4. Wild and Free-Ranging Carnivore Health Issues

4.1. Carnivore Conservation Issues

4.1.1. Wild carnivore health issues

Why do we care?
Threats to worldwide populations?

4.1.2. Human Encroachment

Large carnivores (example: grizzly, cougar) are generallynot tolerated - more likely to die of "acute lead poisoning" (from firearms)
Direct correlation between human/wildlife conflict andthe density of roads (bears and wolves)
Zoonotic disease issues (rabies) highten pressure

4.1.3. Habitat Loss/habitat alteration

Environmental pathology
- A loss of ecological connectivity across the landscape
- Increasing isolation of habitats, wildlife populations and ecosystems
- A continual decline in wildlife numbers, especially large carnivores
- Increasing conversion of natural landscapes to humanscapes
Carnivores can decrease prey density and disease incidence in a variety of ways e.g.
- Brucella abortus in a crowded feedground setting readily expose wolves
- By providing habitat improvements, elk use feedgrounds less and their subsequent dispersal decreases their density and reduces chanceof naive animals coming in contact with infective aborted fetus.
- Wolves accomplished in one month what took managers 10years.

Cockroach theory- By increasing population linkages and distribution, you decrease the chance that disease will wipe out the entire population as may occur in density dependent situations such as on islands.

4.1.4. Loss of Biodiversity

Land protection is skewed heavily toward higher elevation areas (rocks and ice)
- Few species supported
- Little function to link wildlife populations or ecosystems
Low elevation valleys and riparian areas contain the highest biodiversity
- Winter range, migration, sustenance
- Most rapidly developed, fragmented and isolated
Human transportation corridors act as wildlife mortality zones
- Block migration
- Block genetic and demographic exchange between populations

4.1.5. Use of Carnivores as sentinel species to identify potential emerging disease

Relationships among carnivores and their prey, e.g.brucellosis in grizzlies and black bears
Bear seroprevalence to: trichinella, toxoplasmosis,,leptospirosis, canine adenovirus, canine parvovirus, tularemia
Mt. Lion and lynx seroprevalence to: Plague(Yersinia pestis), canine distemper, tularemia
Plague, prairie dogs and black-footed ferrets
Environmental contamination at the top of the food chain -increased hermaphrodism in polar bears

4.1.6. Carnivores in National Parks

Most common disease prevalence in canids: Rabies, sylvatic plague, borreliosis, dirofilaria spp.
Domestic to Wild.
- Gray Wolves and sled dogs in Denali NP share lice, canine distemper, canine parvovirus, infectious canine hepatitis
- Reintroduced Gray Wolves from Idaho to Yellowstone acquire canine parvovirus reducing pup survival from 80% to 60%

4.2. Viral Diseases

4.2.1. Canine Distemper (Morbillivirus)

Terrestrial animals susceptible to infection by canine distemper
Canidae	Wolf, coyote, fox, domestic dog
Felidae	African lion (rare)
Procyonidae	Raccoon
Mustelidae	Ferret, mink, weasel, martin, fisher, otter, badger, skunk, wolverine

4.2.1.1. Description

Widespread and mortality in juveniles is higher than in adults.
Resistant to cold and the majority of distemper cases in domestic dogs are seen in the fall and winter.
In wild animals, since the juveniles are more susceptible to infection, the majority of cases are seen in the spring and summer, but cases are observed year round.

4.2.1.2. Transmission

Aerosol-droplet route, direct contact, or possibly by contact with contaminated objects.
Shed in the feces and urine of infected individuals possible transplacental transmission.
Occasionally infection occurs from ingestion of infective material.
Virus is spread to the tonsils and lymph nodes, where viral replication occurs.
Virus then enters the blood stream where it is transported to epithelial cells throughout the body, including the intestinal and respiratory tract.

