Dermoid cysts in caribou.

Subcutaneous dermoid cysts were identified in eight wild caribou (Rangifer tarandus) from widely dispersed locations in northern Canada and in one wild caribou from Alaska. The dermoid cysts from Canadian caribou were found among 557 diagnostic specimens that had been detected by hunters and submitted by resource officers and biologists between 1 January 1966 and 15 May 2007. All of the cysts were located in the cervical region, and five of nine cysts were found in the throat area. All of the animals for which the age was known were adult; males and females were equally represented. Dermoid cysts were not diagnosed in any of 1,108 white-tailed deer (Odocoileus virginianus), 293 mule deer (Odocoileus hemionus), 174 elk (Cervus elaphus), or 529 moose (Alces alces) examined during the same period at the Canadian laboratory.

Tularemia in deer mice (peromyscus maniculatus) during a population irruption in Saskatchewan, Canada.

Type B tularemia caused by Francisella tularensis subsp. holarctica was diagnosed in deer mice (Peromyscus maniculatus) found dead at four sites in west-central Saskatchewan during April and May 2005. The occurrence of tularemia coincided with a decline in the number of deer mice in part of a large area (>22000 km(2) ) in which deer mice had been extremely abundant during the autumn of 2004 and spring of 2005, and in which mice caused damage to crops in the autumn of 2004. This is apparently the first report of tularemia as a cause of death of wild deer mice. The bacterium isolated from deer mice was atypical in that cysteine was not required in the media used for isolation. Three isolates tested were genotypes not previously identified in Canada. There were no reports of human disease in the area.

Secondary poisoning of eagles following intentional poisoning of coyotes with anticholinesterase pesticides in western Canada.

Records of eagles, coyotes (Canis latrans), and red foxes (Vulpes vulpes) necropsied at the Western College of Veterinary Medicine, Saskatoon, Saskatchewan, Canada, between 1967 and 2002 were reviewed for cases suggestive of anticholinesterase poisoning. From 1993 to 2002, 54 putative poisoning incidents involving 70 bald eagles (Haliaeetus leucocephalus) and 10 golden eagles (Aquila chrysaetus) were identified. Of these, 50 incidents occurred in Saskatchewan, two were in Manitoba, and one occurred in each of Alberta and the Northwest Territories. The diagnosis was confirmed in eight instances by demonstration of pesticide in ingesta from eagles or known use of pesticide at the site together with brain cholinesterase (AChE) reduction of >50% in at least one animal. A presnmptive diagnosis of poisoning was made in 33 incidents based on brain AChE reduction of >50% in at least one animal; 13 incidents were considered suspicious because of circumstantial evidence of the death of eagles in association with other species and limited AChE reduction. Other wild species were found dead in 85% of the incidents involving eagles. Coyotes, foxes, black-billed magpies (Pica pica), and striped skunks (Mephitis mephitis) were associated with 34, six, six, and three incidents, respectively. There were eight additional incidents that did not involve eagles in which poisoning was diagnosed in coyotes. Carbofuran was identified in nine incidents. Carbamate poisoning was indicated on the basis of reactivation of brain AChE activity in two additional incidents. Brain AChE activity was not reduced from normal in eagles in four of seven incidents in which carbofuran was identified. The organophosplorous insecticide terbufos was found together with carbofuran in one incident. Brain AChE activity was measured in wild canids and in eagles in 15 incidents; in all of these incidents, brain AChE was redulced by >50% in at least one mammal, whereas this level of reduction occrred in eagles in only four incidents. Use of anticholinesterase pesticides to poison coyotes is illegal, but the practice continues and secondary poisoning of eagles is a problem of unknown proportions in western North America.

Redescription of the sarcocysts of Sarcocystis rileyi (Apicomplexa: Sarcocystidae).

The intermediate hosts for Sarcocystis rileyi (Stiles 1893) Minchin 1913 are ducks (Anas spp.), and the striped skunk (Mephitis mephitis) is its definitive host. The structure of sarcocysts from an experimentally infected shoveler duck (Anas cylpeata) fed sporocysts from an experimentally-infected M. mephitis was studied and compared with type specimens from a naturally infected duck. The experimentally infected duck was killed 154 d after feeding sporocysts. By light microscopy the sarcocyst wall was 3-5 microm thick with indistinct villar protrusions. Ultrastructurally, the sarcocyst wall was a type-23 cyst wall with anastomosing villar protrusions that were up to 7.5 microm long. The villar projections contained filamentous structures. The bradyzoites were 12-14 microm long. Structurally, the sarcocyst from the naturally infected and experimentally infected ducks appeared similar.

Intracellular survival of Haemophilus somnus in bovine blood monocytes and alveolar macrophages.

