Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: April 2, 2012
Publication Date: N/A
Technical Abstract: Influenza A virus (IAV) infection alone causes significant disease characterized by respiratory distress and poor growth in pigs. Endemic strains of IAV in North America pigs consist of the subtypes H1N1, H1N2, and H3N2. These circulating strains contain the triple reassortant internal gene (TRIG) cassette resulting from incorporation of genes from swine, avian, and human IAVs. Genetic drift and reassortment have resulted in four H1 phylogenetic clusters and all currently co-circulate in US swine. Inactivated IAV vaccines are currently the only platform approved for use in US swine and they do not provide adequate protection to heterologous strains of IAV; thus, IAV infection in swine is becoming increasingly difficult to control. IAV plays a significant role in the porcine respiratory disease complex (PRDC), a multifactorial disease process characterized by coinfection with two or more agents. Previous work from our lab has shown IAV exacerbates Bordetella infection. Other bacterial species of PRDC frequently associated with IAV infection include Mycoplasma hyopneumoniae, Haemophilus parasuis, Streptococcus suis and Actinobacillus suis. Tracheal epithelial cells and alveolar macrophages respond to infection with production proinflammatory cytokines and antimicrobial mediators for controlling pathogen spread; however, exacerbated responses can lead to immunopathology that may be detrimental to the host. IAV is known to predispose to bacterial infection; however, the mechanism by which this occurs is unknown and may depend on the bacterial agent, timing of the secondary infection, and immune status of the animal at the time of secondary infection. Our work has focused on studying the interaction between IAV and secondary bacterial infections in swine, using either a single secondary bacterial agent or a cocktail of bacterial species as well as studying susceptibility and severity as it relates to timing of the secondary bacterial infection. Our work indicates that IAV predisposes to secondary Haemophilus parasuis infection although maternal derived antibody can attenuate this interaction. Pathogen load is often unchanged by coinfection; however local host responses and pathology are enhanced, indicating that secondary immune responses may be dysregulated and lead to immunopathology. With the continued emergence of unique IAV antigenic subtypes, the need for an effective IAV vaccine remains high, and control of bacterial infection and spreading is critical when IAV outbreaks occur.