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Tufts OpenCourseware
Authors: Janet C. Martin, Gretchen Kaufman, DVM, Colin M. Gillin, D.V.M.
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OCW Zoological Medicine 2008
Ungulate 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 Ungulate Medicine will give you a good review of the major husbandry challenges, diseases, and clinical approaches to captive and free-ranging ungulate 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 ungulates and the implications for disease control

  • Understand the importance of good husbandry and preventative medicine in managing captive ungulates

  • Gain a basic understanding of the game ranching industry in the US, including the importance of preventative medicine and good husbandry practices

  • Understand the disease dynamics and social conflicts surrounding Brucella, TB, and Chronic Wasting Disease in North America.

  • Review the global significance of rinderpest and foot and mouth disease with specific reference to wildlife

  • Know the reportable diseases in this lecture


2. Taxonomy

Order Artiodactyla

Suborder Suiformes

Family suidae - pigs

Family tayassuidae - peccaries

Family hippopotamidae - hippos

Suborder Typopoda

Family camelidae - camels and llamas

Suborder Ruminatia

Family tragulidae - chevrotains

Family cervidae - deer

Family giraffidae - giraffe, okapi

Family antilocapridae - pronghorn antelope

Family bovidae - antelope, wild cattle, goats and sheep

Order Perissodactyla

Order Proboscidae

Family equidae - horses and zebra

Family rhinocerotidae - rhinos

Family tapiridae - tapirs

Family Elephantidae

Elephas maximus - Asian, subspecies indian, ceylon, sumatran, malaysian

Loxodonta africana - African, subspecies forest and bush or savannah

Sumatran rhino
Sumatran rhino

Critically Endangered UNGULATES from IUCN

Grey ox


Chiltan goat

Tadjik markhor

Walia ibex

Weems' bighorn sheep

Northern chinese argali

Kara Tau argali

Chartreuse chamois

Tatra chamois

Hunter's hartebeest

Taiwan sika

North and South China sika

Kerama deer

Shansi sika

Manipur brow-antlered deer

Cervus duvaucelii ssp. ranjitsinhi

Pere David's deer

Northern white rhinoceros

Sumatran rhinoceros

Black rhinoceros

Javan rhinoceros

African wild ass

Nubian wild ass

Somalia wild ass



Visayan warty pig

Pygmy hog


Acacia gazelle

Muscat gazelle

Hexaprotodon liberiensis ssp. heslopi

Przewalski's gazelle

Giant sable antelope

Baja California pronghorn

Wild Bactrian Camel

Saiga antelope

Russian saiga

3. Captive Ungulate Health Issues

3.1. Introduction

3.1.1. Captive settings

  • Zoological collections

  • Private collections

  • Game ranches

3.1.2. Management issues

  • Behavioral issues

    • Ungulates are prey animals - their flight response is very strong

    • Runners, climbers, jumpers and pushers

    • Very curious - know their capabilities and their reach

    • Enrichment important in enclosure design

  • Enclosure design -

    • Incorporate natural history

    • Flight distance - instinctive, designed for running, hazards of running into walls, etc. resulting in serious injury/death

    • Take advantage of psychological barriers - e.g. low brush pile for giraffes

    • Fencing - accommodate strength

    • Access/restraint devices (chutes)

    • Pools (water quality), ditches and moats (may be dangerous)

    • Substrate (pasture, dry lot, concrete, straw, rocks) - important for foot health and behavioral needs (rooting in pigs)

    • Shelter - adequate shelter for climate and type of animal, include shade requirements

  • Nutrition

    • Grazers vs. browsers - commercial preparations now available to feed with supplements

    • General feeding based on domestic parallels

    • Hay quality very important

    • Errors occur that do not take into account browser specific requirements and natural nutritional ecology

      • Browse also provides enrichment

  • Transport/Quarantine -

    • Behavioral concerns/safety issues - narrow, tall, dark box may be best

    • Disease testing

    • Quarantine

  • Restraint and handling

    • Operant conditioning extremely valuable - requires adequate administrative commitment and a serious program

    • Physical restraint - "brute-i-caine" no longer acceptable, rely on gates, chutes, crushes and training to avoid anesthesia

    • Standing sedation - very useful in some instances, including use of long acting anxiolytics (e.g. haloperidol)

    • Chemical restraint - fast x 3 days prior to planned anesthesia, keep in sternal recumbency to avoid regurgitation and aspiration pneumonia, reduce light and noise stimulation with eye covers, cotton in ears, use reversible drugs whenever possible

  • Reproduction

    • Generally easy, some problem species (e.g. giraffe)

    • Contraception, surgical options less desirable, reversible options preferred (progesterone implants, PZP vaccines)

    • Surplus issues, "management euthanasia"

    • Aggression issues, especially with too many males


3.2. Preventative medicine

Preventative medicine starts before the animal arrives at the zoo. This is the major activity of a zoo veterinarian. Fire-engine medicine is no longer the rule.

3.2.1. Vaccination recommendations for captive ungulate species

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 .

Some vaccinations to consider:

  • Clostridium (various)

  • Leptospirosis

  • Erysipelas

  • Equine Herpes I


  • Anthrax

  • Rabies

  • West Nile virus vaccination routinely done for equids now.

Killed vaccines should always be used whenever possible.

3.2.2. Annual checkups

  • Performed when possible

  • Risks of anesthesia must be considered (e.g. zebras not routinely examined)

3.2.3. Pre-shipment testing

This is an important first step usually resulting from an agreement between the source institution and the destination institution. Take care of issues before they arrive. Testing will often include:

  • Tuberculosis

  • Serology for various diseases

  • Routine blood work

  • Fecal parasite checks

  • Fecal cultures

  • Include specific inter-state transport requirements

3.2.4. Quarantine

  • 30 day minimum in isolation

  • PE and baseline blood testing

  • Appropriate serology ( brucellosis, leptospirosis, IBR, BVD, MCF, anaplasmosis, blue tongue)

  • Vaccination as appropriate

  • T B testing when possible

  • 3 negative fecal examinations

3.2.5. Routine deworming / Parasite control

  • 2 x yearly monitoring and treatment

  • Quarterly worming when necessary with rotating anthelmintics (annual?)

3.2.6. Stress reduction

Minimizing stress for wildlife in captivity is another important component to preventative medicine. Chronic stress can cause immunosupression and make an animal more susceptible to developing diseases and also potentially produce unhealthy behaviors such as stereotypy and aggression.

  • A well defined enrichment program is an important tool to prevent boredom and maintain healthy behavior.

  • Keep animals in appropriate social groupings to meet their needs (as defined by their natural history)

3.3. Health issues common to many ungulates

3.3.1. Infectious diseases

Beware of the many zoonotic diseases shared between ungulates and people. Take precautions to protect yourself, staff and the public by limiting shared spaces and providing adequate hand washing stations, etc.

  1. Tuberculosis

Management/transport implications; no testing required between zoos by feds, however, states set their own rules; test and slaughter often still prevails (endangered species?). Note that veterinarians need a separate special accreditation for cervid TB testing.

  • M. Bovis

  • M. Paratuberculosis

  • M. Tuberculosis - particularly problematic in elephants

TB testing problems - M. Bovis / M.Avium

  • Single intradermal test - intradermal tests often see cross reactivity with other organisms, caudal fold not very sensitive in cervidae so neck region is preferred

  • Comparative cervical test - compares bovine with avium, but not very accurate especially in cervids for differentiating

  • BTB (blood tuberculosis test, good, but $$) combination of assays: Elisa serology, lymphocyte transformation tests

  • Antigen 85 Dot Blot Immunoassay - detects serum proteins actively secreted by mycobacteria

  • New Rapid Test (RT)/Mapia under development for serologic diagnosis, soon to be approved (Chembio )

  • Culture often definitive, but growth takes time and problematic. Animal must be shedding for culture to be successful.

