Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/16/2001
Publication Date: N/A
Citation: N/A Interpretive Summary: The purpose of this study was to determine if emus, geese, ducks and pigeons could be infected and become ill with the Hong Kong H5N1 bird flu virus. This virus caused illness and death in both chickens and humans during 1997. In this study, the geese, emus, and ducks were infected with the influenza virus, but only geese and emus became ill. Bird flu virus was consistently produced by the geese and emus. Ducks did not show illness and shed only minimal levels of virus. Pigeons were resistant to experimental inoculation.
Technical Abstract: The objective of this study was to ascertain the susceptibility of emus, geese, ducks, and pigeons to intranasal (IN) inoculation with the A/chicken/Hong Kong/220/97 (H5N1) HPAI virus. There was no mortality within 10 days postinoculation (DPI) in the four species investigated, and clinical disease, evident as neurologic dysfunction, was observed only in emus and geese. Grossly, pancreatic mottling and splenomegaly were identified in these two species. Histologically, the emus and geese developed pancreatitis, meningoencephalitis, and mild myocarditis. Influenza viral antigen was demonstrated in areas with histological lesions up to 10 DPI in the geese. Virus was reisolated from oropharyngeal and cloacal swabs and from the lung, brain, and kidney of the emus and geese. Moderate splenomegaly was observed grossly in the ducks. Viral infection of the ducks was pneumotropic, as evidenced by mild inflammatory lesions in nthe respiratory tract and virus reisolation from oropharyngeal swabs and from a lung. Pigeons were resistant to HK/220 infection, lacking gross and histological lesions, viral antigen, and reisolation of virus. These results imply that emus and geese are susceptible to IN inoculation with the HK/220 virus, whereas ducks and pigeons are more resistant. These latter two species probably played a minimal role in the perpetuation of the H5N1 Hong Kong-origin influenza viruses.