|Nemeth, N -|
|Brown, J -|
|Stallknecht, D -|
|Howerth, E -|
|Newman, S -|
Submitted to: Veterinary Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 1, 2013
Publication Date: June 4, 2013
Repository URL: http://handle.nal.usda.gov/10113/59813
Citation: Nemeth, N.M., Brown, J.D., Stallknecht, D.E., Howerth, E.W., Newman, S.H., Swayne, D.E. 2013. Experimental infection of bar-headed geese (Anser indicus) and ruddy shelducks (Tadorna ferruginea) with a clade 2.3.2 H5N1 highly pathogenic avian influenza virus. Veterinary Pathology. 50(6):961-970. Interpretive Summary: Since 2005, clades or families 0, 1, 2.2 and 2.3.2 of the H5N1 highly pathogenic avian influenza (HPAI) viruses have caused infections, disease and death in numerous species of wild waterfowl in Eurasia and Africa. Clade 2.3.2 viruses have become dominant since 2009, being established in poultry in Asia. We conducted studies to determine how clade 2.3.2 viruses affected two wild waterfowl birds; bar-headed geese (Anser indicus) and ruddy shelducks (Tadorna ferruginea). Infected ruddy shelducks had neurologic signs, and died, but infected bar-headed geese were weak with all surviving. All infected birds shed H5N1 HPAI virus from the mouth in larger quantities than from the cloaca. The virus damaged the brains of both species but was more severe in ruddy shelducks. Our studies demonstrated clade 2.3.2 H5N1 HPAI virus can cause infections and disease in some migratory waterfowl potentially serving as short to medium distance disseminators of H5N1 HPAI virus.
Technical Abstract: Since 2005, clade 2.2 H5N1 highly pathogenic avian influenza (HPAI) viruses have caused infections and disease involving numerous species of wild waterfowl in Eurasia and Africa. However, outbreaks associated with clade 2.3.2 viruses have increased since 2009, and viruses within this clade have become the dominant strain of H5N1 HPAI virus detected in wild birds, reaching endemic status in domestic birds in select regions of Eurasia. To address questions relating to the emergence and expansion of clade 2.3.2 viruses, two waterfowl species repeatedly involved in outbreaks of H5N1 HPAI viruses, bar-headed geese (Anser indicus) and ruddy shelducks (Tadorna ferruginea), were inoculated with a clade 2.3.2 H5N1 HPAI virus. Three of four virus-inoculated ruddy shelducks were infected, exhibited neurologic signs, and died between 4-5 days post-inoculation (DPI). All three virus-inoculated bar-headed geese became infected; two were transiently weak, but all survived. Viral shedding occurred between 1-7 DPI in all infected birds and was predominately via the oropharynx. The severity and distribution of microscopic lesions corresponded with clinical disease and immunohistochemical staining of neurons for influenza viral antigen. The predominant lesion in both species was lymphoplasmacytic encephalitis sometimes with neuronal necrosis, which was more severe in ruddy shelducks. Increased caspase-3 reactivity in the brains of all infected birds suggests a role for apoptosis in the pathogenesis of H5N1 HPAI virus in these species. These results demonstrate that similar to clade 2.2 viruses, clade 2.3.2 H5N1 HPAI virus is neurotropic in some species of waterfowl, and can lead to neurologic disease with varying clinical outcomes.