Vet Pathol. 2013 Jun 4. [Epub ahead of print]
Source
College of Veterinary Medicine, University of Georgia, Athens, GA, USA.Abstract
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.
http://www.ncbi.nlm.nih.gov/pubmed/23735616
- PMID:
- 23735616
- [PubMed - as supplied by publisher]
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