Pathogenesis of endocarditis.

The pathophysiology of infective endocarditis comprises at least three critical elements: preparation of the cardiac valve for bacterial adherence, adhesion of circulating bacteria to the prepared valvular surface, and survival of the adherent bacteria on the surface, with propagation of the infected vegetation. It appears that circulating bacteria do not readily adhere to normal endothelial surfaces. Trauma to the valve, however, produces an alteration in the endothelial cells, leading to either disruption of the surface and deposition of platelets and fibrin, or other phenomena that render the surface susceptible to colonization by circulating bacteria. Once the surface is prepared, some bacterial strains appear to adhere to the fibrin-platelet matrix more avidly than others. The bacterial virulence factors that promote adherence are complex, but at least one, an extracellular polysaccharide (dextran), has been identified. Adherence can be blocked by antibodies directed against various surface structures. The survival of bacteria adherent to the surface of the vegetation appears to be complex as well, requiring resistance in situ to the bactericidal properties of complement and phagocytosis by white cells. In addition, vegetation propagation involves activation of the clotting cascade. For at least some streptococci, this occurs partly through perturbation of the valvular cells to produce tissue factor (tissue thromboplastin), which results in the deposition and growth of a fibrin-platelet clot over the rapidly growing bacterial colonies.