Tunkel A R, Wispelwey B, Scheld W M
Division of Infectious Diseases, University of Virginia School of Medicine, Charlottesville.
Infect Dis Clin North Am. 1990 Dec;4(4):555-81.
Advances in the understanding of the pathogenesis and pathophysiology of meningitis have occurred primarily through the use of experimental animal models. These models have proven to be particularly valuable in experimental bacterial meningitis, focusing on the bacterial virulence factors responsible for the initiation of infections, CNS invasion, and induction of SAS inflammation. Recent studies have examined the formation of host inflammatory cytokines in response to these virulence factors. These cytokines may be responsible for many of the pathophysiologic consequences of bacterial meningitis (eg. increased BBB permeability, cerebral edema, and increased intracranial pressure). Meningitis due to C. neoformans occurs most commonly in patients with defects in cell-mediated immunity (eg, AIDS), and the depletion of T helper cells in AIDS patients may allow unrestricted cryptococcal growth. Viral meningitis is an illness of low prevalence when compared with the overall occurrence of viral infections at other sites. CNS infection usually occurs by means of traversal across barriers that normally exclude viral invasion of the CNS, primarily through hematogenous dissemination from initial sites of infection. These advances in the pathogenesis and pathophysiology of bacterial, fungal, and viral meningitis may lead to the development of innovative treatment strategies for these disorders.
对脑膜炎发病机制和病理生理学的认识进展主要源于实验动物模型的应用。这些模型在实验性细菌性脑膜炎中已被证明具有特别重要的价值，主要关注引发感染、中枢神经系统侵袭以及诱导蛛网膜下腔炎症的细菌毒力因子。最近的研究探讨了宿主炎症细胞因子对这些毒力因子的反应。这些细胞因子可能是细菌性脑膜炎许多病理生理后果的原因（例如血脑屏障通透性增加、脑水肿和颅内压升高）。新型隐球菌性脑膜炎最常见于细胞介导免疫缺陷的患者（如艾滋病患者），艾滋病患者辅助性T细胞的耗竭可能会使隐球菌不受限制地生长。与其他部位病毒感染的总体发生率相比，病毒性脑膜炎的发病率较低。中枢神经系统感染通常是通过跨越通常可排除病毒侵袭中枢神经系统的屏障而发生的，主要是通过从初始感染部位的血行播散。细菌性、真菌性和病毒性脑膜炎在发病机制和病理生理学方面的这些进展可能会促使针对这些疾病开发创新的治疗策略。
