A Review of the Diseases and Parasites of Farmed Cervids

For purposes of this paper, the diseases and parasites have been classed as bacterial, viral, fungal, parasitic or other diseases.

Table of Contents

  1. Bacterial Diseases
    1. Anaplasmosis
    2. Brucella abortus
    3. Johne's Disease
    4. Tuberculosis
    5. Yersiniosis
  2. Viral Diseases
    1. Adenovirus infections
    2. Bluetongue
    3. Chronic Wasting Disease (CWD) of Deer and Elk
    4. Epizootic Hemorrhagic Disease (EHD)
    5. Herpesviruses
    6. Malignant Catarrhal Fever (MFC)
    7. Parapoxviruses of Deer
  3. Parasitic Diseases
    1. Ectoparasites
    2. Elaeophoriasis
    3. Elaphostrongylus cervi
    4. Gastrointestinal nematodes
    5. Lungworms

Bacterial Diseases

Anaplasmosis

Anaplasmosis is caused by the vector borne rickettsial organism Anaplasma marginale. It causes subclinical infection in an array of wild ungulates in the United States, and is capable of causing hemolytic disease in cattle (Radostits et al., 1994). Certain species of ticks act as biological vectors while tabanid (horse) flies act as mechanical vectors.

Status in Canada/Ontario

Exotic Species: Subclinical in wild ungulates, including certain species of deer (Haigh and Hudson, 1993); cattle and possibly mule deer (Haigh and Hudson, 1993) are at risk of illness.

Entry/Transmission/Endemicity

Low. Cattle and cervids are tested serologically prior to entry, and reactors are rejected. Entry from United States related to fraudulent documentation of imported cattle; re-use of needles contaminated with infected blood; or unexplained (vector movement). Farmed cervids represent little additional risk beyond that posed by imports of cattle, and movements of free-ranging wild ungulates.

The capacity of the disease to become endemic is related to the availability of effective vector locally. It is more likely in western Canada where Dermacentor andersoni, a known vector, is present. When introduced into Canada with cattle in the past (Manitoba - 1968; Quebec - 1979; Saskatchewan - 1983; Ontario - 1996), it was successfully eradicated with attention to cattle only (Salsberg, pers. com., 1997), suggesting that it did not become established in local vector populations and wildlife.

Degree of harm: Low in wild ungulates

Overall risk: Low

Control/Mitigation

CFIA import control/testing and the eradication or re-export of carrier cattle detected after entry.

Brucella abortus

Brucellosis or B. abortus causes abortions, arthritis and debilitating disease in Bovidae and Cervidae, and undulant fever in people (Smits, 1991; Radostits et al., 1994). Brucellosis is a named disease under the Animal Health Act, therefore control and eradication falls under the jurisdiction of the Canadian Food Inspection Agency (CFIA). Brucellosis was declared eradicated from the Canadian domestic cattle herd in 1985, and the only known reservoir of Brucellosis in Canada, is bison in Wood Buffalo National Park (Tessaro et al., 1993).

Brucellosis is not endemic in wild deer in Canada, nor has it been recognized in farmed deer, tested under CFIA's Captive Ungulate Program. Brucellosis does occur in wild elk in certain refuges in Wyoming, as a result of a spill over of infection from cattle and bison in the Yellowstone National Park region. Its transmission is promoted by congregation associated with winter feeding of elk (see McCorquodale and DiGiacomo, 1985; Smits, 1991). Brucellosis is transmitted mainly by ingestion of organisms shed in body secretions and in the fetal fluids of abortuses.

Status in Canada/Ontario

Brucellosis is endemic in bison in Wood Buffalo National Park, but has been eradicated in cattle and is not present in any species in Ontario.

Species: Cattle, bison, elk can become persistently infected carriers, and under appropriate circumstances of population size, density and management, can develop endemic disease. Other deer are susceptible to infection, but apparently rarely develop endemic infections in populations, or clinical disease. The exception is moose, which get severe disease and may die, but as a result, are unlikely to be able to sustain an endemic disease state in a population (Forbes et al., 1996).

Probability of Entry/Transmission/Endemicity

Low, given efficacy of import testing, rejection at import of animals from infected herds, and CFIA's ongoing testing as part of the Captive Ungulate Program. Brucellosis is unlikely to establish in wild deer in Ontario, based on experience in USA and Ontario, when Brucellosis was common in cattle, and deer were presumably exposed from that source.

Degree of Harm: High (elk, cattle/bison)

Overall Risk: Low

Control/Mitigation

CFIA control and test imported animals and domestic farmed deer under the Captive Ungulate Program. As noted earlier Brucellosis is a named disease and therefore control and eradication falls under the jurisdiction of the Canadian Food Inspection Agency, formerly Agriculture Canada. Eradication has been successful in cattle, and would seem feasible in farmed deer, if the disease were identified. The control of Brucellosis would be difficult in an infected population of susceptible wildlife, without the feasibility of eradication.

Key components to the control of Brucellosis include conformity CFIA regulations, proper animal identification and inventory records, and the containment of farmed deer.

Johne's Disease (ParaTuberculosis)

Johne's disease is caused by Mycobacterium avium paraTuberculosis. All species of ruminants, including deer (Smits, 1991; Haigh and Hudson, 1993), as well as camelids (Stehman, 1996), rabbits (Greig et al., 1997) and some other species are assumed to be susceptible. The disease is common in domestic cattle, sheep, goats and farmed deer (eg. Power et al., 1993; Fawcett et al., 1995) over most of the world, including Ontario (McNab et al., 1991), where it has been diagnosed in farmed fallow and sika deer (Barker, Hazlett and Ernst, 1997).

The organism is transmitted via close contact/ingestion, or transplacentally, from dam to fetus (Sweeney, 1996). The incubation period is long, from perhaps 6-10 months in some species of deer, to about 2 years or more in cattle and sheep. It causes granulomatous enteritis and lymphadenitis, resulting in weight loss progressing to emaciation, and in many species, diarrhea (Clarke, 1997). Reduced productivity and premature loss of the animal due to death contribute to the cost of this disease.

