Type IV Pili of Streptococcus sanguinis Contribute to Pathogenesis in Experimental Infective Endocarditis

  • Anthony M. Martini
    Department of Microbiology and Immunology, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA
  • Bridget S. Moricz
    Department of Microbiology and Immunology, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA
  • Laurel J. Woods
    Department of Microbiology and Immunology, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA
  • Bradley D. Jones
    Department of Microbiology and Immunology, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA

抄録

<jats:p> This work provides evidence that type IV pili produced by <jats:named-content content-type="genus-species">Streptococcus sanguinis</jats:named-content> SK36 are critical to the ability of these bacteria to attach to and colonize the aortic heart valve (endocarditis). We found that an <jats:named-content content-type="genus-species">S. sanguinis</jats:named-content> type IV pili mutant strain was defective in causing platelet-dependent aggregation in a 24-h infection assay but not in a 1-h platelet aggregation assay, suggesting that the type IV pili act at later stages of vegetation development. </jats:p>

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