Managing Zoonoses & Cross-Species Diseases

Question 1

Describe some of the problems that can arise from mixed species exhibits.

What is the most frequent concern with these exhibit types? How can it be addressed?

What nutritional issues may arise?

What diseases are a concern for transmission across species in mammals?

Discuss considerations for malignant catarrhal fever and equine herpesvirus - what considerations should be made for those diseases?

What diseases are a concern for transmission across primates?

What diseases are a concern for transmission across marine mammals?

Birds?

Herps?

Transmission of what parasitic diseases is a concern in mixed species exhibits?

Answer 1

Fowler 7 Ch 4 - Veterinary Challenges of Mixed Species Exhibits

• Larger exhibit size is essential
• Main advantage of mixed species exhibits is behavioral enrichment and educational value
• Veterinary problems arising because of keeping different species together are characterized as: trauma, nutrition-related problems, infectious diseases, parasitic diseases.

TRAUMA

• most serious and frequent cause of health problems
• Competition for nesting sites, establishment of territories, competition for food/water
• Prevention via: large exhibit size, creeps (pole gates) where small animals can flee from larger animals, large obstacles for animals to circle when being chased, hidings places, multiple feed/water stations.

NUTRITION RELATED PROBLEMS

• Need sufficient feeding stations, spread food over large area, feed multiple times per day
• Species specific deficiencies or toxicities should be considered when formulating diets
  
  • Ex: copper deficiency in blesbok/sable antelope, vit. E toxicity in pelicans, iron storage disease in birds/primates.

INFECTIOUS DISEASES

Mammals

Risks in mixed species exhibits include: MCF, equine herpesvirus 1, lepto, brucellosis, IBR, BVD, Tb, paraTb, leucosis, neosporosis, BRSV, CWD, EMC, cowpox, parapoxvirus, monkeypox, rota and corona viruses

Malignant Catarrhal Fever (MCF) - gamma herpesvirus hosted by wildebeest, hartebeest, sheep, goats and is shed around parturition.

• Infects other species (giraffe, musk ox, bison, moose, kudu, deer, banteg, etc)
• Don’t combine wildebeest and giraffe.
• Ideal to rid all sheep and goats (carriers) if possible.

Equine Herpesvirus 1- shed by infected horses, zebra, onager during resp. infection, parturition/abortion.

• Problems with Bactrian camel, llama, gazelle.
• Only use seronegative equids in mixed exhibits

Mixed exhibits with ruminants should monitor for: lepto, brucella, IBR, BVD, paratb, tb, leucosis, neosporosis, BRSV.

• Most of these diseases spread between different ruminant/mammalian species.

Primates

• Spider (Herpes tamarinus, H. saimiri) and squirrel (H. ateles) monkeys should not be housed with other primates as they may transmit herpes virus.
• Don’t mix Asian and African monkeys
  
  • macaques host Herpes simiae, simian varicella group (herpes fatal in patas monkeys and other African cercopithecines)
  • Simian hemorrhagic fever (SHF), simian immunodef. virus (SIV) will also spread.
  • Fecal pathogens (salmonella, campylobacter, shigella) should be monitored in mixed primate exhibits

Marine mammals

• Morbillivirus, Orthopoxvirus, Parapoxvirus infections may occur when water systems are connected between basins.

Birds

• herpes viruses (e.g., Pacheco disease) carried by conures, avipoxvirus variety of avian susceptible

Herptiles

• tortoises carry herpesvirus that can spread to different species and marine turtles carry herpes viruses (fibropapillomatosis),
• ophidian paramyxovirus may be transmitted between snakes (viperids may infect other species)
• chytrid (Batrachochtrium dentrobatidis) risk can increase in mixed species exhibits (frogs, toads, salamanders susceptible)
• adenovirus spread among lizards, snakes, and crocodiles prevented via in-house biosecurity

Broad interspecies diseases

• WNV, Salmonella, Yersinia, C. psittaci, fungi (trichophyton, microsporim, asper, histo, crypto, candida), mycobacteriosis, various bacteria, almost all reportable/notifiable diseases.

PARASITIC DISEASES

• Protozoa easily contaminate substrate –
  
  • Balantidium coli from cercopithecine (baboon, macaque) monkeys to great apes can cause severe illness
• Toxoplasmosis (spread by felids), trichomoniasis (columbiformes to passerines/psittacines become ill), malaria (plasmodium in puffins/penguins), neosporosis (abortion in herbivores)
• endoparasites – nematodes, trematodes, cestodes
  
  • Don’t mix horses and donkeys (lung worms)
• ectoparasites – Sarcoptes, Chorioptes

TOOLS FOR VETERINARIANS:

• knowledge, training, and resources
• diagnostics
• vaccination
• quarantine and pre-transport measures
• parasite control, pathology, and necropsy programs
• biosecurity measures (foot baths, PPE, etc

Question 2

How has the globalization of human civilization affected emerging disease?

What proportion of human pathogens are zoonotic?

Where did HIV come from?

How has growing agriculture become more susceptible to disease outbreaks?

Answer 2

Introduction – General info on Globalization and the interactions with humans, animals and wildlife

• Of 1407 human pathogens, 58% are known to be Zoonotic
• HIV 1 thought to have come from chimpanzees
• HIV 2 from sooty mangabeys (Cercocebus atys)
• International trade is thought to play an important role in transmission of Batrachochytrium dendrobatidis (Chydtidiomycosis).
• Increasingly, diseases are moving amoung people, domestic animals, and wildlife
  
  • Concerns about food safety, public health, and wildlife conservation
• Wildlife species under severe environmental pressure threatened by extinction from spread of novel pathogens
  
  • Chytridiomycosis (Batrachochytriu dendrobatidis) in amphibians
    
    • International trade thought to play a key role in worldlwide dissemination of the disease
• Livestock production and market access to animal protein increasingly threatened by emerging disease
  
  • 2003-UN Food and Agricultural Organization reported 1/3 global meat trade subject to embargoes from disease outbreaks
• Increase in infectious diseases may be linked to anthropogenic pressures of an urbanizing world
• Global movement of people, animals, and their products has profound effects on wildlife, livestock, and public health
• Critical driving forces of globalization:
  
  • Human population increases with intensified agriculture and global climate change
• Effect of Human Population Growth on Agricultural Practices
• By July 2005 the world had an estimated 6.5 billion human inhabitants
• About 95% of all population growth is occurring in the developing world and 5% in the developed world
• By 2050, it is estimated that the world population will increase by 2.6 billion
  
  • Challenge will to feed human populations with declining resources, including water and arable land
• Large-scale agriculture susceptible to outbreaks of disease
  
  • 1982-1984 HPAI in northeast US caused drop in markets by $349 million in a 6-month period
  • 1997-1998 Nipah virus outbreak in Malaysia caused economic impact of $350 to $400 million
  • 2001 FMD outbreak in England and Europe cost markets almost $30 billion
• Developing country livestock practices much different than biosecure facilities in US
  
  • Livestock often share space with people in and around the home
  • In Asia, domestic ducks and geese are given access to recently harvested rice paddies
    
    • Allows wild waterfowl and domestic species to mix and creates an environment conductive to cross-species spread of pathogens

Question 3

How has increased hunting and pet/wildlife trade increased disease transmission?

What are three important diseases that have been the result of increased contact with wildlife?

Answer 3

Hunting, Pets and Globalized Trade in Wildlife

• Bushmeat – the local hunting of wildlife
• Ecologic changes such as human pop density, forest frag due to roads, rural development as well as increased human movement, and the globalized trade of animls alter the relationship of pathogens to hosts;
• Hunting, Pets, and Globalized Trade in WIdlife
  
  • Local hunting of wildlife or bush meat
    
    • Risk of cross-species disease has historically been mitigated through cultural practices
    • Ecologic changes have altered the relationships of pathogens to hosts
      
      • Greater human-patholgen contact
  • World Trade Organization statistics – in 2004 the global merchandise trade rose by 21%
  • Each year approx. 350 million live plants and wild animals are shipped globally
    
    • Poorly regulated wildlife component of global trade facilitates infections via microbial travel

Monkeypox, SARS, Ebola

Question 4

Describe the monkeypox outbreak that occurred in 2003.

Where is this virus endemic to?

How did it get to the US?

What rodents in the US did it affect?

What was the result of that outbreak?

Answer 4

• Monkeypox
  
  • From western and central Africa
  • June 2003 – febrile rash in people from WI, IL, Indiana – total 71 human illnesses, nonfatal from 6 states
  • People had contact with ill prairie dogs that had been held with recent shipment of African rodents that had been shipped from Ghana for the pet trade
  • Now there are restrictions on US importation of African rodents
• Monkeypox
  
  • Viral, smallpox-like disease from central and western Africa
  • 2003- human cases in Wisconsin Illinois and Indiana from prairie dogs (Cynonys ludovicianus)
    
    • Prarie dogs had been held with African rodents shipped from Ghana to the US for the pet trade
      
      • 2 rope squirrels (Funisciurus), 1 Gambian rat (Cricetomys), and 3 dormice (Dryomys) infected with Monkeypox
    • Prior to this, there were no regulatory controls for nonendangered rodents from Africa shipped to the US for pet trade
      
      • Subsequently, restrictions were placed on US importation of African rodents

Question 5

What were the clinical signs associated with SARS?

What is the natural host for that coronavirus? (What else are they hosts for?)

What was the first cross species transmission? What other species were observed to be infected?

