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.

Destructive polyarthropathy in aborted bovine fetuses: a possible association with Ureaplasma diversum infection?

Severe destructive polyarthropathy with fibrillation and erosion of articular cartilage, deformation of articular surfaces, and proliferation of periarticular soft tissue was diagnosed in 5 bovine fetuses aborted in the last trimester. There was involvement of a single coxofemoral joint in 2 fetuses, both elbows, and a stifle in 1, both stifles and tarsal joints in another, and, in the most severely affected fetus, both hips, stifles, and shoulders as well as 1 carpus. In affected joints, the articular cartilage was irregularly reduced in thickness and contained fibrovascular tissue and, in some cases, inflammatory cells and fibrin. Four of 5 fetuses had microscopic placentitis; all had mild lymphoplasmacytic conjunctivitis. Ureaplasma spp. was identified in 4 cases by polymerase chain reaction or culture. Fetal arthropathy and Ureaplasma diversum-associated joint pathology have not been previously reported in the veterinary literature; however, other Ureaplasma spp. are known to cause reproductive disease and arthritis in humans.

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.

Demographic features of Bartonella infections in Richardson's ground squirrels (Spermophilus richardsonii).

The epidemiology of Bartonella infections in Richardson's ground squirrels (Spermophilus richardsonii) was studied at multiple sites in Saskatchewan, Canada, from 2002 to 2004. The overall prevalence of Bartonella infection was 48%. Juvenile squirrels were significantly more likely to be infected with Bartonella than were adults (58% and 37%, respectively), and juvenile animals also were significantly more likely to have high levels of bacteremia compared to adult animals. Prevalence of Bartonella infection appeared to decrease with age; only 24% of animals known to be > or = 2 yr old were infected with Bartonella. Prevalence of infection was lowest in May (27%) and highest in late summer and early autumn (71%). The prevalence of fleas also varied seasonally, and animals were more likely to have fleas in the late summer and early autumn than in early summer. We found no relationship between Bartonella prevalence and host density or flea prevalence.

Effect of experimental ectoparasite control on bartonella infections in wild Richardson's ground squirrels.

The purpose of this study was to investigate the role of ectoparasites in transmitting Bartonella infections in wild Richardson's ground squirrels (Spermophilus richardsonii). Richardson's ground squirrels were trapped, examined for fleas, and tested for Bartonella bacteremia once monthly, at six sites, from April to September 2004. After the initial trapping session in April, burrows at three sites were treated with deltamethrin insecticide. Richardson's ground squirrels trapped on treated sites were less likely to have fleas and had fewer fleas than squirrels on control sites in all months following treatment. We found no difference in the prevalence of Bartonella infections on control and treated sites in May, immediately following treatment; however, significantly fewer squirrels were infected with Bartonella on treated sites in June and July. We conclude that ectoparasites are a main route of transmission for Bartonella infections in Richardson's ground squirrels.

Mortality of geese as a result of collision with the ground.

Two incidents are reported in which groups of migrating wild geese were found dead in agricultural fields in southern Manitoba during spring. In each case, the birds died overnight and poisoning was suspected; however, the birds had lesions of severe traumatic injury. The first incident, in 1985, involved about 150 lesser snow geese (Anser caerulescens caerulescens); the second, in 2003, involved 62 Canada geese (Branta canadensis). Both incidents occurred on dark, moonless nights. One possible explanation is that the birds became disoriented in a manner analogous to spatial disorientation described in aircraft pilots and flew as a flock directly into the earth. In the first incident, geese might have been frightened by sonic booms from aircraft; in the second, there was a thunderstorm with strong gusty winds 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.

Streptococcus equisimilis infection in striped skunks (Mephitis mephitis) in Saskatchewan.

Three radio-collared striped skunks (Mephitis mephitis) found dead during a field study of winter ecology of striped skunks near Willowbrook, Saskatchewan, Canada were examined. Streptococcus equisimilis was identified as the primary agent causing necrotizing purulent pneumonia in one skunk and suppurative meningoencephalitis in another. Both Streptococcus equisimilis and Streptococcus canis were isolated from lesions of purulent myocarditis and pyothorax in the third skunk. These are apparently the first reported cases of S. equisimilis infection in striped skunks and suggest that this opportunistic pathogen may be a significant cause of mortality under some conditions.

Disease management strategies for wildlife.

