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Infective endocarditis (IE) is defined as an infection of the endocardium, generally involving cardiac valves and their valvular apparatus such as the chordae tendinae, interventricular septum, mural endocardium, or intracardiac devices. IE may occur in children with or without antecedent underlying cardiac disease. The diagnosis of IE rests on a constellation of clinical features and laboratory investigations, including blood cultures and echocardiography.1 Most often, IE presents with fever, positive blood cultures, a new murmur, or vegetations by echocardiography. Vascular findings and immunologic phenomena are common. The presenting symptoms, rate of progression, morbidity, and mortality of infective endocarditis depend, in part, upon the underlying heart disease, the etiologic organism, and host factors. Whereas most infective endocarditis is accompanied by positive blood cultures, 5% to 7% are culture negative, sometimes due to administration of antibiotics before blood cultures were obtained.1 Compared to adults, children have a lower incidence and fatality rate of IE.2,3 The most common causes of bacterial endocarditis in children are viridans group streptococci and Staphylococcus aureus; other principal pathogenic agents include coagulase-negative staphylococci, Streptococcus pneumoniae, HACEK organisms (Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella species), and enterococcus species.4-6 Emergence of antibiotic resistance to these common pathogens has serious ramifications for the morbidity and mortality of IE. It is therefore essential that pediatricians and pediatric cardiologists work in concert with specialists in infectious diseases in planning the treatment of IE.


Before the 1970s, rheumatic heart disease was the underlying substrate for infective endocarditis (IE) in 30% to 50% of children.2 As the prevalence of pediatric rheumatic heart disease has declined in developed countries, congenital heart lesions have become the most common form of underlying cardiac disease.4-6 Furthermore, recent series have suggested an ever greater proportion of IE cases without preexisting heart disease, largely a function of nosocomial infections due to greater instrumentation of children with indwelling intravascular catheters and intravenous drug use.2


The relative risk of IE among children with congenital heart lesions is a function of the particular lesion, as well as of host factors. The highest incidence of IE occurs in patients with uncorrected cyanotic congenital heart disease, prosthetic heart valves, or a history of prior IE.9 Compared to patients in the general population, those with prior infective endocarditis have a relative risk 150 times greater, whereas those with prosthetic cardiac valves have a relative risk 400 times greater.10 In general, lesions with high sheer stress or turbulent flow, such as aortic stenosis, seem to be at higher risk than those with low sheer stress, such as atrial septal defect. Patients with unrepaired ventricular septal defects have a higher incidence of infective endocarditis than do those whose defects have been corrected.8


Infective endocarditis is established by the interaction of a bloodstream pathogen with damaged endocardium.1 The process begins when sheer stress, for example, across a stenotic ...

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