Johne's disease has apparently been transmitted from domestic animals to wildlife in several areas of North America: bighorn sheep and Rocky Mountain goats in the Rocky Mountain states (Williams et al., 1983); Tule elk in California (Jessup et al., 1981; Cook et al., 1997); white-tailed deer in the northeastern US (Libke and Walton, 1975; Chiodini and VanKruiningen, 1983), and free-living fallow and axis deer (Reimann et al., 1979).

Status in Canada/Ontario

Johne's Disease is endemic in conventional domestic ruminants and in farmed deer

Species: All species of farmed and wild ruminants, including all species of deer

Probability of Entry/Transmission/Endemicity

Moderate. The probability of spreading and becoming endemic in wild deer populations is difficult to determine. It is fairly common in domestic animals, but has yet to be recognized in wild deer in Ontario. High deer densities or congregations might promote development of endemic Johne's disease. Farmed deer probably add little incremental risk to that already posed by infected conventional domestic ruminants in Ontario.

Degree of harm: Moderate. The disease is insidious, and if it established, might cause incremental mortality in wild populations, that could be difficult to detect or recognize. Population effects on wildlife unstudied.

Overall risk: Moderate, but farmed deer probably add little incremental risk to that already posed by infected conventional domestic ruminants in Ontario.

Control/Mitigation

Tests for the infection in the living animal are unreliable and insensitive (Stehmann, 1996), and so disease control by test and slaughter is not feasible. Surveillance via autopsies on animals sick or dying on farm will detect the disease. There is a slight possibility of confusion of paraTuberculosis with Tuberculosis at autopsy; both are caused by Mycobacterium (but different species), and they should be differentiated by culture or molecular probes if there is any doubt about the diagnosis. Deer farmers should attempt to purchase stock from farms with a veterinary certificate, indicting no history of Johne's Disease, to prevent its spread in the industry.

Management issues relating to control/mitigation of Johne's Disease include the confinement of farmed deer, a herd health program and autopsies of animals dying on farm.

Tuberculosis (Mycobacterium bovis)

Deer are susceptible to bovine Tuberculosis, caused by the bacterium Mycobacterium bovis, which produces a debilitating disease in a proportion of infected animals (Griffin and Buchan, 1994), and can be transmitted to people (Fanning and Edwards, 1991; Grange and Yates, 1994; Liss et al., 1994). Tuberculosis is a named disease under the Animal Health Act and therefore falls under the jurisdiction of CFIA.

With the approaching eradication of this disease from the Canadian cattle herd (Essey and Koller, 1994), Tuberculosis in farmed deer assumes significance for four major reasons: health problems in deer; possibility of transmission back into the cattle population; possibility of transmission to wildlife; and the possibility of transmission to people. In most countries, deer have been a secondary agricultural species, and subsequently resources applied to Tuberculosis control programs centred first on the primary species of concern, cattle. This was also the case in Canada. The upsurge of interest in deer farming in the late 1980's, and associated international trade in deer, exposed weaknesses in standard testing protocols, which had worked well in detecting Tuberculosis-infected cattle, but had relatively low sensitivity in deer (Griffin and Buchan, 1994). As a result, bovine Tuberculosis became an obvious problem in a variety of countries in North America and western Europe, as international and internal trade in deer mushroomed (Clifton-Hadley and Wilesmith, 1991; Mirsky et al., 1992; Rhyan et al., 1992; Thoen et al., 1992; Bolske at al., 1995; Hunter, 1996).

Depopulation of deer herds with Tuberculosis had been ongoing sporadically, but in 1988, Agriculture Canada (now CFIA) established the Captive Ungulate Program, aimed at systematically testing all herds of non-domestic ungulates in the country for Tuberculosis and Brucellosis, with the goal of eradicating these diseases in that segment of the animal population. Testing under this program began in Ontario in 1990.

Tuberculosis in deer may be detected three ways: by skin testing as part of the Captive Ungulate Program; by detection of lesions in tissue during meat inspection at an abattoir (all legal abattoirs in Ontario must be inspected under either provincial OMAF regulations, or under federal CFIA regulations); or if a veterinarian suspects a diagnosis of Tuberculosis (eg. at autopsy, which has occurred several times in Ontario).

Tuberculosis (TB) has been detected on a number of bison, deer and elk farms, and in zoos and menageries in Canada (see Essey and Koller, 1994 for data to 1991; Whiting and Tessaro, 1994; Rohonczy et al., 1996). Most cases seem ultimately to be traceable to the importation of elk from the USA, prior to revision of the cervid TB test protocol, with one possibly attributable to the import of deer from New Zealand. Imports of deer from these countries have not been permitted since 1990/91. In Ontario, 10 premises with Tuberculous deer were detected and depopulated by Agriculture Canada between January 1990 and November 1994. No premises with confirmed Tuberculosis in deer have been detected in Ontario since that time. However, an estimate of over 5,100 deer on about 150 premises (30% and 45% of provincial totals of deer and farms, respectively) remain untested in Ontario as of March 1998. These 150 premises include deer farms as well as non-farm operations such as zoos, menageries, parks and petting zoos.

"Restricted" status herds remain untested for a variety of reasons, mainly related to an absence of satisfactory handling facilities. There is consequently difficulty in reading tests, and physical danger to the CFIA veterinarian, the animals and their handlers, posed by testing under inadequate circumstances (eg. by drug immobilization of unrestrained animals using syringe dart guns etc.). Drug immobilization of deer by syringe dart is expensive. TB testing requires reading skin tests within a specific time frame, good lighting, a clean skin test site and the ability to identify the animal accurately and keep records. This is difficult in an unsheltered paddock, especially if animals are difficult to apprehend reliably and restrain adequately.

