Abstract
Since 2002, H5N1 highly pathogenic avian influenza (HPA1) viruses have been associated with deaths in numerous wild avian species throughout Eurasia. We assessed the clinical response and extent and duration of viral shedding in 5 species of North American ducks and laughing gulls (Larus atricilla) after intranasal challenge with 2 Asian H5N1 HPAI viruses. Birds were challenged at approximately equal to 10 to 16 weeks of age, consistent with temporal peaks in virus prevalence and fall migration. All species were infected, but only wood ducks (Aix sponsa) and laughing gulls exhibited illness or died. Viral titers were higher in oropharyngeal swabs than in cloacal swabs. Duration of viral shedding (1-10 days) increased with severity of clinical disease. Both the hemagglutination-inhibition (HI) and agar gel precipitin (AGP) tests were able to detect postinoculation antibodies in surviving wood ducks and laughing gulls; the HI test was more sensitive than the AGP in the remaining 4 species.
Highlights
Since 2002, H5N1 highly pathogenic avian influenza (HPAI) viruses have been associated with deaths in numerous wild avian species throughout Eurasia
Before 2005, no evidence showed that highly pathogenic avian influenza (HPAI) viruses were maintained in wild bird populations
In 2002, a substantial number of deaths associated with H5N1 HPAI virus infection were reported in captive ducks, geese, and flamingos housed within 2 waterfowl parks in Hong Kong Special Administrative Region, People’s Republic of China [5]
Summary
Since 2002, H5N1 highly pathogenic avian influenza (HPAI) viruses have been associated with deaths in numerous wild avian species throughout Eurasia. Duration of viral shedding (1–10 days) increased with severity of clinical disease Both the hemagglutination-inhibition (HI) and agar gel precipitin (AGP) tests were able to detect postinoculation antibodies in surviving wood ducks and laughing gulls; the HI test was more sensitive than the AGP in the remaining 4 species. One exception occurred in 1961 when a high proportion of deaths in common terns (Sterna hirundo) in South Africa was attributed to an H5N3 HPAI virus without evidence of prior infection in domestic poultry [4]. This tern epizootic was limited, and the virus did not become endemic in any wild bird population. The goal of this study was to determine the susceptibility of critical species of North American waterfowl to 2 H5N1 HPAI viruses and the potential impact of these species on the epidemiology of the viruses in North America
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