The Pathogenesis of H7 Highly Pathogenic Avian Influenza Viruses in Lesser Scaup (Aythya affinis)
- 2 March 2019
- journal article
- research article
- Published by American Association of Avian Pathologists (AAAP) in Avian Diseases
- Vol. 63 (sp1) , 230-234
Abstract
Waterfowl are the natural hosts of avian influenza virus (AIV), and through migration spread the virus worldwide. Most AIVs carried by wild waterfowl are low pathogenic strains; however, Goose/Guangdong/1996 lineage clade 2.3.4.4 H5 highly pathogenic (HP) AIV now appears to be endemic in wild birds in much of the Eastern Hemisphere. Most research efforts studying AIV pathogenicity in waterfowl thus far have been directed toward dabbling ducks. In order to better understand the role of diving ducks in AIV ecology, we previously characterized the pathogenesis of clade 2.3.4.4 H5 HPAIV in lesser scaup (Aythya affinis). In an effort to further elucidate AIV infection in diving ducks, the relative susceptibility and pathogenesis of two North American lineage H7 HPAIV isolates from the most recent outbreaks in the United States was investigated. Lesser scaup were inoculated with either A/turkey/IN/1403-1/2016 H7N8 or A/chicken/TN/17-007147-2/2017 H7N9 HPAIV by the intranasal route. The approximate 50% bird infectious dose (BID50) of the H7N8 isolate was determined to be 10(3) 50% egg infectious doses (EID50), and the BID50 of the H7N9 isolate was determined to be < 10(2) EID50, indicating some variation in adaptation between the two isolates. No mortality or clinical disease was observed in either group except for elevated body temperatures at 2 and 4 days postinoculation (DPI). Virus shedding was detected up to 14 DPI from both groups, and there was a trend for shedding to have a longer duration and at higher titer levels from the cloacal route. These results demonstrate that lesser scaup are susceptible to both H7 lineages of HPAIV, and similar to dabbling duck species, they shed virus for long periods relative to gallinaceous birds and don't present with clinical disease.Keywords
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