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*The pulmonary infection is usually self limited and maybe asymptomatic. | *The pulmonary infection is usually self limited and maybe asymptomatic. | ||
*In most cases of [[fungal meningitis]], the fungi undergo hematogenous spread. | *In most cases of [[fungal meningitis]], the fungi undergo hematogenous spread. | ||
*Patients with immunosuppression are the most vulnerable to fungal meningitis | *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]]: | *Once the fungi cross the [[blood brain barrier]] they cause an inflammation of the [[meninges]] and [[arachnoid space]]: | ||
*The inflammation promotes [[cytokine]] release mainly [[tumor necrosis factor]] (TNF), [[interleukin 1]] and [[interleukin 6]] | *The inflammation promotes [[cytokine]] release mainly [[tumor necrosis factor]] (TNF), [[interleukin 1]] and [[interleukin 6]] | ||
Revision as of 16:48, 22 October 2012
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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 Steps in Meningeal Fungal Infection
- The initial step in fungal meningitis is the 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 promotes cytokine release mainly tumor necrosis factor (TNF), interleukin 1 and interleukin 6
- The cytokines cause the fever observed in meningitis
- The cytokines promotes an increase in the permeability of the blood brain barrier and subsequent cerebral edema and increase in the intracranial pressure
- Cerebral edema leads to decreased blood flow to the brain and hypoxia
- The glucose level in the cerebral spinal fluid (CSF) will decrease due to a decreased transport of glucose coupled to an increased use of glucose by the fungi
- The increase in the permeability of the blood brain barrier is the cause of the observed elevation of the proteins level in the cerebral spinal fluid.[1]
The Underlying Mechanisms of the Symptoms
- Stimulation of the nociceptive fibers by inflammatory processes:
- Cerebral edema and obstructive of the cerebral spinal fluid's pathway:
- Increased intracranial pressure:
- Headache, vomiting, gait disturbance
- Vascular damage:
- Cognitive and behavioral changes, seizures, stroke, myelopathy
- Seeding of inflammatory processes by the cerebral spinal fluid to the brainstem and cranial nerves (CN):
- Vision loss (CN II), facial weakness (CN VII), hearing loss (CNV III), diplopia (CN III, IV, V), other cranial nerves involvement
- Injury to spinal motor and sensory roots:
- Radiculopathy with associated radicular pain, sensory loss, motor weakness[2]
References
- ↑ John Marx. Chapter 107. Central Nervous System Infections. Marx: Rosen's Emergency Medicine, 7th ed.. Mosby: Elsevier; 2009.
- ↑ Koroshetz WJ. Chapter 382. Chronic and Recurrent Meningitis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012.