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

Abstract

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.

Haemagglutinin and neuraminidase characterization of low pathogenic H5 and H7 avian influenza viruses isolated from Northern pintails (Anas acuta) in Japan, with special reference to genomic and biogeographical aspects

“…For instance, HPAI was confirmed in Italy in 1999, caused by subtype H7N1 virus reported to be derived from a low pathogenic progenitor virus of the same subtype, after a period of approximately 9 months of circulation in poultry [6]. Similarly, the causative agent of outbreaks in Mexico from 1994 to 1995 was derived from a LPAI virus [7], as were the viruses that caused outbreaks in British Columbia and Chile [8,9]. Besides, high identity of the HPAI H7N7 virus that caused outbreaks in chicken in Netherlands in 2003 to low pathogenic viruses isolated from wild ducks was reported as well [10].…”

Laboratory Surge Response to Pandemic (H1N1) 2009 Outbreak, New York City Metropolitan Area, USA

“…Attention is given primarily to the hypothetical preparedness of first responders and acute-care facilities, either in the form of surveys ( 9 – 12 ), workflow analysis ( 13 ), or reviews ( 12 , 14 , 15 ). The outbreak of severe acute respiratory syndrome in 2003 generated reports from an actual global outbreak.…”

Amino acids adjacent to the haemagglutinin cleavage site are relevant for virulence of avian influenza viruses of subtype H5

“…HPAIVs evolve from low-pathogenic precursors by acquisition of a polybasic HA cleavage site Garten & Klenk, 2008;Horimoto et al, 1995b;Kawaoka & Webster, 1985;Pasick et al, 2005;Perdue et al, 1997;Suarez et al, 2004). Whereas back-conversion of this polybasic cleavage site to the initial monobasic motif results in a drastic reduction in virulence , the contrary mutation by insertion of a polybasic stretch into the HA cleavage site of a LPAIV may or may not lead to a HPAIV (Bogs et al, 2010;Munster et al, 2010;Stech et al, 2009).…”

“…Remarkably, there are some H5 HPAIVs that have polybasic HA cleavage motifs with threonine at P2 Garten & Klenk, 2008;Horimoto et al, 1995a;Pasick et al, 2005;Perdue et al, 1996Perdue et al, , 1997Saito et al, 1994;Suarez et al, 2004;Wood et al, 1993). These examples indicate that threonine at P2 does not impair the virulence of HPAIVs.…”

“…Several highly pathogenic strains have acquired fragments from the 28S rRNA sequence (Khatchikian et al, 1989) or a gene segment derived from the same or a different virus strain (Morsy et al, 1994;Pasick et al, 2005;Suarez et al, 2004) leading to elongation of the cleavage site region. Polybasic HA cleavage sites may also be generated by polymerase slippage Perdue et al, 1997).…”