The roles of national and provincial diagnostic laboratories in the eradication of highly pathogenic H7N3 avian influenza virus from the Fraser Valley of British Columbia, Canada.

In February 2004 a highly pathogenic avian influenza outbreak erupted in the Fraser Valley of British Columbia, Canada. The index farm was a chicken broiler breeder operation comprising two flocks, 24 and 52 wk of age. Birds in the older flock presented with a mild drop in egg production and a small increase in mortality. Pathological specimens taken from the older flock were submitted to the provincial veterinary diagnostic laboratory from which an influenza A virus was isolated. While still under investigation by the provincial veterinary authorities, a spike in mortality was observed in birds belonging to the younger flock. Diagnostic material from both flocks was forwarded to the Canadian Food Inspection Agency's National Centre for Foreign Animal Disease. A low-pathogenicity H7N3 virus was detected in the older flock and a novel highly pathogenic H7N3 virus was found in specimens collected from the younger flock. Despite destruction and disposal of birds on the index farm, the virus spread to adjacent farms. Given the high density of poultry operations in the Fraser Valley and the high level of integration amongst industry support services, a total of approximately 17 million chickens, turkeys, ducks, geese, and speciality birds were put at immediate risk. Despite movement controls the virus spread and established itself in three distinct clusters. To prevent further spread, healthy, marketable birds outside of the surveillance areas were pre-emptively slaughtered. Although highly pathogenic avian influenza is a federal responsibility, the successful control and eradication of this outbreak would not have been possible without the cooperative involvement of federal and provincial diagnostic laboratories. The success of this collaboration was partly responsible for the formation of a national avian influenza laboratory network.

Relationship between H5N2 avian influenza viruses isolated from wild and domestic ducks in British Columbia, Canada.

In the summer of 2005 a Canadian national surveillance program for influenza A viruses in wild aquatic birds was initiated. The program involved collaboration between federal and provincial levels of government and was coordinated by the Canadian Cooperative Wildlife Health Centre. The surveillance plan targeted young-of-the-year Mallards along with other duck species at six sampling locations along the major migratory flyways across Canada. Beginning in early August, cloacal swabs were taken from 704 ducks on two lakes adjacent to one another near Kamloops, British Columbia. The swabs were screened for the presence of influenza A RNA using a real-time reverse transcription-polymerase chain reaction (RRT-PCR) assay that targets the M1 gene. Swab samples that gave positive results underwent further testing using H5- and H7-specific RRT-PCR assays. One hundred and seventy-four cloacal swab specimens gave positive or suspicious results for the presence of an H5 virus. A portion of these (28/35) were confirmed using an H5-specific conventional reverse transcription-polymerase chain reaction assay and an H5 virus was eventually isolated from 24/127 swab specimens. Neuraminidase typing revealed the presence of H5N2 and H5N9 viruses. In mid-November of 2005 an H5N2 virus was detected in a commercial duck operation in the lower mainland of British Columbia, approximately 120 km from where the H5N2-positive wild ducks were sampled. Molecular genetic analysis of the H5N2 viruses isolated from wild and domestic ducks was carried out to determine their kinship.

Intersegmental recombination between the haemagglutinin and matrix genes was responsible for the emergence of a highly pathogenic H7N3 avian influenza virus in British Columbia.

In February 2004 a highly pathogenic avian influenza (HPAI) outbreak erupted in British Columbia. Investigations indicated that the responsible HPAI H7N3 virus emerged suddenly from a low pathogenic precursor. Analysis of the haemagglutinin (HA) genes of the low and high pathogenic viruses isolated from the index farm revealed the only difference to be a 21 nt insert at the HA cleavage site of the highly pathogenic avian influenza virus. It was deduced that this insert most probably arose as a result of non-homologous recombination between the HA and matrix genes of the same virus. Over the course of the outbreak, a total of 37 isolates with, and 3 isolates without inserts were characterized. The events described here appear very similar to those which occurred in Chile in 2002 where the virulence shift of another H7N3 virus was attributed to non-homologous recombination between the HA and nucleoprotein genes.