Pathophysiology of infective endocarditis

Abstract

Infective endocarditis (IE) is an uncommon infection, occurring as a complication in varying percentages of bacteremic episodes. The ability of an organism to cause endocarditis is the result of an interplay between the predisposing structural abnormalities of the cardiac valve for bacterial adherence, the adhesion of circulating bacteria to the valvular surface, and the ability of the adherent bacteria to survive on the surface and propagate as vegetation or systemic emboli. Certain bacteria, if present in the bloodstream, may colonize the initially sterile vegetation composed of fibrin and platelets; bacterial growth enlarges the vegetation, further impeding blood flow and inciting inflammation that involves the vegetation and adjacent endothelium. The true incidence of endocarditis complicating each of the bacterial species causing IE is difficult to estimate. About 20 %-30 % of individuals with community-acquired staphylococcal bacteremia develop IE [1, 2].