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| Infective Endocarditis | ||
| Etiology •Strepto-, staphylo- and enterococci are most common organisms. Almost all bacterial species, fungi, chlamydiae, and rickettsiae are possible. •Strep most common in non-intravenous drug abuse (IVDA) cases, and mostly S. viridans sp. of low virulence. B-hemolytic strep sp. and S. aureus highly virulent. •IVDA cases: S.aureus most common. Entero- and streptococci, fungi (candida) and gram (-) bacilli (pseudomonas) also seen. Only 20% have previous damaged vaves. Tricuspid valve affected >1/2 cases. | ||
| Pathogenesis •Immunodeficiency, neutropenia, diabetes and IVDA predispose normal hearts to IE. •Any congenital malformation or structual change in the endocardium can result in a barrier to normally flawless blood flow. •The endothelium lining barriers exposed to the pressure of blood flow becomes damaged (hemo- dynamic injury), with deposition of platelet thrombi forming a nidus for the entrapment of circulating organisms and the genesis of IE., | ||
| Epidemiology •Subacute Bacterial Endocarditis (SBE): Typically involves endocardiums subjected to hemodynamic injury: valves deformed by rheumatic heart disease, acquired aortic stenosis, congenital deformaties like septal defects, and prosthetic valves. Usually Strep. viridans or any organism with low virulence. •Acute Bacterial Endocarditis: Highly virulent organisms such as S. aureus and fungi in immunodeficient states infecting normal endocardial surfaces. Right sided valves often involved in IV drug abuse. Inevitable bacteremias (brushing teeth) source of infection. | ||
| General Gross Description •ABE: Usually occurring on normal valves on either side. Vegetations variable in size and shape, some massive up to 3-4 cm, and friable. Often destroy valve leaflets with perforations. Can spread and erode valve base to form annular ring abscess. •SBE: Usually occurring on endocardium lining deformed structures such as healed rheumatic valvulitis, congenital bicuspid aortic valve, and septal defects. Vegetations not as destructive or as large as ABE. •Examples: | ||
| General Microscopic Description •Vegetations have a base of a fibrinous appearing thrombus made mostly of platelets. Bacterial colonies are seen in superficial layers with a prominent infiltrate of neutrophils. Valve structures may be totally destroyed in ABE. •Organisms of low virulence causing SBE can result in a chronic active inflammatory response, even without treatment, with bacteria and neutrophils superficially and active organizing fibrovascular tissue in the basal layers. •Examples: | ||
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 550-4 • Harrison's Principles of Internal Medicine, 13th Ed: Isselbach et. al. (eds). New York, McGraw-Hill, 1994, pp.520-6 This link will directly take you to the relevant new literature Infective Endocarditis
| Synopsis by: J. Hasson M.D. (T39000D72100)[476]
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