Fungal meningitis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor(s)-in-Chief: Rim Halaby

Overview

The pathophysiology of fungal meningitis is not very well studied but it is known to have a lot of similarities with bacterial meningitis. Fungal meningitis usually occurs in immunocompromised patients.

Pathophysiology

• The initial step in fungal meningitis is pulmonary exposure to the fungi by the inhalation of airborne fungal spores.
• The pulmonary infection is usually self limited and maybe asymptomatic.
• In most cases of fungal meningitis, the fungi undergo hematogenous spread.
• Patients with immunosuppression are the most vulnerable to fungal meningitis
• Once the fungi cross the blood brain barrier they cause an inflammation of the meninges and arachnoid space:
• The inflammation promote cytokine release mainly tumor necrosis factor (TNF), interleukin 1 and interleukin 6
  • The cytokines cause the fever observed in meningitis
  • The cytokines promote an increase in the permeability of the blood brain barrier and subsequent cerebral edema and increase in the intracranial pressure
• Cerebral edema leads to decrease blood flow to the brain and hypoxia
• The glucose level in the cerebral spinal fluid (CSF) will decrease due to a decrease transport of glucose coupled to an increase use of glucose by the fungi
• The increase in the permeability of the blood brain barrier is the cause for the observed elevation of the protein level in the cerebral spinal fluid.