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Biology and pathogenesis of thrombosis and procoagulant activity in invasive infections caused by group A streptococci and Clostridium perfringens.
Clinical Microbiology Reviews ( IF 36.8 ) Pub Date : 2003-07-15 , DOI: 10.1128/cmr.16.3.451-462.2003
Amy E Bryant 1
Affiliation  

Group A streptococcal necrotizing fasciitis/myonecrosis and Clostridium perfringens gas gangrene are two of the most fulminant gram-positive infections in humans. Tissue destruction associated with these infections progresses rapidly to involve an entire extremity. Multiple-organ failure is common, and morbidity and mortality remain high. Systemic activation of coagulation and dysregulation of the anticoagulation pathways contribute to the pathogenesis of many diverse disease entities of infectious etiology, and it has been our hypothesis that microvascular thrombosis contributes to reduced tissue perfusion, hypoxia, and subsequent regional tissue necrosis and organ failure in these invasive gram-positive infections. This article reviews the coagulation, anticoagulation, and fibrinolytic systems from cellular players to cytokines to novel antithrombotic therapies and discusses the mechanisms contributing to occlusive microvascular thrombosis and tissue destruction in invasive group A streptococcal and C. perfringens infections. A thorough understanding of these mechanisms may suggest novel therapeutic targets for patients with these devastating infections.

中文翻译:

A组链球菌和产气荚膜梭菌引起的浸润性感染中血栓形成和促凝活性的生物学和发病机制。

A组链球菌坏死性筋膜炎/肌坏死和产气荚膜梭状芽胞杆菌坏疽是人类中最暴发的革兰氏阳性感染中的两种。与这些感染相关的组织破坏进展迅速,涉及整个肢体。多器官功能衰竭很常见,发病率和死亡率仍然很高。凝血的系统性激活和抗凝血途径的失调导致了多种传染病学病因的发病机理,并且我们的假设是微血管血栓形成有助于减少组织灌注,缺氧以及随后的这些区域组织坏死和器官衰竭侵袭性革兰氏阳性感染。本文回顾了凝结,抗凝,和纤溶系统,从细胞因子到细胞因子,再到新型抗血栓形成疗法,并讨论了在A组链球菌和产气荚膜梭菌感染中导致闭塞性微血管血栓形成和组织破坏的机制。对这些机制的透彻了解可能为患有这些破坏性感染的患者提出了新的治疗靶标。
更新日期:2019-11-01
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