank CL Turner GG Meteyer CU Kurta A Britzke ER Frequent arousal from hibernation linked to severity of infection and mortality in bats with whitenose syndrome PLoS One 201276e38920 26 Reichard JD Fuller NW Bennett AB Darling SR Moore MS Langwig KE Interannual survival of Myotis lucifugus Chiroptera Vespertilionidae near the epicenter of whitenose syndrome Northeast Nat 2014214N56 27 Reichard JD Kunz TH Whitenose syndrome inflicts lasting injuries to the wings of little brown myotis Myotis lucifugus Acta Chiropterol 200911457464 28 Russell RE Thogmartin WE Erickson RA Szymanski J Tinsley K Estimating the shortterm recovery potential of little brown bats in the eastern United States in the face of whitenose syndrome Ecol Modell 20153141117 29 Turner GG Meteyer CU Barton H Gumbs JF Reeder DM Overton B Nonlethal screening of batwing skin with the use of ultraviolet fluorescence to detect lesions indicative of whitenose syndrome J Wildl Dis 201450356377 30 Turner GG Reeder DM Coleman JC A fiveyear assessment of mortality and geographic spread of white American Association of Zoo Veterinarians Infectious Disease Manual WHITE NOSE SYNDROME Cutaneous Invasive Ascomycosis in Hybernating Bats nose syndrome in North American bats and a look to the future Bat Res News 2011521327 31 Vanderwolf KJ Malloch D McAlpine DF Detecting viable Pseudogymnoascus destructans Ascomycota Pseuduerotiaceae from walls of bat hibernacula effect of culture media J Cave Karst Stud 201678158162 32 Verant ML Boyles JG Waldrep Jr W Wibbelt G Blehert DS Temperaturedependent growth of Geomyces destructans the fungus that causes bat whitenose syndrome PloS One 20127e46280 33 Verant ML Meteyer CU Speakman JR Cryan PM Lorch JM Blehert DS Whitenose syndrome initiates a cascade of physiologic disturbances in the hibernating bat host BMC Physiol 201414110 34 Verant ML Minnis AM Lindner DL Blehert DS Geomyces and Pseudogymnoascus Emergence of a primary pathogen the causative agent of bat whitenose syndrome In The Fungal Community Its Organization and Role in the Ecosystem Boca Raton FL CRC Press 2017 p 405415 35 Warnecke L Turner JM Bollinger TK Lorch JM MisraV Cryan PM Wibbelt G Blehert DS and Willis CKR 2012 Inoculation of bats with European Geomyces destructans supports the novel pathogen hypothesis for the origin of whitenose syndrome Proc Natl Acad Sci USA 201210969997003 36 Warnecke L Turner JM Bollinger TK Misra V Cryan PM Blehert DS Wibbelt G Willis CKR Pathophysiology of whitenose syndrome in bats a mechanistic model linking wing damage to mortality Biol Lett 20139 20130177 37 Wilcox A Willis CKR Energetic benefits of enhanced summer roosting habitat for little brown bats Myotis lucifugus recovering from whitenose syndrome Conserv Physiol 201641 American Association of Zoo Veterinarians Infectious Disease Manual YABAPOXVIRUS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Primates including human Accidental inoculation insect vectors body fluids wounds Humans infected via skin wounds Benign growths on the face and limbs histiocytoma which may reach several cm in diameter Mild to severe Supportive Usually spontaneous regression in 36 weeks Careful handling of nonhuman primates Disinfection of fomites and vector control Yes Fact Sheet compiled by E Marie Rush Sheet completed on 3 December 2010 25 March 2013 May 1 2018 Fact Sheet Reviewed by Marc Valitutto Susceptible animal groups Primates human and nonhuman Causative organism Yabapoxvirus genus Yatapoxviridae Zoonotic potential Yes Distribution Western Africa originated in Yaba Nigeria Incubation period Unknown but clinical signs can appear within days of inoculation Clinical signs In nonhuman primates subcutaneous tumors begin as small erythematous areas but can quickly proliferate once the histiocytes become infected The infected animal develops a high titer during tumor growth and regression of the tumor is likely caused by in vivo cytopathic effects of virus Signs in humans are similar to nonhuman primates Lesions typically regress spontaneously within 36 weeks Pruritus may accompany lesions This disease is different from Yabalike disease virus which is in the same genus Yatapoxviridae Post mortem gross or histologic findings Grossly apparently subcutaneous tumors that when biopsied show large pleomorphic histiocytic cells loosely arranged in a vascular network Diagnosis History of direct or indirect contact with nonhuman primates or transport from and travel to west Africa ELISA PCR