Pathophysiology of Infective Endocarditis

被引:26
作者
Keynan, Yoav [1 ,2 ,3 ]
Rubinstein, Ethan [1 ,2 ,4 ]
机构
[1] Univ Manitoba, Dept Internal Med, Winnipeg, MB R3E 0J9, Canada
[2] Univ Manitoba, Dept Med Microbiol, Winnipeg, MB R3E 0J9, Canada
[3] Univ Manitoba, Dept Community Hlth Sci, Winnipeg, MB R3E 0J9, Canada
[4] Univ Manitoba, Sect Adult Infect Dis, Winnipeg, MB R3E 0J9, Canada
关键词
Endocarditis; Heart lesions predisposing to endocarditis; Intracardiac hemodynamics predisposing to endocarditis; Bacterial adhesion to endocardial cells; Adhesins; STAPHYLOCOCCUS-AUREUS BACTEREMIA; UNDERLYING CARDIAC LESIONS; PLATELET-AGGREGATION; HEART VALVES; ALPHA-TOXIN; ADHERENCE; BINDING; PROTEIN; PATHOGENESIS; ACTIVATION;
D O I
10.1007/s11908-013-0346-0
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
Infective endocarditis (IE) is an uncommon infection, occurring as a complication in varying percentages of bacteremic episodes. The ability of an organism to cause endocarditis is the result of an interplay between the predisposing structural abnormalities of the cardiac valve for bacterial adherence, the adhesion of circulating bacteria to the valvular surface, and the ability of the adherent bacteria to survive on the surface and propagate as vegetation or systemic emboli. Certain bacteria, if present in the bloodstream, may colonize the initially sterile vegetation composed of fibrin and platelets; bacterial growth enlarges the vegetation, further impeding blood flow and inciting inflammation that involves the vegetation and adjacent endothelium. The true incidence of endocarditis complicating each of the bacterial species causing IE is difficult to estimate. About 20 %-30 % of individuals with community-acquired staphylococcal bacteremia develop IE [1, 2].
引用
收藏
页码:342 / 346
页数:5
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