Staphylococcus aureus, platelets, and the heart

Infective endocarditis (IE) caused by Staphylococcus aureus is serious, burgeoning frequency, and growing increasingly resistant to antibiotics. S. aureus IE is associated with high morbidity and mortality rates in nosocomial and community-acquired settings. S. aureus is the most common, most virulent IE etiologic pathogen. S. aureus IE pathogenesis depends upon complex interaction among the pathogen, platelets, plasma proteins, and vascular endothelial cells. S. aureus coordinates the expression of key virulence factors required for the specific pathogenic phases of IE. Platelets, now appear to play an important role in antimicrobial host defense against S. aureus IE and other endovascular infections. Platelet microbicidal proteins are believed to significantly contribute to the antimicrobial properties of platelets; however, abnormal disposition of native or prosthetic cardiac valves is an important risk factor in S. aureus IE establishment and severity. Thus, the need to define the molecular mechanisms of S. aureus pathogenesis and host defense against IE is urgent. Understanding these mechanisms will yield new approaches for the prevention and treatment of such life-threatening cardiovascular infections due to S. aureus.