Answer 5

• Severe Acute Respiratory Syndrome (SARS)
  
  • 1^st seen in China 2002
  • High fever, resp illness 🡪 pneumonia, diarrhea, death
  • Spread to 25 countries via infected people
  • Coronavirus
  • Palm civet was an artificial market induced host or amplification host
  • Disease also found in raccoon dogs and ferret badgers
  • Horseshoe bats species are the natural reservoir for closely related SARS-like coronaviruses
    
    • Note: bats are also reservoir hosts for Lyssa, Nipah, Hendra and Ebola viruses
• SARS
  
  • 2002- first recognized as an emerging human disease in Guangdong Province, China
  • Spread to Hong Kong, then across 5 continents and 25 countries via infected people
  • April 2003- a new coronavirus discovered to be the causative agent
  • July, 2003- WHO listed probable SARS human cases at 8437, with 813 deaths
  • Evidence of viral infection in palm civets (Paguma), let to cull of more than 10,000 animals
  • Later viral evidence also detected in raccoon dogs (Nyctereutes), ferret badgers (Melogale), and domestic cats
  • Later determined that palm civet was amplification host, and three species of horshoe bat (Rhinolophus) were actually natural reservoir host for the closely related SARS-like coronavirus
  • Bats have also been found to be reservoir hosts for Lyssa, Nipha, Hendra, and Ebola viruses

Question 6

Outbreaks of Ebola hemorrhagic fever have affected what wild species?

What is the natural reservoir?

What are the clinical signs in people?

What are the various strains? Which is the most severe? Which is the least severe?

Answer 6

• Ebola
  
  • Ebola hemorrhagic fever
  • Outbreaks in Africa in 2000 and 2004 where hunters were infected after handling dead animals – gorilla, chimp, duiker. Then spread quickly btwn people
  • First seen in Dem Repub Congo – primarily found in western-central Africa
  • Case fatality 50% (Sudan subtype) -90% (Zaire subtype)
  • Linked to declines in western equatorial African great ape populations – it is believed that Ebola rivals hunting as the major threat to ape populations
  • Other forest animals (ex/ duiker) also affected.
  • Fruit bats, 3 spp, confirmed as reservoirs (Nature article)
  • Ebola Reston does not cause human disease (found in cynomolgus monkey imported from Phillipines into Reston Virginia for biomedical research)
• Ebola Hemorrhagic Fever
  
  • Named after the river in the Democratic Republic of Congo
  • Bush meat poses high risk of cross-species contamination
    
    • Chimpanzees and humans share 98% of their DNA
    • Gorillas and humans share 97% of their DNA
  • First three known Ebola outbreaks occurred btwn 1976 and 1979 in DRC and Sudan
  • Five human Ebola outbreaks documented btwn 2000 and 2004 in western central Africa
    
    • Index cases mainly hunters
    • All cases were infected while handling dead animals, including gorilla, chimps, and duiker
    • Outbreaks quickly spread among people, especially caregivers and almost wiped out entire villages
  • Symptoms in people: effects multiple organs, with internal and external hemorrhaging
    
    • Zaire subtype has case-fatality rate of almost 90%
    • Sudan subtype has case-fatality rate of approximately 50%
  • Linked to declines in western equatorial Africa great ape populations
  • Evidence that other forest animals, such as duikers, are also affected
  • Believed that Ebola rivals hunting as major threat to ape population
  • Three species of fruit bat recently confirmed as reservoir hosts
  • Ebola Reston- strain of disease found in imported cynomolgus monkeys from the Philippines for research in Reston, VA 1989

Question 7

Transmissible spongiform encephalopathies are caused by what etiologic agents?

Give some examples of disease?

What was the suspected cause of the BSE outbreak in cattle in the UK?

Answer 7

• Transmissible Spongiform Encephalopathy
  
  • CWD of cervids, Scrapie sheep, BSE of cattle, Creutzfeldt-Jakob disease (CJD) of people
  • Prions – devoid of nucleic acid, composed of modified isoform of a normal prior protein
    
    • Resistant to inactivation by UV, radiation, steam sterilization, disinfection
  • BSE may have emerged from feeding scrapie infected sheep meat to cattle
  • variant CJD may be due to ingestion of prion infected cattle meat
  • 13 spp of zoo animals incl bovidae and felidae have died from BSE
  • CWD
    
    • 1^st seen in research mule deer in Colorado, 1967
    • Now in free-range and captive herds in multiple places in N. America
    • No evidence yet of “natural” transmission to humans, but conversion of human prion by CWD prion has been demonstrated in an in-vitro cell-free experiment
• Transmissible Spongiform Encephalopathies
  
  • TSEs include:
    
    • Chronic wasting disease of cervids
    • Scrapie of sheep
    • BSE of cattle
    • Creutzfeldt-Jacob disease of humans
  • Caused by pathogenic prions
    
    • Particles devoid of a nucleic acid genome and composed of a modified isoform of normal prion protein
    • Extremely resistant to inactivation by UV light, ionizing radiation, steam sterilization, and almost all disinfection
  • High-volume food production needs caused feeding ruminant protein to cattle, possibly from scrapie-infected sheep
    
    • Believed to be the cause of BSE outbreak in the UK, which spread to Europe, Canada, and the US
  • Likely that ingestion of prion-infected meat from cattle caused variant Creutzfeldt-Jacob disease in humans – 1996
  • 13 species of zoo animals, including Bovidae and Felidae, have died due to BSE infection
  • Chronic wasting disease (CWD) is a prion disease of wild and farmed cervids in North America
    
    • First recognized in a research her of mule deer (Odocoileus hemionus) in Colorado in 1967
    • Since then has been diagnosed in multiple states and regions in both captive and free-ranging cervids

To date, there is no evidence for CWD transmission to humans

Question 8

The avian influenza outbreak was caused by what strain of influenza?

What other species have been affected?

How many different hemagglutinin and neurominidase glycoprotein combinations are there?

Which ones result in highly pathogenic influenza?

What conditions are needed for influenza to be passed from birds to people?

How can pandemic influenza originate?

Answer 8

Avian Influenza

• Type A strain.
• Virus is subtyped based on hemagglutinin (H or HA; 16 total) and neuraminidase (N or NA; 9 total) glycoproteins
• Wildbirds – ducks, geese, shorebirds are the reservoirs for low pathogenic strains (= No disease in these species)
• Subtypes with H5 and H7 have become highly pathogenic in poultry, primarily commercially raised
  
  • Have been detected in mammals, including humans
  • H5N1 influenza A detected in birds, pigs, cats, leopards, tigers, people
• Live bird markets and traditional poultry livestock practices will bring people and domestic fowl together – mixing and spread of flu
• Undetermined if migratory wildfowl are effective carriers or rapidly succumb
  
  • 2005 – H5N1 isolated from migratory waterfowl on Quinghai Lake, China and a whooper swan in Mongolia
• A global pandemic of avian influenza is an important threat to global economy
  
  • Concern that H5N1 will gain ability to spread among people
• Avian Influenza
  
  • Caused by type A strains of the influenza virus
    
    • Subtyped by antigenic properties of hemagglutinin (HA, or H) and neurominidase (NA, or N) glycoproteins
      
      • 16 HA and 9 NA subtypes identified
      • H5 and H7 subtypes have become highly pathogenic (HPAI) in poultry
        
        • Isolated mostly from commercially raised chickens, turkeys, quail, guinea fowl, and ostrich
        • Also detected in mammals, including humans
          
          • H5N1 influenza A viruses detected in birds, pigs, cats, leopards, tigers, and people in Asia
  • Wild birds (ducks, geese, and shore birds) are reservoir species for LPAI in nature
    
    • Does not usually cause illness in these species
  • Live bird markets provide conditions for genetic mixing and spread of flu viruses
    
    • May have caused the H5N1 avian flu outbreak in Hong Kong in 1997 and 2003-2004 throughout Asia
  • 2005- H5N1 HPAI isolated from migratory waterfowl in Quinghai Lake, China
  • Global trade and illegal shipments of domestic and wild birds a great concern
    
    • 2004-illegally imported crested-hawk eagles (Spizaetus nipalensis) into Brussels tested positive for H5N1 HPAI
  • Fear that H5N1 will gain ability to spread effectively among people, causing a global pandemic
    
    • In the 20^th centrury there have been 3 global pandemics thought to have originated from birds
      
      • 1918 Spanish influenza pandemic virus H1N1 was the most severe, caused 20 to 50 million deaths worldwide
    • Pandemic influenza may originate from two mechanisms
      
      • Reassortment between an animal virus and a human virus to create a new strain of virus
      • Direct spead and adaptation of a virus from animals to humans

Question 9

List four important parasitic vector borne diseases.

List 5 important vector spread arboviruses and their families.

What is the etiologic agent of lyme disease? How is it transmitted? What is teh reservoir host?

Describe the spread of the west nile outbreak in the US. What are the typical clinical signs?

What is the most common vector-borne disease of people? What are teh associated clinical signs? How is it transmitted?

Answer 9

• Arthropod Vector-Borne Diseases
  
  • Parasitic organisms spread by vectors include:
    
    • Malaria (Plasmodium)
    • Chagas’ disease (Trypanosoma cruzi)
    • Lyme disease (Borrelia burdorferi)
    • Leishmaniasis (Leishmania)
  • Vector-spread arboviruses
    
    • Flavivirida family – St. Louis encephalitis, dengue fever, yellow fever, WNV
    • Bunyaviridae family – La Crosse virus
    • Togavirida family – eastern, western, and Venezuelan equine encephalitis
• Lyme Disease
  
  • Transmitted primarily by the deer tick, Ixodes scapularis
  • Most common vector-borne disease of people in US
  • Rodent is reservoir host
    
    • White footed mice (Peromyscus leucopus) in eastern North America
    • Apodemus mice in Eurasia
  • Dilution effect model suggest loss of diversity of vertebrate reservoir hosts may increase spread of Lyme disease
• West Nile Virus
  
  • First isolated from blood of a febrile woman in West Nile district of Uganda in 1937
  • Thereafter, isolated from ill people, birds, and mosquitoes during early 1950s
  • Most widespread of the flaviiviruses- geographic distribution in Africa and Eurasia
  • 1999 – entered Western Hemispherre in New York, has spread across North American and into tropics and Caribbean
  • Bird-feeding species of mosquito are the principle vectors, but has been isolated from other species and in ticks
  • Typical illness – encephalitis and fever
• Dengue Fever
  
  • Genus Flavivirus- one of four closely related serotypes
  • Most common vector-borne disease of humans
  • Humans- syptoms range from mild flu-like illness to immune-mediated hemorrhagic fever that may cause death
  • Transmitted between people or between monkeys through mosquitoes of genus Aedes
  • Endemic in approx. 100 countries in southeast Asia, Africa, the western Pacific, the Americas, and eastern Mediterranian
  • Multifactoral cause for global emergence include ineffective mosquito control, urbanization, travel, and climate change

Question 10

What are two important rodent-borne zoonotic diseases?

