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Infective endocarditis (IE) in pediatric patients is often associated with an underlying congenital heart defect. However, structurally normal hearts may also be infected. Accurate diagnosis and appropriate medical management, are required to achieve a satisfactory outcome of this previously uniformly fatal disease.

Establishment of infective endocarditis results from the interaction of several host and microbial factors. Endocardial surfaces damaged by turbulent blood flow attract platelets and fibrin, leading to the formation of a nonbacterial thrombotic lesion. Experimental animal models have demonstrated that healthy, intact endothelium is resistant to colonization by circulating microbes; in contrast, damage of endocardium (as with a plastic catheter or a jet of blood) leads to rapid microbial colonization. The endocardium appears to be a preferential site of microbial adherence and may have some specificity for binding with certain bacteria.1-3

Two mechanisms, the Venturi and jet effects, combine to damage endocardial surfaces as blood is forced from an area of high pressure into a low-pressure sink. The Venturi effect deposits bacterial colonies immediately beyond the orifice that separates high and low pressure areas. Large pressure gradients are essential to these mechanisms, which explains the low risk of infective endocarditis in isolated atrial septal defects and the higher risk of infective endocarditis in small, rather than large ventricular septal defects.

Following endocardial damage, bacterial access to the bloodstream and adherence to endocardial surfaces are required for the establishment of infective endocarditis. It is now thought that the great majority of infective endocarditis develops as the result of transient bacteremia related to activities of daily life,2 but not all bacteria are capable of initiating this process. The presence of several factors, including bacterial surface polysaccharides, endothelial binding proteins, and agglutinating antibodies that clump bacteria, promote adherence of organisms to damaged endocardial surfaces. In some cases, microbial invasiveness may be more important than host or tissue factors in initiating infection.

Many of the classic manifestations of infective endocarditis (IE) are immunologically mediated. In IE patients with arthralgias and arthritis, splenomegaly, Roth spots, glomerulonephritis, and thrombocytopenia, circulating immune complex levels are significantly higher than in IE patients without these manifestations. Levels of immune complexes decline as these physical manifestations resolve.

Bacteremia in patients with infective endocarditis is generally low grade and continuous. As much as 10% of cases of infective endocarditis yield consistently negative blood cultures, most often as a result of prior antibiotic therapy. Fastidious organisms with special growth requirements may be difficult to culture. Bacteria infecting right-sided heart lesions may be filtered by pulmonary phagocytes, significantly reducing the number of bacteria in a peripheral blood sample. In evaluating patients for infective endocarditis, it is preferable to obtain at least three separate blood cultures over a 24- to 48-hour period if the patient is stable. Blood should not be drawn through indwelling vascular catheters because contamination may be misleading. If only one of several ...

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