4.2.1.3. Clinical Signs and Pathology

Respiratory and intestinal problems such as coughing, diarrhea, vomiting, nasal and ocular discharge, anorexia; and hyperkeratosis of the nasal planum and foot pads.
In wild carnivores, signs of abnormal behavior and apparent lack of fear, suggestive of rabies, may be the only signs grossly visible.
Purulent conjunctivitis and nasal discharge and the eyelids may be adhered together with crusty exudate.
Aggressiveness, disorientation, lack of alertness, convulsive movements of the head and paws, and aimless wandering.
Diarrhea, labored breathing and an unkempt appearance to the fur.
Pathological lesions: pulmonary congestion and consolidation leading to focal pneumonitis. Eosinophilic rounded or ovoid bodies with refractile particles are found in the epithelial cells of skin, bronchi, intestinal tract, urinary tract, bile duct, salivary glands, adrenal glands, central nervous system, lymph nodes and spleen. During necropsy an enlarged spleen is usually seen.

Canine distemper viral inclusions in a fox lung.

4.2.1.4. Diagnosis

Presumptive: clinical signs, demonstration of inclusion bodies in neutrophils on blood smear and inclusion bodies in conjunctival smears.
Definitive: laboratory analysis of affected tissues by fluorescent antibody techniques.
Wild carnivores: the presenting signs are often neurological and the disease must be differentiated from rabies and other encephalitides.
Other diseases which may mimic distemper include tularemia, listeriosis, Chastek's paralysis (in captive mink and fox), histoplasmosis (raccoons) and poisonings.

4.2.1.5. Treatment and Control

No treatment to cure but supportive care can save some individuals.
The virus is inactivated by heat, formalin, and Roccal R.
Control
1. Removal of carcasses of animals which have died from the disease
2. Vaccination of susceptible domestic species (pets) to decrease the number of susceptible hosts
3. Reduction in wildlife populations which also reduces the number of potential hosts (?)
4. Eradication not possible or feasible

4.2.1.6. Significance

Die-offs of raccoons and other species due to canine distemper occur yearly. The impact of this disease on other wildlife populations is not known but in the late 1980's the last remaining black-footed ferret population was reduced to 18 animals following an outbreak of distemper. Canine distemper is of no public health significance.

4.2.1.7. Canine Distemper in Felidae

Epizootic killed a third of the lions in Tanzania's Serengeti National Park
Likely infected by spotted hyenas, which share food with lions. May have been infected by free-roaming domestic dogs around the national park.
Unexpected distemper episodes in captive lions in California and javelinas in Arizona. In 1988, a mutation of CDV allowed the virus to kill 90 percent of the harbor seals in the North Sea. And in 1994, a slightly different morbillivirus killed several horses and their trainer in Australia.
Domestic dogs in Tanzania are being vaccinated against CDV, and the approximately 2,000 surviving lions are expected to have immunity for life.

4.2.2. Rabies (Lyssavirus)

All mammals are potentially susceptible to infection by rabies virus.

Rabies viruses (lyssavirus) exists as a disease on every continent in the world, except Antarctica. It maintains itself in a number of different reservoirs (canids, other carnivores, bats) heavily influenced by the interaction between native fauna and human activities.

The major reservoir in developing countries is still primarily domestic dogs. Wildlife reservoirs in many of these countries are poorly understood since most of the attention and limited economic resources have been aimed at the human/domestic animal relationship.

Wildlife reservoirs of rabies are now becoming most important in well-developed areas of the world, including North America and Europe. Domestic animal rabies has been nearly eliminated from these regions allowing the wildlife reservoirs to flourish. This shift began with dog rabies control measures adopted in the 1920's. In 1960 in the United States for the first time, there were more cases of rabies identified in wildlife than in all domestic species combined. Today more than 90% of rabies cases identified are in wildlife species. Within the wildlife reservoir, shifts are also occurring. Distinct species adapted virus strains have developed and are maintained within that species reservoir. Transmission to non-reservoir species, including domestic animals and humans, occurs readily, but may produce atypical clinical signs.

