Location: Location not imported yet.Title: Pathobiology of avian influenza virus infections in wild birds) Author
Submitted to: Meeting Abstract
Publication Type: Abstract only
Publication Acceptance Date: 3/15/2010
Publication Date: 5/10/2010
Citation: Swayne, D.E. 2010. Pathobiology of avian influenza virus infections in wild birds [abstract]. In: Programme and Abstracts of New-Flubird International Symposium. Network for Early Warning of Influenza Viruses in Migratory Birds in Europe. Montpellier, France, May 10-12, 2010. p. 10. Interpretive Summary:
Technical Abstract: Individual avian Influenza (AI) viruses vary in their ability to produce infection, disease and death in different bird species. Based on the pathobiological features in chickens, AI viruses (AIV) are categorized as low pathogenicity (LPAI) or high pathogenicity (HPAI) viruses, and can be of any of the 16 different hemagglutinin (H1-16) and nine neuraminidase (N1-9) subtypes. Typically, LPAI viruses cause asymptomatic infections in wild aquatic birds, but when introduced into domesticated poultry, infections may be asymptomatic or produce clinical signs and lesions reflecting pathophysiological damage to the respiratory, digestive and reproductive systems. Many of the influenza viruses from wild bird are poorly infectious for gallinaceous poultry; i.e., they are not well adapted. The HPAI viruses have primarily been seen in gallinaceous poultry, producing high morbidity and mortality, and systemic disease with necrosis and inflammation in multiple visceral organs, nervous and cardiovascular systems, and the integument. HPAI viruses have only been seen with H5 and H7 hemagglutinin subtypes. HPAI viruses arise from LPAI viruses, following circulation in domestic poultry resulting in specific mutations. Historically, HPAI virus infections have only been seen in two outbreaks in wild birds: 1) common terns in South Africa, during 1961 with H5N3; and 2) various wild birds in Asia, Europe and Africa since 1996 with H5N1. The Eurasian-African H5N1 HPAI virus have evolved over the past decade with the unique capacity to infect and cause disease in domestic ducks and wild birds producing a range of syndromes, including asymptomatic respiratory and digestive tract infections; systemic disease limited to 2-3 critical organs, usually the brain, heart and pancreas; and severe disseminated infection and death. Experimentally, swans and geese have been most severely affected, usually with systemic infection and disease and high mortality, or persistent neurological disease. Mallards have been infected and excrete the virus for short periods of time, but the viruses did not produce illness and death. Although experimental studies using intranasal inoculation have produced infection in other wild bird species, the inefficiency of contact transmission in some of them, for example passerines and Columbiformes, suggests they are unlikely to be a reservoir for the viruses, while others like some wild Anseriformes, can be severely affected and could serve as a dissemination host over intermediate distances.