histopathology of tumors EM Material required for laboratory analysis Serum tissue for histopathology or EM Relevant diagnostic laboratories This is an uncommon disease but has been noted in North American collections Most laboratories that process nonhuman primate samples can either run the PCR for this virus or can direct personnel accordingly to an appropriate laboratory facility for testing of samples Histopathology and EM can be done at most laboratories that normally process tissues and have the capabilities for these procedures Treatment Supportive spontaneous resolution usually in 36 weeks Prevention and control Avoid contact with primates that have had potential exposure Proper quarantine and testing of animals with history of exposure or recent shipment from west Africa Humans should keep all skin wounds cleaned bandaged and covered when working with nonhuman primates Thorough disinfection of all potential fomites in housing areas for primates in collections and protection of animal care staff through education and proper clothing and protective wear gloves long sleeves Vector control Suggested disinfectant for housing facilities Detergents hypochlorite alkalis Virkon and glutaraldehyde Notification Public health officials may need to be notified if zoonotic transmission occurs depending on the state Measures required under the Animal Disease Surveillance Plan Currently none American Association of Zoo Veterinarians Infectious Disease Manual YABAPOXVIRUS Measures required for introducing animals to infected animal Do not introduce animals with clinical disease active or resolving pustuleslesions to noninfected or new animals Allow resolution of all lesions completely prior to introduction and follow proper quarantine measures for individual facility Conditions for restoring diseasefree status after an outbreak Condition typically spontaneously resolves within weeks with supportive care Treatment of any secondary infections should assist in wound healing Immunosuppressed animals may be more susceptible to infection and secondary disease and complications Proper disinfection of animal area and fomites should be done following an outbreak or care of an infected animal prior to housing new animals in the area Experts who may be consulted Centers for Disease Control and Prevention Poxvirus and Rabies Branch Division of HighConsequence Pathogens and Pathology 1600 Clifton Rd Atlanta GA 30333 800CDCINFO References 1 Brunetti CR Amano H Ueda Y Qin J Miyamura T Suzuki T Li X Barrett JW McFadden G Complete genomic sequence and comparative analysis of the tumorigenic poxvirus Yaba monkey tumor virus J Virol 2003771333513347 2 Downie AW Espana C A Comparative Study of Tanapox and Yaba Viruses J Gen Virol 1973193749 3 Downie AW Espana C Comparison of Tanapox virus and Yabalike viruses causing epidemic disease in monkeysEpidemiol Infect 1972 702332 4 International Veterinary Information Service Internet Contageous Ecthyma cited 2013 July 18 Available from httpwwwivisorgadvancesDiseaseFactsheetscontagiousecthymapdf 5 Joslin J Other primates excluding great apes In Fowler ME and RE Miller eds Zoo and Wild Animal Medicine 5th ed St Louis MO Elsevier 2003 p346381 6 USAF Internet Zoonotic Diseases Viral Diseases Yabapox 2006 cited 2013 July 18 Available from httpwwwphsourceusPHZDVDYabapoxhtm 7 Zimmermann P Thordsen I Frangoulidis D Meyer H Realtime PCR assay for the detection of tanapox virus and yabalike disease virus J Virol Method 2005130149153 American Association of Zoo Veterinarians Infectious Disease Manual YELLOW FEVER Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Nonhuman primates humans Mosquito bites Bleeding diathesis fever hepatopathy death Mild to severe to fatal Supportive Mosquito control vaccination Yes Fact Sheet compiled by Ellen Wiedner Sheet completed on 11 November 2010 updated 1 March 2013 Fact Sheet Reviewed by Jim Wellehan Alan Barrett Ramiro Isaza Susceptible animal groups Africa Colobus Cercopithecus Cercocebus Papio Galago Pan South America Alouatta Aotus Saguinus Ateles Callicebus Cebus Saimiri Causative organism Family Flaviviridae Genus Flavivirus at least 7 genotypes Mosquito genera vectors include Aedes Haemagogus and Sabethes Zoonotic potential Yes Sylvatic cycle has monkey reservoir transmission to humans occurs when virus infected mosquito bites a person Urban cycle involves man and mosquitoes only Distribution Disease has been eliminated in North America and Europe but it still occurs