Since 2005, clade 2.2 H5N1 highly pathogenic avian influenza (HPAI) viruses have caused infections and morbidity among 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 the H5N1 HPAI virus detected in wild birds, reaching endemic status in domestic birds in select regions of Asia. To address questions regarding the emergence and expansion of clade 2.3.2 viruses, 2 waterfowl species repeatedly involved in outbreaks of H5N1 HPAI viruses, bar-headed geese (Anser indicus) and ruddy shelducks (Tadorna ferruginea), were inoculated with a representative virus. All of 3 infected ruddy shelducks exhibited neurologic signs and died within 4 to 5 days. Two of 3 infected bar-headed geese had transient weakness but all survived. Viral shedding was predominately via the oropharynx and was detected from 1 to 7 days after inoculation. The severity and distribution of microscopic lesions corresponded with clinical disease and influenza-specific immunohistochemical staining of neurons. The predominant lesions were in the brain and were more severe in ruddy shelducks. Increased caspase-3 reactivity in the brains of all infected birds suggests a role for apoptosis in H5N1 HPAI virus pathogenesis in these species. These results demonstrate that similar to clade 2.2 viruses, a clade 2.3.2 H5N1 HPAI virus is neurotropic in some waterfowl species and can lead to neurologic disease with varying clinical outcomes. This has implications for the role that wild waterfowl may play in transmission of this virus in endemic regions.
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