What species are commonly affected by Leptospirosis in urban settings? What are the typical lesions and clincal signs? When do outbreaks occur?

What are the clinical signs associated with Hantavirus? When and where do outbreaks occur?

Answer 10

Rodent-Borne Diseases

• Leptospirosis
  
  • Reemerging zoonotic disease of global importance
  • Affects domestic and alternative livestock, free-ranging and captive wild mammals, including marine mammals
  • Rodents and dogs are important vectors in urban and agricultural settings
    
    • Transmission most often water contaminated by urine from infected shedders
  • Caused by a filamentous spiral bacterium that has predilection for renal tubules
    
    • Humans- can cause pulmonary hemorrhage, renal failure and jaundice
    • Animals-may appear clinically normal or may have renal and reproductive tract infectection
  • Human outbreaks often associated with increases in rodent populations after heavy rainfall or floods
• Hantavirus
  
  • Zoonotic virus of rodents
  • Genus Hantavirus – causes two major clinical syndromes in people
    
    • Asia and Europe – hemorrhagic fever with renal syndrome
    • Americas – pulmonary syndrome
  • Outbreaks of disease may be associated with weather that promotes rapid increase in rodent populations
    
    • Outbreak in Arizona, New Mexico, Colorado, and Utah regions following El Nino in 1992-1993

Question 11

What is the taxonomy of encaphalomyocarditis virus?

What species have been infected? What species is the most commonly infected?

How is this disease transmitted?

What are the natural hosts?

Describe the pathogenesis of this disease.

How is this diagnosed?

How is this disease controlled?

What are the signs associated with human infection?

Answer 11

Fowler 6 Ch 9 - Encephalomyocarditis virus

ETIOLOGY

• Picornavirus🡪Cardiovirus🡪encephalomyocarditis virus
• Non-enveloped, single stranded RNA virus
• Other cardiovirus
  
  • Columbia SK
  • Mengo virus
  • MM virus

EPIDEMIOLOGY

• Worldwide
• Mammals: humans too
  
  • Suidae
• Pigs are the most commonly and severely infected domestic* animals,
  
  • Proboscidae
  • Pongidae
  • Cercopithecidae
  • Antelopidae
  • Camelidae
  • Tapiridae
  • Lemuridae
  • Cebidae
  • Rodentia
  • Marsupiala
• Free ranging and captive wildlife
• Transmission
  
  • Feco oral
  • Rodent vector - rats
    
    • Shed in feces
• • Outbreaks: states bordering the Gulf of Mexico (unknown why this geography)
    * ??vector species, density, durability (temperature), humidity, other??
    
    • No seasonality

PATHOGENESIS

• Replicative cycle of virus is rapid (8hrs to complete)
• Thought to replicate like enterovirus: attach to cell surface, replicate in pharynx/GI, go to lymph nodes and reticuloendothelial organs
• 2 outcomes: host controls infection or major viremia
• Target tissue: heart (fast->replication->myocardial cell death->failure to conduct->heart failure-> death

DIAGNOSIS

Antemortem

• Death without premonitory signs
• SN titers (can be naturally acquired)

Postmortem

• Gross lesions
  
  • Confined to CV system: myocardium has pale streaks, petechiae on epicardial surface
  • Pulmonary system: congestion (marked fluid accumulation); blood tinged foam in trachea
• Histology
  
  • Confined to CV system: lymphocytic plasmacytic nectrotizing myocarditis
  • Encephalitis in rodents and a bonobo
• Viral Isolation-easy

PREVENTION

• Cornerstone: rodent control; hygienic feeding practices (don’t allow sharing with rodents)
• Survives in moist soil 13 mo
  
  • Remove soil from enclosure
  • Hygiene hygiene hygiene
• Vaccination
  
  • NOT AVAILABLE
• Determine baseline SN titer

ZOONOTIC POTENTIAL

• Human infection is common
  
  • 50% in some countries
  • Most asymptomatic
  • EMCV infection in humans have been associated with fever, neck stiffness, lethargy, delirium, headaches, and vomiting
  • pig-to-human concern from xenotransplantation
• Lethal infections documented in great apes

Question 12

What is larval migrans?

What types of syndromes occur due to Baylisascaris?

Which Baylisascaris species occurs in the following species: racoons, skunks, badgers, martens/fishers, bears, giant pandas, dasyurids, ground squirrels?

How is this disease transmitted?

What species have been affected by larval migrans?

Answer 12

Fowler 6 Ch 34 – Baylisascaris neural larval migrans in zoo animals

Larval migrans – migration of helminth larvae in organs and tissues of humans and animals – normal in intermediate hosts. Causes extensive tissue damage and inflammation in incidental hosts

Syndromes due to Baylisascaris:

• Visceral larval migrans
• Ocular larval migrans
• Neural larval migrans (NLM)– seen most often in zoos
• Cerebral nematodiasis – fatal or severe neurologic disease

Etiology and Epidemiology

• Ascarid nematodes, primarily in carnivores
• Species
  
  • B. procyonis – raccoons
  • B. columnaris – skunks
  • B. melis – badgers
  • B. devosi – martens and fishers
  • B. transfuga – bears
  • B. schroederi – giant pandas
  • B. tasmaniensis – Tasmanian devils, quolls
  • B. laevis – marmots and ground squirrels
• Transmission – ingestion of larvae in small mammal intermediate host or direct infection by ingestion of eggs. Larvae encapsulated in internal organs / tissues, persist for later transmission to an animal which eats the intermediate host
• Ascarid eggs
  
  • are extremely resistant, long lived (years) in environ. Can survive winter
  • Takes 11-14 days for B. procyonis eggs to become infective (L2) under ideal conditions. Usually takes weeks to months under normal conditions
  • Extreme heat and dry can kill eggs by dessication
• Young raccoon infected by ingesting eggs. Older raccoons infected from L3 in intermed hosts
• B. procyonis and B. melis are most pathogenic followed by B. columnaris in terms of neural larval migrans
• Zoo animals infected by contaminated food, bedding, enclosures with raccoons or skunk feces
• B. procyonis is mostly in Midwest, NE and along west coast, but IS found in south
• B. procyonis has been recovered from 2 kinkajou (procyonid)
• Domestic dogs may serve as adult or intermediate hosts
• >90 species have been infected with larval migrans
  
  • rodents, rabbits, primates, birds are most often infected. Cases seen in carnivores
  • No cases in zoo Hoofstock or livestock
  • Cats and raptors appear resistant
• Don’t assume that it is due to B. procyonis, could be from skunks or (less often) badgers

Question 13

What are the clinical signs associated with Baylisascaris?

How is this disease diagnosed?

What are the lesions seen at necropsy?

What are some important differentials?

How is this disease treated? How does it vary for definitive and intermediate hosts?

What are the most effective means for removing eggs from the environment?

Answer 13

Clinical signs

• If migrating larvae leave the brain or become encapsulated and stop migrating – clinical signs may stabilize. Waxing and waning is possible
• Depression, lethargy, rough coat / ruffled feathers
• Tremors, head tilt, circling, ataxia, leaning, falling, opisthotonos, recumbency, stargazing, blindness, nystagmus, weakness, paresis, rigidity, paddling, coma, death

Diagnosis and Clinical pathology

• Seeing ascarids in small intestine at Nx
• Seeing ascarids passed in feces
• Eggs in feces
• NLM is a disease of exclusion. No serologic tests
• CSF eosinophilic pleocytosis, peripheral eosinophilia, brain lesions on MRI or CT
• DDx: rabies, toxo, sarcocystis, amebiasis, fungal, bacterial, viral encephalitis, pesticides, trauma, metabolic causes, neoplasia
• Histopath: brain lesions of diffuse meningoencephalitis, necrosis, spongiosis by eosinophilic and granulomatous inflammation
• Larvae may be seen microscopically
• Larval isolation from brain done with brain squash, artificial digestion, Baermann

Treatment

• Definitive hosts treated with common anthelmintics. Ex. pyrantel, fenbendazole, ivermectin
• Intermediate hosts should only be treated with albendazole and diethylcarbamazine which cross the blood brain barrier
• Once CNS dz is pronounced, treatment will not be effective in reversing NLM
  
  • Tx before the larvae migrate to the CNS is preferable
• Supportive care and steroids to decrease inflammation
• If can’t not id source of infection and can not rid premises of infection, could consider continual pyrantel in feed (experimentally stopped infection in mice)

Prevention

• Prevent the free living species that carry it from access to exhibit, holding, feed, utensils
• General control measures:
  
  • Prevent access to food
  • Discourage digging, block areas under stairways / porches
  • Prune trees
  • Sheet metal barriers to prevent climbing
  • Small mesh size to prevent juveniles from entering exhibit
  • Clean up feces before becomes infective
• Never do mixed species exhibit with the species that normally carry Baylisascaris
• If have open access to free living wild animals, then do a trap and treat or trap and euthanize program
• Contaminated areas
  
  • Small areas treated with 1:1 xylene and ethanol
  • 20% bleach will make eggs non adherent so they can be washed away, but won’t kill
  • Heat (boiling water, autoclave, steam) is recommended to kill eggs **
    
    • Direct flame from propane gun is most effective
  • Surface soil – flamed, broken up, turned over several times with reflaming each time
    
    • Or remove / discard top several inches of soil

Zoonotic

• Young children primarily, but also adults
• The prevalence of asymptomatic infection in humans is not determined
• It is best for zoo personnel to wear disposable coveralls, rubber gloves, washable rubber boats and face mask to prevent inhalation or ingestion of any eggs

Conclusion

• Bayliscascaris infections are probably more common than currently recognized
• Naturalistic exhibits may pose a challenge, vermin feces difficult to see in highly planted
• If disease is suspected, do thorough brain exam at necropsy
• Contaminated skunks and raccoons must be excluded from environment of captive animals

Question 14

What is the taxonomy of cowpox? What other viruses are in this genus?