There are currently in the US: 1 strain in raccoons that has been identified in 19 states and the District of Columbia; 3 skunk strains; 4 fox strains and 1 coyote-strain in Texas. There are also species specific bat strains around the world. Until 1989 the skunk was the most often reported wild animal, and now we see more cases in raccoons than in any other single wildlife species. This change which has impacted us greatly in the Northeast is believed to have begun with human translocation of rabid raccoons from the South to the mid-Atlantic states. Similar human activities are blamed for the recent rise in coyote rabies in Texas.

Bats serve as a natural reservoir in many parts of the world. They are perhaps the best adapted species to this fascinating but deadly virus. Cases of bat rabies in the US are relatively constant. From 1986-95, 14 out of 18 human cases of bat strain rabies in the US were acquired from bats without any "known" exposure. The precise method of transmission in these cases is uncertain, although undetected bites are most likely. A newly discovered lyssavirus in bats in Australia is described below.

There have been very few human cases acquired directly from raccoons in the recent epizootic.

4.2.2.1. Transmission

Bite of an infected animal
Saliva from an infected animal on an open wound
Deep scratch from an infected animal? (considered exposure risk)
Virus replication occurs at the bite site and in the brain
Human non-bite cases have been recorded via inhalation of virus in a bat cave, lab workers sawing through skulls and aerosolizing the virus, and through corneal transplants from a rabid human donor

4.2.2.2. Clinical Signs

"The atypical is typical" especially in wildlife species

Species adapted strains cause a wide variety of clinical signs, often unpredictable in non-host species
Furious rabies: aggressive signs early in the disease and then become paralyzed. Excitation phase lasting several days. Animal is restless and soon becomes vicious, biting at anything and everything but this behavior gradually subsides. Incoordination and tremors are often apparent. Convulsions, paralysis and prostration occur just prior to death.
Dumb rabies: paralyzed and die shortly thereafter.
Important consideration in reaching a clinical diagnosis: no sign (or series of signs) is typical or characteristic. Signs mimic distemper, hepatitis, listeriosis, tetanus, botulism and some parasitic diseases. Encephalitic syndromes can also be caused by plant or chemical toxins.
Only sure way to diagnose rabies is with post-mortem laboratory tests.

4.2.2.3. Diagnosis

Wild animals that have bitten or exposed humans should be killed immediately and their heads submitted to the proper health authorities as soon as possible.
Bats should be sent in whole.
Wear rubber gloves and mask as a precautionary measure.
No gross pathology evident
Diagnosis is made by examining brain tissue with IFA, and/or by identifying Negri bodies with histopathology.
- Microscopic lesions of the central nervous system are inflammatory and similar to those seen in other virus infections.
- Negri bodies (inclusion bodies in the cytoplasm of neurons of infected animals) are positive proof of rabies infection.
Only a physician should advise the person as to what course of medical treatment should be followed.

4.2.2.4. Control

Vaccination and immediate treatment post-exposure in people and domestic animals have resulted in good control where possible.
There is no successful treatment for humans or animals with symptoms of rabies.
Successful control has been achieved with oral baiting programs in certain areas of the world (see below)

4.2.2.5. Significance

Human health is of primary importance. Occupational risks to veterinarians are important. ARE YOU PROTECTED?

Also some economic loss to farmers from cattle and horses coming in contact with rabid animals.

Rabies may pose a significant threat to some fragile carnivore populations

4.2.2.6. Wildlife rabies control in New England

Raccoon rabies was first recognized in FL in late '40s. In 1977 translocation resulted in spread to Virginia and then further North. The first case in MA occurred in September, 1992.

Raccoon vaccination programs began with VRG (vaccinia vectored recombinant vaccine in a fish-meal bait) in 1984. This technique is now being employed in NJ, MA, NY, FL, VT,OH and other states. The fish-polymer bait has been found to be best accepted by raccoons.

In 1994 Massachusetts began to bait the area around the Cape Cod canal to prevent the spread of rabies to the Cape, taking advantage of the natural barrier. Baiting has occurred every year since (Spring and Fall) and successfully prevented spread of raccoon rabies on the Cape.