in tropical South America Caribbean and SubSaharan Africa Incubation period In humans 36 days in monkeys 23 days Clinical signs New World monkeys fever leukopenia death Old World monkeys none except in Galago which has high mortality rate and may show signs as in New World monkeys In Galago serum may turn green for 2 to 5 days during period of viremia Humans variable ranging from mild and selflimiting febrile disease to severe hepatitis to fulminant hemorrhagic fever In humans mortality rate from up to 50 Post mortem gross or histologic findings New world monkeys bleeding diathesis shock severe hepatocellular necrosis Diagnosis Serology paired serum titers showing fourfold increase in IgG or presence of yellow fever specific IgM Isolation of virus in tissues particularly liver can be performed or PCR identification of viral genome in blood or tissues Immunohistochemical detection of viral antigen in tissues is possible Material required for laboratory analysis Liver other organ tissues whole blood serum Relevant diagnostic laboratories CDC Arbovirus Diagnostic Laboratory For details and contact information refer to httpwwwcdcgovncidoddvbidmiscarboviralshippinghtm Treatment Symptomatic including fluids antiinflammatories and blood transfusions Ribavirin has been used in some cases Prevention and control Vaccination is recommended for travelers and for personnel in face of outbreak Specific documentation required for movement into and between yellow fever endemic countries per International Health Regulations guidelines Yellow fever 17D vaccine is a live attenuated vaccine Mosquito control necessary in primate facilities Suggested disinfectant for housing facilities Mosquito control required Notification As eliminated it is a reportable disease and state health department should be contacted All yellow fever cases must be reported to WHO within 24 hours of confirmation American Association of Zoo Veterinarians Infectious Disease Manual YELLOW FEVER Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal The disease is arthropod borne However infected animals can infect mosquitoes and contribute to the transmission cycle Thus insect control is essential Experimentally contact with contaminated blood can infect some primate species so do not introduce animals to each other when they are clinically sick Conditions for restoring diseasefree status after an outbreak Outbreak control requires elimination of infected mosquitoes and their larvae Experts who may be consulted Centers for Disease Control Prevention Division of VectorBorne Diseases Arboviral Diseases Branch 3156 Rampart Road Ft Collins CO 80521 970 2216400 World Health Organization Department of Pandemic and Epidemic Diseases Avenue Appia 20 1211 Geneva 27 Switzerland httpwwwwhointcsrdiseaseen References 1 Beeching NJ TE Fletcher DR Hill and GL Ghomson 2010 Travelers and viral haemorrhagic fevers what are the risks Intl J Antimicrob Agents 365 526535 2 Centers for Disease Control 2007 Yellow fever fact sheet National Center for Zoonotic VectorBorne and Enteric Diseases 3 Holzmann I I Agostini JI Areta H Ferreyra P Beldomenico and MS Di Bitetti 2010 Impact of yellow fever outbreaks on two howler monkey species Alouatta guariba clamitans and A caraya in Misiones Argentina Am J Primat 72 475480 4 Kalter SS 1989 Infectious diseases of nonhuman primates in a zoo setting Zoo Biol 8 6176 5 Monath TP 2008 Treatment of yellow fever review Antiviral Res 78 116124 6 Pastorino B A Nougairede N Wurtz E Gould and X de Lamballerie 2010 Review role of host cell factors in flavivirus infection implications for pathogenesis and development of antiviral drugs Antiviral Res 87 281294 7 Smithburn KC and AJ Haddow 1949 The susceptibility of African wild animals to Yellow Fever I Monkeys Am J Trop Med S129 389423 8 World Health Organization 2003 Yellow fever In WHOrecommended standards for surveillance of selected vaccinepreventable diseases World Health Organization Geneva Pp 4044 American Association of Zoo Veterinarians Infectious Disease Committee Manual 2013 PLAGUE Yersinia pestis Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Rodents human and nonhuman primates felids mustelids lagomorphs 1 Vector borne 30 species of fleas possibly lice and ticks 2 Aerosol 3 Direct contact with infected tissues bite from infected animal 4 Oral ingestion of infected tissue or feces 5 Fomites Peracute mortality without signs swelling abscess and hemorrhage at inoculation site lymphadenopathy