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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #222114
Title: Contribution of Bordetella bronchiseptica Filamentous Hemagglutinin and Pertactin to Respiratory Disease in Swine

Author
item Nicholson, Tracy
item Brockmeier, Susan
item Loving, Crystal

Submitted to: American Society for Microbiology Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 2/22/2008
Publication Date: 6/1/2008
Citation: Nicholson, T.L., Brockmeier, S., Loving, C.L. 2008. Contribution of Bordetella bronchiseptica Filamentous Hemagglutinin and Pertactin to Respiratory Disease in Swine [abstract]. American Society for Microbiology Meeting, June 2-4, 2008, Boston, Massachusetts. 2008 CDROM.

Interpretive Summary:

Technical Abstract: Respiratory disease in pigs is the most important health concern for swine producers today. Bordetella bronchiseptica is widely prevalent in swine populations and has multiple roles in respiratory disease. It is the primary etiologic agent of atrophic rhinitis, bronchopneumonia in young pigs, and has been demonstrated to increase the frequency and severity of respiratory disease due to other viral and bacterial pathogens. Most studies addressing virulence factors of B. bronchiseptica are based on isolates derived from hosts other than pigs. Swine isolates of B. bronchiseptica possess unique genetic and phenotypic traits as compared to isolates from other host species. Two well-studied virulence factors implicated in the adhesion process are filamentous hemagglutinin (FHA) and pertactin (PRN). We hypothesized that both FHA and PRN would serve critical roles in the adhesion process and be necessary for colonization of the swine respiratory tract. To investigate the role of FHA and PRN in Bordetella pathogenesis in swine, we constructed mutants containing an in-frame deletion of the FHA or the PRN structural gene in KM22, a virulent B. bronchiseptica swine isolate. We compared both of these mutants to KM22, the wild-type swine isolate, for their ability to colonize and cause disease. Except for day one post-infection, colonization of the PRN mutant was indistinguishable from wild-type and caused similar disease severity. In contrast, colonization of the FHA mutant was lower than wild-type at all respiratory tract sites and time points examined and caused limited to no disease. Our results indicate that FHA, but not PRN, is required for optimal colonization throughout the respiratory tract, including the nasal cavity, in swine.