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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #273096
Title: Host response to secondary bacterial infection associated with antecedent influenza virus infection in pigs – exacerbation associated with vaccination

Author
item Loving, Crystal
item Baker, Amy
item Brockmeier, Susan
item Henningson, Jamie
item Braucher, Douglas
item DE SOUZA RAJAO, DANIELA - Universidade Federal De Minas Gerais

Submitted to: Autumn Immunology Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 9/19/2011
Publication Date: 11/18/2011
Citation: Loving, C.L., Vincent, A.L., Brockmeier, S.L., Henningson, J.N., Braucher, D.R., De Souza Rajao, D. 2011. Host response to secondary bacterial infection associated with antecedent influenza virus infection in pigs - exacerbation associated with vaccination [abstract]. Autumn Immunology Conference. Poster No. 140.

Interpretive Summary:

Technical Abstract: The increasing number of annual influenza (IAV) cases, coupled with the recent IAV pandemic, has amplified concerns about its impact on human and animal health. It is appreciated that Flu is complicated by bacterial pneumonia. Vaccine-associated enhanced respiratory disease (VAERD) can occur following IAV vaccine/challenge mismatch in pigs, and may explain increased disease severity observed in vaccinated people during the 2009 pandemic. Using a working VAERD model in conjunction with secondary bacterial (bacT) challenge, we evaluated implications of VAERD and bacterial pneumonia. Pigs were challenged with pH1N1 IAV and one day later with a bacT cocktail of Haemophilus, Streptococcus and Actinobacillus. A subset of IAV challenged pigs was vaccinated with a killed-adjuvanted whole-influenza virus vaccine (H1N2). Disease was more severe in coinfected (IAV/bacT) pigs, regardless of vaccination, through day 5 post-IAV challenge. However, IL-1b, IL-6, TNFa, IFNg, IL-10 and IL-2 were significantly increased in the lungs of VAERD/bacT pigs. Pathogen load cannot explain observed differences, but instead, VAERD likely predisposes to exacerbated responses to bacT through aberrant recruitment and activation of cells.