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United States Department of Agriculture

Agricultural Research Service

Research Project: COUNTERMEASURES TO PREVENT THE PORCINE RESPIRATORY DISEASE COMPLEX (PRDC) Title: Contribution of Bordetella bronchiseptica Filamentous Hemagglutinin and Pertactin to Respiratory Disease in Swine

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

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 12, 2009
Publication Date: May 15, 2009
Citation: Nicholson, T.L., Brockmeier, S., Loving, C.L. 2009. Contribution of Bordetella bronchiseptica Filamentous Hemagglutinin and Pertactin to Respiratory Disease in Swine. Infection and Immunity. 77(5):2136-2146.

Interpretive Summary: Respiratory disease in pigs is the most important health concern for swine producers today. Bordetella bronchiseptica is pervasive in swine populations and has multiple roles in respiratory disease. Two well-studied Bordetella virulence factors are filamentous hemagglutinin (FHA) and pertactin (PRN). To investigate the role of these in swine, we constructed mutants containing a deletion of the FHA or the PRN structural gene in a virulent B. bronchiseptica swine isolate. We compared both of these mutants to the wild-type swine isolate for their ability to colonize and cause disease. 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. In contrast, the PRN mutant caused similar disease severity relative to wild-type, however, colonization of the PRN mutant was reduced during early and late infection. The decreased colonization observed early suggests that PRN plays a role in attachment, while the decreased colonization levels observed late implies a role for PRN in persistence in the swine respiratory tract. Higher anti-Bordetella antibodies were also detected in pigs infected with the PRN mutant. These results provide a crucial understanding of the role of PRN and FHA in swine respiratory disease, which will expedite the discovery of new vaccine therapy.

Technical Abstract: Respiratory disease in pigs is the most important health concern for swine producers today. Bordetella bronchiseptica is pervasive in swine populations and plays multiple roles in respiratory disease. It is a 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. 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 the wild-type swine isolate for their ability to colonize and cause disease. 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. These results indicate that FHA is required for optimal colonization throughout the respiratory tract, including the nasal cavity, in swine. In contrast, the PRN mutant caused similar disease severity relative to wild-type, however, colonization of the PRN mutant was reduced relative to wild-type during early and late infection. The decreased colonization observed early suggests that PRN may play a role in aiding early attachment. The decreased colonization levels observed late in the infection occurred in the lung and coincided with higher anti-Bordetella antibody titers in pigs infected with the PRN mutant. The elevated serum antibody response induced by the PRN mutant may have contributed to the clearance of this mutant from the lower respiratory tract.

Last Modified: 4/20/2014
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