Where is this disease endemic?

What zoo species is most commonly affected? What is the second most commonly affected group?

What are some potential sources of exposure?

Describe the pathogenesis of this disease.

Mortality is high in which group?

How is this disease diagnosed? What inclusion bodies are present?

Vaccines have been used in which species?

What treatments should be employed? Which should be avoided?

Is this disease zoonotic?

Answer 14

Fowler 7 Ch 5 - Cowpox in Zoo Animals

CAUSE:

• Cowpox Virus (CPXV) = genus Orthopoxvirus, family Poxviridae (an enveloped virus)
  
  • also known as elephantpox, catpox, or ratpox – depending on affected species
• Other members of the orthopoxvirus family:
  
  • monkeypox, vaccinia, camelpox, raccoon pox, skunk pox, vole pox

HISTORY:

• 1960 infection of 2 captive Asian elephants in German zoo, originally thought to be vaccinia virus (VACV) transmitted from recently vaccinated kids (with smallpox vaccine) but later retrospectively characterized as CPXV.

EPIDEMIOLOGY:

• Endemic in Europe and western Russia and naturally infects a broad range of hosts:
  
  • domestic animals, zoo animals, humans.
• Cowpox is NOT enzootic in cattle, cattle are incidental hosts of CPXV.
  
  • elephants are the most frequently infected exotic animal
  • exotic felids are the second most affected group (UK, Europe, Russia)
• Exotic zoo animals that are housed in close proximity to other zoo animals and come in direct contact with wild rodents and animal keepers are at higher risk.
• Despite the wide host range of CPXV, only few infections of different species have been reported to be cause by the same CPXV strains.
• Wild rats and white rats bred as food for carnivores are most likely source of transmission of CPXV to exotic animals. Rats could either be a primary reservoir or an amplifying host.
  
  • mice have never been found to be CPXV (+) but are still speculated to be a main reservoir/source of infection.

PATHOGENESIS:

• Localized/multiple lesions on skin and mucous membranes.
  
  • Less often, pulmonary symptoms without skin lesions or from a generalized rash.
• CPXV infections are epitheliotropic, starting as vesicular lesions and developing into pustule with indented center and raised erythematous border.
• CPXV infections result in eosinophilic A-type cytoplasmic inclusion bodies.
• Mortality among exotic animals/felids is high.

DIAGNOSIS:

• Swab or biopsy samples can confirm cowpox virus infection.
  
  • histo examination of biopsy tissues for inclusions, EM for detection of poxvirus particles, or PCR assay to detect OPV DNA.
• After the onset of clinical signs poxvirus antibodies can be detected on ELISA, immunoflourescence assay, or plaque reduction test.
  
  • detected Ab is not cowpox specific but can indicate an OPV infection.

TREATMENT AND VACCINATION:

• Prophylactic vaccination might protect susceptible species, as no treatment has been approved.
  
  • Elephants have been routinely vaccinated with attenuated modified vacinnia Ankara (MVA) strain of vaccinia virus resulting in prolonged immune response.
  • Vaccines have not been widely used in other species.
• The early establishment of a significant OPV-specific antibody titer during a cowpox outbreak seems crucial for survival.
• In a study without CPXV challenge, a significant increase in antibody titer was achieved in all vaccinated felids (cheetah, jaguar, tiger, snow leopard, serval) and red panda.
• Treat secondary bacterial infections with broad-spectrum antibiotics and avoid glucocorticoid therapy as this will result in a significantly higher viremia and mortality.
• Animals known to be susceptible to CPXV that reveal signs of infection should be immediately quarantined and observed closely for minimum weeks.
  
  • Impossible to segregate zoo animals permanently from wild rodents that can move freely around the zoo enclosures and transmit CPXV.

ZOONOTIC POTENTIAL

• Infections of humans have become more numerous during the last decade, perhaps due to inadequate immune status of the population after ridding smallpox vaccinations in 1980s.
  
  • In humans, CPXV infections remain localized and are self-limiting, but can be fatal in immunocompromised patients.

Question 15

Describe a 7 point plan for managing a zoonotic disease outbreak.

Answer 15

Fowler 7 Ch 7 - Guidelines for the Management of Zoonotic Diseases

• Zoonotic disease- any infectious disease that may be readily transmitted between animals and humans
• Steps in managing a Zoonotic case
  
  • Trigger—zoonotic disease identified
    
    • Test result, postmortem examination (confirmed or suspected), less often employee, volunteer, or guest who is diagnosed with an infectious disease may have been acquired from contact with animals in collection
  • Notifications
    
    • Critical that employees are informed- will take proper precautions and report signs and symptoms of disease
    • Written disease fact sheet is helpful- many good ones online
  • Animal isolation
    
    • Veterinary and animal care staff- determine whether appropriate to isolate infected animal and/or facility in which it is located
    • Quick risk assessment performed based on severity and contagiousness of disease be balanced against feasibility of performing isolation safely and effectively
    • Separate tools and equipment should be used; footbath may be helpful to reduce spread of contamination and remind workers of isolation entry control point
    • Importance of proper hygiene (hand washing) and use of appropriate personal protective equipment
  • Waste management- especially bedding, follow regional reg on biomedical waste, use appropriate disinfection
  • Regulatory reporting- if required based on region and disease
  • Medical management- if indicated, treat animal with appropriate antimicrobials and perform follow-up diagnostics as appropriate
  • Establish criteria for case resolution and endpoint for patient and facility isolation (e.g., test negative and/or clinically normal)

Question 16

What are the responsibilities of the veterinarian in preventing zoonotic disease?

How can exhibit design prevent transmission?

What sort of signage needs to be present?

What type of hand-washing or hand sanitizer

Answer 16

Responsibilities of the Zoo Veterinarian

• Disease prevention and treatment in animal, if reportable, education of staff, exhibit and hand-washing station design, signage development

Zoonotic Disease Transmission and Prevention

• Zoonotic organisms may
  
  • Only be shed intermittently
  • Not be easily detected in the animal
  • Not be cleared in the animal
• Prevention of Transmission
  
  • Staff/Volunteer education
  • Exhibit design
    
    • Exhibits placed away from food stations
    • Appropriate drainage systems
    • One-way traffic flow
  • Signage
    
    • Hand hygiene education = most important factor in preventing dz transmission (Aiello, et al. 2008. Am J Publ Health 98)
  • Design of hand-washing stations
    
    • Non-antibacterial soap more effective than antibacterial (Aiello)
    • Benzylalkonium chloride-based hand sanitizers more protective than alcohol based sanitizers to prevent respiratory dz (Aiello)

Question 17

Discuss the challenges in managing enteric bacterial zoonoses from ruminants.

What type of bacteria is E coli? What is the strain of concern? Is this normal flora? When is shedding the highest?

Salmonella causes what signs in ruminants? Describe latent and passive carriers?

What campylobacter species affect ruminants?

Answer 17

Ruminants

Bacterial Dz:

Ruminant Zoonoses

• Enteric Bacterial Dz
  
  • Usually asymptomatic carriers, shed intermittently, contaminate environment
  • Fecal culturing may reduce risk
  • Antimicrobial tx ineffective – won’t eliminate infection, prevent shedding or protect against reinfection; may prolong shedding and increase antimicrobial resistance
  • Escherichia coli O157:H7
    
    • Gram neg, motile or non-motile, facultative anaerobe; Enterobacter family
    • Usually food borne pathogen, but reported from petting zoos
    • Normal ruminant GI flora – No clinical signs!
    • Shedding higher in summer (May – Nov)
    • Stress – increased shedding, transient colonization
    • Fecal-oral transmission
  • Salmonella
    
    • Gram negative, motile, facultative anaerobe, Enterobacter family
    • Asymptomatic (adults) to diarrhea (usually neonates)
    • Abortion in sheep & goats
    • Not a major prob in New world camelids
    • Latent carriers – bacteria lodge in LN and tonsils so organism not shed in the feces
    • Passive carriers – intermittent fecal shedding
    • Dx: fecal culture – may not detect passive or latent carriers
    • Fecal-oral transmission
  • Campylobacter
    
    • C. jejuni and C. fetus
    • Curved, non-spore forming, gram neg
    • C. jejuni – asymptomatic
      
      • Dx: fecal culture
    • C. fetus – most common cause abortion in sheep
      
      • Late-term abortion, stillbirth, weak lambs
      • Ewes become immune after OR persistently infected
    • Transmission – fecal-oral or handling aborted fetuses

Question 18

List 6 non-enteric zoonotic bacteria that ruminants may carry.

What are the mycobacteria of concern? What nonruminant groups are highly susceptible? Intradermal skin testing is approved for which groups? How is this transmitted?

What is the etiologic agent of Q fever? What are the clinical signs? How is it diagnosed? How is it transmitted? Risk is highest in what settings?

What are the clinical signs, diagnosis and transmission of Leptospirosis, Listeria, Brucella, and Chlamydophila in ruminants?

Answer 18

Non-enteric Bacteria of Zoonotic Concern in Ruminants

• Less concerning / common than enteric dzs
• Tuberculosis
  
  • M. tuberculosis complex – M. tuberculosis most common cause of animal-origin human TB
  • New world camelids highly susceptible
  • Intradermal skin test USDA approved for cattle, bison, goats and captive cervids
  • Transmission via aerosol, ingestion, contamination scrapes
  • Viable in feces or carcasses for months
• Q Fever
  
  • Coxiella burnetii – Gram neg coccobacillus
  • Asymptomatic carriers to mild fever, abortion
  • Dx: serology, placental findings, organism isolation
  • Transmission via inhalation, contact w/ contaminated fluids, handling infected animals
  • Mostly problematic for institutions with indoor birthing exhibits
• Other Nonenteric Bacteria
  
  • Low risk of transmission
  • Leptospira interrogans
    
    • Asymptomatic to abortions, sepsis w/ hemolysis
    • Dx: spirochetes on dark field microscopy of urine, plasma; serology;
    • Transmission: contact w/ urine (may be in water source), infected tissue
  • Listeria monocytogenes
    
    • Usu food-borne pathogen, but may be fecal-oral
    • Depression, anorexia progress to neurologic syndrome (facial, vestibular lesions)
    • No specific dx tests
    • Shed by sick, recovering, or normal animals in milk, feces for long time periods
  • Brucella spp
    
    • B. melitensis = goats, sheep
    • B. abortus = cattle
    • Problem in reindeer, but not really in NW camelids
    • Abortion; Also, mastitis, lameness, orchitis
    • Dx: serology
    • Transmission: contact w/ infected tissue, ingestion, inhalation
  • Chlamydophila psittaci
    
    • Sheep, goats, cattle
    • Abortion, pneumonia, keratoconjunctivitis, epididymitis, polyarthritis
    • Dx: culture, serology
    • Transmission: fecal-oral, contact w/ infected placenta,
      
      • Mammalian forms < zoonotic than avian strain

Question 19

What ruminant viruses are zoonotic? What are the typical clinical signs of these viruses? How are they transmitted?