  • Johnes culture can take >3 months which may be too long for pre-shipment requests?

  • Treatment? Isoniazid +

Take care at necropsy to protect yourself for possible unknown cases! - gloves and mask Malignant Catarrhal Fever in artiodactylids

  • Wildebeest natural reservoir

  • Sheep domestic reservoir

  • R/O IBR, blue tongue, EHD, BVD, rinderpest, F & M

3.3.2. Non-infectious diseases Neonatal care (<72 hr.)


  • Birthing area substrate issues - need good footing that is also clean (outdoors best)

  • Dam vs. hand rearing - behavioral issues with hand reared ungulates

  • Neonatal examination

    • Generally wait 24 hr. to allow for maternal bonding, observation only unless there is an obvious problem

    • Sometimes not possible e.g. with zebra foals

    • Check for suckle reflex, fully formed soft palate, patent anus, palpate abdomen, auscult for heart and lung problems, determine sex, take body weight and dip navel (iodine)

    • Colostrum, FPT assessment

    • Vitamin E/selenium

    • Vaccination

    • Iron (suidae) etc. Hoof problems

Rocky mountain goat
Rocky mountain goat

  • Abscesses

  • Overgrowth

  • Pododermititis, leading to osteomyelitis

  • Substrate and adequate exercise important

  • Trimming may become part of routine care Skin problems

Pyoderma in the skin folds of a captive rhinoceros.
Pyoderma in the skin folds of a captive rhinoceros. Dental care

  • Tooth root abscesses (lumpy jaw)

  • Overgrown molars (as in a horse)

  • Congenital malformations

  • Trauma

  • Hippos overgrown teeth

  • Tusk issues in pigs may need regular trimming Trauma

  • Dominance aggression - capping horns?

  • Stress induced Capture myopathy

  • Common to most ungulates

  • Can be induced by conspecifics (chasing) as well as during capture/restraint

  • Can have delayed effects

  • Relationship with hyperthermia

  • Prevention is key! Vitamin E deficiency

  • May be linked to feed quality

  • Dietary concerns (specialized requirements often not well-defined, absence of fresh fodder, availability of nutrients)

  • Variation in Vitamin E metabolism across species Neoplasia

3.4. Focus on Elephants

  • Zoo and circus elephant ethics

  • Working elephants


3.4.1. Anatomy/Physiology

  • Male African avg. 4100-5000kg

  • Sinus filled skull

  • Teeth

  • Skin - routine care very important, especially bathing

  • Intra-abdominal testicles

  • Tusks (modified incisors)

  • Trunk

  • Lungs - absent pleura

  • Accessible veins - venipuncture sites

Blood sampling
Blood sampling

3.4.2. Captive restraint and handling

  • Chaining & target training

  • Free contact vs. protected contact

    • Free contact involves some negative reinforcement in training

    • Veterinarian at very high risk in free contact situations

    • Protected contact provides for a barrier between human caretakers and the elephant. The keeper or vet never goes into the same space as the elephant at the same time.

    • Protected contact uses positive reinforcement, operant conditioning

    • See AZA standards for elephant care at

  • Narcotics and anesthesia



3.4.3. Infectious diseases

  • Anthrax

  • Salmonellosis

  • TB - M. TB, M. bovis

    • Testing recommended annually

    • Trunk wash technique

  • Tetanus

  • Enterotoxemia

  • Herpesvirus

  • Pasteurellosis

  • Rabies

  • Foot and mouth

  • Elephant pox (zoonotic)

  • Encephalomyocarditis virus

3.4.4. Noninfectious diseases

  • Colic

  • Dental problems

    • Problems with molar teeth progression

    • Cracked or broken tusks

  • Skin problems

  • Foot problems

    • Routine care by keepers critical

    • AZA requires annual radiographs of feet

  • Degenerative joint disease

  • Trauma

  • Colic

  • Foreign body ingestion, choke

  • Heatstroke

  • Frostbite (margins of ear)

  • Ear slough

  • Parasites

  • Nutritional problems, esp. baby elephants


Sole infection
Sole infection

3.4.5. Reproduction in captivity

Bull elephant
Bull elephant

  • Sexual maturity 6-7 years (don't breed until 8 yrs.)

  • Estrus 13-16 weeks (plot serum progesterone weekly)

  • Pregnancy diagnosis with increased progesterone longer than expected

  • Gestation 20-22 mos.

  • Natural breeding issues - have to have bull facilities? or ship animals (challenging)

  • AI is starting to work out, but very intensive and expensive. Use a fiberoptic colonoscope.

3.5. Focus on Giraffe


  • Captive management

  • Reproduction/hybridization issues

  • Restraint issues

  • Foot problems

  • Diseases: common to most ruminants; peracute mortality syndrome - stress and poor or inadequate (?) nutrition

3.6. Focus on Rhino

White rhino
White rhino

  • Captive management

  • Handling/restraint - training helpful

  • Vitamin E issues - free-ranging black rhinos have much higher alpha-tocopherol levels, also need to use d-alpha-tocopherol polyethylene 1000 succinate to supplement; encephalomalacia in black rhino calves

  • Acute hemolytic anemia in black rhinos (leading cause of death in captives)

  • Creosote poisoning in black rhinos

  • Ulcerative stomatitis/dermatitis

  • Fungal pneumonia

  • Hemosiderosis

Young rhino
Young rhino

3.7. Focus on Game Farming/Ranching

3.7.1. Economics

Captive elk
Captive elk Products

  • Exhibition, hunting, sale of breeding stock

  • Venison, antlers, hides, etc.

  • Antlers sold for trophies and medicinal purposes in Asia (tx. for lumbago, mastitis, ecchymosis, carbuncles, tuberculosis in bones and joints, impotence, spermathorrea, frequent urination, wet dreams, vertigo and anemia, pharmacologically shown to have gonadotrophic, hematopoietic, hypotensive effects, protective against shock, growth stimulant, retarding aging, etc.).

  • Antler also used in combination with acupuncture Species involved

  • White-tailed deer

  • Axis deer

  • Blackbuck

  • Mouflon

  • Aoudad

  • Fallow deer

  • Sika

  • Nilgai

  • Bison

  • Wapiti (American elk)

  • Reindeer

  • Red deer

  • Others Regulation

  • Much looser than for domestic livestock

  • Endangered Species Act and Animal Welfare Act

  • Require TB testing of all cervids moved interstate (test not reliable)

  • Variable individual state regulations, must check for exact requirements

CWD regulations
  • Ban on selling meat or velvet products from infected herds is part of the CWD eradication and control program developed by the United States Department of Agriculture (USDA) and the Canadian Food Inspection Agency (CFIA).

  • Mandatory CWD "surveillance" of herds. This mandate requires each and every brain of a farmed elk or deer that perishes for any reason to be submitted to the USDA's National Veterinary Services Laboratory in Ames, Iowa for examination.

  • It is prohibited to move ANY animal off of a farm where any CWD case has been diagnosed. Herds identified with CWD are being depopulated.