Three basic forms of management strategies exist for wildlife disease, as follows: prevention of introduction of disease, control of existing disease or eradication. Management may be directed at the disease agent, host population, habitat or be focused on human activities. Disease agents may be dealt with in the environment through disinfection or in the host through treatment. Disinfection and pesticides used to destroy agents or vectors are limited to local situations, may have serious environmental effects and may result in acquired resistance. Difficulty in delivering treatment limits chemotherapy to local situations. Host populations may be managed by immunisation, by altering their distribution or density, or by extirpation. Immunisation is best suited for microparasitic exogenous infections with a low reproductive rate and in populations which have a low turnover. Mass immunisation with oral baits has been effective, but this strategy is limited to a few serious diseases. It is difficult to move wild animals and techniques to discourage animals from entering an area become ineffective rapidly. The setting up of fences is feasible only in local situations. Selective culling is limited to situations in which affected individuals are readily identifiable. General population reduction has had little success in disease control but reducing populations surrounding a focus or creating a barrier to disease movement have been successful. Population reduction is a temporary measure. Eradication of a wildlife population has not been attempted for disease management. Habitat modification may be used to reduce exposure to disease agents, or to alter host distribution or density. Management of diseases of wild animals usually requires a change in human activities. The most important method is by restricting translocation of wild animals to prevent movement of disease.

Histology and ultrastructure of the chorioallantoic membrane of the mallard duck (Anas platyrhynchos).

The histology and fine structure of the chorioallantoic membrane of the mallard duck (Anas platyrhynchos), and the density of vessels per millimeter of membrane were assessed between days 12 and 24 of incubation. Light and transmission electron microscopy of the chorioallantoic membrane of the mallard duck after various days of incubation was carried out. Blood vessels within the mesoderm were counted per millimeter of membrane by light microscopy (40x). The chorioallantoic membrane had three distinct layers from day 12 to 24 of incubation, the chorionic epithelium, the mesoderm, and the allantoic epithelium. After day 12, chorionic epithelium consisted of two layers of flattened, elongated epithelial cells interfaced by numerous desmosomes, and separated from the underlying mesoderm by a basement membrane. At this stage, the allantoic epithelium consisted of a single layer of flattened, overlapping cells. Blood capillaries were observed in the mesoderm close to the chorionic epithelium on days 12 and 13; by day 14, these capillaries were located within the chorionic epithelium, forming a capillary sinus. Between days 14 and 16, the chorion underwent cellular and cytological differentiation into three cell types: capillary covering cells, villus cavity cells, and less differentiated basal cells. The mesoderm was composed of a loose matrix of mesenchymal cells and collagen fibrils through which coursed blood and lymphatic vessels. The vascular density in the mesoderm increased rapidly from 4.2+/-0.6 vessels per mm (n = 12) on day 12 to a maximum of 9.4+/-0.3 vessels per mm (n = 15) by day 16. From day 16, the allantoic epithelium had two to three layers of elongated and overlapping cells. The luminal layer of allantoic epithelial cells had microvillus projections and varying numbers of membrane-bound dense vesicles at all stages from day 12 onward. The histologic and ultrastructural features of mallard duck chorioallantoic membrane from day 12 to 24 of incubation were very similar to those described in the chorioallantoic membrane of the chicken (Gallus gallus) from day 8 to 20 of incubation. Much of the information available concerning the CAM of the chicken also may apply to the CAM of the mallard, with timing adjusted to match the developmental time-frame recorded here.

Immunization of ducks for type C botulism.

A single subcutaneous immunization with a vaccine used for protecting ranch mink (Mustela vison) against type C botulism reduced morbidity and mortality in mallard (Anas platyrhynchos) and northern pintail (Anas acuta) ducks challenged with approximately 4.5 x 10(4) and 2.25 x 10(4) mouse lethal doses (MLD50), respectively, of botulinum toxin at 10 and 15 days post-immunization (pi). There was no significant protection at 5 days pi. Protection persisted in mallards for 90 days pi. To simulate use of vaccine as a part of treatment of sick birds in the field, mallards were exposed to toxin and, when clinical signs were evident, each bird was treated by intraperitoneal injection of type C botulinum antitoxin and one-half of the birds were immunized. Immunization had no significant effect on recovery from intoxication. At 10 days posttreatment, all birds were challenged with toxin. Clinical signs and mortality were significantly less frequent among immunized birds than among non-immunized birds after the second exposure. Immunization might be useful as part of the treatment regimen in botulism outbreaks.

