In the past, Bb was considered to play only a secondary role in feline respiratory disease but it is now established as a primary pathogen in this species. Respiratory disease has been reproduced in specific pathogen free cats following both aerosol and nasal challenge [Jacobs et al., 1993; Coutts et al., 1996] and a number of field cases associated with Bb have also been reported [Willoughby et al., 1991; Welsh, 1996]. However, it is likely in the field that other factors may be involved in disease including environmental factors such as stress or overcrowding, or in some cases, pre-existing viral infection.
Their is little data available on the pathogenicity of Bb in the cat but much can be inferred from infections in other species. Features of Bb that are responsible for acting as a primary pathogen in the feline respiratory tract are its motility (mediated by flagellin), the presence of adhesins and production of toxins.
This microorganism colonizes the ciliated epithelium of the respiratory tract of the host, establishing chronic infections. Bordetella have evolved many often shared mechanisms that allow them to colonize this site, a surface designed to eliminate foreign particles [Mattoo et al., 2001]. These include adhesins such as filamentous hemagglutinin, fimbriae and periactin. Fimbriae are required for efficient establishment and persistent colonization of the trachea. They also play an important role in the development of humoral immunity to Bordetella infection [Mattoo et al., 2000].
Once attached, toxins such as a bifunctional adenylate cyclase/hemolysin, dermonecrotic toxin, tracheal cytotoxin, and Bb-specific type III secreted proteins result in ciliostasis and destruction of the cilia.