Tuberculosis has rarely been reported from free-ranging cervids anywhere in the world (see Clifton-Hadley and Wilesmith, 1991; Griffin and Buchan, 1994; Hunter, 1996; Schmitt et al., 1997, for reviews). Tuberculosis is known to be established in wildlife in Canada, only in bison in Wood Buffalo National Park (Essey and Koller, 1994). Hadwen (1942) reported Tuberculosis in elk, mule deer and moose in Alberta. A single Tuberculous elk was encountered in the vicinity of a farm with TB-infected cattle in Manitoba (Rhyan et al., 1992) and a single case was reported in a white-tailed deer from Ontario (Belli, 1962). Sporadic cases of TB have also been reported in wild cervids in the USA (see Hunter, 1996; Schmitt et al., 1997). With the exception of the single Ontario white-tailed deer, all cases listed were in association with Tuberculosis in farmed animals, including farmed elk, or feral swine (Rhyan et al., 1995).

In 1994, a population of white-tailed deer with endemic bovine Tuberculosis was identified in northeastern Michigan (Schmitt et al., 1997). The origin of the infection in this population is unclear, and its duration is unknown, although a Tuberculous deer was reported in the vicinity in 1975 (Schmitt et al, 1997). Michigan at one time had a very high prevalence of Tuberculosis in cattle (Schmitt et al., 1997), and it is probable that the disease spilled over into deer decades ago, and went unrecognized. It seems unlikely that it originated with farmed deer, since only one case of TB has been identified in farmed cervids in Michigan, despite extensive surveillance (Michigan DNR, c. 1997), and the genetic fingerprint of M. bovis isolated from wild white-tailed deer resembles that of cattle isolates, and is dissimilar from the Michigan elk isolate (Whipple et al., 1998).

Tuberculosis is a density-dependent disease in ruminants, since close contact promotes successful transmission, mainly by the respiratory route, or by ingestion (Radostits et al., 1994). Variations in herd behaviour and density have been invoked to explain differences in prevalence of Tuberculosis in wild cervids. Hadwen (1942) considered that elk, as herd animals, were more prone to transmission of TB than mule deer, and Schmitt et al. (1997) suggest that artificial feeding, with attendant close contact among animals, may be the factor which has permitted Tuberculosis to remain endemic in wild deer in the affected area of Michigan. A computer model suggests that the rate of transmission among deer will have to drop by more than 50% before the prevalence of the disease will begin to decline (Corso et al., 1997). Michigan initially proposed attempting to reduce transmission by voluntary restrictions on supplementary winter feeding and by increasing hunting pressure (Schmitt et al., 1997). However, more recently, they have initiated stringent compulsory restrictions on feeding deer in the affected area (Anony mous, 1998c).

While white-tailed deer densities in Ontario do not approach those in the affected area of Michigan. Supplementary winter feeding on deer yards might set up circumstances favourable for maintenance of Tuberculosis in a local population in this province, were the disease introduced, especially if escaped farmed deer commingled with wild.

Status in Canada/Ontario

Rare, sporadic; eradication program advanced

Species: Cattle, bison, all species of deer, other species of ruminants, carnivores (eg., especially zoos, menageries)

Probability of Entry/Transmission/Endemicity

Low probability of entry currently, due to CFIA testing (cattle) or non-issuance of permits for imports (deer). Moderate to high probability of transmission and subsequent endemicity in wildlife, while potentially infected deer remain in the farmed population

Degree of harm: High

Overall risk: High, until the disease is eradicated.

Control/Mitigation

Universal and full compliance with the CFIA's control program is the key to controlling, mitigating and eventually eradicating Tuberculosis from the deer farming industry. Important components of the CFIA's Captive Ungulate Program include import testing/controls, on-farm testing and eradication, and movement controls. Other important elements contributing to the success of the control program include adequate animal identification and deer inventory records, as well as proper on-farm containment of deer.

Yersiniosis

Yersiniosis is caused by enteric bacteria of the genus Yersinia, mainly Y. pseudotuberculosis. Yersiniosis is a disease predominantly of red deer, though it also occurs in other species of deer, and in sheep and cattle (Haigh and Hudson, 1993; Radostits et al., 1994; Sanford, 1995; Diseases Diagnosed at Autopsy in Farmed Deer in Ontario, Barker, Hazlett and Ernst). The organism is present in soil, water and feces, and strains with particular virulence attributes invade the intestinal mucosa, causing diarrhea, weight loss, and sometimes systemic infection. Losses can be severe in farmed deer, and treatment is difficult. The disease is most common in stressed weaners in their first fall, when adverse weather conditions seem able to precipitate outbreaks (Sanford , 1995). Yersiniosis is a sporadic disease in a variety of wild mammals and birds other than deer, causing mortality in beaver and musk-ox, among other species, but apparently has not been recognized in free-ranging deer in Ontario.

Status in Canada/Ontario

Yersiniosis is endemic in farmed deer and sporadic in wildlife.

Species: Cervids, especially red deer, fallow deer; sporadic in other wildlife

Probability of Entry/Transmission/Endemicity

Low, difficult to determine if effect of deer farming is additive, given that the agent is in the environment in the wild.

Degree of harm: Moderate. The probability of overt disease is slight, but outbreaks may occur.

Overall risk: Low

Control/Mitigation

Ensuring deer remain on-farm (containment) and limiting environmental contamination (manure runoff) are best management practices that will assist in controlling the spread of Yersiniosis.

Viral Diseases

Adenovirus infections

Adenoviruses are common infectious agents of ungulates, often causing subclinical infection, but occasionally producing respiratory or gastrointestinal disease, or hemorrhagic syndromes, due to replication in vascular endothelium (Mattson, 1992). Antibodies to adenoviruses have been detected in several species of deer (Haigh and Hudson, 1993). Adenovirus infections have been diagnosed in red deer (Horner and Read, 1982) and fallow deer (Boros et al., 1985), but in neither species can adenoviruses be considered a significant cause of disease. In 1993 an epidemic of adeno virus infection caused high mortality among free-ranging mule deer in northern California (Woods et al., 1996, 1997). The viruses involved are incompletely characterized, and their epidemiology in deer is undefined, though adenoviruses generally are transmitted by close contact or by environmental contamination in other species.

Status in Canada/Ontario

Unknown

Species: With certainty, red deer, fallow deer, mule deer; others unknown.

