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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.
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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
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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
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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 ...