Fungal meningitis pathophysiology: Difference between revisions
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Rim Halaby (talk | contribs) Created page with "__NOTOC__ {{Fungal meningitis}} {{CMG}}; '''Assistant Editor(s)-in-Chief:''' Rim Halaby ==Overview== The pathophysiology of fungal meningitis is not ve..." |
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*The inflammation promote [[cytokine]] release mainly [[tumor necrosis factor]] (TNF), [[interleukin 1]] and [[interleukin 6]] | *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 cause the [[fever]] observed in meningitis | ||
**The cytokines | **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 decrease blood flow to the brain and [[hypoxia]] | *[[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 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]].<ref>John Marx. Chapter 107. Central Nervous System Infections. Marx: Rosen's Emergency Medicine, 7th ed.. Mosby: Elsevier; 2009.</ref> | *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]].<ref>John Marx. Chapter 107. Central Nervous System Infections. Marx: Rosen's Emergency Medicine, 7th ed.. Mosby: Elsevier; 2009.</ref> | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 15:26, 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 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 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 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.[1]
References
- ↑ John Marx. Chapter 107. Central Nervous System Infections. Marx: Rosen's Emergency Medicine, 7th ed.. Mosby: Elsevier; 2009.