Probability of Entry/Transmission/Endemicity

Moderate/high; infection may be endemic, but is unrecognized in some farmed species. The current infection status of wild cervids in Ontario is unknown.

Degree of harm: Moderate. The California outbreak, though regionally significant, appears to have been transient, with no long-term after-effects reported.

Overall risk: Moderate

Control/Mitigation

Seropositive animals are likely recovered, and not shedding virus; seronegative animals are either uninfected or incubating, so serologic testing to exclude animals carrying the virus is difficult. Control entry of susceptible species; in theory, quarantine and exclude lots of deer which seroconvert in quarantine. There are no controls currently in place. Adenovirus infections are not considered sufficiently significant in domestic ungulates to warrant specific control measures or vaccination (Mattson, 1992); in fact they are not even considered as a disease problem in the major text on large animal veterinary medicine (Radostits et al., 1994). The containment of farmed deer would reduce, but not eliminate, whatever probability there is, of transmission to wildlife.

Bluetongue

An orbivirus infection of ruminants, transmitted by Culicoides midges (certain strains of C. variipennis in North America), endemic in the southern USA, periodically epidemic in the western states (occasionally spilling over into the Okanagan Valley in BC [Sterritt and Dulac, 1992; Dulac et al., 1992]) and mid-eastern states, but not those abutting the border in Ontario (Walton et al., 1992). The virus does not appear to over-winter in arthropods, and the disease dies out as the vector arthropods die in fall/winter (Radostits et al., 1994).

Status in Canada/Ontario

Exotic, with periodic incursions at long intervals into south-central British Columbia (last in 1987 - Shapiro et al., 1991); has never been recognized in Ontario.

Species: Cattle are the major reservoir. Goats and elk can be sub-clinical carriers, though wapiti may develop very mild signs. Odocoileus spp., pronghorns and bighorn sheep may develop fatal hemorrhagic disease, but the effect on red deer is unknown (Hoff and Trainer, 1981; Haigh and Hudson, 1993).

Entry/Transmission/Endemicity

Entry could be via infected cattle or elk, not detected by serologic screening, but this is an unlikely event. Entry of this disease by regulated animal imports is not considered significant (Gibbs, 1992). Disease is now recognized as regionalized with respect to risk, based on origin of animal in North America (Walton et al., 1992). This recognizes the fact that the disease has never been reported from some areas, and the agent does not over-winter in vectors in the north. Controls are placed by the Canadian Food Inspection Agency on animal movements from infected areas, until risk is deemed negligible, based on vector activity and incubation/transmission period (Sterritt and Dulac, 1992).
It could also enter by wind-borne transportation of vector from south. Local transmission would require presence of suitable vector; the subspecies of C. variipennis in Ontario may be an incompetent vector (Walton et al., 1992). Based on experience in northwestern American states, infected vectors likely would not persist over winter in Ontario, resulting in a transient epidemic impact if the disease did occur. Farmed deer (elk) pose essentially no incremental probability of introduction of Bluetongue to Ontario, beyond the already very low probability posed by importation of cattle and by wind-borne vectors.

Degree of harm: Moderate

Overall risk: Low to negligible in Ontario, due to extremely low probability of vector transmission.

Control/Mitigation

CFIA controls the imports into Canada from the USA, based on source, season, and serologic status of herd of origin. There are no other issues directly relevant to BMPs for farmed deer, other than conformity to CFIA regulations and animal identification.

Chronic Wasting Disease (CWD) of Deer and Elk

A prion-associated transmissible spongiform encephalopathy analogous to scrapie in sheep, bovine spongiform encephalopathy (BSE), transmissible mink encephalopathy, and Creutzfeldt-Jakob Disease and Kuru of people. CWD was first described in mule deer in 1980 (Williams and Young, 1980), but had been recognized as a clinical syndrome since 1967 (Williams and Young, 1992). Animals develop behavioural changes, increased drinking/urination, excess salivation and difficulty swallowing, occasionally some ataxia, and in all cases, loss of body condition progressing to emaciation.

The pattern is sporadic, and the minimum incubation period seems to be about 18 months in mule deer and elk. Transmission is horizontal, by contact, and possibly vertical/maternal, from dam to offspring, even with minimum contact after birth. The disease has been recognized in wild elk, mule deer and white-tailed deer in Colorado and Wyoming (Spraker et al., 1997), and in captive elk, mule deer and mule x white-tailed deer hybrids in research facilities and zoos in Colorado, Wyoming and Ontario which had exchanged animals during the 1960's and 1970's (Williams and Young, 1992). The disease in Ontario involved a small herd of black-tailed/mule deer at the Toronto Zoo, established in the mid-1970's. This herd had connections to a zoo in Colorado in which a syndrome compatible with CWD occurred, and which had exchanged animals with other affected facilities. Animals gradually succumbed to a syndrome compatible with CWD during the late 1970's; the herd died out and was not replaced. A spongiform encephalopathy was diagnosed histologically in one case that died in 1978 (Barker, unpublished), but the syndrome of emaciation was not associated with the spongiform encephalopathy until CWD was described by Williams and Young (1980). Spongiform encephalopathy has not been recognized in any species at the Toronto Zoo since (Barker, unpublished).

The origin of CWD is unknown. There is no clear epidemiologic association with spongiform encephalopathies of domestic animals. Since the affected captive herds were established with wild animals prior to recognition of the disease in free-ranging animals, it is possible that CWD was introduced from the wild population, where it was unknown at the time. This may have occurred following depopulation and re-population of one of these facilities with wild animals in an attempt to eradicate the disease (Williams and Young, 1992). However, surplus animals from affected captive herds had been released to the wild, prior to definition of the disease (Williams and Young, 1992), possibly introducing CWD to the wild population.

CWD was diagnosed in January 1996 in Saskatchewan in a farmed elk which had been imported from South Dakota, USA in 1989. The Saskatchewan herd was depopulated and the first generation progeny of the affected elk which had moved to other farms were also destroyed under Agriculture and Agri-Food Canada supervision (Agriculture and Agri-Food Canada, 1997). As a result of compulsory reporting of illness in farmed deer, required by state regulations, CWD has subsequently been recognized on 2 elk farms in South Dakota, where control measures are underway (Anonymous, 1998a, b).

