Contributor: John M. Kissane and John D. Pfeifer
Acute bacterial endocarditis is commonly caused by Staphylococcus aureus [staphylococcal infection]. It is a rapidly progressive and destructive febrile illness with early embolization, valvular regurgitation, and myocardial abscess formation. Streptococcus viridans [streptococcal infection], enterococci, and tend to cause subacute bacterial endocarditis. Fungi [fungal infection] also cause a subacute endocarditis.Vegetations on thev heart valves can emolize to various organs including the eye [embolism]. Streptococci collectively are the commonest cause of bacterial endocarditis. Groups A and B typically cause acute bacterial endocarditis, while alpha hemolytic (viridans group) streptococci cause subacute bacterial endocarditis. Staphylococci cause 20 to 30 % of cases of bacterial endocarditis. Most of these (80-90 %) are caused by Staphylococcus aureus. In about one-third of cases, the staphylococci attack normal valves producing acute bacterial endocarditis. The organisms give rise to bulky friable vegetations typically at the lines of closure of valves, usually those of the left side of the heart. In parenteral drug abusers, however, staphylococcal endocarditis involves the right side of the heart. The endocarditis is characterized by the development of vegetations (friable excrescences that consist of bacteria, fibrin, and leukocytes) on the heart valves or less commonly on the mural endocardium. Bacterial vegetations consists of three zones: 1) a mantle of sparsely cellular fibrin that separates the vegetation from flowing blood, 2) an intermediate zone of leukocytes, predominantly neutrophils, and bacteria, and 3) a basal layer, more sparsely inflamed, that consists of damaged valvular or endocardial tissues. In cases of chronic deforming valvular disease, historically most often due to rheumatic fever, it is the vascularization extending from the valve annulus into the base of the leaflet that predisposes the damaged valve to the lodgement of otherwise minimally pathogenic bacteria (in the most common scenario, Streptoccoccus viridans from the patient's mouth cause a transient bacteremia following a dental procedure or teeth-brushing, although often the bacteremia is without an identifiable antecedent). Vegetations of acute endocarditis are bulkier and more friable than those of subacute bacterial endocarditis and are more prone to erode, ulcerate, or even perforate the underlying valve. Either form of vegetation is far commoner on the left-sided cardiac valves, but lesions occur on right-sided valves, particularly in intravenous drug abusers who share needles. Fragments of vegetations frequently dislodge and embolize to peripheral organs, often resulting in infarcts. In acute endocarditis, such infarcts are often infected, while those in subacute bacterial endocarditis are frequently sterile. Focal or diffuse glomerulonephritis may complicate either form of endocarditis. Although antibiotic therapy currently blurs the differences between the two forms of endocarditis, the distinction remains clinically useful. Bacterial endocarditis is an important complication of cardiac valve replacement. A ring abscess is a distinctive lesion that results from growth of organisms in the suture ring of a prosthetic valve. About one third are staphylococcal, the remainder usually streptococcal. Streptococci are also important agents in infection of prosthetic valves; included in these processes is the striking ring abscess, an infection of the sewing ring of a prosthetic valve that not only disturbs the valve's function but also constitutes a focus of sepsis.In cases of chronic deforming valvular disease, historically most often due to rheumatic fever, it is the vascularization extending from the valve annulus into the base of the leaflet that predisposes the damaged valve to the lodgement of otherwise minimally pathogenic bacteria (in the most common scenario, viridans streptococci from the patient's mouth cause a transient bacteremia following a dental procedure or teeth-brushing, although often the bacteremia is without an identifiable antecedent). Emboli, often septic, are common in patients with bacterial endocarditis and may involve the myocardium, kidneys or brain. Purulent pericarditis complicates myocardial abscess formation. In acute endocarditis, such infarcts are often infected, while those in subacute bacterial endocarditis are frequently sterile. Focal or diffuse glomerulonephritis may complicate either form of endocarditis.