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What causes infective endocarditis?
Last reviewed: 04.07.2025
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Normally, the heart is relatively resistant to infections. Bacteria and fungi have difficulty attaching to the endocardial surface because the constant blood flow prevents this. Two factors are necessary for the development of infective endocarditis: predisposing changes in the endocardium and the presence of microorganisms in the blood (bacteremia). Sometimes massive bacteremia and/or particularly pathogenic microorganisms cause endocarditis of intact valves.
Endocardial causes of infective endocarditis
Endocarditis usually affects the heart valves. The main predisposing factors are congenital heart defects, rheumatic valvular disease, bicuspid or calcified aortic valves, mitral valve prolapse, and hypertrophic cardiomyopathy. Prosthetic valves pose a particular risk. Infection of intracavitary thrombi, ventricular septal defects, and areas of the patent ductus arteriosus sometimes occurs. The primary site of infection is usually the sterile vegetations of platelets and fibrin formed by endothelial damage when the cells of the latter synthesize tissue factor.
Infective endocarditis most often occurs in structures on the left side of the heart (e.g., the mitral or aortic valve). Approximately 10-20% of cases are right-sided (tricuspid or pulmonary valve). Injecting drug users have a much higher incidence of right-sided endocarditis (approximately 30-70%).
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Bacterial causes of infective endocarditis
Microorganisms infecting the endocardium may migrate from distant infected sites (e.g., skin abscess, urinary tract) or have visible portals of entry (e.g., central venous catheters or drug injection sites). Almost any implanted foreign material (e.g., ventricular or peritoneal shunt, prosthetic valve, etc.) is at risk of bacterial colonization, thus becoming a source of bacteremia and endocarditis. Endocarditis may also result from asymptomatic bacteremia, such as that which occurs during invasive dental or other medical procedures or surgery. Even tooth brushing and chewing can cause bacteremia (usually streptococcal) in patients with gingivitis.
The organisms vary with the site of infection, the source of bacteremia, and host risk factors (eg, intravenous drug use), but generally streptococci and Staphylococcus aureus account for 80% of cases. Enterococci, gram-negative bacteria, anaerobes, and fungi account for most of the remainder. It is unclear why streptococci and staphylococci frequently infect vegetations while gram-negative aerobic bacteria rarely do. However, the ability of Staphylococcus aureus to adhere to fibronectin, as well as the synthesis of viridans streptococci to dextran, may play a role.
After colonizing the vegetation, microorganisms become covered with a layer of fibrin and platelets, which block access to neutrophils, immunoglobulins and the complement system, thus blocking the immune defense.