Frederick A. Leighton

Wild bird influenza survey, Canada, 2005.

Of 4,268 wild ducks sampled in Canada in 2005, real-time reverse transcriptase–PCR detected influenza A matrix protein (M1) gene sequence in 37% and H5 gene sequence in 5%. Mallards accounted for 61% of samples, 73% of M1-positive ducks, and 90% of H5-positive ducks. Ducks hatched in 2005 accounted for 80% of the sample.

Emergence of Sylvatic Echinococcus granulosus as a Parasitic Zoonosis of Public Health Concern in an Indigenous Community in Canada

Within a remote Canadian Indigenous community, at least 11* of people had antibodies against Echinococcus granulosus and E. granulosus eggs were detected in 6* of environmentally collected canine fecal samples. Dog ownership, hunting, and trapping were not risk factors for seropositivity, suggesting that people are most likely exposed to E. granulosus through indirect contact with dog feces in the environment. In this situation, human exposure could be most effectively curtailed by preventing consumption of cervid viscera by free-roaming dogs.

Multiple Zoonotic Pathogens Identified in Canine Feces Collected from a Remote Canadian Indigenous Community

Five genera of potentially zoonotic bacteria and parasites were detected in environmentally collected fecal samples from a remote indigenous community in Northern Saskatchewan, Canada. Organisms identified include Toxocara canis, Echniococcus granulosus, Giardia duodenalis, Cryptosporidium spp., and Campylobacter spp. The prevalence and intensity of Giardia spp. and Campylobacter spp. in fecal samples was particularly remarkable. Three-quarters of samples tested contained at least one zoonotic species of Campylobacter, and C. jejuni-containing feces had an average of 2.9 x 10(5) organisms/g. Over one-half of samples tested contained Giardia spp. with an average of 9,266 cysts/g. Zoonotic G. duodenalis Assemblage A was the only Giardia spp. genotype identified. These data suggest that canine feces have the potential to pose a significant health risk to Canadians in rural and remote indigenous communities.

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.

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 DoréLake (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 (≤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).

The morphology and pathology of Besnoitia sp. in reindeer (Rangifer tarandus tarandus).

Four of five reindeer (Rangifer tarandus tarandus) obtained from a Besnoitia sp.-infected herd at the Assiniboine Park Zoo in Winnipeg, Manitoba, Canada, in October 1989, had evidence of mild dermatitis over the articular surfaces of carpal and tarsal joints. Cysts of Besnoitia sp., either surrounded by inflammatory reactions or without evident host response, were present within the dermis, submucosa of the nasal turbinates, periosteum, tendons, testes and hooves. The light microscopic and histochemical features of Besnoitia sp. from reindeer were indistinguishable from those of other Besnoitia spp. described in cattle, rodents and horses.The Besnoitia sp. cysts and organisms from reindeer were unique in that bradyzoite membrane micropores and cytoplasmic enigmatic bodies were not observed. Two cats were fed cysts of Besnoitia sp. but no oocysts were detected in feces for 90 days post-infection.

Sampling strategies and biodiversity of influenza A subtypes in wild birds.

Wild aquatic birds are recognized as the natural reservoir of avian influenza A viruses (AIV), but across high and low pathogenic AIV strains, scientists have yet to rigorously identify most competent hosts for the various subtypes. We examined 11,870 GenBank records to provide a baseline inventory and insight into patterns of global AIV subtype diversity and richness. Further, we conducted an extensive literature review and communicated directly with scientists to accumulate data from 50 non-overlapping studies and over 250,000 birds to assess the status of historic sampling effort. We then built virus subtype sample-based accumulation curves to better estimate sample size targets that capture a specific percentage of virus subtype richness at seven sampling locations. Our study identifies a sampling methodology that will detect an estimated 75% of circulating virus subtypes from a targeted bird population and outlines future surveillance and research priorities that are needed to explore the influence of host and virus biodiversity on emergence and transmission.

Survey of Influenza A Viruses Circulating in Wild Birds in Canada 2005 to 2007

Abstract A multi-agency, Canada-wide survey of influenza A viruses circulating in wild birds, coordinated by the Canadian Cooperative Wildlife Health Centre, was begun in the summer of 2005. Cloacal swab specimens collected from young-of-year ducks were screened for the presence of influenza A nucleic acids by quantitative, real-time reverse transcription-polymerase chain reaction (RRT-PCR). Specimens that produced positive results underwent further testing for H5 and H7 gene sequences and virus isolation. In addition to live bird sampling, dead bird surveillance based on RRT-PCR was also carried out in 2006 and 2007. The prevalence of influenza A viruses varied depending on species, region of the country, and the year of sampling, but generally ranged from 20% to 50%. All HA subtypes, with the exception of H14 and H15, and all NA subtypes were identified. The three most common HA subtypes were H3, H4, and H5, while N2, N6, and N8 were the three most common NA subtypes. H4N6, H3N2, and H3N8 were the three most common HA–NA combinations. The prevalence of H5 and H7 subtype viruses appears to have a cyclical nature.

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 (104.8 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.

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.