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Title:   Author  item
                                            Loving, Crystalitem
                                            Brockmeier, Susanitem
                                            Baker, Amyitem
                                            Palmer, Mitchellitem
                                            Sacco, Randyitem
                                            Nicholson, Tracy
  Submitted to: Conference Research Workers Disease Meeting
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 11/1/2009
                                    Publication  Date: 12/6/2009
                                    Citation: Loving, C.L., Brockmeier, S.L., Vincent, A.L., Palmer, M.V., Sacco, R.E., Nicholson, T.L. 2010. Swine influenza virus co-infection with Bordetella bronchiseptica enhances bacterial colonization and host immune responses exacerbating pulmonary lesions [abstract]. Conference Research Workers Disease Meeting. Paper No. 130.Interpretive Summary:
                                Technical Abstract: Swine influenza virus (SIV) is one of the most important disease causing agents for the U.S. swine industry, not only as a primary pathogen but as a predisposing agent to secondary bacterial infection. Bordetella bronchiseptica (Bb) is often isolated from swine and has been shown to contribute to the porcine respiratory disease complex, a multifactorial complex of respiratory pathogens. To investigate the course of disease during SIV/Bb co-infection, a study was completed in which pigs were inoculated with SIV-only, Bb-only or both agents (SIV/Bb). We measured SIV titers and Bb burden in the respiratory tract on days 1, 5 and 10 post-challenge and examined host immune responses in the lung and trachea. Results indicate that the course of influenza disease is not altered by Bb infection, but SIV does enhance Bb colonization in the lung. Pulmonary lesions in the SIV/Bb group were more severe on days 1 and 10 post-challenge when compared to pigs challenged with SIV-only or Bb-only. Further-more, Bb did not cause significant pulmonary lesions unless pigs were also challenged with SIV.  The type I interferon response was elevated on day 1 following challenge in co-infected pigs, but enhanced expression of antiviral genes Mx and PKR did not appear to contribute to SIV clearance in the co-infected pigs because viral clearance was similar between the SIV/Bb and SIV-only groups.  Proinflammatory mediators IL-1beta and IL-8 were elevated in the lungs of co-infected pigs on days 1 and 10 following inoculation, which may contribute to the enhanced pulmonary lesions observed on those days.  Overall, these data suggest that SIV infection increases Bb colonization in the lung leading to enhanced production of proinflammatory mediators that likely contribute to exacerbated pulmonary lesions.


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