Pathogenesis of Bacterial Meningitis

Infect Dis Clin North Am. 1999 Sep;13(3):527-48, v-vi. doi: 10.1016/s0891-5520(05)70093-3.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Blood-Brain Barrier
  • Cerebral Ventricles / microbiology
  • Cerebrovascular Circulation / immunology
  • Cytokines / metabolism
  • Excitatory Amino Acids / metabolism
  • Humans
  • Immunity, Cellular
  • Intracranial Pressure
  • Meninges / microbiology
  • Meninges / pathology
  • Meningitis, Bacterial / cerebrospinal fluid
  • Meningitis, Bacterial / immunology
  • Meningitis, Bacterial / microbiology*
  • Metalloendopeptidases / metabolism
  • Neutrophils / metabolism
  • Nitric Oxide / metabolism
  • Reactive Oxygen Species / metabolism
  • Subarachnoid Space / microbiology

Substances

  • Cytokines
  • Excitatory Amino Acids
  • Reactive Oxygen Species
  • Nitric Oxide
  • Metalloendopeptidases