lethargy fever Three classic forms in humans 1 Bubonic 2 Septicemic 3 Pneumonic Subclinical in resistant species 80100 mortality in others Streptomycin gentamicin tetracyclines ciprofloxacin sulfonamides Flea and rodent control program quarantine prairie dogs and other rodents personal protective equipment Yes Fact Sheet compiled by Rae Gandolf Sheet completed on 1 January 2011 updated 1 November 2012 Fact Sheet Reviewed by Tonie E Rocke Mark Drew Genevieve Vega Weaver Susceptible animal groups 200 different species of mammals including humans rodents felids and blackfooted ferrets Between 30 and 40 rodent species are considered important as reservoir hosts In the literature susceptible species have commonly been grouped into four categories 1 enzootic hosts California voles deer mice grasshopper mice 2 epizootic hosts prairie dogs ground squirrels 3 resistant nonrodent hosts coyotes badgers domestic dogs ungulates and 4 susceptible nonrodent hosts bobcats mountain lions Canada lynx blackfooted ferrets lagomorphs primates including humans domestic cats More recently however the distinction between enzootic and epizootic host species has become less clear it appears that both cycles can occur in the same species Causative organism Yersinia pestis is a small nonspore forming Gramnegative facultative anaerobic coccobacilli in the Enterobacteriaceae family consisting of one serotype that is divided into four biovars Antiqua Medievalis Orientalis and Microtus Zoonotic potential Yes Primary disease concerns Urban human plague pandemics may occur sylvatic plague is a major threat to blackfooted ferret and prairie dog populations felids domestic cats Canada lynx are susceptible they can develop a highly contagious form of the disease pneumonic plague and can further represent a health threat to people who come in contact with them Distribution Y pestis has a patchy global distribution in semiarid regions of Africa Middle East Asia and South America In North America it occurs in the western one third of the continent from Canada to Mexico Plague is also divided into two epidemiologic forms sylvatic and urban Incubation period 16 days in humans 14 days in felids 37 days in blackfooted ferrets Clinical signs Rodent species such as prairie dogs frequently present with peracute mortality and without American Association of Zoo Veterinarians Infectious Disease Committee Manual 2013 PLAGUE Yersinia pestis demonstrating signs of disease In all animal species affected swelling and hemorrhage can develop at the inoculation site and progress to abscessation Other signs may include fever depression and lymphadenopathy In resistant species such as canids and some rodents infection may be subclinical or mild Wild ungulates mule deer and the blacktailed deer have been reported to acquire ocular plague characterized by keratoconjunctivitis endophthalmitis and panophthalmitis In humans there are three classic forms of plague bubonic septicemic and pneumonic Similar signs may be seen in animals although this terminology is generally restricted to human and felid cases 1 Bubonic fever anorexia lethargy lymphadenopathy draining lymph nodes abscesses cellulitis oral ulceration vomiting diarrhea ocular discharge dehydration and weight loss If acquired via ingestion severe pharyngitis and tonsillitis can occur If not treated this form can progress to the septicemic or pneumonic form 2 Septicemic shock DIC respiratory distress due to secondary pneumonia No obvious involvement of the lymph nodes in primary septicemic plague may be seen but the other signs of bubonic plague may be present 3 Pneumonic dyspnea hemoptysis cough neurologic signs This form can occur via primary inhalation of the organism or following bloodborne dissemination to the lungs from bubonic or septicemic plague Post mortem gross or histologic findings Lesions are variable depending on host susceptibility and route of infection and may include large numbers of the organism in lesions necrotic foci in liver spleen lungs and other internal organs hepatomegaly and splenomegaly enlarged hemorrhagic and necrotic lymph nodes soft tissue abscesses with cellulitis hemorrhagic gastritis and colitis interstitial pneumonia pulmonary edema and pulmonary hemorrhage keratoconjunctivitis panophthalmitis and endophthalmitis subcutaneous vascular hemorrhage Diagnosis Presumptive diagnosis can be made by identifying the characteristic organism in stained samples of lymph node aspirates or