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ENDOCARDITIS

INTRODUCTION

Infective endocarditis (IE) in pediatric patients is rare (5–12 per 100,000 pediatric admissions) and often associated with an underlying congenital heart defect or, increasingly, central indwelling intravascular catheters. However, structurally normal hearts may also be infected. Premature infants now account for 10% of pediatric IE. Endovascular infections outside the heart and infected thrombi are close cognates of IE.

PATHOGENESIS AND EPIDEMIOLOGY

Establishment of IE results from the interaction of several host and microbial factors. Experimental animal models have demonstrated that damage to the endocardium (as with a plastic catheter or a high-velocity jet of blood) leads to formation of a nonbacterial thrombotic lesion. Following endocardial damage, bacterial access to the bloodstream from elsewhere and subsequent adherence to endocardial surfaces are required for the establishment of IE. It is now thought that the great majority of IE develops as the result of transient bacteremia related to activities of daily life, but not all bacteria are capable of initiating this process. The endocardium appears to be a preferential site of microbial adherence and may have some specificity for binding with certain bacteria. The presence of several factors, including bacterial adhesins, endothelial binding proteins, and agglutinating antibodies that clump bacteria, promotes adherence of organisms to damaged endocardial surfaces. The Venturi effect (the reduction in fluid pressure that results when blood flows through a constricted area) deposits bacterial colonies immediately beyond the orifice that separates high- and low-pressure areas.

Bacteremia in patients with established endocarditis is generally low grade and continuous. As many as 10% of cases of IE yield consistently negative blood cultures, most often as a result of prior antibiotic therapy or organisms that are 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.

Classically, viridans streptococci have been the most common cause of IE, progressing along a subacute course in patients with preexisting cardiac lesions in which fever, fatigue, and immune complex–mediated clinical manifestations develop slowly over weeks or months. Enterococci behave in a fashion similar to the viridans streptococci. IE caused by Staphylococcus aureus has historically followed an acute course with rapid progression and poor outcome, including death, often in patients with normal hearts. Prosthetic heart valves within 2 months after implantation are prone to infection with coagulase-negative staphylococci and S aureus, as are neonates who require intensive care and intracardiac central lines. Gram-negative infections of the heart, although infrequent, are increasing in frequency and are most often associated with intravenous drug use, prosthetic or otherwise abnormal valves, invasive procedures, or nosocomial acquisition.

HACEK is an acronym for a group of small, fastidious gram-negative coccobacilli (Haemophilus aphrophilus, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae). These organisms that normally inhabit the upper respiratory tract are often ...

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