Causes of morbidity and mortality and their effect on reproductive success in double-crested cormorants from Saskatchewan.

The objectives of this study were to describe causes of morbidity and mortality in a breeding colony of double-crested cormorants (Phalacrocorax auritus) on Doré Lake (Saskatchewan, Canada), and to determine cause-specific mortality rates of juvenile birds. Morbidity and mortality were monitored every third day during the breeding season from 1994 to 1996 from inside a tunnel-and-blind system. Affected eggs and birds were collected for examination and diagnosis. The cause of mortality was determined for 105 eggs, 178 nestlings (< or = 4-wk-old), 1393 post-nestling chicks (> 4-wk-old), and 10 adults. The main causes of mortality were infertility or embryonal death, avian predation, displacement of eggs and chicks from the nest, starvation from sibling competition, Newcastle disease, coyote predation, human-induced suffocation, and entrapment. In 49% of the cases, avian predation and displacement from the nest of eggs or nestlings was associated with human disturbance. Thirty-six nestlings, 40 post-nestling chicks, and three adults were examined for the presence of parasites. Contracaecum spiculigerum was found in the proventriculus; Amphimerus elongatus in the liver. Piagetiella incomposita in the gular pouch; Eidmanniella pellucida, Pectinopygus farallonii, and Ceratophyllus lari in the plumage; and Theromyzon sp. in the nasal and oral cavity. Contracaecum spiculigerum was associated with ulcerative gastritis, A. elongatus with multifocal hepatitis and bile duct hyperplasia, and P. incomposita with ulcerative stomatitis, but these lesions were not considered fatal. Other diseases included beak deformity, abnormal rotation of the carpal joint, hypopigmentation, and eye loss. Overall mortality of cormorant chicks between hatching and the end of the breeding season varied from 25 to 48%. The most important causes of mortality were Newcastle disease, which killed 21% of hatched chicks in 1995, sibling competition (maximum 12% in 1994), and coyote predation (2% in 1994).

Pathology of Newcastle disease in double-crested cormorants from Saskatchewan, with comparison of diagnostic methods.

Newcastle disease (ND) in juvenile double-crested cormorants (Phalacrocorax auritus) occurred several times since 1975, but there are relatively few studies on its pathology and diagnosis. In order to describe the distribution of Newcastle disease virus (NDV) and associated lesions in cormorants with ND and to compare diagnostic methods, 25 cormorants with nervous signs from a ND epizootic in Saskatchewan in 1995 (NDE cormorants) were compared with 18 negative control cormorants. Tissues of these birds were examined by necropsy, histology, virus isolation, immunohistochemistry, serology, and reverse transcriptase-polymerase chain reaction (RT-PCR) methods. The NDE cormorants had a characteristic non-suppurative encephalomyelitis, with a significantly higher prevalence of neuronal necrosis, gliosis, perivascular infiltration with mononuclear cells, and endothelial hypertrophy than control cormorants. These lesions were found more frequently in the cerebellum and brain stem than in other parts of the central nervous system. Immunohistochemically, NDV antigen was limited to neurons, glial and endothelial cells in the central nervous system, and to tubular epithelial cells in the kidney. Newcastle disease virus was isolated with the highest prevalence (4/5) and the highest concentration (10(4.8) ELD50/g) from the kidney. The virus isolates often did not agglutinate erythrocytes in the standard hemagglutination test; the presence of NDV was confirmed by use of an indirect immunoperoxidase assay. By RT-PCR, NDV was detected in kidney and jejunum of a NDE cormorant. There was no significant difference between sensitivity of histology, virus isolation, and serology for detecting ND in NDE cormorants.

An epidemic of Newcastle disease in double-crested cormorants from Saskatchewan.

A Newcastle disease epidemic in double-crested cormorants (Phalacrocorax auritus) occurred in July and August 1995, during a 1994-96 study of a breeding colony of this species on Doré Lake (Saskatchewan, Canada). Clinical signs and mortality were observed from a tunnel-and-blind system, and moribund and freshly dead birds were examined virologically. Yolks from cormorant eggs and sera from cormorants and other birds were tested for hemagglutination inhibiting antibodies to Newcastle disease virus (NDV). Evidence of Newcastle disease was limited to juvenile double-crested cormorants, despite close contact with other birds, including American white pelicans (Pelecanus erythrorhynchos) and gulls (Larus spp.). Clinical signs included limb, head or neck paralysis, head or body tremors, ataxia, and blindness; pathogenic NDV was isolated from affected birds. The mortality rate of juvenile cormorants was 32 to 64%, which was high relative to overall first-year mortality in years without epidemics. Thirty-seven of 63 (59%) cormorant sera collected during the epidemic tested positive for antibodies to NDV. Antibody status of cormorant egg yolks depended on stage of incubation, likely due to changes in the amount of water in the yolks. The departure of juvenile cormorants from their nests at 4 wk of age, resulting in an increased contact rate among individuals, may have been important in triggering the epidemic.