draining lesions Yersinia pestis has a bipolar or safety pinlike staining pattern with WrightGiemsa or Wayson stain and will be positive with an immunefluorescence stain for the presence of Y pestis F1 antigen Definitive diagnosis is made by Y pestis isolation rapid immunoassays PCR and paired sera demonstrating a four fold titer increase to Y pestis F1 antigen using agglutination testing Differentials include bacterial infections such as Pasteurella Franciella tularensis Y pseudotuberculosis and Y enterocolitica Material required for laboratory analysis Blood nasaloral swabs lymph node aspirates swabs of draining lesions transtracheal aspirates tissue samples from liver spleen lungs and lymph nodes Relevant diagnostic laboratories Plague diagnosis should be conducted by state public health laboratories or the CDC under Biosafety level2 practices Contact the laboratory before collecting samples Treatment Prompt treatment within 24 hours is necessary for survival from pneumonic plague Yersinia pestis is susceptible to streptomycin fluoroquinolones trimethoprimsulfamethoxazole and tetracyclines Personal protective gear consisting of gown gloves surgical maskrespirator and eye protection is important to prevent transmission when treating affected animals Clinical cases should also be given a flea treatment Prevention and control Close parks and campgrounds during plague outbreaks to prevent transmission to humans from rodents Quarantine any wild caught rodents including prairie dogs for at least two weeks and treat all animals with an insecticide Flea and rodent control programs are critical in facilities that are located in plague endemic regions Insecticides like deltamethrin and flea growth regulators like pyriproxyfen can be sprayed into prairie dog burrows to control flea populations to slow or stop outbreaks Private ownership of prairie dogs is restricted or prohibited in some states in the US Interstate shipment in American Association of Zoo Veterinarians Infectious Disease Committee Manual 2013 PLAGUE Yersinia pestis the US is regulated by the Center for Disease Control Personal protective gear should be used when handling any potential cases including during postmortem examinations An F1V fusion protein vaccine for subcutaneous injection is used in blackfooted ferrets An oral vaccine has been recently developed for use in prairie dogs and appears to confer better immunity than the subcutaneous vaccine Suggested disinfectant for housing facilities 1 sodium hypochlorite 70 ethanol 2 glutaraldehyde iodines phenolics formaldehyde moist heat 121 C for at least 15 min dry heat 160170 C for at least 1 hour Notification Nationally notifiable infectious disease Report cases to the CDC Measures required under the Animal Disease Surveillance Plan Reportable disease Measures required for introducing animals to infected animal Not recommended Potential carrier animals should be screened for disease before introduction and diseased animals must be quarantined during curative course of treatment Conditions for restoring diseasefree status after an outbreak Yersinia pestis is endemic to certain regions of the world Sporadic and seasonal outbreaks occur in endemic regions Within a limited environment such as a zoological facility elimination of the rodent and flea population along with proper disposal of infected tissues is critical to eliminating disease Experts who may be consulted Tonie E Rocke PhD Epizootiologist National Wildlife Health Center 6006 Schroeder Rd Madison WI 53711 6082702451 References 1 Abbott RC and TE Rocke 2012 Plague US Geological Survey Circular 1372 79 p plus appendix Also available at httppubsusgsgovcirc1372 Accessed 11 July 2013 2 Eisen R and K Gage 2009a Adaptive strategies of Yersinia pestis to persist during interepizootic and epizootic periods Vet Res 40 1 3 Gage KL and MY Kosoy 2005 Natural history of plague perspectives from more than a century of research Ann Rev Entomol 50 50528 4 Gasper PW and RP Watson Plague and yerisniosis In Williams ES and IK Barker eds Infectious Diseases of Wild Mammals Ames Iowa 2001 Iowa State University Press Pp 313329 5 Matchett MR DE Biggins V Carlson B Powell and T Rocke 2010 Enzootic plague reduces blackfooted ferret Mustela nigripes survival in Montana 2735 VectorBorne Zoonot 10 2735 6 Rocke TE 2012 Sylvatic plague vaccine and management of prairie dogs US Geological Survey Fact Sheet 20123087 2 p Also available at httppubsusgsgovfs20123087 Accessed 11 