What are the dermatophytes that affect ruminants?

What are two important zoonotic protozoa of ruminants? What are the typical clinical signs in these species?

Answer 19

Ruminant Zoonoses

Viral Dz:

• Rabies
  
  • Rarely exhibit aggressive form
  • Neuro signs, lameness or CHOKE
  • New world camelids not able to spit when infected (per Med/Sx of SA Camelids by Fowler)
  • Direct fluorescent Ab testing on brain
• Orf: Contagious Pustular Dermatitis, Sore Mouth , Contagious Ecthyma
  
  • Parapox
  • Sheep, goats, NW camelids, reindeer
  • Self-limiting, proliferative crusting lesions of mucocutaneous junctions
    
    • Esp mouth, nose; also feet, genitalia, teats
  • Dx: Histopath i.d. of virus in tissue
  • Environmentally hardy
  • Transmission to humans via direct contact w/ infected or recently vaccinated (non-attenuated live virus vaccine designed to create a controlled outbreak) animal

Fungal Dz:

• Dermatophytosis: Ringworm, Lumpy Wool, Club Lamb Fungus
  
  • Trichophyton verrucosum, T. gypseum, T. mentagrophytes, Microsporum canis
  • All ruminants and NW camelids
  • May be asymptomatic carriers or clinical
  • Transmission direct or indirect
    
    • Remains viable in crusts & hair in environment for years

Parasitic Dz:

• Cryptosporidiosis
  
  • Cryptosporidium parvum – protozoal parasite
  • Adults = asymptomatic; Juveniles = diarrhea
  • Dx: fecal exam
    
    • Intermittant shedding makes difficult to pick up
  • Transmission: fecal-oral
• • Esp 2-4 wk old lambs or kids w/ diarrhea
    
    • Self-limiting
    • Shed cysts for long periods
    • Dx: fecal
    • Fecal-oral transmission

Question 20

Rabbits in petting zoos can be a source of zoonoses.

What are two potential bacteria of concern, what clinical signs do they cause, and what is the transmission?

What are the dermatophytes that affect rabbits?

What protozoa can be transmitted to people?

What mite is a potential zoonotic concern?

Answer 20

Rabbit Zoonoses

Bacterial Dz:

• Pasteurella multocida
  
  • Grm neg, non-motile, coccobacillus
  • Snuffles
  • Dx: deep nasal culture, PCR, paired serology
  • Transmission: aerosol or fomites
• Salmonella
  
  • Not a common prob in rabbits
  • Causes high morbidity and mortality – rapidly fatal
  • Transmission: fecal-oral

Viral Dz:

• Rabies

Fungal Dz:

• Ringworm
  
  • Trichophyton mentagrophytes & Microsporum canis

Parasitic Dz:

• Encephalitozoon cuniculi
  
  • Intracellular protozoal parasite
  • CS depend on organ affected
  • Dx: Serology
  • Lives up to 1 month in environment
  • Transmission to people via contaminated urine
    
    • Shed intermittently
• • Cheyletiella parasitovorax – nonburrowing mite
    * Pruritus, flakes, oily dermatitis
    * Direct contact

Question 21

Rodents in zoos can pose several zoonotic risks.

What bacterial disease is most likely to be transmitted from contact rodents, particularly gerbils? What clinical signs occur in these animals?

What viral disease is an important zoonotic risk?

List three zoonotic protozoa.

Identify 8 zoonotic diseases in rodents.

Answer 21

Rodents: Mice, Rats, Hamsters, Gerbils

Bacterial Dz:

• Salmonella
  
  • Salmonella enteriditis and S. typhimurium most common
  • Very important in gerbils
  • Asymptomatic or anorexia, weight loss, enteritis, lymphadenopathy or sepsis
  • Fecal-oral transmission

Viral Dz:

• Lymphocytic choriomeningitis virus (arenavirus)
  
  • Rodent carriers
  • Rodents may be asymptomatic or show weight loss, tremors, convulsions or photophobia
  • Dx: serology
  • Transmission: exposure to feces, urine, bites
• Rabies

Fungal Dz:

• Rare
• Trichophyton and Microsporum spp.

Parasitic Dz:

• Cryptosporidium parvum
• Giardia spp
  
  • Hamster & gerbil
  • Asymptomatic or diarrhea
• Hymenolepiasis
  
  • Hymenolepis nana or H. diminuta
  • Asymptomatic carrier
  • Dx: fecal
  • Transmission: fecal-oral

Other Zoonotic Diseases:

• Minor significance
• Acinetobacter spp
• Dermatophytosis
• Streptobacillus moniliformis
• Spirillum minus = rat bite fever
• Streptococcus pneumonia
• Leptospira interrogans
• Hantavirus
• Yersinia pestis – plague
  
  • Not a problem in zoos, but is in wild rodents
• Allergic reactions to dander and urine

Question 22

What is the major bacterial zoonoses that can be acquired from Hedgehogs? What serotype? What are the clinical signs?

What are the dermatophytes that affect hedgehogs?

What zoonotic protozoa can hedgehogs carry?

Answer 22

Hedgehogs

Bacterial Dz:

• Salmonella serotype Tilene
  
  • CS: anorexia, diarrhea, weight loss or asymptomatic
  • Dx: fecal culture
  • Transmission: direct and indirect contact

Viral Dz:

Fungal Dz:

• Trichophyton mentagrophytes var. erinacei
• Microsporum spp.

Parasitic Dz:

• Cryptosporidiosis has been diagnosed, but zoonotic potential unknown

Question 23

There are several important zoonotic bacterial diseases that can be acquired from birds.

Chlamydophila psittaci is most common in what groups? What are teh most common clinical signs? How is it diagnosed? How is it transmitted?

What salmonella species are of concern from birds? What are the typical signs in birds? How is it transmitted?

Campylobacter produces what signs in birds? What groups have a higher incidence of shedding?

What avian species are particularly susceptible to Yersinia? What are the typical presenting signs?

How big of a zoonotic risk is Mycobacterium? And what species are common to birds?

Answer 23

Birds

Bacterial Dz:

• Chlamydophila psittaci
  
  • Obligate intracellular bacteria
  • Most common in psittacines; frequent in pigeons, canaries, finches
  • CS: mucopurulent ocular, nasal d/c; green urates; non-specific
  • May be asymptomatic shedders
  • Dx: culture, immunoflurescent detection of Ag, paired serology, i.d. of Chlamydiaceae in macrophages; Also ELISA, PCR, FAB on feces cloacal or ocular swabs
  • Transmission: inhalation dried feces, respiratory secretions, nose to beak contact, handling infected feathers/tissues
• Salmonella
  
  • S. gallinarum, S. pullorum, and S. typhimurium in galliforms
  • S. typhimurium in wild and pet birds
  • Symptomatic or asymptomatic
  • Dx: fecal culture
  • Fecal-oral
• Campylobacter
  
  • C. jejuni in poultry and wild and pet birds
  • CS: weight loss, yellow diarrhea, non-specific
  • Poultry and many other spp have high rate of intestinal inf and may shed in feces
  • Dx: fecal culture
  • Fecal-oral
• Yersinia
  
  • Y. pseudotuberculosis and Y. enterocolitica
  • Gram neg coccobacilli
  • Much more important in birds than mammals
  • Canaries and toucans more susceptible
  • CS: non-specific, per-acute mortality
  • Dx: necropsy, culture of liver and spleen
  • Fecal-oral
• Other Bacterial Dzs
  
  • Low zoonotic risk
  • M. avium, M. intracellulare, M. scrofulaceum reported in all types of birds
    
    • Not a major zoonotic pathogen
  • P. multocida, E. rhusiopathiae, C. brunette, E. coli, L. monocytogenes

Question 24

What are two important viral zoonoses of birds? What clinical signs occur in birds and how are they transmitted?

What two fungal diseases are commonly associated with soil enriched with avian feces?

Parasitic diseases from birds represent a low zoonotic risk to people, but what two mites may cause issues?

Answer 24

Viral Dz:

• Influenza
  
  • A (=most important), B, C
  • Dx: serology, virus isolation from tracheal swabs, cloacal swabs, fecal samples
  • Shedding in resp secretions, conjunctiva, feces
  • Transmission: inhalation from environmental sources (?)
• Newcastle
  
  • Avian paramyxovirus 1
  • Very prevalent in poultry, ostriches, pigeons
  • CS: none to resp dz, green diarrhea, neurologic signs, swelling of neck and eyes
  • Dx: serology, necropsy
  • Fecal-oral or aerosolization transmission

Fungal Dz

• Histoplasmosis
  
  • Histoplasma capsulatum
  • In soil enriched w/ avian feces in Ohio and Mississippi river valley
  • Inhalation of airborne spores
  • Birds = mechanical vectors (no dz in birds)
• Cryptococcosis
  
  • Cryptococcus neoformans
  • Contaminated soil, esp under roosting sites
  • Inhalation of spores or direct contact w/ skin
  • Limit exposure to pigeon feces

Parasitic Dz:

• Very low zoonotic risk
• Ornithonyssus spp and Dermanyssus spp mites
  
  • Mites visible
  • Pruritus and anemia in people
• Giardia spp
  
  • No documented transmission from birds to people

Question 25

What are two important bacterial zoonoses carried by reptiles?

