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Background: The lack of animal models to experimentally study how infectious agents transmit between hosts limits our understanding of what makes some pathogens so contagious.Methods: We recently developed a Bordetella bronchiseptica mouse model to study transmission and have used it to assess, for the first time, which of several well-studied "virulence factors" common to classical Bordetella species contribute to transmission.Results: Among 13 mutants screened, a mutant lacking an extracellular polysaccharide (EPS) locus consistently failed to transmit. The loss of EPS had no obvious effect on in vitro characteristics of growth, adherence, cytotoxicity, or serum resistance, though it profoundly reduced the ability of the mutant to colonize the lower respiratory tract of mice. While wild-type B. bronchiseptica was shed from colonized mice and efficiently transmitted to cage-mates, the mutant colonized less efficiently, shed at lower numbers, and consequently did not transmit to naive animals.Conclusions: These results have important implications for potential roles of polysaccharides in the pathogenesis and transmission of Bordetella species as well as other respiratory pathogens. Cases of pertussis (whooping cough) caused by Bordetella pertussis are on the rise, and understanding factors that contribute to their spread is critical to its control. [ABSTRACT FROM AUTHOR]