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Title: PATHOBIOLOGY OF A/CHICKEN/HONG KONG/220/97 (H5N1) AVIAN INFLUENZA VIRUS IN SEVEN GALLINACEOUS SPECIES

Author
item Perkins, Laura
item Swayne, David

Submitted to: Veterinary Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/14/2000
Publication Date: 3/31/2001
Citation: N/A

Interpretive Summary: The purpose of this study was to determine the disease-causing potential of an influenza virus in seven species of birds. This influenza virus had caused severe natural disease in both chickens and humans. The species investigated included chickens, turkeys, guineafowl, quail (2 species), pheasants, and partridges. In all seven species of birds, rapid disease and ddeath occurred as a result of the influenza virus infection, with the viru being identified in multiple organs.

Technical Abstract: The pathogenicity of A/chicken/Hong Kong/220/97 (H5N1) (HK/220) HPAI virus infection was investigated in chickens, turkeys, Japanese and Bobwhite quail, guineafowl, pheasants, and partridges. The HK/220 virus was highly pathogenic, producing near 100% mortality within 10 days of inoculation in these species. Depression, diarrhea, and neurologic signs were common clinical manifestations in these species. Grossly, the most remarkable an consistent lesions included splenomegaly, pulmonary edema and congestion, and hemorrhages in enteric lymphoid areas, on serosal surfaces, and in skeletal muscle. Histologic lesions, characterized by exudation, hemorrhage, necrosis, and/or inflammation, were observed in multiple organs, but were most severe in the lung, heart, brain, spleen, and adrenal glands. The histologic lesions corresponded to the presence of parenchymal viral antigen detected by immunohistochemistry. Moderate to severe lymphoid depletion also was a prominent histologic feature of lymphoid tissues. The earliest mortality occurred at 1 to 2 DPI and corresponded to the presence of severe pulmonary edema and congestion and virus localization within the vascular endothelium. The second phase of mortality occurring after 2 DPI likely related to systemic biochemical imbalance, multiorgan failure, or a combination of factors.