Reptiles are reservoirs for what arboviruses that may infect people?

What parasitic diseases of reptiles are potential zoonoses?

Answer 25

Reptiles

Bacterial Dz:

• Salmonella
  
  • Intermittant fecal shedding
  • Fecal-oral
• Aeromonas
  
  • Dx: culture of mouth or feces
  • Transmission: direct contact or fecal-oral
• Mycobacterium
  
  • M. marinum, M. avium, M. tuberculosis
  • Transmission: scratches, bites, aerosol
• Other Bacteria
  
  • Study suggests turtles may be Campylobacter reservoir
  • Citrobacter, Enterobacter, Klebsiella, Proteus, Serratia, Erysipelothrix, Yersinia (enterocolitica and pseudotuberculosis), Pseudomonas
    
    • Transmission: scratches, bites, inhalation, ingestion

Viral Dz:

• Snakes = WEE reservoirs
• Alligators = WNV reservoirs
• Viremia may be significant enough to infect IH (mosquito)
• Unknown role of reptiles in epidemiology of the dzs

Fungal Dz:

• Zygomycoses
  
  • Inhabitants of gastrointestinal tract
  • Inhalation ingestin inoculation, contamination of skin w/ spores
• Mucor, Asper, Candida, Trichosporon
  
  • All isolated from reptiles – possibility of transmission

Parasitic Dz:

• Cryptosporidium carried asymptomatically by reptiles
  
  • No evidence reptilian form is zoonotic
• Pentastomes
  
  • Primitive arthropods
  • Esp in wild animals
  • CS: none to oral infection
  • Transmission to humans: direct contact, then placing hands in mouth
• Ophionyssus natricis = snake mite
  
  • No dz in humans, but may bite

Question 26

Occupational health is important for zoological veterinarians.

How can chemical hazards be reduced?

How do controlled drugs need to be managed?

How is radiation safety achieved?

How can infectious disease risks be minimized?

Answer 26

Fowler 9 Chapter 10: Veterinary Occupational Health and Safety in the Zoo and Wildlife Setting

• Occupational Health and Safety Administration (OSHA) regulates and monitors human health hazards in the workplace in the United States.
  
  • Employers initiate Occupational Health and Safety Programs (OHSP), which is a group with a safety coordinator and multiple other individuals, often including facilities director, veterinarian, HR representative, attorney, etc.
    
    • OHSP components include employer commitment and employee involvement, worksite analysis and risk assessment, hazard prevention and control, and safety health training.
    • Safety committees ensure participation of relevant stakeholders.
• Safety training is critical for new staff, as is yearly re-training.
  
  • Documentation of training is crucial.
• Protocols should be in place and advertised so employees know who to contact if injured on the job.
  
  • OSHA must also be contacted within 8 hours for work-related death or 24 hours for work-related hospitalization, amputation or loss of eye.
• Veterinary services ranked 15^th in terms of most non-fatal workplace injuries and illnesses.
• Chemical Hazards
  
  • All chemicals must be labeled with appropriate Safety Data Sheets (previously MSDS).
  • Bleach and ammonia cannot be stored together, i.e. the “don’t make chlorine gas” principle.
• Scheduled Drugs
  
  • Scheduled drugs should be inventoried at a minimum of every two years, records kept for 2yr
  • Schedule II drug logs are kept separate from Schedule III-V drugs.
  • Wear appropriate PPE (face shield, gloves, etc.) when handling ultra-potent narcotics. Avoid recapping needles as much as possible when using these agents.
  • Profound respiratory depression can occur with accidental exposure to ultra-potent narcotics. Intranasal naloxone spray should be brought wherever immobilizations occur, and staff should be trained how to use it.
• Radiology
  
  • Dosimetry badges should be worn.
  • Try to keep radiation exposure As Low As Reasonably Achievable (ALARA) through use of sand bags when possible, lead shielding, and most importantly, distance (inverse square law).
• Infectious Disease
  
  • Wash hands! Minimum 15s. Cold and warm water equally effective. Soap from disposable container.
  • Alcohol solutions are also acceptable provided gross debris is removed first. Do not eliminate destroy clostridial spores, cryptosporidium, and some other pathogens (e.g. non-enveloped viruses).
  • No eating or drinking should be allowed in animal or laboratory spaces.
  • Dedicated work clothes, washed on site, are also important.
  • Staff should be educated on zoonoses, rabies, hepatitis B, MRSA, psittacosis, salmonellosis, and herpes B in particular.
    
    • Staff should be vaccinated according to their potential exposure.
• Sharps
  
  • Don’t recap needles if possible, use one-handed method if not.
• Various Hazards
  
  • Wear appropriate PPE during necropsies. Consider wearing a respirator when using power tools.
  • Store gas cylinders upright or they might explode.
  • Dangerous animals and venomous snakes are beyond the scope of this chapter.

Question 27

What is the etiologic agent of anthrax?

What groups of animals are commonly affected in the wild? What about in zoos?

What environments allow anthrax to thrive?

How resistant are anthrax spores? Why are they so resistant?

What triggers germination?

Describe the pathogenesis of anthrax.

What are the toxins? How do they work?

Answer 27

Fowler 7 Ch 13 - Anthrax in Free-Ranging Wildlife

Introduction:

• Bacillus Anthracis – gram positive, endospore-forming, non-motile rod
• Contrast to other bacteria/viruses: Lifecycle thrives on high virulence and acute mortality of hosts
• Many unreported outbreaks in wildlife

Recorded Wildlife Host Range

Wildlife:

• Infects most mammals
• Ruminants and hind-gut fermenters most susceptible
• Carnivores, primates, humans moderately resistant
• Ostrich = only bird known to get natural infections
• Carcass scavengers usually highly resistant

Zoos

• Cases usually in carnivores and associated with feeding anthrax infected carcasses, meat or bone meal
• Natural cases in South Africa

Bio-Ecologic Considerations

Organism and Sources of Infection:

• Spores:
  
  • Environmental preference for:
    
    • Alkaline soils;
    • High calcium;
    • High organic material;
    • High moisture
  • Resistant to:
    
    • Time (can survive centuries)
    • Dessication, UV, Heat
    • Digestion by carnivores/scavengers – these animals become mechanical vectors for spores
  • Highly resistant d/t:
    
    • hydrophobic exosporium & spore coat;
    • low water content of spore (= resistant to heat & UV light);
    • Calcium cations + dipicolinic acid (DPA) = Immobilization of enzymes, DNA}metabolism and heat resistance
  • Germination
    
    • Triggered by warmth, moisture and L-alanine in blood serum
    • Followed by exponential replication

Molecular groups: Two Major Clonal Groups (A & B)

• A and B2 = worldwide
• B1 = South Africa

Vegetative Form (bacillus)

• Cannot sporulate in anaerobic conditions (ie in carcass not open to air)
• Susceptible to putrefactive bacteria (which take over in unopen carcass)
• Opening carcass helps disperse bacilli to aerobic microclimates where nutrients become scarce and sporulation occurs

Pathogenesis:

• NOT a highly invasive organism, but undergoes explosive replication once inside body / lymph nodes
• Germination – Replication in regional lymph nodes – enters lymphatics – sepsis – replication in reticuloendothelial system (esp spleen) (=secondary centers)
• Endotoxins = source of clinical signs
  
  • Protein Toxins (2)
    
    • Edema Factor (EF)
    • Lethal Factor (LF)
  • Cell-receptor binding protein
    
    • Protective Antigen (PA)
  • Function together to:
    
    • Reduce phagocytosis
    • Increase capillary permeability
    • Damage blood-clotting mechanisms
  • Net effect = Massive edema (inc in brain & lungs), hemorrhage, renal failure and terminal hypoxia
  • Different spp have different sensitivity to endotoxins
    
    • Highly sensitive spp have low blood bacterial counts at death
    • Less sensitive spp have high blood bacterial counts at death

Question 28

What are some environmental variables that lead to dispersion of anthrax spores?

What are the three methods of anthrax transmission?

Which is most common?

What species are affected by these routes and how are they affected?

Answer 28

Routes of Infection, Transmission & Seasonality

Exposure:

• Outbreaks associated with low-lying depressions and rock land seep areas meeting above criteria (alkaline pH, etc) = concentrator areas
• Flood-drought/evaporation cycles concentrate spores in these areas
• Run-off pools and seasonal drought reduces water availability leading wildlife to drink from these concentrator areas
• Water and wind erosion may expose spores or affected carcasses
• Spores may surface from seismic events

Transmission:

• Several Methods:
  
  • Ingestion – generally most common
    
    • Carcasses
    • Water contaminated by vectors (wading vultures) or carcasses
    • Browse contaminated by non-biting, necrophilic flies
    • Osteophagia – by pregnant, lactating animals or in areas w/phosphorus deficient soil is an important mechanism of transmission in specific locations
  • Innoculation – second most common;
    
    • carnivores from bone chunks
    • Fly bites (mechanical vector) – especially common in suids & equids
    • People - handling carcasses
    • Creates localized infection – phagocytosis minimal – infection spreads to lymphatics – may progress to sepsis if not treated
    • cellulitis, edema of initially affected area most profound:
      
      • Carnivores and suids – Oral and pharyngeal edema, cellulitis
      • Browsers – necrohemorrhagic lesions in Peyer’s patches or segmental regions of small intestion – sepsis
  • Inhalation – rare; spores difficult to aerosolize;
    
    • Rapid septicemia and death
    • Spores do NOT germinate in airways, but are phagocytized by macrophages and transported to local lymph nodes

Question 29

Describe the transmission factors, including potential vectors, for the development of anthrax in the following species and geographical areas.