Baits had to be labeled clearly in case a person found them (highly populated area) and dogs were tested that ate the baits. They have achieved an estimated 63% vaccination rate that has been successful.

The raccoon strain has moved north into Canada, and the fox strain is moving south from Canada into New England (NH).

4.2.2.7. Coyote and Gray fox rabies in Texas

In 1988, an epizootic of canine rabies occurred along the Mexican border and included coyotes as the primary reservoir, also targeted domestic dogs, and dog/coyote hybrids . Rabies moved into the rest of South Texas from there. In 1995 the threat to the San Antonio area prompted action, where only 1/4 of the pet population was vaccinated!. They identified 3 strains of rabies in the area: south-central skunk, Texas gray fox, and domestic dog/coyote.

VRG was used with a tetracycline marker with a bait made up of dog food or fishmeal with warning label in English and Spanish. Baits were distributed using an automated delivery system from an airplane (pioneered this technique) utilizing 2 aircraft. Baiting began in Feb. 1995. Supplemental baiting by helicopter targeted problem areas (Aug. 1995) Greater than 87% bait uptake on the first pass!

Gray foxes were added to the target population in 1996. The total area covered 41,000 square miles of South and West-Central Texas.

The program has been very successful at keeping rabies close to the Mexican border.

4.2.2.8. European fox rabies

Historically foxes were the major wildlife reservoir of rabies in Europe. The main method of control was culling or elimination of wild foxes in any given area. This proved ineffective. Why?

Switzerland in the mid- 1970's tried an oral attenuated vaccine in their wild carnivores, but some problems arose with its ineffectiveness in raccoons and with vaccine induced rabies in skunks. This problem prompted development of a recombinant vaccine (VRG). This vaccine is effective for a wide range of animals.

Baits now used in Europe include: Vaccinia recombinant (VRG-Merieux) and SAG2, highly attenuated live vaccine. Both sanctioned by WHO.

Facts proven from the program in Europe:

Foxes: life expectancy 1.5-2.5 years.
VRG immunity lasts 12-18 mos.
Baiting in prescribed areas produced successful vaccination in up to 81% of adult foxes.
Need to bait several times to catch animals already infected, or animals missed by first pass and to get juveniles missed because they were in the den at the time.

November 1997 fox rabies was declared as eliminated from France and in1999 Switzerland declared they had "eliminated" rabies

4.2.2.9. Australian Bat lyssavirus - an emerging infectious disease!

In 1996, a new lyssavirus was discovered in fruit bats (flying foxes). Within months the first human case occurred and initiated intensive research into this virus in a country heretofor declared "rabies free". Only two cases have occurred to date in humans, both resulting in their deaths.

This virus is genetically very similar to classical rabies virus and produces very similar signs in humans. The human diploid recominant vaccine is felt to be protective. It is a distinct and separate virus however and is classified as genotype 7 of the Lyssavirus genus. The virus has been found in 5 different species of fruit bats (or flying foxes).

For more on RABIES see the CDC Rabies site...

4.2.3. Feline Leukemia Virus

Retroviridae subfamily oncovirinae
Spread by nasal and saliva secretions
Lymphoma, leukemia, and cytosuppressive disease
Not endemic, not widespread in the wild (domestic and feral cats believed to be source)
Several published accounts of cougars, European wildcat (felis silvestris) with transient viremia.
Surveillanced in lynx and cougar serum in CO, WY, MT, BC, Yukon, AK, have not seen to date.