Status in Canada/Ontario

CWD has not been reported in wild cervids in Canada. CWD is currently not recognized, but has occurred in captive animals in Saskatchewan and Ontario. CFIA, in consultation with Canadian Venison Council, has formulated a policy of surveillance and eradication, though CWD is not a "named disease" under the Health of Animals Act.

Species: Mule deer, white-tailed deer, mule deer x white-tailed deer hybrid, elk are susceptible. The susceptibility of other Cervidae is unknown.

Probability of Entry/Transmission/Endemicity

High in the absence of effective antemortem tests, unless moderated by effective federal import controls (currently in place) and surveillance/eradication program (see below). At the time of the triennial Tuberculosis test, CFIA veterinarians observe captive cervids for signs of disease compatible with CWD (Agriculture and Agri-Food Canada, 1997). Some further infected animals may have entered Canada before the current ban on importation of farmed cervids from USA, and gone undetected. They, the progeny or contacts may be present on farms in Canada.

Degree of harm: High in both captive and wildlife populations.

Overall risk: High

Control/Mitigation

CFIA control/ban on imports from regions of endemic or unknown status with respect to presence of CWD (currently in place via effective ban on farmed deer imports from USA until import protocols developed [Agriculture and Agri-Food Canada, 1997]). Control/mitigation factors include the on-farm containment of deer, CFIA traceback (identification) and eradication under Captive Ungulate Program and the implementation of an effective internal surveillance for CWD in farmed animals, including the necropsy of deaths.

Epizootic Hemorrhagic Disease (EHD)

This disease is caused by an orbivirus closely related to Bluetongue virus. The two viruses often cocirculate (Shapiro et al., 1991), and the diseases are indistinguishable without virus isolation. It is transmitted by Culicoides midges (certain strains of C. variipennis in northern latitudes), endemic in the southern USA, periodically epidemic in the western and mid-eastern states. Three incursions into Canada are known, in the Cypress Hills area of southern Alberta in 1962; in the Okanagan Valley of BC in 1987 (Sellers and Maarouf, 1991; Shapiro et al, 1991); and on the basis of antibody in cattle, but no disease, in southern Saskatchewan in 1988 (Dulac et al., 1992). The virus does not appear to over-winter in arthropods, and the disease dies out as the vector arthropods die in fall/winter.

Status in Canada/Ontario

The disease is exotic to Canada, with rare incursions into western Canada at long intervals. EHD has never been recognized in Ontario.

Species: A variety of domestic and wild ruminants likely form the reservoir in the southern United States. The disease is rarely recognized in domestic animals. Among wildlife, white-tailed deer are especially susceptible to EHD, while other species, including elk, may develop mild or subclinical disease.

Probability of Entry/Transmission/Endemicity

Low to negligible. EHD is not listed for import control by CFIA under Health of Animals Act, since there is little risk to domestic ruminants, and specific testing is not carried out, though the virus cross-reacts with bluetongue. Entry to Canada is most probable via wind-blown infected vectors from the south (Sellers and Maarouf, 1991). The epidemiology and risk with respect to vectors in Ontario, is like Bluetongue. Farmed deer pose little incremental probability of introduction of EHD to Ontario, beyond the already very low probability posed by importation of domestic ruminants and by wind-borne vectors.

Degree of harm: Moderate

Overall risk: Low to negligible, due to extremely low probability of vector transmission in Ontario.

Control/Mitigation

There is no practical means of control.

"Herpesviruses"

Herpesvirus infections are ubiquitous among ruminants. In cervids, infections occur with "herpesviruses apparently native to deer, and with the sheep or wildebeeste origin ( herpesviruses, which cause malignant catarrhal fever.
Alpha herpesviruses of ruminants typically cause mucosal infections and may produce latency in neurons (Engels and Ackermann, 1996). Two "herpesviruses, CHC-1 and CHV-2 have been isolated from red deer (Vanderplasschen et al., 1993); the former was associated with conjunctivitis in farmed red deer calves in Scotland (Nettleton et al., 1986). Rangiferine Herpesvirus-1 was isolated from a reindeer (Ek-Kommonen et al., 1986). CHV-1 and RHV-1 are related to Bovine herpesvirus-1, the cause of infectious bovine rhinotracheitis (Lyaku et al., 1992). A herpesvirus related antigenically to Equine Herpesvirus-1 was isolated from fallow deer in Alberta (Kinyili and Thorsen, 1979). Only CHV-1 has been associated with disease in farmed deer, and no herpesviruses have been firmly associated with disease in wild deer. However, antibodies that react with BHV-1 have been detected in Quebec caribou (Elazhary et al., 1981), and in black-tailed deer and white-tailed deer in the USA (Ingebrigtsen et al., 1986; Haigh and Hudson, 1993), and in white-tailed deer on Anticosti Island, where the herpesvirus was circumstantially associated with unusual mortality that occurred in deer in 1985 (Sadi et al., 1991).

Although these herpesviruses cross-react, indicating that they are antigenically related, they are distinct, and may very well not cross-infect significantly between hosts (Reid et al., 1986).

Status in Canada/Ontario

The status in Ontario is unknown. Herpesvirus has been isolated from fallow deer in Alberta, and antibody to an "herpesvirus has been demonstrated in parts of the USA and Canada.

Species: Fallow deer, red deer have been affected with (CHV-1, 2), and an uncharacterized herpesvirus has affected white-tailed deer and mule deer.

Probability of Entry/Transmission/Endemicity

Overall, Low. There is high probability of entry, because these viruses may be latent, and serology can be difficult. But a herpesvirus is circumstantially already present in white-tailed deer in North America. The transmission of herpesvirus requires close contact and the likelihood of establishment across host species barriers is low. In these circumstances, the incremental likelihood of transmission from farmed deer is likely low.

Degree of harm: Low-to-moderate. Clinical disease can be severe with related herpesviruses in housed cattle. In deer, so far, the disease, known to be due to herpesviruses has been mild to non-existent. The association with high mortality on Anticosti Island is retrospective and speculative, but cannot be discounted.