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.

Excretion of pathogenic Newcastle disease virus by double-crested cormorants (Phalacrocorax auritus) in absence of mortality or clinical signs of disease.

Pathogenic Newcastle disease virus (NDV) caused several epidemics of Newcastle disease in double-crested cormorants (Phalacrocorax auritus) in recent years. Eleven 16-week-old cormorants were infected with, or exposed to, pathogenic NDV from one of these epidemics and monitored for 70 days. No birds died, four birds had transient ataxia between 12 and 27 days post-infection (d.p.i.), and one bird had neuronal necrosis and non-suppurative encephalitis characteristic for Newcastle disease. The mean haemagglutina-tion inhibiting antibody titre to NDV peaked at 1:630, 21 d.p.i., and decreased to 1:56 70 d.p.i. Duration of NDV excretion from the cloaca was 15 +/- 6.2 d.p.i., with a maximum of 28 d.p.i. The absence of mortality in these birds may have been due to age-related resistance. The excretion of NDV by cormorants in the absence of mortality or clinical signs of disease suggests that the cormorant population could maintain pathogenic NDV through serial infection of susceptible birds. The greatest risk of NDV transmission from cormorants to poultry probably is during autumn migration, through contact with infected birds, excreta or contaminated water.

Ecosystem health as a clinical rotation for senior students in Canadian veterinary schools.

We describe 4 years of an experimental rotation in ecosystem health offered to senior veterinary students in Canada. Faculty from the 4 Canadian veterinary colleges collaborated in offering the rotation once annually at 1 of the colleges. The 1st rotation was held in Guelph in 1993, followed in successive years by rotations at Saskatoon, Saint-Hyacinthe, and Charlottetown. The rotation is a predominantly field-based experience that allows students to work with veterinary and other role models who are actively engaged in clinical research related to ecosystem health. Five specific field studies that worked particularly well during the rotations are presented. These studies involved investigating mortality in wildlife due to botulism, designing an environmental surveillance system around herds of beef cattle, using belugas to evaluate the health of the St. Lawrence River, dealing with competition for water use by aquaculture and agriculture, and exploring the role of veterinarians during major coastal oil spills. The experience has resulted in our developing the subject matter, field examples, teaching approach, and confidence necessary to make ecosystem health the focus of a productive clinical rotation for senior year veterinary students.

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.

Epidemiology of Mycobacterium bovis infection in feral ferrets (Mustela furo) in New Zealand: II. Routes of infection and excretion.

Detailed necropsies of 228 ferrets captured from eight areas in the North and South Islands provided material for an investigation into the epidemiology of tuberculosis in wild ferrets. Seventy-three of the 228 (32%) animals examined were diagnosed as tuberculous, by culture of pooled lymph nodes and detailed histopathological examination. The prevalence of bovine tuberculosis was 96% in 24 ferrets taken from areas in which tuberculous possums were common. None of 35 animals under 4 months of age were found to be infected, and the prevalence of infection was shown to rise with age, such that for each 6 month age increment there was a 2.8 times greater risk of becoming infected. The most common route of infection appeared to be via the alimentary tract, as 79% of 38 animals, in which the initial lesions could be reasonably determined, had these lesions associated with the digestive tract. Samples from potential sites of excretion from infected ferrets were submitted for culturing. The most common route of excretion was via the oral cavity, with M. bovis recovered from 15 of 64 (23%) oral swabs. Mycobacterium bovis was also isolated from four of 64 (6%) tracheobronchial lavage samples, ten of 63 (16%) faecal samples, two of 29 (7%) urine samples and one of 8 (12.5%) mammary glands. The disease in ferrets appears to be principally maintained by ingestion of tuberculous carrion. Although a moderate number of ferrets excrete M. bovis orally, there appears to be only minor intraspecific transmission by bite wounding. The findings provided no evidence to support the occurrence of pseudo-vertical transmission.