Subacute Bacterial Endocarditis Due to Streptococcus Viridans

Smith, C. Daniel; Sauls, H. Cliff; Stone, Charles F.

doi:10.1001/jama.1942.02830230012003

Cited by 19 publications

(3 citation statements)

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“…Although the mitis group of streptococci is known to be the major causative agent for IE, there have been many IE cases induced by S. mutans, a major pathogen of dental caries (Lockwood et al, 1974;McGhie et al, 1977;Moore et al, 1977;Robbins et al, 1977;Smith et al, 1977;Vose et al, 1987;Ullman et al, 1988;Gauduchon et al, 2001;Nomura et al, 2006). In our previous studies, the serotypes of four blood isolates of S. mutans were analysed and showed that none of the strains belonged to serotype c, the major serotypes in the human oral cavity (Fujiwara et al, 2001).…”

Section: Discussionmentioning

confidence: 94%

Identification and characterization of a collagen‐binding protein, Cbm, in Streptococcus mutans

Nomura

Nakano

Naka

et al. 2012

Molecular Oral Microbiology

111

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Streptococcus mutans, a major pathogen of dental caries, is occasionally isolated from the blood of patients with infective endocarditis. Bacterial attachment of exposed collagen tissue in the impaired endothelium is an important step in the onset of infective endocarditis. In our previous studies, some S. mutans strains were shown to possess collagen-binding activities and most of them had an approximately 120-kDa cell-surface collagen-binding protein called Cnm. However, several strains without Cnm proteins show collagen-binding properties. In the present study, another collagen-binding protein, Cbm, was characterized and its coding gene cbm was sequenced in these strains. The amino acid alignment in the putative collagen-binding domain of Cbm was shown to have approximately 80% identity and 90% similarity to the comparable region of Cnm. Cbm-deficient isogenic mutant strains constructed by insertional inactivation of the cbm gene, lacked collagen-binding properties, which were recovered in the complemented mutant. Analyses of a large number of clinical isolates from Japan, Thailand and Finland revealed that cbm-positive strains were present in all of these countries and that cnm-positive and cbm-positive strains were detected in the oral cavity of approximately 10 and 2% of systemically healthy subjects, respectively. In addition, cnm-positive strains were predominantly identified in the serotype f group, whereas cbm-positive strains were frequently detected in serotype k. These results suggest that Cbm as well as Cnm are major cell surface proteins of S. mutans associated with binding to type I collagen and predominantly identified in serotype k strains.

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Section: Discussionmentioning

confidence: 94%

Identification and characterization of a collagen‐binding protein, Cbm, in Streptococcus mutans

Nomura

Nakano

Naka

et al. 2012

Molecular Oral Microbiology

111

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“…Streptococcus mutans is a viridans streptococcus which does not react with Lancefield grouping sera, but which is easily confused with group D streptococci because of the ability of many isolates to grow in the presence of 40% bile and to hydrolyze esculin and ferment mannitol. (332,333) Another feature of this streptococcus worth emphasizing is that it may appear like a diphtheroid on primary isolation from blood cultures and risks being discarded as a contaminant. (334) The classic streptococcal morphology became evident upon subculture in glucose broth.…”

Section: Viridans Streptococcimentioning

confidence: 99%

Infective Endocarditis and Other Intravascular Infections

Freedman¹

1982

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“…Streptococcus mutans, known to be a major pathogen of dental caries, is occasionally isolated from the blood of patients with infective endocarditis (IE) (Nakano and Ooshima, 2009). Although the mitis group of oral streptococci, such as S. sanguinis, are major pathogens of IE, S. mutans has also been reported to be associated with the disease (Lockwood et al, 1974;McGhie et al, 1977;Moore et al, 1977;Robbins et al, 1977;Smith et al, 1977;Vose et al, 1987;Ullman et al, 1988;Gauduchon et al, 2001;Nomura et al, 2006). One of the important steps in the pathogenesis of IE is adhesion of pathogenic bacteria onto the endothelial cells of heart tissues (Moreillon and Que, 2004).…”

Section: Introductionmentioning

confidence: 99%