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OCW Zoological Medicine 2008
Carnivore Medicine (2008)
J. Martin, DVM, G. Kaufman, DVM, C. Gillin, DVM
Cummings School of Veterinary Medicine at Tufts University
1. Learning Objectives
This section on Carnivore Medicine will give you a good review of the major husbandry challenges, diseases, and clinical approaches to captive and free-ranging carnivore health issues. Color coded topics indicate learning objectives that the student should become familiar with. Cases will be presented in class to illustrate these topics. At a minimum, you will be expected to be familiar with the following:
Gain an appreciation for the similar disease issues across wild and domestic carnivores and the implications for disease control
Understand the importance of good husbandry and preventative medicine in managing captive carnivores
Know the vaccination recommendations for rabies, canine distemper and feline panleukopenia for the more important carnivores
Understand the disease dynamics and social conflicts surrounding Rabies, Canine Distemper and the Feline retroviruses
Understand the public health significance of Baylisascaris in raccoons.
Appreciate the role of sentinel species in conservation medicine.
2. Basic Information
dogs, wolves, foxes
bears, giant panda
raccoons, coati, kinkajou
weasels, otters, badgers, ferrets
civets, genets, fossas, linsangs, binturong
Taxonomy table based on DNA hybridization for some new thoughts on carnivore taxonomy.
Critically Endangered CARNIVORES from IUCN
South China tiger
South Arabian leopard
North African leopard
Malabar large-spotted civet
2.3. General Characteristics
Size - great variation from the least weasel 35-70 g to the grizzly bear 780 kg
Carnassial teeth and prominent canine teeth
Simple stomach, short intestinal tract (procyonids - no cecum)
Anal glands for marking
Few have a clavicle
Prehensile tails in kinkajou, binturong
Coat color seasonal change in mustelids (weasels), canids (arctic foxes)
digitigrade in canids, felids
plantigrade in ursids, procyonids
solitary (bears), pairs, or small groups (fox, otters)
usually one litter per year
altricial young - therefore often lengthy period of parental care and instruction
delayed implantation in ursids
3. Captive Carnivore Husbandry and Health Issues
3.1.1. Captive carnivore settings
Private collections - breeders
Private collections - pets
Diggers, climbers, chewers
Environmental enrichment very important for carnivores used to traveling long distances and hunting in the wild. Toys, training exercises and activities can be very useful enrichment tools.
Water quality - Marine Mammal Protection Actfor seals, polar bears and sea otters
Carnivores, Piscivores, Insectivores, Omnivores - not all carnivores eat only meat!
Natural diets vs. commercial diets - some very specialized diets available
Enrichment items and supplements
Preparation and storage important to maintain quality
live food sources must be kept clean and healthy (crickets, mice)
quality fish stocks very important, handling and preparation (DO NOT thaw fish in warm water - leaches out nutrients)
rotate frozen fish/food stocks
vary types of fish offered to keep animal from becoming dependant on one fish type
3.2.1. Manual restraint
Hand around the throat mimics dominance behavior and will make the animal relax (subordinate), scruffing is not recommended
Straw broom best for pinning in back of cage
Snare/rabies pole pretty dangerous
Squeeze cage, shift doors
3.2.2. Chemical restraint
Proper planning with team assignments and clear decision making hierarchy very important
Procedures often done on exhibit or in the den - this is the safest place for large dangerous animals
remote delivery systems
conditioning for hand injection
beware of fat layer in bears - preferable to inject in shoulder (triceps)
Oral - Carfentanil
Inhalant for long-term restraint/anesthesia
Recover in dry warm safe place (den)
3.3. Preventative medicine
3.3.1. Vaccination Recommendations for Captive Carnivora
Weigh the risks of exposure in the particular setting, modes of transmission, individual risks, and take into account regional epidemiology for particular diseases. Consult the American Association of Zoo Veterinarians Guidelines for Zoo and Aquarium Veterinary Medical Programs for recommendations.
Some vaccinations to consider:
Canine infectious hepatitis
Killed vaccines should always be used when available.