  • See also discussion below

3.7.2. Management issues Types of operation

  • Game and Ranch operations involve fenced production systems

  • Farming is more intensively managed

  • Sport game hunting is not permitted in very many places Fencing

  • Fencing specific for the species

  • Fences as high as 10' may be required

  • System of paddocks and alleyways and sheds, with appropriate chutes, gates and squeezes or crushes

  • Animals must be appropriately acclimated to the system to avoid panic and injury. Animal handling

  • Handling and restraint facilitated by management practices, farm layout, fence design, etc.

  • Safety for the animals and handlers is an important issue

  • Danger from the head (antlers, horns, crushing blows, biting), forelimbs, hindlimbs, and body slams

  • Use of remote injection systems sometimes needed, requires knowledge of anesthetics

3.7.3. Preventative medicine Quarantine

  • Usually not carried out

  • Recommended to have separate quarantine site (connected by chute to main herd)

  • 30 day quarantine depending on place of origin

  • TB testing and fecal examination during quarantine

  • Animals should be tagged/identified Parasite control

  • Parasite control program essential (may represent > 50% of health problems seen!)

  • Beware of exotic parasites as well as domestic ones

  • Pasture rotation, routine fecal checks and anthelmintic administration similar to domestic schemes Vaccination and testing

  • Vaccination: polyvalent clostridial vaccines, leptospirosis, pasteurellosis (?)

  • Testing for brucellosis, Johnes (?), bovine TB (problematic), Anaplasmosis

3.7.4. Health issues

Nutritional issues are important as in any intensive farming/production system. Must be knowledgeable about the species, seasonal requirements, nutritional ecology in the wild state. Noninfectious diseases

  • Trauma (mostly management related)

  • Malnutrition (Under and overfeeding - management related)

  • Reproductive problems related to mismanagement Infectious diseases

  • MCF (wildebeest/AHV1 and domestic sheep/AHV2 carriers) - bison, white-tailed deer, axis deer, moose, red deer most susceptible; wapiti moderately sensitive; fallow deer resistant

  • Blue tongue and EHD - white-tailed deer

  • Bovine TB (+ herd slaughtered in Canada routinely) - issues with testing methods, unreliable caudal fold test in cervids

  • Johnes disease

  • Brucellosis, etc.

  • Chronic wasting disease - especially in elk herds in US and Canada Parasitic diseases

Important management issue as in domestic ranching.

  • Parelaphostrongylus tenuis, elaeophora schneideri

  • Lungworm

  • Fascioloides magna - fallow deer, red deal, sambar deer, sika, mule deer as well as white-tailed deer and elk

  • Ticks

  • Intestinal parasitism

4. Wild and Free-Ranging Ungulate Health Issues

4.1. Introduction

4.1.1. Significance of disease in wildlife

  • How does disease and health of wildlife affect us?

  • Why does it matter?

    • Zoonoses - Direct (Rabies, TB, Hantavirus, SARS) & Indirect (West Nile, Tick Borne)

    • Socioeconomic - Livestock & Industry

    • Biodiversity and Ecosystem Health Habitat - Human/animal relationship

4.2. Malnutrition and Starvation

  • Causes: injuries, poor teeth, parasitism, disease, digestive tract foreign bodies, tumors, increased mobility of digestive tract

  • Eliminates young, old, weak, sick

  • Winter: cold, deep snow, increased energy demands, snow covered food, stress

  • Clinical signs: lethargic, listless, unsteady skin appear loose swollen face, sunken eyes lack of subcutaneous, visceral, bone marrow fat, fat tissue and femur marrow red and gelatinous

  • Diagnosis: overall physical condition, lack of adipose tissue, examination of femur marrow in adults (production of RBC in juveniles)

  • Prevention:

    • supplemental feeding - habitat carrying capacity philosophical questions interfering with nature's checks and balances disease transmission (TB, brucellosis) expensive

    • start early - continued and surplus provided

4.3. Infectious Diseases




Morbilliviruses (6)


Bluetongue, EHD (Orbiviruses)





Rodent-borne Hemorrhagic Fever Viruses

Herpesviruses (Many)

Orthomyx- & Paramyxoviruses




Transmissible Spongiform Encephalopathy




Plague & Yersiniosis








Miscellaneous (Actinomyces, Campylobacter, Helico-bacter, Leptospirosis, Salmonellosis, Shigellosis, etc.)

Other Rickettsia diseases (Anaplasmosis, Erlichia, Heartwater, Salmon Poisoning Disease)














Biting flies



Bot Flies

Filarioid Nematodes






Hepatic Capillariasis


Liver Flukes




Amebiasis, Trichomoiasis

Piroplasms (Babesia)




4.3.1. Chronic Wasting Disease

Chronic Wasting Disease (CWD): a spongiform encephalopathy (prion disease , TSE) in deer and elk that is closely related to mad cow disease, scrapie in sheep, and Creutzfeldt-Jakob disease in humans.


The brain of a sheep with scrapie
The brain of a sheep with scrapie

CWD has been reported in mule deer, black-tailed deer, white-tailed deer, Rocky Mountain elk, and possibly one pronghorn antelope. Red deer are likely susceptible as well. CWD transmits efficiently to mink and then to hamster experimentally. There is no known documentation of transmission to humans. For the latest information see Supplemental Readings Theory of origin of CWD

  • First case of CWD was seen in 1967 in a captive mule deer at the Foothills Wildlife Research Station (operated by the Colorado Dept. of Wildlife) in Ft. Collins and was attributed then by station employees [10] to close confinement of deer to former (scrapie) sheep pasture or to horizontal transmission from sheep allowed into the pens.

  • Shortest known incubation time in deer is 17 months, dating the exposure back to 1965-66 or earlier. Surplus does were released back into the wild after fawning in the facility; the first case in free-ranging wild deer was seen in 1981. Other infected animals were shipped to zoos (Denver, Toronto, Laramie), game farms and similar research facilities in Colorado and Wyoming.

  • The origin of chronic wasting disease (CWD) is not known. It was first recognized in captive mule deer and probably was transmitted from deer to elk within the same facilities in Colorado and Wyoming. These animals were not fed British meat and bone meal and strain typing has shown that CWD is NOT BSE. CWD occurs in free-ranging mule deer, white-tailed deer, and elk in a geographically limited area of southeastern Wyoming and northeastern Colorado. The origin of CWD in farmed elk has not been determined. CWD affected farmed elk herds have been identified in 8 states and 2 Canadian provinces.

Alternate theories include:

  • A naturally occurring prion genetic disease; possible but not supported by recent genotyping studies

  • Transmission at winter feeding stations via rendered downer cow protein (i.e., a non-UK strain of bovine spongiform encephalopathy) or CWD deer or elk recycled as rendered road kill. CWD deer are commonly observed at a feeding station on Lexington Lane in Estes Park, Colorado Clinical signs

  • Loss of fear of humans

  • Ataxia, weakness, inability to stand

  • Dehydration

  • Rough dull haircoat

  • Excessive salivation

  • Drooping of head and ears

  • Severe emaciation Diagnosis

  • Antemortem test on lymph node aspirate/biopsy shows promise.

  • Examination of brain medulla tissue

  • Histopathology: brain fixed in formalin, stained

  • Antigen EIA quick screen test (IDEXX )

  • Immunohistochemistry (IHC): formalin-fixed brain and/or retropharyngeal lymph node tissue (Gold standard). Prion antibody stains cells around vacuoles seen with hematoxylin and eosin staining. Amyloid plaque is most obvious in white-tailed deer, present but less conspicuous in mule deer, not usable diagnostically in elk. Parasympathetic vagal nucleus is first site of prion deposition in sub-clinical animals.

