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Pathophysiology of bacterial meningitis: mechanism(s) of neuronal injury

W Michael Scheld1, Uwe Koedel, Barnett Nathan

  • 1Division of Infectious Diseases, Department of Internal Medicine, University of Virginia School of Medicine, PO Box 801342, Charlottesville, VA 22908, USA. wms@virginia.edu

The Journal of Infectious Diseases
|November 9, 2002
PubMed

Insights

Acute bacterial meningitis epidemiology is changing. Understanding neuronal injury mechanisms, involving cytokines, chemokines, and oxidants, is key to developing new therapies.

Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Pathophysiology

Background:

  • Acute bacterial meningitis epidemiology has significantly changed over the last decade.
  • Recent research enhances understanding of meningitis pathogenesis and pathophysiology.
  • Neuronal injury and its role in mortality and sequelae are central concerns.

Purpose of the Study:

  • To review the changing epidemiology of acute bacterial meningitis.
  • To explore recent findings on the pathogenesis and pathophysiology of meningitis.
  • To detail mechanisms of neuronal injury and their contribution to adverse outcomes.

Main Methods:

  • Review of recent experimental studies and existing literature.
  • Analysis of the inflammatory cascade in bacterial meningitis.
  • Exploration of molecular mechanisms of oxidant-induced neuronal injury.

Main Results:

  • Evidence implicates cytokines, chemokines, proteolytic enzymes, and oxidants in meningitis-related tissue destruction.
  • Specific molecular mechanisms of oxidant-induced neuronal injury are detailed.
  • The inflammatory cascade plays a critical role in neuronal damage.

Conclusions:

  • Targeting implicated pathways through genetic or pharmacologic means offers potential therapeutic strategies.
  • Adjunctive therapies alongside antimicrobial agents may improve outcomes for acute bacterial meningitis.
  • Further research into molecular mechanisms can guide the development of novel treatments.

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