The mechanisms used by Haemophilus somnus to survive and multiply within bovine mononuclear phagocytes are not fully understood. In order to study the interaction between bovine mononuclear phagocytes and H. somnus, a colorimetric assay using 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenylItetrazolium bromide (MTT) was developed to assess the survival of H. somnus within cultured bovine blood monocytes (BBM). Using this system, it was found that H. somnus was able to survive within BMM in vitro, and the kinetics of its survival were similar to that seen in BBM isolated from experimentally infected cattle. Using ultrastructural studies, it was possible to demonstrate the survival of H. somnus in freshly isolated bovine mononuclear phagocytes in membrane-bound vacuoles. To determine if activation of macrophage function would result in elimination of intracellular H. somnus, BBM were treated with E. coli lipopolysaccharide (LPS) or recombinant bovine (rBo) cytokines, interferon-gamma (IFN-gamma), granulocyte macrophage colony stimulating factor (GM-CSF), tumour necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta). Treatment of BBM with rBoIFN-gamma, rBoGM-CSF or E. coli LPS resulted in decreased intracellular survival of H. somnus at 18 and 48 h, whereas BBM treated with rBoTNF-alpha or rBoIL-1beta had reduced intracellular survival of H. somnus only at 18 h. However, none of these treatments resulted in complete elimination of the intracellular bacteria. The ability of H. somnus to survive and multiply in both freshly isolated and cytokine-treated cultured BBM demonstrated the capability of H. somnus to escape from macrophage killing mechanisms. This capability may play a role in the dissemination of H. somnus infection in the body.

Epidemiology of Mycobacterium bovis infection in feral ferrets (Mustela furo) in New Zealand: I. Pathology and diagnosis.

Necropsies from 228 ferrets captured from eight areas in the North and South Islands provided material for an investigation into the epidemiology of tuberculosis in feral ferrets. Mycobacterial culture of pooled lymph nodes (retropharyngeal, respiratory and jejunal) identified the prevalence of infection to be much higher than that estimated from gross lesions only. Seventy-three of the 228 animals examined (32%) were diagnosed as tuberculous. Fifty-three culture-positive ferrets and 18 seemingly uninfected animals were subjected to detailed histopathological examination. The outcomes of these investigations, including the characteristics of the disease, distribution of lesions and aids to diagnosis, are presented. Of the feral carnivores found in New Zealand, the disease persists at high prevalence only in ferrets, and is probably the maintained principally by ingestion of tuberculous carrion. The course of the disease may be prolonged in some ferrets, but tuberculosis eventually causes death of many infected animals. Microscopic hepatic granulomas may be considered pathognomonic of the disease, and have potential to be used as a rapid diagnostic tool in ferrets with no gross lesions.

Experimental vitamin A deficiency in mallards (Anas platyrhynchos): lesions and tissue vitamin A levels.

Captive mallards (Anas platyrhynchos), fed an all-grain diet for up to 5 months during the winters of 1991 to 1992 and 1992 to 1993, developed lesions of squamous metaplasia; some had no detectable hepatic vitamin A. Vitamin A deficiency in mallards was defined as hepatic levels of retinyl palmitate < 2 micrograms/g liver. Lesions were found only in ducks with low levels of hepatic vitamin A, but not all ducks with these low levels of hepatic vitamin A had histological lesions. The prevalence of lesions in the esophagus was greatest cranially and caudally and less common in the central region. Palatine salivary glands rarely were affected. Mallards with liver stores > 600 micrograms of hepatic retinyl palmitate per g liver, fed a diet deficient in vitamin A were unlikely to become deficient over a 5 month period. Birds fed an all-grain diet had significantly lower vitamin A concentrations in their liver compared to those fed an all-grain diet with vitamin A added. Liver weight, when corrected for body size, did not affect vitamin A concentration. Serum retinol levels were conserved over a large range of hepatic vitamin A levels but levels below 300 micrograms retinol/l were useful in detecting vitamin A deficiency in captive mallards. Based on the findings, the presence of lesions provides a conservative measure of vitamin A status in ducks and tissue levels should be measured in instances when mallards have questionable vitamin A status.

Starvation, staphylococcosis, and vitamin A deficiency among mallards overwintering in Saskatchewan.

During January to March 1991, 38 mallards (Anas platyrhynchos) found dead from a group of approximately 600 overwintering on the South Saskatchewan River were examined. Thirty birds died from starvation, four had disseminated Staphylococcus aureus infection, and the cause of death of four birds was not determined. All six birds from which the esophagus was examined microscopically, including the four birds with staphylococcosis, had squamous metaplasia of the submucosal glands, a lesion pathognomonic for vitamin A deficiency. Vitamin A deficiency may occur in mallards and other waterfowl that overwinter north of traditional wintering areas and rely on grains deficient in carotenoids.