  • Western blot: Fresh, non-fixed tissue. Prion protein resistant to protease K is stained on a molecular weight gel with prion antibody.

  • Capillary gel electrophoresis: a very sensitive new method for detecting tiny amounts of rogue prion protein, tests on elk and deer now underway at ARS, Ames, Iowa to measure degree of contamination of blood.

  • In vitro conversion: the efficiency of CWD prion at converting normal prion of other species to rogue prion of that species. This test showed BSE and scrapie equally capable of converting normal human prion to the form associated with disease. Results with CWD and human prion are expected to be published shortly.

  • Strain-typing: Different strains of CWD may exist. These involve different degrees of glycosylation, different fragments of the full prion protein, and varying 3-dimensional conformations. Strain properties are generally maintained fairly well during passage to a new species, possibly allowing a dietary source of human infection to be identified. CWD strains expected to pass easily to sheep and cattle because the prion gene sequences are very similar; deer and elk commonly share pastures with cow and sheep. Where is it now, where is it going?

Visit the USDA APHIS site for the latest information. CWD regulations & management strategies

  • A ban on selling meat or velvet products from infected herds (United States Department of Agriculture (USDA) and the Canadian Food Inspection Agency (CFIA)).

  • Mandatory CWD "surveillance" of herds. This mandate requires each and every brain of a farmed elk or deer that perishes for any reason to be submitted to the USDA's National Veterinary Services Laboratory in Ames, Iowa for examination.

  • It is prohibited to move ANY animal off of a farm where any CWD case has been diagnosed. Herds identified with CWD are being depopulated.

  • Wild herds managed by State programs utilize direct intervention or regulated hunting. Translocation from infected zones prohibited.

  • Current moratorium on importation of all cervids into Massachusetts

4.4. Viral Diseases

4.4.1. Rinderpest (morbillivirus)

  • Rinderpest is enzootic in parts of eastern Africa, India, Pakistan and Sri Lanka, where it may cause only mild or inapparent infection. The disease spread through Africa at the turn of the century, killing around 90% of all cloven-hoofed animals in its path.

  • The devastating pan-African epizootic that started in the Horn of Africa in 1889 took a mere seven years to spread the length of the continent to South Africa. As it raced southwards it decimated between 80% and 95% of all cloven-footed animals; domestic cattle, sheep, goats, and pigs along with buffalo, giraffe, wildebeest, and antelope. In South Africa alone two and a half million cattle died before rinderpest was eradicated in 1905. This southerly spread of rinderpest was one of the most devastating impacts of a disease on an animal populations in recorded history.

  • Pandemic affected buffalo, cattle, eland, and wart hog peracutely and acute disease seen in bongo, bushbuck, African bush pig, dik-dik, duiker, giant forest hog, giraffe, wildebeast, hippopotamus, impala, kudu, oryx, topi, gazelle Clinical Signs

  • Animals affected by the virus experience a sudden onset of clinical signs, manifested by high fever, nasal and ocular discharge, erosive lesions of the mucous membranes, and dysentery.

  • Clinical signs can vary greatly depending of the strain of virus and the susceptibility of the host. Generally there is a high fever 6-9 days after infection with inflammation and swelling of the mouth, nasal cavity, and vagina/vulva. Severe lacrimation (tearing) and salivation occurs, eventually turning purulent and possibly blood-stained. Necrotic lesions occur in the area, and they eventually join together so that the mucosa will slough off leaving an underlying raw exposed area. The same type of lesions occur in the intestine, leading to diarrhea and dysentery. After 3-5 days the temperature becomes subnormal, and shock and prostration lead to death.

  • High morbidity and high mortality are key indicators of this disease. Transmission

  • The major form of virus transmission is by direct contact between animals. The virus is present in the affected animals' exhaled breath, nasal and ocular discharges, saliva, feces, urine and milk.

  • Virus does not survive for long outside the infected host. Indirect transmission is not an important feature of this disease. Significance

Rinderpest is targeted for global eradication by the WHO. It still occurs in isolated outbreaks in Eastern Africa. The fear in people comes from knowing how quickly and easily rinderpest spreads through and between herds. It is usually introduced by infected goats or sheep, with catastrophic effects in susceptible cattle and wild buffalo. OIE List A REPORTABLE Disease

Current global status of Rinderpest (OIE)
Current global status of Rinderpest (OIE)

4.4.2. Foot and Mouth Disease

  • Foot-and-mouth disease affects all cloven hoofed animals producing vesicles in the mouth, on the teats, and on the skin between and above the hoofs.

  • Low adult mortality, decreased production.

  • Distribution - Asia, the Middle East, parts of Europe, Africa and South America.

  • Genus Aphthovirus; family Picornaviridae

  • Wild buffalo (Africa) and domestic cattle may act as carrier reservoir species for the disease for several years following infection

  • Other than buffalo, wildlife is sporadically affected as "spill-over"

  • Look-a-likes: Vesicular stomatitis, MCF

  • OIE List A REPORTABLE Disease - U.S. is classified as FMD free

4.4.3. Parapoxvirus (Contagious ecthyma)

  • Similar to "orf" or contagious ecthyma in sheep

  • Only deer species of virus is found in New Zealand (separate from virus in sheep but similar disease)

  • There was a single reported case in Saskatchewan in a wapiti calf Transmission

  • Direct contact with active lesions, exudate or scabs in the environment (hardy virus)

  • Rough pasture may play a role Clinical signs

  • Usually scabby lesions on muzzle, lips, face, ears, perineal area and growing velvet

  • A more serious disseminated disease including leg lesions

  • Secondary bacterial infections can complicate healing Diagnosis

  • Diagnosis is through electron microscopy (EM) as a member of the parapoxvirus group Treatment

  • None, the animal usually recovers spontaneously

  • Antibiotics may be indicated if a secondary bacterial infection has occurred Control

  • No vaccine for deer

  • Suggested that farmers keep incoming animals isolated Significance

  • Financial loss associated with infections in hinds and calves near calving, stags in velvet, and recently stressed or transported animals

  • Zoonosis from sheep, goats, and potentially from deer, self limiting, painful lesions

  • Wild ovids, caprids and other ungulates

  • In Bighorn Sheep see with overpopulation and other stress factors

  • Seen in Bighorn Sheep lambs (AK, CO, NV, NM, CA, Canada)

4.4.4. Malignant Catarrhal Fever

Malignant catarrhal fever (MCF) is a disease which occurs worldwide in cattle, buffalo, deer and other wild bovidae (bongo, Pere David's deer, gaur, Sika deer, European and American bison). The disease occurs in two forms; wildebeest-associated MCF which is caused by alcephaline herpesvirus-1 and sheep-associated MCF from which the causal virus has not yet been isolated. However, recent DNA studies indicate a herpesvirus, provisionally called ovine herpesvirus 2, related to the wildebeest virus, is the cause of the disease.

The wildebeest-associated form of MCF is transmitted to cattle by wildebeest and possibly hartebeest and does not occur outside Africa except where these animals are held in zoos with other susceptible bovidae.

  • Wildebeest-Associated herpes virus causes MCF in cattle

  • Shed in nasal and ocular lesions of wildebeest calves during the first 3 months of life

  • In wildebeest calves, is in cell-free state. In cattle and adult wildebeest the virus is cell associated.