Northern Canada - Wood Bison

Southwest Texas

South Africa & Zimbabwe - Greater Kudu

Botswana & Namibia - Elephants, African Buffaloes, Springbok

South Africa Northern Cape

Zambia & Uganda Rivers & Lakes

Reindeer in Northeastern Europe

Answer 29

North America:

• Northern Canada
  
  • Wood bison (Bison bison) outbreaks
    
    • Hot, dry summer months
    • Associated/overlaps w/ rut
    • More common in adult males – rare gender/age association – likely due to year-to-year use of wallows which may be concentrator areas
    • Also Tabanid (biting) fly increase
    • Scavengers (mammalian, avian) thought to increase spread of dz
    • Moose and black bear occasionally also affected during outbreaks
• Texas, U.S.A.
  
  • Southwest TX - endemic
  • Shallow, lime rich, humus soil overlying limestone (perfect environment)
  • Cases during hot, dry weather following wet spring
  • WTD and unvaccinated cattle most affected
  • Biting flies (Charbon flies) = important mechanical vector
    
    • Cause centrifugal spread of infection

Sub-Saharan African Wildlife:

• South Africa and Zimbabwe – Southeastern, subtropical savannahs
  
  • Greather kudu (Tragelaphus strepsiceros) = most important host
    
    • 3.7% population in Kruger, but 42-62% deaths during outbreaks
    • High bacteremia at death
    • Thin skin easily opened by scavengers makes them important anthrax amplifiers
  • Nyala also commonly affected
  • Contamination of graze by blowflies (Chrysomyia and Lucilia spp) = most important mode of transmission
  • Dry season outbreaks associated w/ overpopulation and/or limited resources
• Botswana and Namibia – more arid southern African savannah
  
  • Elephants, African buffaloes, zebras, springbok = important players
  • Transmission mainly via grazing or infected water
  • Etosha National Park – unusual in that anthrax is endemic and causes clusters of elephant deaths at the end of the dry season followed by a summer (wet season) outbreak in ungulates (zebra, wildebeest, springbok) related to contamination rain pools by wading vultures or of grazing by carcasses
• Northern Cape, South Africa
  
  • Endemic areas
  • Outbreaks associated with WET summer season (opposite most areas)
  • Dz propagation d/t huge numbers biting flies (Hippobosca spp)
• Zambian Luangwa river system & Ugandan Greath Lakes
  
  • Hippos primarily affected, followed by cape buffalo
  • Outbreaks preceded by overpopulation and resource stress

European Wildlife:

• Northeastern Europe
  
  • Species: Reindeer
  • Transmission: Hematophagus flies

Asian Wildlife:

• Species: Water buffalo, sambar deer, Asian elephants (Elephas maximus), Indian rhino (Rhinoceros unicornis)
• Transmission: ingestion contaminated graze or water

Question 30

What makes male Wood Bison and African Buffaloes more susceptible to anthrax?

What age group is rarely affected by anthrax?

How do outbreaks typically resolve?

Answer 30

Other Epidemiologic Determinants

Gender Predilection:

• Adult males - Wood bison in Canada and African Buffalo in South Africa
• Similar behavior during rut/reproduction – wallowing and digging in holes, dirt

Age Predilection:

• Not typically seen in unweaned juveniles

Patterns of Disease:

• Endemic region pattern: sporadic cases interspersed with outbreak clusters occur on irregular basis with seasonal pattern
• Propagating epidemics – generally linked to densities/concentrations of preferred host species in the system
  
  • Self-limiting
  • Follow normal epidemic curve pattern
  • In South Africa – epidemics/outbrks dramatically terminated by onset of summer rains

Question 31

What are the typcal clinical signs associated with anthrax?

What is teh typical appearance of carcasses?

How do clinical signs vary between hoofstock adn carnivores?

What are the gross adn histologic lesions associated with anthrax?

Answer 31

Clinical Signs

• Peracute or Acute
• Disoreintation, ataxia, respiratory distress, apoplectic seizures, acute death
• Good body condition at death
• Opisthotonus with extensor rigidity of the forelimbs freq observed in carcasses
• Equids & Suids: Abdominal pain/colic, diarrhea and cutaneous/localized swellings common
• Predators: Less susceptible, but at high risk of massive exposure during feeding
  
  • Lions: Massively swollen heads, faces
  • Clinical cases more common during early outbreak as predators gain immunity if they survive initial exposure – eventually resistant
  • Cheetah (Acinonyx jubatus) – unique among carnivores b/c sig. morts reported in Namibia
    
    • Suspected that cheetah don’t build up acquired immunity b/c don’t scavenge much

Postmortem and Gross Pathology:

• Externally: Incomplete or absent rigor mortis, bloating, leaking bloody fluid, petechiae & ecchymoses
• Necropsy: Unclotted blood, blood in body cavities, widespread edema, hemorrhage & necrosis, splenomegaly w/ currant jelly appearance of red pulp, hemorrhagic & edematous LNs, pulmonary and mediastinal edema are common
• Lions & Leopards: variable severity; Freq localized to head/oropharynx
  
  • Glossitis, stomatitis to severe cellulitis of entire face & oral cavity (severe edema seen)

Histopathology:

• Large numbers bacilli in blood and tissues
• Edema
• Extravasation of blood, large amts blood in spleen, LN
• Loss of splenic and LN architecture

Question 32

Anthrax diagnosis must be done at a lab with what biosafety level?

How should you confirm your suspicion that an animal diet of antrhax?

What diagnostic techniques are available to confirm the diagnosis?

What are some important differentials to consider?

Answer 32

Laboratory and Differential Diagnosis

• Biosafety Level 2 required for cx
• Do not open carcass – take blood sample from superficial vein (ear, tail, etc)
  
  • Older or scavenged carcasses – can get drop of blood from coronary band or hoof lamellae (skin it) for blood smear

Laboratory Diagnosis:

• Blood and Tissue Smear Examination:
  
  • Stains: Gram, McFadyean, malachite green or Giemsa (bacilli) or Ziehl-Neelsen (spores)
    
    • Giemsa preferred b/c can distinguish anthrax bacilli from post-mortem putrefactive organisms
      
      • Anthrax: singles or short chains, magenta, flat ends, all equally sized (monomorphic), no endospores visible, ghost cells (capsular remains) appear pink
      • Putrefactive bugs: polymorphic, rounded ends, deep purple, form long chains, may produce spores
  • Lions – anthrax often not detectable in blood smears, but may be seen in fluid from edema of face/head
  • African buffalo – typically have low terminal bacteremias

Culture and Phage Typing:

• Placed in warm water bath to eliminate other bacteria (only clostridium survives)
• Aerobically cultured (clostridium=anaerobe)
• Colonies are white w/ frosted glass appearance +/- tailing, difficult to remove with loop
• Confirmed identification if non-hemolytic

Serologic Testing:

• Ascoli precipitin test – detects antigens using hyperimmunized serum from rabbits; oldest test; precipitin line develops at Ab:Ag interface
• Rapid, hand-held immunochromographic device – detects Ag; not commercially available;
• Rapid, hand-held ELISA for on-site diagnosis

Molecular Techniques:

• PCR – detects various genes including capsular (capB) and protective antigen (pagA)
• Commercial kits available
• Nucleotide sequencing important to i.d. strain

Differential Diagnosis:

• Wild herbivores: Clostridial infection, lightening strikes, cyanobacterial intoxications, acute plant poisonings, acute organic or inorganic poisoning, snake bite
• Carnivores: acute infections, envenomations

Question 33

What is the public health risk of an anthrax outbreak?

What are the three forms of disease in humans?

Answer 33

Domestic Animal and Veterinary Public Health Concerns

• Response to Outbreak:
  
  • Mass vaccination
  • Multimedia public awareness campaigns
• Human Cases:
  
  • Cutaneous form = 95% cases
    
    • Pruritic skin lesion – vesicle – surrounding edema – vesicle rupture – black, non-painful necrotic lesion – low grade fever,
    • sepsis and death may occur if untreated
  • Enteric – most common in rural areas of third world countries
    
    • Acute diarrhea, vomiting – hematemesis, bloody diarrhea, acute abdomen – shock and death
  • Inhalation – occupational dz of wool-sorters (18^th-20^th centuries); musicians playing drums made of infected carcasses
    
    • Little evidence of pneumonia on rads
    • Pleural effusion, hilar lymphadenopathy, widened mediastinum

Question 34

How is anthrax controlled?

Is there a vaccine? Do any species react poorly?

How do carcasses need to be disposed of?

What environmental control options exist?

Is treatment ever an option?

Answer 34

Control and Treatment

Control Measures:

• Vaccination: Non-encapsulating strain 34F of B. anthracis (=Sterne spore vaccine) + adjuvant
  
  • Mainstay of protection
  • Repeat annually – makes it difficult to vaccinate wildlife
  • Caprines and Llamas = severe reactions
  • Wildlife:
    
    • Small numbers/groups – darts or biodegradable ballistic implants (thin-skinned spp)
    • Large herds – mass capture and pole syringe as released (difficult, costly, but effective)
    • Need oral vaccine

Carcass Disposal:

• Dispose of carcass intact
  
  • Burn – best
  • Bury – not recommended:
    
    • May be uncovered later
    • Bury at 2m depth & mix chloride of lime with dirt (1:3parts) when covering carcass (reduces spore survival)
• Canada – 5% formaldehyde spray of carcass and surrounding area kept scavengers away allowing time for putrefaction and disinfected surrounding soil (flies??)
• Wrap carcass in agricultural plastic to prevent scavengers and inverts from accessing it – allows for putrefaction; then bury/burn

Other Control Techniques:

• Insect control
• Rangeland burning – destroys spores, kills invert vectors, removes grass making area undesirable for herbivores
  
  • Used in African Savannah systems with anthrax winter-dry season pattern

Treatment:

• Highly susceptible to antibiotics
• BUT – usually too late once symptomatic except in some more resistant spp (lions and leopards have been treated)
• Prophylactic tx recc when moving animals out of outbreak area, then vaccinate later
• NEVER vaccinate and give antibiotics together

Question 35

What are the routes by which West Nile Virus can be transmitted?

What are some of the long term sequelae of west nile infection?

How long can West Nile virus persist in th brain?

