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Acute endocarditis is a febrile illness that rapidly damages cardiac structures, seeds extracardiac sites hematogenously, and can progress to death within weeks. Subacute endocarditis follows an indolent course, rarely causes metastatic infection, and progresses gradually unless complicated by a major embolic event or a ruptured mycotic aneurysm.

  • Epidemiology In developed countries, the incidence of endocarditis ranges from 2.6 to 7.0 cases per 100,000 population per year, with higher rates among the elderly.

    • – Predisposing conditions include congenital heart disease, illicit IV drug use, degenerative valve disease, and intracardiac devices.

    • – Chronic rheumatic heart disease is a risk factor in low-income countries.

    • – Of endocarditis cases, 16–30% involve prosthetic valves, with the greatest risk during the first 6–12 months after valve replacement.

  • Etiology Because of their different portals of entry, the causative microorganisms vary among clinical types of endocarditis.

    • – In native valve endocarditis (NVE), viridans streptococci, staphylococci, and HACEK organisms [Haemophilus spp., Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae] enter the bloodstream from oral, skin, and upper respiratory tract portals. Streptococcus gallolyticus (formerly S. bovis) originates from the gut and is associated with colon polyps or cancer. Enterococci originate from the genitourinary tract.

    • – Health care–associated NVE, frequently due to Staphylococcus aureus, coagulase-negative staphylococci (CoNS), and enterococci, can have a nosocomial onset (55%) or a community onset (45%) in pts who have had extensive contact with the health care system in the preceding 90 days.

    • – Prosthetic valve endocarditis (PVE) developing within 2 months of surgery is due to intraoperative contamination or a bacteremic postoperative complication and is typically caused by CoNS, S. aureus, facultative gram-negative bacilli, diphtheroids, or fungi. Cases beginning >1 year after valve surgery are caused by the same organisms that cause community-acquired NVE. PVE due to CoNS that presents 2–12 months after surgery often represents delayed-onset nosocomial infection.

    • – Endocarditis occurring among IV drug users, especially that involving the tricuspid valve, is commonly caused by S. aureus (often a methicillin-resistant strain). Left-sided valve infections among IV drug users are caused by Pseudomonas aeruginosa and Candida, Bacillus, Lactobacillus, and Corynebacterium spp. in addition to the usual causes of endocarditis.

    • – About 5–15% of endocarditis cases are culture negative, and one-third to one-half of these cases are due to prior antibiotic exposure. The remainder of culture-negative cases represent infection by fastidious organisms, such as the nutritionally variant bacteria Granulicatella and Abiotrophia, HACEK organisms, Bartonella spp., Coxiella burnetii, Brucella spp., and Tropheryma whipplei.

  • Pathogenesis Endothelial injury allows direct infection by more virulent pathogens (e.g., S. aureus) or the development of an uninfected platelet-fibrin thrombus [referred to as nonbacterial thrombotic endocarditis (NBTE)] that may become infected during transient bacteremia. NBTE arises from cardiac conditions (e.g., mitral regurgitation, aortic stenosis, aortic regurgitation), hypercoagulable states, and the antiphospholipid antibody syndrome. After entering the bloodstream, organisms adhere to the endothelium or sites of ...

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