  • Disease associated with wildebeest calving season

  • No clinical disease described in free-living wildebeest, topi, hartebeest, oryx. Clinical signs

  • In deer, the disease occurs as an acute hemorrhagic enteritis, although more typical chronic forms of the disease have also been reported.

  • Rapid onset of bloody diarrhea, dark stained urine, depression and death within 48 hrs.

  • Pathogenesis of the disease showed the cause of death was vasculitis with terminal disseminated intravascular coagulation with consumption coagulopathy. Significance

Wildebeest and sheep and goats are considered to be the principal reservoirs of the virus. No vaccine presently available.

4.4.5. Epizootic Hemorrhagic Diseases (EHD)

  • Orbivirus, Reoviridae

  • An acute, infectious, often fatal viral disease of some wild ruminants.

  • Characterized by extensive hemorrhages; responsible for significant epizootics in white-tailed and mule deer, pronghorn antelope in northern U.S. and Canada.

  • Bluetongue also occurs throughout the U.S. and Canada and the two diseases are antigenically different. However Bluetongue is REPORTABLE as an OIE List A disease. Distribution

  • Since 1890, deer die-offs from diseases which might have been EHD have occurred in various parts of North America.

  • First identification of EHD occurred in 1955 when several hundred white-tailed deer (Odocoileus virginianus) succumbed in both New Jersey and in Michigan. It was considered a new disease of deer and the name 'epizootic hemorrhagic disease' was suggested to describe its main clinical and pathological features.

  • Since these initial confirmed outbreaks of EHD, documented epizootics have occurred in white-tailed deer in South Dakota, North Dakota, Wyoming and Alberta, Canada. Suspected EHD outbreaks have occurred in Missouri, Washington, Nebraska, Iowa and British Columbia. South Dakota, Missouri and Nebraska have experienced periodic outbreaks of EHD and the disease might be considered enzootic in these areas.

  • Since the initial 1955 outbreak, this malady has occurred primarily among white-tailed deer, although occasionally mule deer (O. hemionus) and pronghorn antelope (Antilocapra americana) have succumbed.

  • For news of current outbreaks, see Supplemental Readings Transmission and development

The mode of transmission of EHD in nature is via a Culicoides biting fly or gnat. Culicoides variipennis is the most commonly incriminated vector in North America. A common observation in outbreaks involving large numbers of deer - as in Michigan, New Jersey and Alberta - is that they are single epizootics which do not recur. Die-offs involving small numbers of deer - as experienced in South Dakota and Nebraska - occur almost annually, and the disease appears to be enzootic in these areas. All documented outbreaks of EHD have occurred during late summer and early fall (August-October) and have ceased abruptly with the onset of frost. Clinical signs

  • Clinical signs of EHD and bluetongue are very similar.

  • White-tailed deer develop signs of illness about 7 days after exposure.

  • A constant characteristic of the disease is its sudden onset.

  • Deer initially lose their appetite and fear of man, grow progressively weaker, often salivate excessively, develop a rapid pulse and respiration rate, and finally become unconscious.

  • Hemorrhage and lack of oxygen in the blood results in a blue appearance of the oral mucosa, hence the name 'bluetongue'.

  • Death in 8-36 hours: deer pass into a shock-like state, become prostrate and die. Diagnosis

  • Case history, characteristic signs and lesions, and the isolation of the virus. The epizootic nature of the disease, its seasonal occurrence, and its spectacular hemorrhagic lesions are important diagnostic signs.

  • Gross and histological lesions characterized by extensive hemorrhage. Hemorrhages range from pin-point to massive in size, and involve different tissues and organs in individual animals. No organs appear to be exempt from hemorrhage, with the most regularly involved being the heart, liver, spleen, kidney, lung and intestinal tract. Extensive hemorrhaging is the result of interference with the blood-clotting mechanism together with degeneration of blood vessel walls.

  • Generalized edema and increased pericardial fluid are consistently found in EHD. These changes also reflect the widespread interference with normal blood circulation.

  • The virus can be recovered from blood, liver, spleen, kidney, lung, heart and muscle.

  • Due to similarity of EHD symptoms to bluetongue and malignant catarrhal fever, isolation and identification of the virus is essential.

  • Methods used for virus isolation include:

    • inoculation of cell cultures

    • inoculation of susceptible sheep or deer combined with serologic monitoring

    • intravenous inoculation of embryonating chicken eggs. Treatment and control

No known effective treatment or control of EHD. Theoretically, an oral vaccine could be developed for administration through a supplementary winter feeding program. Significance

Due to high mortality rate, EHD can have a significant effect upon deer numbers in a given area, reducing the population size drastically. Hemorrhagic disease can be transmitted to other wild ruminants. The EHD virus can infect domestic animals but rarely causes disease. The virus does not infect humans.

4.5. Bacterial Diseases

4.5.1. Brucellosis (Brucella sp.)


Target species

B. melitensis

Sheep, goats and cattle

B. suis

Swine, reindeer, and cattle

B. abortus

Cattle, bison, and elk

B. canis


B. ovis

Sheep and goats

B. neotomae

Wood rats

B. maris(?)

Marine animals

Brucellosis is REPORTABLE to the USDA. Disease in humans - Zoonosis

  • Ranges from complicated, eventually fatal disease (rarely) to fever of unknown origin, frequently asymptomatic- case fatality of 0 - 1%.

  • Transmission by contact with body fluids of infected animals, ingestion, aerosol, and (rarely) by tissue transplants or sexual contact

  • Symptoms: fever, chills, night sweats, headache, arthralgia, arthritis, anorexia, nausea, weight loss, weakness, backache, abortions (rare)

  • B. melitensis principle cause of human brucellosis - clinically most severe - in USA due to ingestion of imported unpasteurized goat cheese.

  • B. ovis and B. neotomae - no known human disease Brucellosis in feral swine

  • 3 million feral swine in 23 states

  • B. suis biovars I and 3

  • Transmission: venereal, ingestion/contact with infected fetuses, placentas, fluids

  • Signs/lesions- abortion at any stage of gestation, stillbirths, weak pigs, sterility, lameness, orchitis, arthritis

  • Seroprevalence: 4% (CA) - 53% (FL) - majority of seropositives are culture positive

  • Human disease: packing plant employees, livestock owners, hunters (3 1/2 weeks after cleaning wild hog)

  • Spread to other species: cattle, dogs

  • Prevention strategies: population control, oral RB51 vaccine

  • Emerging disease issue due to disease eradication in domestic swine, increased hunting and transport of feral swine Brucellosis in reindeer and caribou

  • Reindeer: 14 herds on Seward Peninsula totaling 20,000 reindeer; caribou: several hundred thousand in western arctic herd

  • B. suis biovar 4

  • Transmission via ingestion/contact with infected fetuses, placentas, fluids- venereal(?)

  • Signs/lesions: abortion, retained placenta, lameness, sterility, orchitis, epididymitis, seminal vesiculitis, metritis, mastitis, nephritis, bursitis/synovitis

  • Seroprevalence: reindeer - cyclic - <1% - >20%; caribou - 1% - 24%

  • Human disease: 5 - 20% are seropositive where caribou is eaten

  • Spread to other species: dogs, foxes, wolves, bears, muskox, moose, cattle (experimentally)

  • Prevention strategies: 2/3 of AK herds are vaccinated ( killed vaccine 45/20)- RS I

  • Emerging disease issue due to eradication of other Brucella diseases and desire to export Brucellosis in Greater Yellowstone Area (GYA) elk

  • 120,000 elk in GYA-25,000 winter on 23 feedgrounds

  • B. abortus biovars I and 4

  • Transmission: ingestion/contact with infected fetuses, placentas, fluids

  • Signs/lesions: abortion, stillbirth, bursitis, arthritis, hygromata

  • Seroprevalence in feedground elk - 24%; non-feedground elk - <2%

  • Human disease is rare

  • Spread to other species: bison, cattle, horses, bears, moose, canids(?)

