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| Endocarditis | ||
| Etiology •Strep-, staph- and enterococci are most common organisms. Almost all bacteria, fungi, chlamydiae, and rickettsia occur. •Non-intravenous drug abuse (IVDA) cases mostly S. viridans of low virulence. B-hemolytic strep. sp. and Staph. aureus highly virulent. •IVDA cases: S. aureus common. Strep- and enterococci, gram neg. bacilli and fungi (candida, aspergillus) also seen. | ||
| Pathogenesis •Non-IVDA cases. Transient bacteremias from obvious infections or from trivial injuries (teeth brushing) seed valves. •IVDA cases. High doses of pathogens delivered with dirty needles affecting right side commonly. •Existing immunosuppression (HIV, organ transplants, alcoholism) increases risk., | ||
| Epidemiology •Non-IVDA cases. Most have some existing abnormality: Congenital septal or valve defects; healed rheumatic valvulitis; prolapsed mitral valve; calcific aortic stenosis. Some have apparently normal valves with minimal degenerative changes. •IVDA cases. Most have normal valves. Left sided lesions predominate, but right sided valves commonly affected. | ||
| General Gross Description •Vegetations are often bulky, with irregular friable surfaces, and may extend to adjoining endocardium and chordae tendinae. Destructive, with defects in valve structure, and with invasion along annulus to form a "ring" abscess. Size and destuctiveness of vegetations directly proportional to virulence of organism. •Less virulent organisms may have flatter vegetations, invisible on echocardiography. •Examples: | ||
| General Microscopic Description •Varies with virulence of organism and duration of process. Bulky vegetations show a suppurative exudate of neutrophils with fibrinous thrombi and large bacterial colonies destroying valve substance. •Smaller, flatter vegetations of longer duration will also show the same surface reaction, but with a deeper chronic inflammatory component including a vascular fibrous tissue healing response. •Flat vegetations may be missed on an echocardiogram. •Examples: | ||
| References • • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 550-554. This link will directly take you to the relevant new literature Endocarditis
| Synopsis by: J. Hasson, MD (T36000D72100)[369]
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