Leib S L, Täuber M G
Institute for Medical Microbiology, University of Bern, Switzerland.
Infect Dis Clin North Am. 1999 Sep;13(3):527-48, v-vi. doi: 10.1016/s0891-5520(05)70093-3.
Bacterial meningitis is fatal in 5% to 40% of patients and causes neurologic sequelae in up to 30% of survivors. Much has been learned recently about the mechanisms that lead to brain injury during meningitis. Once bacteria have gained access to the central nervous system, their multiplication triggers a complex host response consisting of humoral and cellular immune mediators, reactive oxygen intermediates, matrix-metalloproteinases, and other host-derived factors. Alterations of the cerebral vasculature, with disruption of the blood brain barrier and global and focal ischemia, ultimately lead to functional and structural brain damage. This article reviews current concepts of the pathophysiology of bacterial meningitis and emphasizes possible therapeutic strategies to prevent its harmful consequences.
细菌性脑膜炎在5%至40%的患者中是致命的，并且在高达30%的幸存者中会导致神经后遗症。最近，人们对脑膜炎期间导致脑损伤的机制有了很多了解。一旦细菌进入中枢神经系统，它们的繁殖就会引发复杂的宿主反应，包括体液和细胞免疫介质、活性氧中间体、基质金属蛋白酶和其他宿主衍生因子。脑血管系统的改变，伴随着血脑屏障的破坏以及全身性和局灶性缺血，最终导致脑功能和结构损伤。本文综述了细菌性脑膜炎病理生理学的当前概念，并强调了预防其有害后果的可能治疗策略。