  • Prevention strategies: ballistic vaccination with Strain 19, habitat improvement, RB5 I (probably is not effective), oral vaccination(?)

  • Emerging disease issue due to eradication of brucellosis Brucellosis in GYA bison

  • 3000 bison in YNP and GTNP

  • B. abortus biovars 1 and 2

  • Transmission: ingestion/contact with infected fetuses, placentas, fluids- milk; venereal(?)

  • Signs/lesions: third trimester abortion, stillbirth, weak calves, retained placentas, arthritis, bursitis, hygromata, orchitis, epididymitis, seminal vesiculitis, metritis

  • Seroprevalence: 50% (YNP); 70% (GTNP); 46% of seropositives are culture positive

  • Human disease (?)

  • Spread to other species: cattle, elk, bears, canids, moose(?)

  • Prevention strategies: historically - strain 19 vaccination and test and slaughter- RB 5 1 (?)

  • Emerging disease issue due to eradication of brucellosis Brucellosis in Northwest Territories

  • Wood Buffalo National Park

  • 3,000 Wood Bison

  • TB, Brucellosis, Johne's, Anthrax

  • Population replacement with disease-free animals from captive herd (300-500 animals) Brucellosis in marine mammals

  • B. maris(?)

  • Transmission- ?, fecal, shedding

  • Signs/lesions: abortion with placentitis (bottlenose dolphin), subcutaneous lesions (harbor porpoise, common dolphin, striped dolphin)

  • Seroprevalence: ringed seal (4 - 40%); Atlantic walrus (12%); grey seal (23%); harbor seal (32%)-, harbor porpoise (22%)-, common dolphin (1 of 1), striped dolphin, bottlenose dolphin, killer whale, pilot whale, hooded seal (35%); harp seal (2%)- minke whale (8%)- fin whale (I 1%); sei whale (14%); California sea lion 5 of 89 (5.6%)

  • Culture positive: harbor seal, harbor porpoise, common dolphin, bottlenose dolphin, hooded seal, grey seal, Atlantic white-sided dolphin, European otter, minke whale

  • Human disease - ? (1 case in laboratory worker)

  • Spread to other species- ? (cattle-experimental inoculation caused seroconversion and abortion)

  • Prevention strategies - ?

  • Emerging disease: earliest report was in 1994

4.5.2. Tuberculosis (Mycobacterium spp.)

  • The natural reservoir for M. bovis is domestic cattle. Wild animals have become sylvatic reservoirs in some cases:

    • wild deer (US)

    • buffalo (Africa)

    • non ungulate species such as badgers (UK) and possums (NZ)

  • Bovine TB once relatively common in cattle in the U.S., it has historically been a very rare disease in wild deer. Prior to 1994, only eight wild white-tailed or mule deer had been reported with bovine TB in North America.

  • In 1994, a Michigan hunter shot a 4-year old male white-tailed deer infected with bovine TB

  • To assess the extent of the bovine TB infection in the deer population from the area surrounding where the 1994 TB deer was taken, over 17,721 deer were examined from the fall of 1995 to the summer of 1999 and 228 have tested positive for bovine TB.

  • Aerosol transmission in deer from close contact at feeding stations

  • Bovine TB has also been found in coyotes, raccoons, black bear and bobcat. The most likely source of infection for these is through eating the lungs and lymph nodes of a TB-infected deer.

    • Michigan: 1,363 carnivores tested (16 species: badger, black bear, bobcat, coyote, opossum, raccoon, red fox, gray fox, weasel, skunk, feral cat, feral dog, porcupine, otter, mink, snowshoe hare)

    • 30 Tested positive: 13 coyotes, 2 raccoons, 7 black bear, 4 bobcat, 2 red fox, 2 opossum

  • Bovine TB is occasionally a problem in captive game farms in the western U.S. (Montana) Management strategies used to eliminate bovine TB in wild deer in Michigan

  • Ban deer feeding and restrict baiting of deer

  • Reduce the population of deer

  • Reduce the average age of the deer population

  • Reduce nose-to-nose contacts between animals

  • Ban new captive deer/elk enclosures Clinical findings

  • Usually observed only after advanced stage of disease.

  • Infected animals become shedders of the bacteria.

  • Enlarged superficial lymph nodes useful diagnostic sign.

  • General signs are weakness, anorexia, dyspnea, emaciation, and low grade, fluctuating fever.

  • Organs may be involved including granulomas in the lung parenchyma and associated lymph nodes of the thoracic cavity. Diagnosis

  • Clinical signs, observance of acid-fast staining bacteria, Elisa

  • Lymphocyte blastogenic assays (bison, llama, deer, non-human primates)

  • Gene probes

Bovine TB is REPORTABLE to the USDA.

4.5.3. Mycobacterium paratuberculosis

  • Infectious bacterial disease of livestock

  • Clinical disease in Rocky Mountain bighorn sheep (CO, WY), Rocky Mountain goats (CO), tule elk (CA), captive herds of bison (MT, WY, NE), wild bison in Northwest Territories.

  • Estimated mortality 5%

  • Survives desiccation, but susceptible to UV and heat

  • Transmitted through ingestion from feces, milk

  • Management Options: no relocations and herd reduction through either sex harvest

  • Infected animals show decreased productivity and physical condition and become predisposed to predation

  • Diagnosis: thickened and folded walls of distal ileum, enlarged pale or mineralized lymph nodes, subserosal and mesenteric edema, and Thickening and cording of mesenteric lymphatic vessels.

  • Acid-fast stains of phagocytic cells (filled with bacteria), sloughed cells in feces

  • Culture of feces or tissues (Mesenteric lymph nodes, ileocecal junction) most sensitive


4.5.4. Anthrax (Bacillus anthracis)

  • Worldwide distribution

  • North American hot spots : Texas, North and South Dakota, Minnesota, Canada (S. Northwest Territories, Alberta, Manitoba)

  • All mammals, hoofstock usually first - Bison and deer. Elephants highly sensitive.


  • Soil type and climatic conditions

  • Spores when conditions not favorable

  • Infection by inhalation, ingestion, break in skin Encounter from infected grazing areas

4.5.5. Lungworm (Protostrongylosis sp.) / Pasteurella Pneumonia Complex

  • Associated with large die-offs of bighorn sheep

  • 1800's - 2 million bighorns; 1940 - 14,000 BHS, present - 40,000

  • Causes: Market hunting, association with domestic sheep, stress, poor forage and habitat conditions from competition, human development, and fire suppression, disease

  • Complicating factors: 13 different strains of Pasteurella, viruses, lungworms, scabies mites, internal parasites, fleas, and ticks

  • Pasteurella tends to be the nail in the coffin.

  • Often find Pasteurella multocida, P. haemolytica (also in healthy sheep)

  • Fibrinopurulent broncho-pneumonia often follows predisposing factors such as lungworm, viruses, nutritional, cold, behavioral stress, immunosuppression

  • See lungs bilaterally reddened, wet and consolidated, in an anterioventral distribution. Fibrinous pleural adhesions and pulmonary abscesses with cavitations. Purulent exudate expressed from sectioned bronchioles. Bloody intra-tracheal froth.