Overall risk: Low

Control/Mitigation

The best means of control is to ensure deer are contained on-farm.

Malignant Catarrhal Fever (MFC)

MFC is caused by a cell-associated (herpesvirus, either Alcelaphine Herpesvirus-1 transmitted from wildebeest (an issue in zoos), or Ovine Herpesvirus-2 (OHV-2) transmitted from domestic sheep. Until recently, tests were not available to detect carrier sheep or wildebeest, and they are still not routine (Baxter et al., 1993; Tham et al., 1994). The hosts of origin (wildebeest, sheep) do not develop disease, but the carrier state is widespread and common among them (Li et al., 1994, 1995). Disease occurs in cattle, bison, and most species of cervids. Transmission is by exposure of the susceptible species to the carrier host, usually by close contact, since the virus is not persistent in the environment. There is little, if any, horizontal transmission of disease among individuals of the susceptible species, despite the fact that they show severe signs (ocular; nervous; orocutaneous, respiratory, gastrointestinal mucosal ulceration). They are considered "dead end" hosts from the standpoint of disease transmission. Virtually all deer which develop clinical MCF go on to die (Haigh and Hudson, 1993).

Status in Canada/Ontario

Endemic infection with OHV-2 in sheep

Species: Virtually all cervid species are susceptible to MCF, except fallow deer, which seem refractory to the disease. Sika deer, white-tailed deer, and red deer are highly susceptible; elk and perhaps mule deer seem less-so, but still may get the disease. Moose are also susceptible.

Probability of Entry/Transmission/Endemicity

Negligible. OHV-2 is present in sheep in Ontario, and farmed deer. Cattle and bison do become infected, but deer are dead end hosts, and endemic infection will not establish in farmed or wild deer.

Degree of harm: High in captive deer, in which outbreaks can be devastating (Brown and Bloss, 1992); low in wild deer, in which it has rarely been reported (Jessup, 1985).

Overall risk: The risk to the wild population, from farmed deer is negligible, since deer-to-deer transmission is not significant.

Control/Mitigation

Prevent exposure of deer to sheep.

Parapoxviruses of Deer

Parapoxviruses usually cause mild transient infections in their native host, but can cause severe disease in unnatural hosts; however, the capacity to cross-infect, and the reaction in the unnatural host, are unpredictable. No parapox infections have been recognized in native deer in North America, and the only cervid in which a parapox infection is described is the red deer. In red deer, lesions of the skin and velvet antler were associated with cutaneous trauma due to thistles in paddocks (Haigh and Hudson, 1993). The overall impact of the disease was mild.

Status in Canada/Ontario

Unknown; red deer have been imported to Canada, but to Barker's knowledge, no disease compatible with parapox infection has occurred in that species here. A single case of uncharacterized parapox infection has occurred in an elk in western Canada (Haigh and Hudson, 1993), and there may be undescribed parapox viruses in elk and other deer. However, if present, they would seem to be uncommon.

Species: Red deer and presumably elk can be infected. Infectivity to other deer is possible but unproven.

Probability of Entry/Transmission/Endemicity

High. The virus may be spread by clinically-infected animals, which would likely get picked up in pre-shipment quarantine. However, incubating animals would not be detected, unless they got sick in quarantine here. The virus is also transmitted environmentally, and contact with an infected animal is not required. The capacity to cross-infect to other deer species is unknown, but other parapoxviruses readily cross species barriers.

Degree of harm: Low in red deer; unpredictable in other species, but likely no worse than moderate.

Overall risk: Moderate

Control/Mitigation

Containment of deer.

Parasitic Diseases

Ectoparasites

The principal ectoparasites (external parasites) of concern on deer are mites, especially Psoroptes. sp., and ticks, especially the winter tick Dermacentor albipictus and the black-legged tick Ixodes scapularis.

Psoroptes causes scabies on deer, including elk (Colwell and Dunlap, 1975; Samuel et al., 1991) and white-tailed deer (Bubenik, 1989; Garris et al., 1991), in which it may also cause otitis (Rollor et al., 1978), and it also infects mule deer (Roberts et al., 1970). Psoroptic scabies does not seem to be a clinical problem in red deer and fallow deer, but Sarcoptes mites have been recorded from red deer in Europe (Haigh and Hudson, 1993).

Dermacentor albipictus causes severe alopecia in moose, and does infect elk and white-tailed deer (Haigh and Hudson, 1993). Ixodes scapularis is the vector of Lyme borreliosis. It is endemic in parts of the northeastern and upper midwest USA, but is known to be endemic in Canada at only two localities in southern Ontario, Long Point peninsula (Barker et al., 1992), and Point Pelee National Park (Barker, unpublished).

Status in Canada/Ontario

Psoroptes, Dermacentor albipictus and Ixodes scapularis endemic on deer in Ontario, though Dermacentor albipictus is mainly associated with moose, and Ixodes scapularis is limited in distribution.

Species: Particularly white-tailed deer and elk, though any species of deer, as well as other medium-sized to large mammals, such as dogs, may be hosts for Ixodes scapularis.

Probability of Entry/Transmission/Endemicity

High, if animals come from endemic areas at a time of year when infestation is present (if seasonal). Establishment of endemicity in a new locality is dependent on local environment and climate. There is a high probability of establishment for Psoroptes, Dermacentor in Ontario and regionally variable for Ixodes scapularis (Lindsay et al., 1995). It is probably a greater issue with translocation of wild animals into or within the province, than with farmed deer.

Degree of harm: There is no incremental harm, unless introduced into currently non-endemic locality and able to establish; then the degree of harm would be low to moderate. In endemic areas, deer farms pose no incremental risk. The impact of Ixodes scapularis is on people, not directly on wildlife.

Overall risk: Low

Control/Mitigation

It is difficult to prevent introduction of ectoparasites by inspection or treatment with parasiticides. Animals should be moved at times of year when not infested with seasonal parasites (ticks). Confinement will limit contact transmission of mites somewhat; but confinement is unlikely to be effective with ticks.