Viral tracheitis in goslings in Saskatchewan.

Up to 12% mortality occurred in goslings between 4 and 11 days of age in two sequential hatches from a single breeder flock. Respiratory signs were noted before the birds died. The most consistent necropsy finding was a white opaque plug of fibrin and cellular debris in the trachea. The tracheal epithelium was hyperplastic and metaplastic with intranuclear inclusion bodies present in superficial cells. An adenovirus was isolated in both chicken and goose embryo liver cells.

Multicentric intramuscular lipomatosis/fibromatosis in free-flying white-fronted and Canada geese.

Over a period of 9 yr, seven white-fronted geese (Anser albifrons) and one Canada goose (Branta canadensis) with multiple intramuscular mesenchymal tumors were encountered in Saskatchewan (Canada) and one similarly affected Canada goose was seen on Prince Edward Island (Canada). The tumors in these birds consisted either of adipose tissue, fibroblastic tissue, or a mixture of both types of tissues. The high prevalence of this condition in white-fronted geese suggested a genetic influence.

An adenovirus infection of the kidney of Franklin's ground squirrels (Spermophilus franklini) in Saskatchewan, Canada.

During routine pathological studies of Franklin's ground squirrels (Spermophilus franklini) collected during a predator control program, basophilic intranuclear inclusions were found in the collecting tubule epithelium of the renal papillae in seven of 13 squirrels. This was associated with marked karyomegaly in affected cells. An inflammatory response was not seen in the adjacent tissues. Electron microscopic examination of affected cells demonstrated that the enlarged nuclei contained numerous virus-like particles. Autoculture and serial passage of renal medullary cells resulted in the isolation of virus particles producing intranuclear inclusions and cytopathic effect. The virus possessed properties typical of adenoviruses, but showed no evidence of hemagglutinating activity with a range of species of erythrocytes tested under several temperature conditions. The isolates were relatively host-cell specific; they failed to grow in hamster and rabbit kidney cell lines and in ground squirrel kidney cortical cells.

Characteristics of the labile neurotoxin associated with nervous coccidiosis.

Reported are the results of preliminary attempts to characterize the molecular weight, heat sensitivity and other features of a labile neurotoxin identified in the serum of calves exhibiting neurological signs in association with coccidial enteritis. The labile neurotoxin activity is heat labile (60 degrees C for 30 min) and is lost upon exposure to acidic pH (5.5) and cysteine (1.75 g/100 mL serum). Activity can be recovered from the precipitate of a 30% wt/vol solution of (NH4)2SO4 in serum. Ultrafiltration trials suggest that labile neurotoxin activity may be linked to a molecule of over 300,000 MW.

Subacute toxic effects of dietary T-2 toxin in young mallard ducks.

Young Mallard ducks (Anas platyrhynchos) were fed diets containing purified T-2 toxin at levels of 20 or 30 ppm for two or three weeks. Ingestion of T-2 toxin was associated with reduced weight gain and delayed development of adult plumage. Affected ducks developed caseonecrotic plaques throughout the upper alimentary tract, especially in oropharynx and ventriculus. Several ducks also developed severe ulcerative, proliferative esophagitis and proventriculitis. Generalized atrophy of all lymphoid tissues consistently occurred. The manifestations of T-2 mycotoxicosis in Mallard ducks were mostly attributable to irritant toxicity to the alimentary mucosa. The T-2 toxin caused neither hematopoietic suppression nor a hemorrhagic syndrome in ducks. These alimentary lesions of T-2 mycotoxicosis in ducks do not resemble diseases of native waterfowl presently being recognized in routine surveillance of waterfowl mortality in Saskatchewan.

Experimental transmission of Sarcocystis sp. (Protozoa: Sarcocystidae) between the shoveler (Anas clypeata) duck and the striped skunk (Mephitis mephitis).

Muscle containing macroscopic cysts of Sarcocystis sp. from naturally infected wild shoveler (Anas clypeata) ducks was fed to two captive striped skunks (Mephitis mephitis). The skunks passed sporocysts in their feces beginning 19 and 22 days post-infection, and continued to pass small numbers of sporocysts sporadically to 63 and 51 days post-infection, respectively. Sporocysts from the skunks were administered orally to four laboratory-reared shovelers. No cysts were found in ducks examined 56 and 84 days post-infection. One duck examined at 85 days post-infection had many microscopic cysts in its skeletal muscle. The remaining duck had numerous small macroscopic cysts in muscle at 154 days post-infection. A skunk fed muscle from this duck began to pass sporocysts on day 18 post-infection. All cysts in muscle (natural and experimental infection) had irregular cauliflower-like projections of the primary cyst wall.