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Clonal structure of Streptococcus sanguinis strains isolated from endocarditis cases and the oral cavity
Author(s) -
Do T.,
Gilbert S.C.,
Klein J.,
Warren S.,
Wade W.G.,
Beighton D.
Publication year - 2011
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/j.2041-1014.2011.00618.x
Subject(s) - biology , microbiology and biotechnology , housekeeping gene , multilocus sequence typing , genetics , gene , genotype , gene expression
Summary A collection of Streptococcus sanguinis strains from patients with endocarditis ( n = 21) and from the oral cavity ( n = 34) was subjected to a multi‐locus sequence typing analysis using seven housekeeping genes, carbamoyl‐phosphate synthetase ( carB ), Co/Zn/Cd efflux system component ( czcD ), d ‐alanyl‐ d ‐alanine ligase ( ddl ), DNA polymerase III ( dnaX ), glucose‐6‐phosphate dehydrogenase ( gdh ), DNA‐directed RNA polymerase, beta subunit ( rpoB ) and superoxide dismutase ( sodA ). The scheme was expanded by the inclusion of two the putative virulence genes, bacitracin‐resistance protein ( bacA ) and saliva‐binding protein ( ssaB ), to increase strain discrimination. Extensive intra‐species recombination was apparent in all genes but inter‐species recombination was also apparent with strains apparently harbouring gdh and ddl from unidentified sources and one isolate harboured a sodA allele apparently derived from Streptococcus oralis . The recombination/mutation ratio for the concatenated housekeeping gene sequences was 1.67 (95% confidence limits 1.25–2.72) and for the two virulence genes the r/m ratio was 3.99 (95% confidence limits 1.61–8.72); recombination was the major driver for genetic variation. All isolates were distinct and the endocarditis strains did not form distinct sub‐clusters when the data were analysed using C lonal F rame . These data support the widely held opinion that infecting S. sanguinis strains are opportunistic human pathogens.