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Pathogenesis of streptococcal and staphylococcal endocarditis

2002; Elsevier BV; Volume: 16; Issue: 2 Linguagem: Inglês

10.1016/s0891-5520(01)00009-5

1557-9824

Philippe Moreillon, Yok‐Ai Que, Arnold S. Bayer,

Antimicrobial Resistance in Staphylococcus

Although streptococcal and S. aureus IE share the same primary site of infection, their pathogenesis and clinical evolution present several major differences. Streptococci adhere to cardiac valves with pre-existing endothelial lesions. In contrast, S. aureus can colonize either damaged endothelium or invade physically intact endothelial cells. These interactions are mediated by multiple surface adhesins, some of which have been only partially characterized. Streptococci produce surface glucans (gtf and ftf), ECM adhesins (e.g., fibronectin-binding proteins, FimA), and platelet aggregating factors (phase I and phase II antigens, pblA, pblB, and pblT), all of which have been.