Elaeophoriasis

The nematode Elaeophora schneideri, which inhabits arteries in the head and neck, infects mule deer with little effect, but causes problems with mastication in white-tailed deer; blindness, brain damage and gangrene of the tissues of the head in moose and elk; and less severe effects in sika deer and sheep and goats (Haigh and Hudson, 1993). The normal host in the western United States is the mule deer, and white-tailed deer are usually not infected. In the southeastern USA, white-tailed deer are the normal host. Elaeophora uses certain species of tabanids (horse flies) as vectors.

Status in Canada/Ontario

Present in British Columbia, never known in Ontario.

Species: Likely all species of farmed deer, plus moose.

Probability of Entry/Transmission/Endemicity

Low to negligible. The species of tabanid flies which are suitable vectors for this parasite do not seem to be present in Ontario, based on the natural absence of this worm from wild populations of white-tailed deer. Hence, even if an infected animal were imported, it would likely not transmit and establish.

Degree of harm: Moderate, if it could establish

Overall risk: Negligible

Control/Mitigation

Not necessary under current circumstances.

Elaphostrongylus cervi

This protostrongylid nematode, though it lives at sites distant from the lungs, produces eggs which reach the lungs via the circulatory system. The eggs hatch in the lungs and the first-stage larvae move up the trachea, and are swallowed, to be passed in feces (Mason, 1989). They use molluscs (snails or slugs) as intermediate hosts. Suitable molluscs are present and widespread in Canada (Gajadhar and Tessaro, 1995). Infectious larvae in molluscs accidentally ingested by deer, migrate from the gut to the spinal cord and brain, then, in most cases, to intermuscular tissues, where they mature. During their migration in the central nervous system, these worms can cause damage which may result in clinical disease.

Elaphostrongylus cervi is endemic in red deer populations in western Europe (English et al., 1985; Hollands, 1985; Eriksen et al., 1989) and New Zealand (Mason et al., 1976), though not in fallow deer (Mason, 1989). It is unknown in native species of cervids in North America, though elk in New Zealand have become infected spontaneously (Mason and McCallum, 1976). A related species, originally identified as E. cervi (Lankester and Northcott, 1979), but now considered to be E. rangiferi (Carreno and Lankester, 1993), a parasite of reindeer in Scandinavia (Bye and Halvorsen, 1984), probably was introduced by the translocation of European reindeer into Newfoundland, where it causes disease in caribou and moose (Lankester and Fong, 1989).

Elaphostrongylus alces is found in moose in Scandinavia (Steen et al., 1989). These parasites, though they do cross-infect hosts, seem to be distinct species (Steen et al., 1997), and separate from E. cervi, with which they were once lumped (Mason, 1995).

E. cervi has very low pathogenicity in red deer, causing usually minor lesions (Sutherland, 1976) detected at low frequency at meat inspection, and uncommonly in farmed animals (Mason and Gordon, 1994). In mule deer it will produce patent infections (animals pass larvae), but it causes significant central nervous system disease, resulting in ataxia and other neurologic deficits (Gajadhar and Tessaro, 1995) which may be fatal, or render the animal more prone to predation. White-tailed deer do not develop patent infections following experimental inoculation with E. cervi, and developing worms seem to be overcome by the host during their migration, without producing disease (A. Gajadhar, personal communication, 1998). Both E. rangiferi and E. alces also seem capable of causing disease in some other species of cervids, in addition to their natural host (Lankester and Fong, 1989).

In 1991 presumptive infection with Elaphostrongylus cervi was detected in several consignments of quarantined red deer imported to Canada from New Zealand, all of which were slaughtered (Gajadhar et al., 1994; deWith et al., 1998). Since the Baermann technique for detection of larvae in feces is insufficiently sensitive to reliably detect larvae in all infected animals (see Mason, 1989; Agriculture Canada, Position Paper, February, 1992; de With et al., 1998) importations of red deer and fallow deer from New Zealand (or elsewhere) that are not known to be free of E. cervi were halted in 1991 by Agriculture Canada, so as not to further imperil Canadian wildlife populations. The burden of proof with respect to freedom from infection is on the exporting country, and deer have not been imported into Canada from New Zealand since that time.

Of over 92,000 deer (?all species) examined in quarantine in New Zealand before export to Canada and Australia up to the end of 1990, 0.28% were detected shedding E. cervi larvae (P. Mason, Meeting on Elaphostrongylus cervi Risk Management for the Importation of Deer, Agriculture Canada, 1991). Among about 8,000 red deer in quarantine in Canada examined by the Baermann technique, about 0.1% were found to be infected (Meeting on Elaphostrongylus cervi Risk Management for the Importation of Deer, Agriculture Canada, 1991), though since all affected animals were detected in 1991, after an increase in sensitivity of the testing protocol, up to about 1% of animals may have been infected (de With et al, 1998). Probably no more than about 80 E. cervi-infected deer entered Canada, and of those, one can assume that about 20% were slaughtered without being released from quarantine (all those detected, and any undetected infected cohorts in the same consignments). The prevalence of infection with E. cervi among animals released from quarantine must have been very small (<~1%), if it was present at all.

Some red deer destined for slaughter from a consignment detected with E. cervi in quarantine, escaped as they were unloaded at an abattoir in southern Ontario; however, all were subsequently accounted for. Agriculture Canada took the position that, as of November 28, 1991, "Elaphostrongylus cervi has not been detected in continental Canada and that we can reasonably assume that it is not present." To our knowledge, this position has not been tested by seeking this parasite in red deer populations on farms in Ontario. Elaphostrongylus cervi infection would be unlikely to be detected in red deer unless sought specifically. Though the Baermann technique is relatively insensitive on an individual animal basis, it would likely detect established infections at the herd level if the prevalence of infection in individuals in herds of over 50-100 animals were substantial (>5-10%).

