Bryant Amy E
Infectious Diseases Section, Veterans Affairs Medical Center, Boise, and Department of Microbiology, University of Idaho, Moscow, Idaho.
Clin Microbiol Rev. 2003 Jul;16(3):451-62. doi: 10.1128/CMR.16.3.451-462.2003.
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.
A组链球菌坏死性筋膜炎/肌坏死和产气荚膜梭菌气性坏疽是人类最严重的两种革兰氏阳性感染。与这些感染相关的组织破坏迅速进展，累及整个肢体。多器官功能衰竭很常见，发病率和死亡率仍然很高。凝血的全身激活和抗凝途径的失调促成了许多不同感染性病因疾病实体的发病机制，我们的假设是微血管血栓形成导致这些侵袭性革兰氏阳性感染中组织灌注减少、缺氧以及随后的局部组织坏死和器官衰竭。本文从细胞成分到细胞因子再到新型抗血栓治疗，综述了凝血、抗凝和纤维蛋白溶解系统，并讨论了侵袭性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。对这些机制的透彻理解可能为患有这些毁灭性感染的患者提示新的治疗靶点。