4.2.4. Feline Immunodeficiency Virus

Stephen O'Brien (Natl Cancer Institue)/ Craig Packer identified in Serengeti Lions 1990 (domestic cats in 1987, CA)
In wild cats: 84 % infection rate but no AIDS: Appears to be a balance between host and virus.
See in over 25 species of cats including african lions, cougars, snow leopards, Pallas's cat of Siberian steppes, etc.
FIV first entered the FELIDAE family 3-6 million years ago
Each species infected with its own strain of FIV
Seldom infects a new, even closely related species, but when virus jumps to new host there is little resistance (high morbidity and mortality)
Sequences from lion to Puma strains are 25 % different (this much difference takes a long time)
Domestic cats are new conquest for FIV.
In the wild, don't see it in young animals so is probably not passed sexually or during birth or while nursing. Spread through aggressive playing and biting in prides (see lower infection rate in solitary cats; leopards and cheetahs)
Closest among the lentivirus genetically are HIV, SIV, FIV, BIV. FIV has 1/2 genes of SIV or HIV, may indicate it is a more primitive virus

Theoretical Scenario:Several Million years ago in Africa or Middle East, an ancestor of today's lion killed and fed on a BIV infected bovid (buffalo). Somehow it made the rare species transition in the cat and figured out its new host immune system- became FIV. Disease passed from cat to cat through typical transmission mode. Some pre-historic cats in turn passed it onto other cat species. Eventually one bit a monkey which escaped the attack and survived. FIV again figured out the monkey's immune system to become SIV. Some thousand years later through humans hunting and butchering monkeys, SIV found a way to infect humans.

4.2.4.1. Significance

FIV research involving evolutionary studies of lions and other cats may provide a lead to combating HIV. Lions are still around because some natural engineering has taken place. The lions' T-Cells hold up against the virus. Because FIV is constantly evolving it may one day again start killing lions
FIV in Lions indicates that AIDS is similar to many immunodeficiency viruses and they affect many species and that human suffering of AIDS is typical of this stage of virus-host coevolution.
Relationship between FIV infection and susceptibility to new viruses such as Canine distemper?

4.2.5. Panleukopenia

Feline panleukopenia (also called feline distemper, cat plague, cat fever, feline agranulocytosis, and feline infectious enteritis), is an acute, highly infectious parvoviral disease affecting members of the Felidae, Procyonidae and Mustelidae.

4.2.5.1. Transmission and Development

Shed in all body secretions and excretions of affected animals.
Recovered animals may shed virus for months.
Fleas and other insects, especially flies, may play a role in transmission of the disease.
The route of infection is either inhalation or ingestion of infective material by a susceptible host. Virus affects all rapidly dividing cells including cells of the intestinal mucosa, bone marrow and reticulo-endothelial system.

4.2.5.2. Clinical Signs

High fever with some animals dying peracutely.
Usually, high fever is followed by depression, vomiting, anorexia, diarrhea, and a profound leukopenia and subsequent severe dehydration.
In a wild animal, disease may progress similarly or may be characterized by an encephalitis syndrome with central nervous system disturbances, convulsions, or ataxia.
The course of the disease is short and rarely lasts over one week. Mortality is high and may reach 100% in susceptible animals.

4.2.5.3. Diagnosis

Presumptive diagnosis: necropsy findings and the demonstration of leukopenia with a marked absence of granulocytes on differential blood cell count.
Definitive diagnosis: based on histological examination and laboratory analysis of affected tissues.
Pathological lesions of feline panleukopenia are found primarily in the bone marrow and small intestine. Necropsy findings include an empty intestinal tract, hemorrhagic small intestine, hemorrhagic and edematous mesenteric lymph nodes, and a fluid-like appearance of the bone marrow of the long bones.

4.2.5.4. Treatment and Control

No treatment practical in wild felids. Supportive care and prevention of secondary bacterial infection for domestic cats. Vaccination of susceptible domestic species to decrease the number of potential hosts which may infect wild felids.

4.2.5.5. Significance

Impact on wild populations thought to be small. Bobcats are very susceptible however, only one animal has been positively diagnosed with the disease. Disease is not transmitted to humans.

4.3. Parasitic Diseases

4.3.1. Sarcoptic Mange (Sarcoptes scabiei)

4.3.1.1. Description and Distribution

Skin disease of mammals caused by a tissue-burrowing arthropod, the mange mite.
Several identified mange mites in wildlife including Sarcoptes scabiei and Notoedres douglasii among others.
Too small to be seen with the naked eye, but skin pathology can be dramatic.
Skin diseases caused by these species of mites are sarcoptic and notoedric mange.
Sarcoptic mange has been reported in red fox, coyote, gray wolf, porcupine, black bear and cottontail rabbit.
Notoedric mange has been reported in North America in the eastern fox squirrel and the gray (black) squirrel.
Sarcoptic mange mites are less host-specific. Notoedric mange mites are host specific for squirrels.