  • Generally no sex or age difference. Outcome almost always fatal.

  • Non-pathogenic strain in domestic sheep becomes pathogenic in bighorns; Domestic sheep may harbor other bacteria, viruses, mycoplasma that predispose to pneumonic bacterial overgrowth

  • Lungworm infestations often associated with higher lamb mortality but does not have to be present in all sheep to act as a predisposing factor.

  • Other species: Pasteurella multocida causes septicemic pasteurellosis in elk, bison, water buffalo (depression, salivation, congestion, petechial ecchymotic hemorrhages in lymph nodes, diaphragm, lungs and endocardium. P. multocida isolated from marrow and other tissues. Death in 24 hours.

4.6. Parasitic Diseases

4.6.1. Parelaphostrongylus tenuis

The adult brainworm (Parelaphostrongylus tenuis) is a roundworm or nematode normally found in the venous sinuses and subdural space of the brain of white-tailed deer in eastern North America. Moose, wapiti, caribou, reindeer, mule deer, sheep, goats, llamas and guinea pigs are susceptible to infection. However, they are abnormal hosts, resulting in aberrant migration and cerebrospinal nematodiasis. Distribution

  • Eastern North America where white-tailed deer exist in abundance

  • Naturally occurring cerebrospinal nematodiasis is found fairly often in moose on the southern fringe of its distribution in eastern and central North America where white-tailed deer are abundant (Nova Scotia, New Brunswick, Quebec, Ontario, Maine, Minnesota and Michigan).

  • It also occurs in elk (wapiti), caribou and reindeer introduced into areas in eastern North America where there are white-tailed deer. Transmission and development

  • Adult worm lives in the subdural space of the brain, deposits eggs on the dura mater surrounding the brain, or in adjacent small blood vessels.

  • Eggs hatch on the dura mater and young larvae emerge. The larvae penetrate small blood vessels and are swept into the lungs. Eggs deposited in blood vessels are carried directly to the lungs where they lodge in the smallest capillaries.

  • Eggs hatch and young larvae emerge. Once larvae are in the lungs, they enter bronchioles and move up the respiratory tract until they reach the throat. They are swallowed and carried through the gastrointestinal tract, and eventually leave the deer in the mucus coat surrounding the fecal pellets.

  • The mucus is fed upon by numerous species of snails or slugs and the mollusks thereby become infected.

  • After a period of development, the larvae become infective for deer. An infected snail or slug is ingested by a deer, probably accidentally, while browsing or grazing. The tiny larvae penetrate the wall of the small intestine and enter the body cavity. From there, they migrate to the spinal cord; the route they follow is not known.

  • Once in the spinal cord, they begin to grow. They remain there only a short time before they migrate to the space surrounding the cord. They then migrate along the outside of the cord to the subdural space surrounding the brain. Here they grow to maturity, thus completing their life cycle. From the time a deer is infected, 82-91 days are required before the worm matures and larvae start appearing in the feces.

parelaphostrongylus Clinical signs

  • Infection is largely silent in white-tailed deer, although temporary lameness and spasms of one front limb have been noted in fawns experimentally infected. There have been a few reports of neurologic signs in naturally infected adult white-tailed deer.

  • In naturally infected elk: an individual tends to leave its herd and remains near a road, field, or woodland clearing, and becomes less wary. Vision may be impaired. In advanced cases, the animal often walks aimlessly or in circles, and may carry its head in a tilted position. The disease is generally progressive and terminates in death, although there may be short periods of remission when the animal appears quite normal.

  • Severe neurologic disease terminating in paralysis has been produced experimentally in the young of moose, elk, mule deer, caribou, goats, sheep and guinea pigs, all of which may be regarded as unfavorable hosts. Signs of illness in these animals consisted of ataxia, lameness, stiffness, general and lumbar weakness, circling associated with blindness, abnormal positioning of the head and neck, and finally, paraplegia. Signs were variable in onset and character. Moose, elk and mule deer appeared listless and showed slight ataxia 10-60 days after infection. Signs appeared 5-7 days after infection in young caribou. In all the experimental cases, there were remissions of a short duration. Diagnosis

  • Tentative diagnosis can usually be made by finding larvae in the feces of infected animals.

  • Positive diagnosis can be made only by recovering and identifying the adult worms. In animals which develop clinical signs, worms are hard to find and diagnosis must often be based only on signs of illness and microscopic lesions.

  • The lack of pathological lesions is consistent with the absence or slightness of neurologic signs in infected deer. The neural parenchyma rather quickly assumes a normal appearance after the departure of worms, between 25 and 40 days. Lesions in the central nervous system are usually not visible grossly. In general, the lesions in elk, moose, caribou, and other abnormal hosts are similar to those in white-tailed deer, but much more severe. Treatment and control

Control of deer populations is obviously desirable, especially in areas where priority should be given to moose, elk or caribou. Control of mollusk populations is probably neither feasible nor desirable. Medical treatment of infected animals has not been reported. Significance

Cerebrospinal nematodiasis caused by P. tenuis may be responsible for the decline of moose in some areas of the United States and Canada and is a major factor preventing the establishment of moose, elk and caribou in areas where white-tailed deer are abundant. The worm is of no public health significance. The parasite is of importance to veterinarians since sheep, goats and llamas are susceptible.

4.6.2. Scabies (Psoroptes sp.)

  • Host spectrum includes sheep (wild sheep), cattle, equids, wild ruminants, goats, rabbits

  • Geographic distribution is worldwide

  • Sites of infestation are the ears ( Psoroptes cuniculi ) or on the skin of parts of the body well covered with wool or hair ( Psoroptes ovis, bovis, equi ) Clinical signs

  • Hair loss, scabs

  • Lesions are pruritic, animals rub against fences, etc.

  • Physical damage, reduced weight gain, damage to hide, possibly death Diagnosis

Diagnosis made by finding the organism in skin scrapings from the edges of active lesions

psorptes cuniculi
psorptes cuniculi Treatment

Herd capture of wild sheep and treatment with ivermectin (Subcutaneous implants). Use of biobullet in some populations of free-ranging animals. Significance

No Public health significance. Bighorn sheep may serve as a reservoir of scabies in western North America. The disease may be partially responsible for the decline and low numbers of populations in North America (Desert and Rocky Mountain bighorn sheep). REPORTABLE disease to the USDA.

5. References and Resources

5.1. Professional Organizations

American Association of Wildlife Veterinarians

American Association of Zoo Veterinarians

Wildlife Disease Association

5.2. Websites

Elk Breeders Home Page

Maine Deer and Elk Farmer's Association

North American Deer Farmer's Association

North American Elk Breeders Association

APHIS Information on

The Ultimate Ungulate Page

Wisconsin Department of Natural Resources site on CWD

National Wildlife Health Center site for CWD

5.3. Articles

Fowler, Murray E. and Miller, R. Eric. Zoo and Wild Animal Medicine, 5th ed. Saunders, 2003. Chapters: 53 - 64, 78

American Association of Zoo Veterinarians. Guidelines for Zoo and Aquarium Veterinary Medical Programs

AAZV Report of the Committee on Captive Wildlife & Alternative Livestock

Ballweber, L.R. 1999. Parelaphostrongylus tenuis and Elaphostrongylus cervi in free-ranging artiodactylids. In Fowler, M. E. and R. E. Miller (eds.) Zoo and wild animal medicine: current therapy. Fourth ed. W. B. Saunders Co. 626-628 pp.

