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The prototypic lesion of infective endocarditis, the vegetation(Fig. 124-1), is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inflammatory cells. Infection most commonly involves heart valves (either native or prosthetic) but may also occur on the low-pressure side of a ventricular septal defect, on the mural endocardium where it is damaged by aberrant jets of blood or foreign bodies, or on intracardiac devices themselves. The analogous process involving arteriovenous shunts, arterioarterial shunts (patent ductus arteriosus), or a coarctation of the aorta is called infective endarteritis.

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Figure 124-1
Graphic Jump Location

Vegetations (arrows) due to viridans streptococcal endocarditis involving the mitral valve.

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Endocarditis may be classified according to the temporal evolution of disease, the site of infection, the cause of infection, or a predisposing risk factor such as injection drug use. While each classification criterion provides therapeutic and prognostic insight, none is sufficient alone. Acute endocarditis is a hectically febrile illness that rapidly damages cardiac structures, hematogenously seeds extracardiac sites, and, if untreated, progresses to death within weeks. Subacute endocarditis follows an indolent course; causes structural cardiac damage only slowly, if at all; rarely metastasizes; and is gradually progressive unless complicated by a major embolic event or ruptured mycotic aneurysm.

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In developed countries, the incidence of endocarditis ranges from 2.6 to 7 cases per 100,000 population per year and has remained relatively stable during recent decades. While congenital heart diseases remain a constant predisposition, predisposing conditions in developed countries have shifted from chronic rheumatic heart disease (which remains a common predisposition in developing countries) to illicit IV drug use, degenerative valve disease, and intracardiac devices. The incidence of endocarditis is notably increased among the elderly. In developed countries, 30–35% of cases of native valve endocarditis (NVE) are associated with health care, and 16–30% of all cases of endocarditis involve prosthetic valves. The risk of prosthesis infection is greatest during the first 6–12 months after valve replacement; gradually declines to a low, stable rate thereafter; and is similar for mechanical and bioprosthetic devices.

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Etiology

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Although many species of bacteria and fungi cause sporadic episodes of endocarditis, a few bacterial species cause the majority of cases (Table 124–1). Because of their different portals of entry, the pathogens involved vary somewhat with the clinical types of endocarditis. The oral cavity, skin, and upper respiratory tract are the respective primary portals for the viridans streptococci, staphylococci, and HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella; Haemophilus aphrophilus and Actinobacillus actinomycetemcomitans have been reclassified into the genus Aggregatibacter). Streptococcus gallolyticus (formerly S. bovis) originates from the gastrointestinal tract, where it is associated with polyps and colonic tumors, and enterococci enter the bloodstream from the genitourinary tract. Health care–associated NVE, commonly caused by Staphylococcus aureus, coagulase-negative staphylococci ...

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