4.3.1.2. Transmission and Development

Spread to new hosts is through direct body contact or by use of common nests and burrows.
Stages in the life cycle include the egg, larva, 2 nymphs and the adult. The parasite lives and burrows in the skin layers. Fertilized females deposit eggs as they tunnel through the skin, and the eggs hatch in 3 to 4 days. Males complete their development in 13 to 16 days, females in 18 to 23 days. Fertilization apparently takes place when the female is in its final stage of development.

4.3.1.3. Clinical Signs

Thinning and loss of hair, thickening and wrinkling of the skin, and scab and crust formation.
In advanced cases, animals are emaciated and weak.

4.3.1.4. Diagnosis

Skin scrapings examined under a microscope for the presence of mites.

Disease particularly pathologic to foxes, especially in pups in the summer. The hair becomes sparse, the skin inflamed and irritated. Tissue serum and pus resulting from bacterial infection in the damaged skin combine to form a thick, odorous crust over the affected areas. Skin changes around the eyes, ears and mouth may cause blindness, impaired hearing and difficulty in eating. Disease can be fatal to red foxes.

4.3.1.5. Treatment and Control

Mange is effectively controlled through application of acaricidal compounds: ivermectin is the treatment of choice.
Treatment generally not feasible for wild free-ranging mammals except in very isolated populations.
Elimination of mangy animals to reduce opportunities for transmission of the parasite is sometimes suggested but effectiveness of procedure is questionable, because the parasite is likely widespread before infestations become obvious.

4.3.1.6. Significance

A marked decline of foxes in several states has been attributed to mange. Mange appears to be a contributing factor, if not a primary one, in squirrel mortalities in cold weather.
Zoonotic: wear rubber gloves and wash promptly after handling a diseased animal. Freezing kills the mites, therefore freeze carcasses of deceased animals before examination.

4.3.2. Baylisascaris Procyonis (Raccoon roundworm)

4.3.2.1. Description

Zoonoses
A large roundworm parasite that spends a portion of its life cycle in the intestines of raccoons. Worm does not harm the raccoon, but can cause serious illness in humans and other non-target species (e.g. birds).
The single most common cause of clinical larval migrans in animals (Mammals/birds)

4.3.2.2. Transmission

Adult worms shed millions of microscopic eggs daily that are passed in the raccoon's feces. Eggs can survive for months to years in the environment. Parasite is transmitted when the eggs are ingested by another animal.
Humans generally become infected from accidentally ingesting eggs from soil, water, hands, or other objects contaminated with raccoon feces.
Young children are at greatest risk due to their tendency to put their fingers or objects into their mouths (reported deaths in PA, IL, MN, NY, CA). Hunters, trappers, taxidermists, and wildlife rehabilitators are also at increased risk if they handle raccoons.

4.3.2.3. Clinical Signs

Severity of disease depends on how many eggs are ingested. Eggs hatch into larvae which then cause disease by migrating through the central nervous system, eyes, and other organs.
Symptoms include nausea, lethargy, liver enlargement, ataxia, loss of muscle control, coma, and blindness. Fatalities are rare. Symptoms appear one to three weeks post-infection, although they may take as long as two months. Interval depends on the number of eggs ingested.

4.3.2.4. Treatment and avoidance

There are no consistently effective treatment regimens.
Keeping raccoons as pets should be discouraged. Young and neonate raccoons are often infected. Raccoons used in education or on exhibit should not be allowed direct contact with the public.
Discourage raccoons near houses by eliminating access to food sources (garbage cans and bird feeders.) Raccoons may nest in (and defecate on) places like woodpiles, attics, chimneys, sheds, and barn lofts.
Contaminated wood, soil, hay or straw should be removed and burned or deeply buried in a site remote from houses. Wear disposable gloves, boots, and a dust mask (such as a painter's mask) when disposing of such material. Contaminated surfaces can be decontaminated by flaming with a propane torch (used for concrete and other non-flammable surfaces) or with boiling Lysol.

