Abstract
Streptococcus gordonii, a member of the human indigenous oral microflora, colonizes smooth tooth surfaces and contributes to dental plaque formation. Although it is not recognized as being a cariogenic pathogen, it may cause endocarditis following invasion of the bloodstream. Using allelic exchange mutagenesis, we have constructed a mutant of S. gordonii (Challis) which is defective in its single functional glucosyltransferase gene and, hence, is unable to synthesize glucan exopolymers from sucrose. When examined in a rat endocarditis model, the sucrose-grown mutant did not differ significantly from S. gordonii wild-type, suggesting that glucan polymers did not contribute to infectivity. This result was in striking contrast to that previously observed with a polymer-defective S. mutans mutant.
Original language | English (US) |
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Pages (from-to) | 301-306 |
Number of pages | 6 |
Journal | FEMS microbiology letters |
Volume | 112 |
Issue number | 3 |
DOIs | |
State | Published - Sep 15 1993 |
Externally published | Yes |
Keywords
- Endocarditis
- Glucosyltransferase
- Streptococcus gordonii
ASJC Scopus subject areas
- Microbiology
- Molecular Biology
- Genetics