3.3.1.1. 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.)

Oryx

• 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.

3.3.2.2. Hoof problems

Rocky mountain goat

• Abscesses

• Overgrowth

• Pododermititis, leading to osteomyelitis

• Substrate and adequate exercise important

• Trimming may become part of routine care

3.3.2.3. Skin problems

Pyoderma in the skin folds of a captive rhinoceros.

3.3.2.4. 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

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

• Relationship with hyperthermia

• Prevention is key!

3.3.2.7. 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

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 regulations, 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 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

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 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.

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.

• 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

4.4.1.1. 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.

4.4.4.2. Significance

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

4.4.5.1. 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

4.4.5.2. 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.

4.4.5.3. 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.

4.4.5.4. 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.

4.4.5.5. 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.

4.4.5.6. 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.

4.5.1.1. 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

4.5.1.2. 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

4.5.1.3. 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

4.5.1.4. 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

4.5.1.5. 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

4.5.1.6. 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)

4.5.1.7. 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

4.5.2.1. 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

4.5.2.2. 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.

4.5.2.3. 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.

4.6.1.1. 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.

4.6.1.2. 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

4.6.1.3. 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.

4.6.1.4. 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.

4.6.1.5. 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.

4.6.1.6. 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.

4.6.2.1. Clinical signs

• Hair loss, scabs

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

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

4.6.2.2. Diagnosis

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

psorptes cuniculi

4.6.2.3. Treatment

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

4.6.2.4. 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.