4.3.3. Other Parasitic Infections

4.3.3.1. Heartworm

Dirofilaria immitis
Found in coyotes, foxes, otters, ferrets
Effects on wild populations of canids are unknown but it does not appear to be limiting them in the NE.

4.3.3.2. Lice

Trichodectes sp.
American Black Bears trombiculid mites (25% of some southern pop.)

4.3.3.3. Fleas

Ctenocephalides sp.
Most free-ranging carnivores
Clinical signs includepruritis and flea allergy dermatitis, chronic scratching and rubbing
Severe infestations may lead to exsanguination and debilitation.

4.3.3.4. Ticks

Ixodes, Dermacentor, Amblyomma spp.
tick borne diseases (piroplasmosis, borreliosis, tularemia, rickettsiosis, tick borne encephalitis)
Anemia in young animals

4.3.3.5. Demodectic Mange

Demodex sp.
Cigar shaped mites live within the hair follicles
Iinfestation transmitted from lactating female
Usually see clinical signs following an immunodeficiency and then will see erythema and alopecia primarily on head region

4.3.3.6. Toxoplasmosis

Toxoplasma gondii
Enteric sporozoan of felids.
Domestic cat is definitive host.
Also see in Jaguarundi, leopard cat, ocelot, cougar, bobcat, cheetah where they may act as an intermediate host in the intestinal form or with a tissue form
200 + intermed. hosts identified in mammals and birds.
Wild significance: none at this time.

4.3.3.7. Piroplasmosis

Babesia sp.
Hemolytic anemia.
In southern US bobcat is the natural host involving a nonclinical parasitemia.
Trypanosoma sp., Hepatozoon sp., Theileria sp. found in wild lions and cheetah with no pathogenic lesions.

4.3.3.8. Giant Kidney Worm

Dioctophyma renale
Affects carnivores and swine. Definitive host is the mink.
Reported in red wolf, gray wolf, coyote, maned wolf, grey fox, raccoon, coati, otter, and other mustelids.
Eggs are passed in urine and are ingested by an oligochaete annelid.
Fish and frogs are paratenic hosts and when eaten infect carnivore (e.g carnivores feeding on salmon)
Usually go to the right kidney but have been found in other abdominal sites in wolves

4.3.3.9. Echinococcus

Most important in dogs, however wild carnivores can also be infected.
E. granulosus in dogs, large canids and felids
E. multilocularis in dogs, small canids and felids

4.3.3.10. Trichinella

Some wild species infected: Hogs (feral, wild) Bear, Fox, Wolf, Cougar, Seal, Walrus
Consumption of raw meat containing cysts
Cases do occur in people associated with eating game

1. Learning Objectives

2. Basic Information

2.1. Taxonomy

2.2. Conservation

2.3. General Characteristics

3. Captive Carnivore Husbandry and Health Issues

3.1. Husbandry

3.1.1. Captive carnivore settings

3.1.2. Housing

3.1.3. Nutrition

3.2. Restraint

3.2.1. Manual restraint

3.2.2. Chemical restraint

3.3. Preventative medicine

3.3.1. Vaccination Recommendations for Captive Carnivora

3.3.2. Quarantine

3.3.3. Routine examination

3.4. Health Issues

3.4.1. Reproduction

3.4.2. Non-infectious diseases

3.4.2.1. Dental

3.4.2.2. Nutritional

3.4.2.3. Perinatal

3.4.2.4. Traumatic

3.4.2.5. Neoplastic

3.4.2.6. Behavioral

3.4.3. Infectious diseases

3.4.3.1. Bacterial

3.4.3.2. Viral

3.4.3.3. Parasitic