30 day minimum in isolation
PE and baseline blood testing
Appropriate serology (FIV, FeLV, FIP, Toxoplasma, Heartworm)
Vaccination as appropriate
3 negative fecal examinations
3.3.3. Routine examination
Annual PE and diagnostics
Routine maintenance (dentistry, etc.)
Reproductive exam and contraception
Neonatal exams - is it worth the stress and risks of disruption of the mother?
3.4. Health Issues
Captive propagation generally successful and easy, very important for endangered species programs
Contraception is the bigger challenge
surgical sterilization - consider this permanent, lose genetic material
chemical contraception - side effects (uterine cancer with MGA implants)
Vasectomies may be preferred - retain secondary sexual characteristics and behavior
3.4.2. Non-infectious diseases
Preventative maintenance is important
Soft commercial diets are a problem - tartar buildup
Fence chewing, trauma - especially broken canines, may need root canal
Urolithiasis in Asian small clawed otter
Metabolic bone disease especially in young growing animals
Hypothermia due to maternal neglect
Ammonia toxicity in poorly ventilated dens
Hit by car
Aggression between exhibit mates
Hepatic and biliary tumors in older bears
Carcinomas in snow leopards (viral?)
Self mutilation and over-grooming
3.4.3. Infectious diseases
Helicobacter gastritis in cheetahs
Canine distemper - gray fox, pandas, felids
Adenovirus type 1
FIV, FIP, FeLV
Avian influenza? - H5N1
Baylisascaris procyonis (raccoons and bears)
Dirofilaria (heartworm) - prevention important for all carnivores
scabies, fleas, etc.
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?
Population studies especially important in fragmented landscapes
4.1.2. Human Encroachment
Large carnivores (example: grizzly, cougar) are generally not tolerated
Direct correlation between human/wildlife conflict and the density of roads (bears and wolves)
Zoonotic disease issues (rabies) heighten pressure
4.1.3. Habitat Loss/habitat alteration
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 human-scapes
Carnivores can decrease prey density and disease incidence in a variety of ways e.g.
Brucella abortus in a crowded feed ground setting readily expose wolves
By providing habitat improvements, elk use feed grounds less and their subsequent dispersal decreases their density and reduces chance of naive animals coming in contact with infective aborted fetus.
Wolves accomplished in one month what took managers 10years.
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 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
Wolf, coyote, fox, domestic dog
African lion (rare)
Ferret, mink, weasel, martin, fisher, otter, badger, skunk, wolverine
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.
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.
22.214.171.124. 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.
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.
126.96.36.199. Treatment and Control
No treatment to cure but supportive care can save some individuals.
The virus is inactivated by heat, formalin, and Roccal R.
Removal of carcasses of animals which have died from the disease
Vaccination of susceptible domestic species (pets) to decrease the number of susceptible hosts
Reduction in wildlife populations which also reduces the number of potential hosts (?)
Eradication not possible or feasible
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.
188.8.131.52. 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.
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
184.108.40.206. 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.
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.
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)
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)
220.127.116.11. 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).
18.104.22.168. 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.
22.214.171.124. 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
126.96.36.199. 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).
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. See Recent reports in Florida Panthers (2004). ProMED-mail: 20041003.2722. <http://www.promedmail.org>. Accessed April 2009.
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 (National Cancer Institute)/ 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.
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?
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.
188.8.131.52. 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.
184.108.40.206. 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.
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.
220.127.116.11. 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.
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)
18.104.22.168. 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.
22.214.171.124. 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.
126.96.36.199. 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.
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.
188.8.131.52. 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.
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)
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)
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.
184.108.40.206. 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.
220.127.116.11. 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. Other Parasitic Infections
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.
American Black Bears trombiculid mites (25% of some southern pop.)
Most free-ranging carnivores
Clinical signs include pruritis and flea allergy dermatitis, chronic scratching and rubbing
Severe infestations may lead to exsanguination and debilitation.
Ixodes, Dermacentor, Amblyomma spp.
tick borne diseases (piroplasmosis, borreliosis, tularemia, rickettsiosis, tick borne encephalitis)
Anemia in young animals
18.104.22.168. Demodectic Mange
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
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.
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.