July 2013 7 Rocke TE N Pussinis SR Smith J Williamson B Powell and JE Osorio 2010 Consumption of baits containing raccoon poxbased plague vaccines protects Blacktailed prairie dog Cynomys ludovicianus VectorBorne Zoonot 10 5358 8 Rocke TE S Smith PJ Marinari J Kreeger JT Enama and BS Powell 2008 Vaccination with F1V fusion protein protects blackfooted ferrets Mustela nigripes against plague upon oral challenge with Yersinia pestis J Wild Dis 44 17 9 The Center for Food Security and Public Health at Iowa State University httpwwwcfsphiastateeduFactsheetspdfsplaguepdf Accessed 11 July 2013 10 United States Department of Agriculture National Wildlife Disease Program Plague Surveillance American Association of Zoo Veterinarians Infectious Disease Committee Manual 2013 PLAGUE Yersinia pestis httpwwwaphisusdagovwildlifedamagenwdpplagueshtml Accessed 11 July 2013 11 United States Geological Survey National Wildlife Health Center Protecting BlackFooted Ferrets and Prairie Dogs Against Sylvatic Plague httpwwwnwhcusgsgovdiseaseinformationsylvaticplaguepublicationsprotectingblack footedferretspdf Accessed 11 July 2013 12 Williams ES 2003 Plague In Fowler M E and RE Miller eds Zoo and Wild Animal Medicine 5th ed Elsevier Science St Louis Missouri Pp 705709 American Association of Zoo Veterinarians Infectious Disease Manual YERSINIOSIS Animal Groups Affected Transmission Clinical Signs Severity Treatment Prevention and Control Zoonotic Mammals including humans Birds Reptiles Fish Ingestion of fecal contaminated food and water ingestion of raw meat and milk blood transfusions humans Diarrhea abdominal pain fever weakness septicemia weight loss enlarged lymph nodes sudden death Ranges from subclinical to acutely fatal or a chronic wasting form depending on individual and species Third generation cephalosporins fluoroquinolones supportive therapy Good hygiene protocols pest control program vaccination minimize stress Yes Fact Sheet compiled by Rae Gandolf and Genevieve Vega Weaver Sheet completed on 15 January 2018 Fact Sheet Reviewed by Lynnette Waugh Disease Significance Yersiniosis is considered among the most important diseases of farmed deer in the US as well as New Zealand and Australia Among zoological facilities in the US major outbreaks with mortalities have occurred among captive antelope birds and nonhuman primates with sporadic events in other species such as a cougar lion and Siberian tiger Enzootics have affected freeranging musk ox in Canada and brown hares and hedgehogs in Europe Yersiniosis is also zoonotic human exposure is typically foodborne Susceptible animal groups Yersinia pseudotuberculosis has been detected in 110 species including humans other mammals squirrels and other rodents nonhuman primates hedgehogs hares meerkats domestic dogs ruminants bats suids and felids birds guinea fowl turkey collared doves parrots reptiles and fish Rodents wild boar deer insects and wild birds are believed to be reservoirs however there has been some debate about their exact role in transmission In Amazona spp parrots hemosiderosis may predispose to systemic infection with Y pseudotuberculosis after enteric disease Outbreaks occur in farmed 48 mo old deer in fallwinter in the US Yersinia pseudotuberculosis can also survive for months to years in the soil water and vegetation Sensitive species and groups include callitrichids capybaras agouti mara turacos toucans lemurs guenons fruit bats squirrels and deer Yersinia entercolitica in contrast is a less common cause of yersiniosis and has only been reported to cause disease in a few species of nonhuman primates such as the African Green monkey chinchillas guinea pigs domestic pigs wild boars deer dogs cats and humans Young old immunosuppressed and animals with chronic liver illness appear to be most susceptible to severe disease associated with both Yersinia species Alpine ibex have been identified as a potential carrier of pathogenic Y enterocolitica Pathogenic Y enterocolitica has also been detected in asymptomatic dogs cats Djungarian hamsters pigs cattle goats rats mice voles shrews mongooses and beavers and a bird species the dunnock Carriers have the potential to cause water and soil contamination as well as direct zoonotic transmission Outbreaks of Y pseudotuberculosis most commonly occur during winter months due to stress and overcrowding as well as the enhanced virulence factors of the organism at lower temperatures In contrast Y entercolitica occurs more commonly