Update on pathogenesis of infective endocarditis

Specific interactions between pathogens and host factors contribute to the apparent tissue and microbial selectivity in infective endocarditis. Streptococci and staphylococci can produce exopolysaccharides and peptides that have been implicated in adherence to host factors. The presence of a platelet-fibrin matrix on the surface of endothelium can serve as a nidus for colonization by gram-positive cocci, which in turn can promote further aggregation of platelets. Tissue factor expression by valvular endothelial cells is low but can be turned on by endocytosis of staphylococci—this could favor infected thrombus formation. The presence of a foreign body such as a prosthetic heart valve increases the risk of endocarditis. Platelets can promote adherence of staphylococci to foreign body surfaces. Infection of heart valves is the result of influences that in the end will favor microbial attachment and survival. Normal endothelium is resistant to colonization by microorganisms. Antibodies and phagocytes offer some protection against the development of endocarditis. Platelets produce microbicidal proteins that appear important in containing the infection. New diagnostic criteria for endocarditis take into account the pathogenetic characteristics of the disease.