The pathophysiology of pneumococcal meningitis.
The interactions between pneumococcal surface components and host defence systems that initiate pneumococcal meningitis have been studied in considerable molecular detail over the past decade. In this sense, the pneumococcus has served as a prototype for the unravelling of the genesis of inflammation caused by gram-positive bacteria. This review outlines the progression of these early events involving the cytokine cascade, the coagulation cascade, and leukocyte migration, and relates these processes to the production of blood-brain barrier permeability, the hallmark of injury in meningitis. This new understanding has radically altered the therapy of disease with the promise of greatly improved outcome.
Spellerberg
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B
Laboratory of Molecular Infectious Diseases, Rockefeller University, New York, NY 10021.
Tuomanen
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EI
D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001812:Blood-Brain Barrier; D001929:Brain Edema / Q000209:etiology; D002463:Cell Membrane Permeability; D002560:Cerebrovascular Circulation; D016207:Cytokines / Q000134:cerebrospinal fluid; D004727:Endothelium / Q000502:physiology; D006801:Humans; D008586:Meningitis, Pneumococcal / Q000188:drug therapy / Q000503:physiopathology*; D009504:Neutrophils / Q000502:physiology
D000900:Anti-Bacterial Agents; D000893:Anti-Inflammatory Agents; D016207:Cytokines