CFIA is currently developing an ELISA test capable of detecting animals with E. cervi early in the course of infection. This test is very promising, but, pending technical refinements and validation, is likely several years away from field application (A. Gajadhar, personal communication, 1998). No ELISA test has 100% sensitivity; however, such a test could be used effectively to detect infected herds, if not all infected individuals. Over a course of several herd tests at intervals, herds of susceptible species might be certified free of infection. Indeed, the same might be accomplished in herds of sufficient size now, using the Baermann technique, with repeated sampling, though infections with Parelaphostrongylus tenuis might yield false positive results. Infected herds would likely persist, due to the difficulty of eliminating infected molluscs from a premises. Since E. cervi is not amenable to successful therapy using anthelmintics currently available, potentially infected deer could not be placed in secure quarantine, treated, and safely moved to uninfected premises.

Other Elaphostrongylus spp. are not reviewed since their hosts are not permitted to be farmed in Ontario.

Status in Canada/Ontario

Not present in western Canada (west of Ontario, since red deer are not permitted); officially not present in eastern Canada/Ontario, but a slight possibility exists that it escaped quarantine.

Species: Red deer from New Zealand and their descendants are potential hosts for endemic infection in Ontario. Elk are a susceptible farmed and indigenous wild species. Mule deer are a susceptible farmed species; while white-tailed deer and fallow deer are apparently insusceptible.

Probability of Entry/Transmission/Endemicity

Moderate, based on the possibility that it may have escaped quarantine, and could be endemic in red deer. Apparently there is no possibility of the establishing of Elaphostrongylus spp. in wild white-tailed deer. There is a possibility of the transfer of Elaphostrongylus spp. to elk, were infected deer to be farmed in an area where elk are established.

Degree of harm: Low to moderate; potential impact on elk rather than white-tailed deer, even if difficult to eradicate from red deer. This is a potential issue in inter-provincial trade if established, or status unknown.

Overall risk: Moderate

Control/Mitigation

Control measures include CFIA import controls, possible testing and herd certification, zoning of deer farming away from elk range and the identification and confinement of farmed deer.

Gastrointestinal nematodes

Gastrointestinal nematodes, predominantly Trichostrongyloidea, are common in all ruminants, including deer. Infections typically involve a complex of species of worms, but are usually dominated by one. Those found in deer are usually species related, but not identical, to those in domestic ruminants, and even when they are the same species, they seem to be host-adapted. Parasites exotic to the new world certainly have been imported with their hosts to North and South America (Suarez at al., 1991; Rickard et al., 1993). Parasites of deer non-indigenous to Ontario may not transmit effectively to indigenous species of deer, although cross-infection by some species clearly can occur from white-tailed deer to exotics in areas of sympatry (Richardson and Demarais, 1992).

Worms parasitizing the abomasum (true stomach), belonging to the genus Ostertagia or its relatives, are pathogenic in fallow deer, red deer and wapiti, causing diarrhea and weight loss (Mylrea et al., 1991; Haigh and Hudson, 1993; Connan, 1996), as do their relatives in sheep and cattle. Related worms are found in wild white-tailed deer in Ontario (Baker and Anderson, 1975). Haemonchus species cause anemia in white-tailed deer in the southeastern United States, where, under warm, humid conditions, parasite burdens can be heavy. Under conditions prevailing there, worm burdens are host-density dependent, and have been used as a management tool in measuring deer population density in relation to habitat quality (Prestwood and Pursglove, 1981).

Status in Canada/Ontario

Endemic in farmed and wild deer, but species and host range of parasites may differ.

Species: All farmed cervids and all wild cervids

Probability of Entry/Transmission/Endemicity

Moderate. The probability of entry is high, but likelihood of establishment across host species barriers is moderate-to-low.

Degree of harm: Low; probability of overt disease slight.

Overall risk: Low

Control/Mitigation

Control measures include ensuring the deer are properly contained on the farm premises and limiting environmental contamination (runoff).

Lungworms

Lungworms of the genus Dictyocaulus occur in all species of deer and seem to be particularly pathogenic in red deer and elk. Most lungworms of deer (red deer, elk, white-tailed and black-tailed deer, reindeer and caribou, and moose) on morphologic grounds are termed D. viviparus (Anderson and Prestwood, 1981), which is the lungworm of cattle. Transmission is direct (no intermediate host). Cross infections do occur, but cross-infectivity of these worms among hosts in some cases seems to be incomplete (Anderson and Prestwood, 1981). When it has been attempted (ie. infectivity is best or pathogenicity is greatest in the host of origin, compared with the alternative host). There is argument about the nomenclature of the Dictyocaulus species of fallow deer in Europe, which seems to be a distinct species D. eckerti (Epe et al., 1997).

Dictyocaulus is an important pathogen of red deer, elk and fallow deer in captivity, including in Ontario (Appendix 6; Barker unpublished). Heavy infections can occur in wild deer, especially elk in the northern Pacific coast region (Haigh and Hudson, 1993) and white-tailed deer in the southeastern United States (Anderson and Prestwood, 1981). In Ontario, it seems only to be a minor parasite of wild deer, although it was implicated as a contributory agent in multi-factorial winter deaths of deer in NewYork (Anderson and Prestwood, 1981).

Status in Canada/Ontario

Endemic in farmed deer and wild deer

Species: all cervids

Probability of Entry/Transmission/Endemicity

High. Dictyocanlus or lungworm are already endemic in farmed and wild deer.

Degree of harm: Low. The probability of overt disease is slight in wild deer in Ontario, and the incremental harm associated with deer farms, if any, probably would be very localized.

Overall risk: Low

Control/Mitigation

Containment of deer and minimizing runoff.


For more information:
Toll Free: 1-877-424-1300
E-mail: ag.info.omafra@ontario.ca
Author: Frank Miller - The Independent Study Panel for the Development of Best Management Practices for Farmed Cervids to Protect Native Wildlife in Ontario; Dr. Ian Barker - The Independent Study Panel for the Development of Best Management Practices for Farmed Cervids to Protect Native Wildlife in Ontario; John Williamson - The Independent Study Panel for the Development of Best Management Practices for Farmed Cervids to Protect Native Wildlife in Ontario; Brian Tapscott - Alternative Livestock Specialist/OMAFRA
Creation Date: 01 March 1998
Last Reviewed: 28 September 2015