Beard, P. M. et al. Paratuberculosis Infection of Nonruminant Wildlife in Scotland. Journal of Clinical Microbiology, April 2001, p. 1517-1521, Vol. 39, No. 4.

Chatkupt, Thomas T. and Albert E. Sollod. Elephants in Thailand: determinants of health and welfare in working populations. Journal of Applied Animal Welfare Science, Vol 2 (3), 1999, pp.187-203

Cook, R. A. 1999. Mycobacterium bovis infection of cervids: diagnosis, treatment, and control. In Fowler, M. E. and R. E. Miller (eds.) Zoo and wild animal medicine: current therapy. Fourth ed. W. B. Saunders Co. 650-657 pp.

Corbel MJ. 1997. Brucellosis: an overview. Emerging Infectious Diseases 3: 213-230.

Davis DS. 1990. Brucellosis in wildlife. In: Nielsen K, Duncan JR eds. Animal Brucellosis. CRC Press. Boca Raton, FL. pp. 322-334.

Dobson, A. and M. Meagher. 1996. The population dynamics of brucellosis in the Yellowstone National Park. Ecology 77:1026-1036.

Guidelines for Zoo and Aquarium Veterinary Medical Programs and Veterinary Hospitals , prepared by the Veterinary Standards Committee, American Association of Zoo Veterinarians, 1998.

Guidelines for Comprehensive Elephant Health Monitoring , American Association of Zoo Veterinarians, March 2005.

Gross, John E., and Michael W. Miller. Chronic wasting disease in mule deer: disease dynamics and control. Journal of Wildlife Management, 65(2), 2001: 205-215.

Haigh, Jerry C. Farming Wapiti and Red Deer. Mosby, 1993.

Heuschele, W.P. 1993. Malignant Catarrhal Fever. In: Fowler, M. E.. Zoo and wild animal medicine: current therapy. Third ed. W.B. Saunders Co. 504-506 pp.

Hunter, D. L. and T. J. Kreeger. Brucellosis caused by Brucella abortus in free-ranging North American artiodactylids. 1999. In Fowler, M. E. and R. E. Miller (eds.) Zoo and Wild Animal Medicine: current therapy. Fourth ed. W. B. Saunders Co. 621-625 pp.

Jessup, D. A. and E.S. Williams. 1999. Paratuberculosis in free-ranging wildlife in north America. In Fowler, M. E. and R. E. Miller (eds.) Zoo and Wild Animal Medicine: current therapy. Fourth ed. W. B. Saunders Co. 616-620 pp.

Jessup, D.A. and W.M. Boyce. 1993. Diseases of wild sheep. In: Fowler, M. E.. Zoo and Wild Animal Medicine: current therapy. Third ed. W.B. Saunders Co. 554-560 pp.

Kaneene, Johyn B., et al. Prevalence of Mycobacterium bovis infection in cervids on privately owned ranches. JAVMA, v. 220 (5), 2002: 656-659.

Kirkwood, J.K. and A.A. Cunningham. 1999. Scrapie-like spongiform encephalopathies (Prion diseases) in nondomesticated species. In Fowler, M. E. and R. E. Miller (eds.) Zoo and Wild Animal Medicine: current therapy. Fourth ed. W. B. Saunders Co. pp. 662-668

Manning, Elizabeth J.B., and Michael T. Collins. Johne's disease (paratuberculosis in zoo animals, Proc. of the Joint Conference of AAZV and AAWV, 1998, pp. 128-130.

Manning, Elizabeth J.B., et al. Epizootic of paratuberculosis in farmed elk. JAVMA, 213 (9), 1998, pp.1320-1322.

Meagher, M. and M.E. Meyer. 1994. On the origin of brucellosis in bison of Yellowstone National Park. Conservation Biology 8 (3): 645-653.

Mikota, Susan K., et al. Investigation of diagnostic paramters and treatment regimens for tuberculosis in bongo antelope (Tragelaphus eurycerus). Proc. of the Joint Conference of AAZV and AAWV, 1998, pp. 116-118.

Mikota, Susan K., et al. Medical Management of the Elephant. Indira Publishing House, W. Bloomfield, MI, 1994.

Mikota, Susan K.,et al. Epidemiology and diagnosis of Mycobacterium tuberculosis in captive asian elephants (Elephas maximus). Journal of Zoo and Wildlife Medicine 2001 32: 1-16.

Miller MW, Williams ES, McCary CW, Spraker TR, Kreeger TJ, Larsen CT, Thorne ET. Epizootiology of chronic wasting disease in free-ranging cervids in Colorado and Wyoming. Journal of Wildlife Diseases 36(4), 2000:676-690.

Montali, Richard J., et al. Factors influencing interpretation of indirect testing methods for tuberculosis in elephants. Proc. of the Joint Conference of AAZV and AAWV, 1998, pp. 109-112.

Moore CG, Schnurrenberger PR. 1998 1. A review of naturally occurring Brucelia abortus infections in wild mammals. J Am Vet Med Assoc 179: 1105-1112.

Murray, Suzan, et al. Idiopathic hemorrhagic vasculopathy syndrome in seven black rhinoceros. JAVMA, 216 (2), 1999: 230-233.

Palmer, Mitchell V., et al. Naturally occurring tuberculosis in white-tailed deer. JAVMA, 216 (12), 2000: 1921-1924.

Priola SA. Prion protein and species barriers in the transmissible spongiform encephalopathies. Biomedical Pharmacother. 53 (1), 1999:27-33.

Proceedings of the Workshop on Diagnosis, Prevention, and Control of Johne's Disease in Non-Domestic Hoofstock. White Oak Conservation Center, Yulee, FL, June 26-28, 1998.

Richman, Laura K., Richard J. Montali, and Gary S. Hayward. Review of a newly recognized disease of elephants cause by endotheliotropic herpesviruses. Zoo Biology , v.19, 2000: 383-392.

Rossiter, P.B. 1994. Rinderpest. In Coetzer, J.A.W., Thompson, G.R., Tustin, R.C. (eds.): Infectious diseases of livestock with special reference to southern Africa. New York, Oxford University Press. Pp. 735-757.

Sayer, P. and D. Rottcher. 1993. Wildlife management and utilization in East Africa. In: Fowler, M. E.. Zoo and wild animal medicine: current therapy. Third ed. W.B. Saunders Co. pp. 101-111.

Spraker, T.R., et al. 1997. Spongiform encephalopathy in free-ranging mule deer (Odocoileus hemionus), white-tailed deer (Odocoileus virginianus), and rocky mountain elk (Cervus elaphus nelsoni) in northcentral Colorado. Journal of Wildlife Diseases. 33 (1):1-6.

Thoen, C. O., K. J. Throlson, L.D. Miller, E.M. Himes, and R.L. Morgan. 1988. Pathogenesis of Mycobacterium bovis infection in American Bison. American Journal of Veterinary Research. 49:1861-1865.

Williams, E. S. and S.Young. 1992. Spongiform encephalopathies in Cervidae. Rev. sci. tech. Off. Int. Epiz. 11: 551-567.

Wywialowski, A. P. and M. J. Gilsdorf. 1998. Historical relationships among brucellosis and wildlife with emphasis on Brucella abortus. In: International Symposium on Bison Ecology and Management in North America. L. R. Irby and J. E. Knight (eds.) Montana State University, Bozeman, Montana pp. 45-54.