3.3.1.1. 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?)

• M. Bovis
• M. Paratuberculosis
• M. Tuberculosis
• 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
• Culture often definitive
• Treatment? Isoniazid +

Take care at necropsy to protect yourself for possible unknown cases! - gloves and mask

3.3.1.2. Malignant Catarrhal Fever in artiodactylids

• Wildebeest natural reservoir
• Sheep domestic reservoir
• R/O IBR, blue tongue, EHD, BVD, rinderpest, F & M

3.3.2.1. Neonatal care (<72 hr.)

• Birthing area substrate issues - need good footing that is also clean (outdoors best)
• Dam vs. handrearing - behavioral issues with handreared ungulates
• Neonatal examination
  • Generally wait 24hr. to allow for maternal bonding
  • Sometimes not possible e.g. with zebra foals
  • Check for suckle reflex, fully formed soft palate, patent anus, auscult for heart and lung problems, take body weight and dip navel (iodine)
  • Colostrum, FPT assessment
  • Vitamin E/selenium
  • Vaccination
  • Iron (suidae) etc.

3.3.2.2. Hoof problems

• Substrate and exercise
• Trimming restrictions

3.3.2.3. Skin problems

Pyoderma in a rhino

3.3.2.4. Dental care

• Tooth root abscesses (lumpy jaw)
• Hippos overgrown teeth
• Tusk issues in pigs

3.3.2.5. Trauma

• Dominance aggression - capping horns?
• Stress induced

3.3.2.6. Capture myopathy

• Common to most ungulates
• Can be induced by conspecifics (chasing) as well as during capture/restraint
• Can have delayed effects
• Prevention is key!

3.3.2.7. Vitamin E deficiency

• Dietary concerns (specialized requirements often not well-defined, absence of fresh fodder, availability of nutrients)
• Variation in Vitamin E metabolism across species

3.3.2.8. Neoplasia

3.7.1.1. 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

3.7.1.2. Species involved

• White-tailed deer
• Axis deer
• Blackbuck
• Mouflon
• Aoudad
• Fallow deer
• Sika
• Nilgai
• Bison
• Wapiti (American elk)
• Reindeer
• Red deer
• Others

3.7.1.3. 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 regs, must check for exact requirements

3.7.2.1. 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

3.7.2.2. 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.

3.7.2.3. 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

3.7.3.1. 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

3.7.3.2. 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

3.7.3.3. Vaccination and testing

• Vaccination: polyvalent clostridial vaccines, leptospirosis, pasteurellosis (?)
• Testing for brucellosis, Johnes (?), bovine TB (problematic), Anaplasmosis

3.7.4.1. Noninfectious diseases

• Trauma (mostly management related)
• Malnutrition (Under and overfeeding - management related)
• Reproductive problems related to mismanagement

3.7.4.2. 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

3.7.4.3. 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

4.3.1.1. 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 province.

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 (ie, 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

4.3.1.2. 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

4.3.1.3. 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 hematolxylin 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.

4.3.1.4. Where is it now, where is it going?

Visit the USDA APHIS site for the latest information

4.3.1.5. 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. See Certifiction Program athttp://www.aphis.usda.gov/vs/nahps/cwd/farmed-cwd.html
• 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.

4.4.1.1. 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.

4.4.1.2. 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.

4.4.1.3. 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)

4.4.3.1. Transmission

• Direct contact with active lesions, exudate or scabs in the environment (hardy virus)
• Rough pasture may play a role

4.4.3.2. 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

4.4.3.3. Diagnosis

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

4.4.3.4. Treatment

• None, the animal usually recovers spontaneously
• Antibiotics may be indicated if a secondary bacterial infection has occurred

4.4.3.5. Control

No vaccine for deer

Suggested that farmers keep incoming animals isolated

4.4.3.6. 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)

4.4.4.1. 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.