Submitted to: American Society for Microbiology General Meeting
Publication Type: Abstract Only
Publication Acceptance Date: March 2, 2010
Publication Date: May 23, 2010
Citation: Nicholson, T.L., Brockmeier, S., Loving, C.L., Lu, H., Sloan, G.P., Deora, R. 2010. Contribution of the Bordetella Bps Polysaccharide to Biofilm Formation and Respiratory Disease in Swine [abstract]. American Society for Microbiology. p. 123. Technical Abstract: Bordetella bronchiseptica is pervasive in swine populations and plays multiple roles in respiratory disease. Additionally, B. bronchiseptica is capable of establishing long-term or chronic infections in swine. Bacterial biofilms are increasingly recognized as important contributors to chronic bacterial infections. Recently the polysaccharide locus bpsABCD has been demonstrated to serve a critical role in the development of mature biofilms formed by the sequenced laboratory strain of B. bronchiseptica. We hypothesized that swine isolates would also have the ability to form mature biofilms and the bps locus would serve a key role in this process. Using a micotiter plate assay, a virulent B. bronchiseptica swine isolate was found to form a robust biofilm. A mutant containing an in-frame deletion of the bps structural genes was constructed in this wild-type swine isolate and found to be negative for PNAG-like material by immunoblot assay. To investigate the role of the bps locus in Bordetella pathogenesis in swine, we compared this mutant to the wild-type swine isolate for its ability to colonize and cause disease in swine. The bps mutant strain was recovered from the nasal cavity at similar or higher levels than the wild-type swine isolate up to twenty-eight days post infection. Together the data demonstrate a biofilm mode of existence for B. bronchiseptica swine isolates and suggest that the Bps polysaccharide is not required for early colonization of the swine respiratory tract.