Pathobiology of A/Chicken/Hong Kong/220/97 (H5N1) avian influenza virus inseven Gallinaceous species

Direct bird-to-human transmission, with the production of severe respirator y disease and human mortality, is unique to the Hong Kong-origin H5N1 highl y pathogenic avian influenza (HPAI) virus, which was originally isolated fr om a disease outbreak in chickens. The pathobiology of the A/chicken/Hong K ong/ 220/97 (H5N1) (HK/220) HPAI virus was investigated in chickens, turkey s, Japanese and Bobwhite quail, guinea fowl, pheasants, and partridges, whe re it produced 75-100% mortality within 10 days. Depression, mucoid diarrhe a, and neurologic dysfunction were common clinical manifestations of diseas e. Grossly, the most severe and consistent lesions included splenomegaly, p ulmonary edema and congestion, and hemorrhages in enteric lymphoid areas, o n serosal surfaces, and in skeletal muscle. Histologic lesions were observe d in multiple organs and were characterized by exudation, hemorrhage, necro sis, inflammation, or a combination of these features. The lung, heart, bra in, spleen, and adrenal glands were the most consistently affected, and vir al antigen was most often detected by immunohistochemistry in the parenchym a of these organs. The pathogenesis of infection with the HK/220 HPAI virus in these species was twofold. Early mortality occurring at 1-2 days postin oculation (DPI) corresponded to severe pulmonary edema and congestion and v irus localization within the vascular endothelium. Mortality occurring afte r 2 DPI was related to systemic biochemical imbalance, multiorgan failure, or a combination of these factors. The pathobiologic features were analogou s to those experimentally induced with other HPAI viruses in domestic poult ry.