Answer 35

Flower 8 Ch 75 Updates on West Nile Virus

• At the time of publication it had been 13 years since WNV appeared in North America
• Originally thought to only be spread by mosquito bite, now we know that it can be spread by multiple routes
• Even mild infections can have long term sequelae like fatigue and cognitive deficits
• Many avian species other than crows are susceptible to disease (rather than asymptomatic carriers)
• Many diverse species such as alligators, polar bears, reindeer, seals, killer whales, macaques and psittacines can succumb to WNV
• Species such as fox squirrels, chipmunks and rabbits have been found to develop viremias sufficient to infect mosquitoes and play a role in transmission
• WNV has also had a significant impact on raptors
  
  • Ocular signs seen in both humans and raptors
• Can also be transmitted from bird to bird, orally, via breast milk, via the intrauterine root, and via blood transfusions
• WNV can persist for months in infected animals (up to years in humans and is associated with the development of CKD)
• The WNV has several key structural proteins: the capsid protein C, the premembrane protein prM and an E protein that mediates viral attachment and membrane fusion
  
  • Most neutralizing antibodies are directed against the E protein
• How WNV crosses the blood–brain barrier (BBB) and whether central nervous system (CNS) damage is caused by direct viral infec- tion, indirectly by the host’s immune response, or both, is a question that has been the subject of many studies
  
  • Likely through hematogenous spread with the help of TNF alpha and MMPs which increase permeability of the BBB

Long term sequelae

• Parkinsonian-like disorders have been described
• Patients with mild disease are just as likely to suffer long term health problems as encephalitis cases
• Sequelae may be a result of viral persistence

Viral persistence

• Studies in zoo animals demonstrate that subclinical seropositivity can also produce CNS pathology
• A 2010 study found viral persistence in the face of a robust antibody response and in the presence of inflammation in the brain even in subclinical infections and showed that WNV persisted in the CNS for up to 6 months in mice with subclinical infections
• Estimated 1.2 million people in the US with asymptomatic infections and possible subclinical CNS disease
• Kidney disease has also been reported
• It is not known what impact viral persistence may have on zoo species, but any seropositive animal should have longterm follow up even if asymptomatic

Vaccination

• A variety of vaccines and vaccine protocols have been used in many different (mostly avian) species with varying results
• Some human vaccines have shown immunity in geese
• Measles vaccine expressing the WNV E protein showed immunity in squirrel monkeys

Question 36

Describe the significance of clostridium perfringens in zoo animals.

What type of bacteria is this?
- Since they are part of the enteric flora, what is required for a true infection to occur?
- What does most of the damage?

Where is the bacteria found?
- What are some predisposing factors for enterotoxemia?

Answer 36

Intro
- Clostridium perfringens (CP) is the most important enteric clostridial pathogen of animals.
- Dynamic and has the ability to adapt to different hosts
- Disease expression of CP is determined by the specific toxin, species and age of the host, and site of infection

Microbiology and pathogenicity
- Encapsulated rod - capsule plays an important role in wound virulence
- Anaerobic but relatively aerotolerant
- Identifying CP infection in intestines post mortem can be confounded by post mortem overgrowth
- CP infections require a break of the skin or alteration of the GI microbiota
- CP infections are true infections, but much of the damage is secondary to the toxins produced
- CP can produce as many as 17 different toxins, each with specific tissue tropism

Epidemiology
- CP is an environmental bacterium (soil, forage, cadavers), but can also be present within the intestinal tract of many species, without any symptoms.
- Transmitted orally or by wound infection
Reservoirs for toxinotype summarized in table 29.2 below
- Foods rich in protein and energy as well as young age predispose to enterotoxemia

Question 37

How does Clostridium perfringens affect reptiles?
- What are some predisposing factors?

How does Clostridium perfringens affect birds?
- What are the typical lesions?
- What are the unique lesions of lories and chickens?
- What toxin causes necrotic enteritis?
- What dietary supplement in poultry decreases CP?

Answer 37

Reptiles
* Clostridiacae are a normal part of gut flora in burmese pythons
* Has also been cultured from the blood and oral cavity of clinically normal reptiles
* Reports of clinical disease due to CP in reptiles are rare, and metronidazole and transfaunation have been suggested as the most efficient therapies
* Clostridial abscesses or gangrene can occur secondary to loss of blood supply and subsequent creation of anaerobic sites
* Enteric clostridial disease can be triggered by a shift in the gut microbiota following the use of antibiotics

Birds
* Avian CP infections typically manifest as necrotic enteritis, nectarivorous bird emphysematous ingluvitis (NBEI, reported only in Loriinae), cholangiohepatitis (reported only in chickens), or gangrenous dermatitis
* Often normal flora in birds with well developed caeca, rarely found in species with small or absent caeca
* Avian necrotic enteritis (ANE) is typically caused by a type G CP
* ANE occurs in many species but is common in lorikeets
* ANE is generally secondary to a change to a protein-rich feed
* It is also a common finding in lead-poisoned trumpeter swans
* Contaminated feed has been implicated in some cases of ANE
* Nectarivorous birds are at higher risk, due to clostridial proliferation and toxin production favored by the nectar
* Dietary putrescine supplementation, widely used in poultry production, has been shown to significantly reduce fecal excretion of CP in zoo-housed azurewinged magpies (Cyanopica cyanus)
* NBEI is a disease of lorikeets and lories characterized by crop subepithelial pseudocysts, lytic necrosis, and granulomatous to pyogranulomatous ingluvitis, with multifocal intralesional bacteria.
* CPA typically the causative agent
* Gangrenous dermatitis, although rare in birds, can occur secondary to cutaneous trauma, particularly in warm and humid environments, and can be associated with Staph coinfection

Question 38

Describe clostridial perfringens infection mammals.

How does it affect carnivores?
- What species have been affected?
- What lesions have been seen?
- What toxins have been isolated?

How does it affect marine mammals?
- What lesions have been observed?

How does it affect terrestrial ungulates?
- What toxin is most commonly affected - what lesions does it produce?
- What species are commonly affected and which toxins affect them?

Answer 38

Carnivores
* CP type A has been implicated in fatalities in several species of nondomestic carnivores such as black-footed ferrets, siberian tigers, and lions
* Affected ferrets and some tigers displayed marked gastric distention and dyspnea, acute depression, anorexia, and bloody diarrhea for several days prior to death.
* CPE isolated from amur leopards and cheetahs–intermittently hemorrhagic diarrhea, successfully treated
* CP type B ETX isolated from a fecal sample of a tiger that presented with acute neuro signs
* CPB2 was reported in two Asiatic black bears – acute death, necrohemorrhagic intestinal lesions
* CP found in NAROs –acute death or diarrhea - intestinal mucosal necrosis on histo

Marine Mammals
* CP type A is reported as part of normal flora of several cetacean, and pinniped GI tracts
* Myositis or enterotoxemia reported in several species
* CP septicemia reported in a estranged long-beaked common dolphin
* acute necrotizing colitis with pneumatosis intestinalis was reported in a manatee

Terrestrial Ungulates
* Significant disease is most frequently associated with type C, which causes hemorrhagic enteritis
* Lesions in nondomestic bovids are comparable to those described in domestic ruminants, including necrotizing ulcerative enteritis and peritonitis.
* CP type D enterotoxemia associated with diarrhea affects mostly young cervids, while adults present with rumen acidosis, enteritis, and/or colitis
* Reindeer (Rangifer tarandus tarandus) are susceptible to CP types A to E
* In Tragulidae and Moschidae, CP type D enterotoxemia often results in sudden death or peracute disease
* CP type A and C enterotoxemia is well described in neonatal and adult camelids
* CP type A has been implicated as the cause of fatal hemorrhagic enteritis in a neonatal Nile hippopotamus as well as sudden death and peracute syndrome in white and black rhinos
* CPB2 has been found in an African and an Asian elephants under human care with severe diarrhea, ulcerative enteritis, and acute fatal myonecrosis.
* CP reported as a coinfection with EEHV
* Contrary to CP type C that is often fatal in swine, CP type A is part of the normal flora in pigs.

Question 39

Describe the diagnosis and management of Clostridium perfringens.

What diagnostics are available for the various toxxins?

What husbandry measures can be made to prevent CP infection?
- FOr ungulates?
- For carnivores?
- For marine mammals?

What vaccinations are available?
- When should they be administered to pregnant hoofstock?

How is it treated?
- What antibiotics should be considered?
- How are gangrenous lesions treated?

Answer 39

Diagnosis
* Diagnosis based off of clinical signs plus gross and microscopic findings
* ELISA currently available for detection of CPA, CPB, and ETX
* PCR for multiple toxins and for the CPA gene cpa (highly conserved).
* As CPB is rapidly destroyed in the intestine, a type B infection (CPA, CPB, and ETX producing toxin) can be misdiagnosed as type D (CPA and ETX producing toxins) if a diagnosis only relies on toxin detection
* Mouse Bioassay - In vivo rabbit/mouse toxin-neutralization test is the gold standard to identify CP toxins and assess protection tests. No longer used routinely due to ethical concerns

Prophylaxis
* Animal husbandry, population density, environment, and spore abundance are risk factors
* In ungulates, decrease of animal density, appropriate diet high in fiber, and limited amount of concentrates or access to lush pasture help to decrease sporulation rates and fecal-oral transmission
* In carnivores avoid 1) abrupt dietary change, 2) partial thawing of meat diets, and 3) overeating
* In marine mammals, ubiquitous CP is not killed by chlorination and could enter a skin lesion–combined with anaerobic conditions from diving, can lead to clostridial proliferatiton and disease

Vaccination and treatment
* Multivalent clostridial vaccines are available for prophylaxis in domestic ruminants but not licensed for zoological species
* CP type C and D vaccination is highly recommended for South American camelids.
* Recommendations include vaccination of pregnant exotic hoofstock 4 to 8 weeks before parturition to increase specific colostral immunoglobulins
* Antibiotic prophylaxis such as metronidazole, penicillin, and antitoxins (Type C and D) administration may be considered in case of outbreak.
* Therapy includes intravenous large-spectrum antibiotics, to protect bacteremia induced by intestinal damage, and supportive care.
* Gangrenous lesions require surgical debriding and local asepsis.
* Enterotoxemia is often rapidly fatal.