22.214.171.124. Giant Kidney Worm
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
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
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
5. References and Resources
5.1. Professional Organizations
American Association of Wildlife Veterinarians http://www.aawv.net/
American Association of Zoo Veterinarians http://www.aazv.org/
Wildlife Disease Association http://www.wildlifedisease.org/
Wildlife Disease Association http://www.wildlifedisease.org/
Emerging Infectious Diseases Journal http://www.cdc.gov/ncidod/EID/index.htm
Promed: an online journal for emerging diseases http://www.fas.org/promed/
Virology on the WWW http://www.virology.net/ATVarticles.html
5.3. Texts and Articles
American Association of Zoo Veterinarians. Guidelines for Zoo and Aquarium Veterinary Medical Programs
Fowler, Murray E. and Miller, R. Eric. Zoo and Wild Animal Medicine, 5th ed. Saunders, 2003. Chapters: 47-51
Bacon, Philip J. (ed.) Population Dynamics of Rabies in Wildlife. Academic Press, 1985.
Baer, G. M. 1994. Rabies-an historical perspective. Infectious Agents and Disease.3:168-80.
Childs, James E., et al. Surveillance and spatiotemporal associations of rabies in rodents and lagomorphs in the United States, 1985-1994. Journal of Wildlife Diseases, 33 (1), 1997, pp. 20-27.
Compendium of animal rabies prevention and control, 2007. The National Association of State Public Health Veterinarians Committee
Conservation Biology. Special Section: Large carnivore conservation in the Rocky Mountains of the United States and Canada . Vol. 10 No. 4, 1996: pp. 936-1058.
Deem, Sharon L., et al. Canine distemper in terrestrial carnivores: a review.Journal of Zoo and Wildlife Medicine, 31 (4): 441-451.
Fearneyhough, M. Gayne. Results of an oral rabies vaccination program for coyotes. JAVMA, 212 (4), 1998, pp.498-502.
Gould, S. E. (ed.) Trichinosis in man and animals. Charles C. Thomas, Springfield, Ill. 390 pp.
Kennedy-Stoskopf, S. 1999. Emerging viral infections in large cats. In Fowler, M. E. and R. E. Miller (eds.) Zoo and wild animal medicine: current therapy 4. Fourth ed. W. B. Saunders Co. 401-409 pp.
Krebs, John W., et al. Rabies surveillance in the United States during 2003. JAVMA, 221 (12), 2002: 1690-1701.
Laurenson, M.K., et al. Approaches to disease control in domestic canids for the conservation of endagnered wild carnivores. In: Conservation and Development Interventions at the Wildlife/Livestock Interface . IUCN SSC Occasional Paper no. 30. 2005.
McCall, Bradley J., Jonathan H. Epstein, et al. Potential human exposure to Australian Bat Lyssavirus, Queensland, 1996-1999. Emerging Infectious Diseases, 6 (3), 2000 .
Mondul, Alison M., John W. Krebs, and James E. Childs. Trends in national surveillance for rabies among bats int he United States (1993-2000). JAVMA, vol. 222 (5), 2003: 633-639.
Robbins, Alison H. Prevention of the spread of rabies to wildlife by oral vaccination of raccoons in Massachusetts. JAVMA, 213 (10), 1998, pp.1407-1412.
Roelke-Parker, M. E., Munson, L, Packer,C. et. al: A canine distemper virus epidemic in Serengeti lions (Panthera leo). Nature 379:441-445, 1996.
Roken, B. O. 1993. Parasitic diseases of carnivores. In: Fowler, M. E.. Zoo and wild animal medicine: current therapy 3. Third ed. W.B. Saunders Co. 399-403 pp.
Rupprecht, C. E., J. S. Smith, F. Makonnen, and J. E. Childs. 1995. The ascension of wildlife rabies: a cause for public health concern or intervention? Emerging Infectious Diseases. Vol. 1 No. 4
Worley, D. E., J. C. Fox, J. B. Winters, and K. R. Greer. 1974. Prevalence and distribution of Trichinella spiralis in carnivorous mammals in the United States northern Rocky Mountain Region. In Proceedings of the Third International Conference on Trichinella, C. W. Kim (ed.), Intext Press, New York, New York, pp.597-602.