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Pathogenesis of vegetation formation in infective endocarditis

Daniel J Sexton, MD
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Elinor L Baron, MD, DTMH


Infective endocarditis arises when an adherent platelet-fibrin nidus becomes secondarily infected and produces vegetations, which in turn may directly damage the endocardial tissue and/or valves. The pathogenesis of infective endocarditis will be reviewed here.

Other aspects of infective endocarditis, including clinical consequences of vegetation formation, are discussed separately. (See "Epidemiology, risk factors, and microbiology of infective endocarditis" and "Epidemiology, clinical manifestations, and diagnosis of prosthetic valve endocarditis" and "Infective endocarditis in injection drug users" and "Infective endocarditis in children" and "Clinical manifestations and evaluation of adults with suspected native valve endocarditis" and "Antimicrobial therapy of native valve endocarditis" and "Antimicrobial therapy of prosthetic valve endocarditis" and "Surgery for left-sided native valve endocarditis" and "Complications and outcome of infective endocarditis".)


Vegetation formation — The endothelial lining of the heart and its valves is normally resistant to infection with bacteria and fungi. Experiments in animal models have demonstrated that a sequence of interrelated events must occur before microbes can establish an infective nidus or vegetation on the endocardium:

The initial step in the establishment of a vegetation is endocardial injury, followed by focal adherence of platelets and fibrin. Some organisms with high virulence are capable of infecting normal human heart valves, such as Staphylococcus aureus.

The initially sterile platelet-fibrin nidus becomes secondarily infected by microorganisms circulating in the blood, either from a distant source of focal infection or as a result of transient bacteremia from a mucosal or skin source [1,2].


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Literature review current through: Sep 2016. | This topic last updated: Jul 9, 2015.
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