in the summer and autumn Causative organisms Yersinia pseudotuberculosis and Y entercolitica are nonspore forming Gramnegative aerobic coccobacilli belonging to the Enterobacteriaceae family They are facultative intracellular bacteria Yersinia pseudotuberculosis consists of 15 serotypes plus additional subtypes while Y entercolitica has over 60 serotypes of which four O3 O527 O8 and O9 are believed to be pathogenic Zoonotic potential Yes Distribution Worldwide except Antarctica especially in temperate climates Highly prevalent in Europe Incubation period 10 days Clinical signs Disease is predominantly gastrointestinal although extraintestinal yersiniosis also occurs American Association of Zoo Veterinarians Infectious Disease Manual YERSINIOSIS Disease may be acute subacute or chronic Signs vary by species and individual but most typically consist of gastroenteritis Severe cases progress to septicemia Signs may include lethargy anorexia green to bloody diarrhea respiratory distress incoordination emaciation and sudden death Other forms of the disease include abortion and mastitis in ungulates chronic disease resulting in wasting syndrome and enlarged palpable mesenteric lymph nodes in various species skin rash desquamation erythema nodosum and arthritis caused by certain serotypes granulomatous conjunctivitis in dairy goats and appendicitis gastroenteritis abdominal pain and reactive arthritis in humans A carrier state can also develop Clinical symptoms are similar to salmonellosis Post mortem gross or histologic findings Yersina pseudotuberculosis can cause ulcerative enterocolitis hepatomegaly and splenomegaly multifocal necrosis seen as whitegray nodules on the liver and spleen and possibly the lungs and kidneys organisms are seen in the lesions interstitial pneumonia enlargement and abscessation of abdominal lymph nodes and adhesive peritonitis Yersinia entercolitica often results in lesions in the lymphoid tissue of the head and neck particularly the tonsils and submandibular lymph nodes Subclinical cases may demonstrate minimal gross and histologic changes Diagnosis Diagnosis is based on characteristic gross and histopathologic lesions with the presence of gram negative coccobacilli identification from bacterial culture cold enrichment and identification using conventional or realtime PCR A commercially available IgM ELISA for domestic pigs has been used with muscle and tonsillar tissue Serotyping can be done by slide agglutination or PCR Isolates can be further characterized using pulse field gel electrophoresis PFGE Rule out similar diseases including salmonellosis by culture Yersinia enterocolitica O9 shares common antigenic epitopes with B abortus and is known to cross react in diagnostic testing of African buffalo Material required for laboratory analysis The organism is most reliably cultured from organs demonstrating lesions particularly liver and spleen but also lungs mesenteric lymph nodes and intestines Blood culture is used in humans and can be used in nonhuman primates in cases of suspected septicemia Culture may also be performed on feces and postmortem tissues showing lesions However shedding of the organism can be intermittent therefore fecal culture is not always reliable For PCR Rectal or cloacal swab 05 g feces 05 g fresh frozen or fixed tissue or Y pseudotuberculosis 05 ml whole blood in EDTA purple top or ACD yellow top tube Relevant diagnostic laboratories Any diagnostic laboratory with Biosafety Level 2 practices that can perform bacterial culture and sensitivity Care should be taken because of the zoonotic potential Yersinia pseudotuberculosis and Y entercolitica do not grow well on routine culture media therefore submitted samples should indicate that these organisms are suspected For more rapid detection PCR is available Zoologix B0062 for qualitative ultrasensitive detection of Yersinia pseudotuberculosis and B0073 for detection of Yersinia enterocolitica Treatment There has been little success with treatment of clinical cases Prophylactic treatment of animals in contact with an individual demonstrating clinical signs is recommended Antibiotic treatment should be based on sensitivity Although different strains have demonstrated variable sensitivities most strains are susceptible to third generation cephalosporins fluoroquinolones and chloramphenicol There have been reports of some resistance by certain strains particularly those of Y enterocolitica to amoxicillinclavulanic acid