3.4.2.1. Dental

• Preventative maintenance is important

• Soft commercial diets are a problem - tartar buildup

• Fence chewing, trauma - especially broken canines, may need root canal

• Congenital

3.4.2.2. Nutritional

• Urolithiasis in Asian small clawed otter

• Obesity

• Metabolic bone disease especially in young growing animals

Lion cub - Metabolic bone disease in a lion cub fed a steak diet

3.4.2.3. Perinatal

• Maternal neglect

• Hypothermia due to maternal neglect

• Ammonia toxicity in poorly ventilated dens

Handfeeding fisher kits

3.4.2.4. Traumatic

• Trap injuries

• Hit by car

• Aggression between exhibit mates

Hit-by-car

3.4.2.5. Neoplastic

• Hepatic and biliary tumors in older bears

• Carcinomas in snow leopards (viral?)

• Many others

3.4.2.6. Behavioral

• Stereotypy common

• Self mutilation and over-grooming

• Stress-associated problems

Tiger

3.4.3.1. Bacterial

• Leptospirosis

• Clostridium

• Ehrlichiosis

• Helicobacter gastritis in cheetahs

3.4.3.2. Viral

• Rabies

• Canine distemper - gray fox, pandas, felids

• Parvovirus

• Adenovirus type 1

• Feline panleukopenia

• FIV, FIP, FeLV

• Avian influenza? - H5N1

Raccoon

3.4.3.3. Parasitic

• Internal

  • Baylisascaris procyonis (raccoons and bears)

  • Trichinella spiralis

  • Toxoplasma

  • Dirofilaria (heartworm) - prevention important for all carnivores

• External

  • scabies, fleas, etc.

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.

Distemper raccoon

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.

4.2.2.1. 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.

IFA	Negri bodies

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 are 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 heretofore 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).

Flying foxes

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

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?

4.2.5.1. 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.

4.3.1.1. 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.

4.3.2.1. 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 disinfectant.

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 include pruritis 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

• Infestation 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+ intermediate hosts identified in mammals and birds.

• Wild significance: none at this time.

4.3.3.7. Piroplasmosis

• Babesia sp.

• Hemolytic anemia.

• In southern U.S. 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