Abstract
Streptococcus sanguinis is an important component of dental plaque and a leading cause of infective endocarditis. Genetic competence in S. sanguinis requires a quorum sensing system encoded by the early comCDE genes, as well as late genes controlled by the alternative sigma factor, ComX. Previous studies of Streptococcus pneumoniae and Streptococcus mutans have identified functions for the >100-gene com regulon in addition to DNA uptake, including virulence. We investigated this possibility in S. sanguinis. Strains deleted for the comCDE or comX master regulatory genes were created. Using a rabbit endocarditis model in conjunction with a variety of virulence assays, we determined that both mutants possessed infectivity equivalent to that of a virulent control strain, and that measures of disease were similar in rabbits infected with each strain. These results suggest that the com regulon is not required for S. sanguinis infective endocarditis virulence in this model. We propose that the different roles of the S. sanguinis, S. pneumoniae, and S. mutans com regulons in virulence can be understood in relation to the pathogenic mechanisms employed by each species.
Highlights
Apart from caries formation by Mutans group species, oral streptococci generally play a benign or beneficial role within the oral cavity
The transformation efficiency was low, we succeeded in isolating a mutant, JFP45, in which the comX gene was replaced by the Knr cassette
We expected a comX mutant to exhibit little or no competence in the presence or absence of competence-stimulating peptide’’ (CSP), as the sigma factor it encodes is required for upregulation of DNA uptake genes in other species [16]
Summary
Apart from caries formation by Mutans group species, oral streptococci generally play a benign or beneficial role within the oral cavity. Because of their habitat and the rich vasculature of the gingival tissue, the oral streptococci may be seeded into the bloodstream through oral surgery or everyday activities including brushing and chewing [1,2]. S. sanguinis virulence for IE has been examined in a number of studies [6,7,8,9,10,11] but very few genes or functions required for virulence have been identified. Virulence reduction could require simultaneous elimination or downregulation of multiple genes
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