ampicillin tetracyclines sulfonamides macrolides florfenicol and fluorquinolones Multidrug resistant strains of Y enterolitcia have been found in humans and pigs In patients with chronic liver lesions long term antibiotic treatment might be needed Fluid therapy should be administered as dehydration is a common development Prevention and control The bacteria can survive in animal and environmental reservoirs Outbreaks of are associated with stressors such as cold and wet weather decreases or changes in food availability overcrowding intestinal parasitism or animal capture Measures should therefore be taken to minimize these stressors Affected animals should be isolated and enclosures should be disinfected In some cases euthanasia of groups of animals may be necessary Preventive measures include implementing a rodent and bird control program practicing good hygiene including disinfection changing substrate removing contaminated or old food and water from enclosures minimizing stress competition and overcrowding in enclosures and avoiding raw meat in nonhuman primates American Association of Zoo Veterinarians Infectious Disease Manual YERSINIOSIS A killed whole cell vaccine for Y pseudotuberculosis Pseudovac Department of Veterinary Pathology Utrecht University The Netherlands is available and used mainly in European zoos before the winter and a killed vaccine Yersiniavax Intervet used for cervid farms in New Zealand A new vaccine of a live attenuated strain IP32680 of Y pseudotuberculosis administered orally has shown to provide adequate protection against severe infection in experimentally infected guinea pigs and mice and has demonstrated superior efficacy over Pseudovac The development of a recombinant vaccine for Y pseudotuberculosis is in the research phase but has also had positive results Suggested disinfectant for housing facilities 1 sodium hypochlorite 70 ethanol 2 glutaraldehyde iodines phenolics formaldehyde moist heat 121 C for at least 15 min dry heat 160170 C for at least 1 hour Be aware that organic material such as soils plant debris blood manure can inactivate some disinfectants e g chlorinebased products Removal of organic material should be conducted prior to disinfection Notification Notification of public health officials is required in human cases Measures required under the Animal Disease Surveillance Plan None Measures required for introducing animals to infected animal Not recommended In some cases euthanasia of symptomatic individuals may be warranted to avoid a carrier state Following exposure only animals free of clinical signs and with multiple negative cultures should be allowed to comingle with new animals Conditions for restoring diseasefree status after an outbreak Since the organism is ubiquitous in the environment and appears sporadically in some zoos it is problematic to designate an institution diseasefree Yersiniosis appears to be endemic in some European zoos Experts who may be consulted Shuping Zhang DVM PhD Professor and Director of VMDL University of Missouri zhangshupmissouriedu References 1 Allchurch AF Yersiniosis in all taxa In Fowler ME Miller RE eds Zoo and wild animal medicine 5th edition St Louis MO Elsevier 2003 p 724727 2 Food and Drug Administration Internet Bad Bug Book Yersinia enterocolitica 2012 cited 2019 February 20 Available from httpswwwfdagovdownloadsFoodFoodborneIllnessContaminantsUCM297627pdf 3 Galosi L Farneti S Rossi G Cork SC Ferraro S Magi GE Petrini S Valiani A Cuteri V Attili AR Yersinia pseudotuberculosis serogroup O1A infection in two amazon parrots Amazona aestiva and Amazone oratrix with hepatic hemosiderosis J Zoo Wild Med 2015463588591 4 Gasper PW Watson RP Plague and yerisniosis In Williams ES and Barker IK eds Infectious diseases of wild mammals Ames IA Iowa State University Press 2001 p 313329 5 Gorsich EE Bengis RG Ezenwa VO Jolles AE Evaluation of the sensitivity and specificity of an enzymelinked immunosorbent assay for diagnosing brucellosis in African buffalo Syncerus caffer J Zoo Wild Med 2015511918 6 Quintard B Petit T Ruvoen N Carniel E Demeure CE Efficacy of an oral live vaccine for veterinary use against pseudotuberculosis Comp Immunol Microbiol Infect Dis 201033e59e65 7 WildPro Internet Yersiniosis cited 2019 February 20 Available from httpwildprotwycrosszooorgS0zMGracilicutesyersiniaYersiniahtm 8 Williams C Approaches to control Yersinia pseudotuberculosis in European zoos In Proc European Assoc Zoo and Wildl Vet 2004 p 1925