Fungal meningitis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===The Steps in Meningeal Fungal Infection=== | |||
===Pathogenesis=== | |||
====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 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. | *The pulmonary infection is usually self limited and maybe asymptomatic. | ||
| Line 20: | Line 23: | ||
*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]].<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 of the observed elevation of the proteins 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 Underlying Mechanisms of the Symptoms=== | ====The Underlying Mechanisms of the Symptoms==== | ||
*Stimulation of the [[nociceptive fibers]] by inflammatory processes: | *Stimulation of the [[nociceptive fibers]] by inflammatory processes: | ||
**[[Headache]], [[neck pain]], [[back pain]] | **[[Headache]], [[neck pain]], [[back pain]] | ||
| Line 33: | Line 36: | ||
*Injury to spinal motor and sensory roots: | *Injury to spinal motor and sensory roots: | ||
**[[Radiculopathy]] with associated radicular pain, sensory loss, motor weakness<ref>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.</ref> | **[[Radiculopathy]] with associated radicular pain, sensory loss, motor weakness<ref>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.</ref> | ||
===Gross pathology=== | |||
===Microscopic pathology=== | |||
==References== | ==References== | ||
Revision as of 18:37, 31 January 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby; Prince Tano Djan, BSc, MBChB [2]
Overview
The pathophysiology of fungal meningitis is not very well studied however, it is known to have a lot of similarities with bacterial meningitis. Fungal meningitis usually occurs in immunocompromised patients.
Pathophysiology
Pathogenesis
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.
- Fungal infections are not contagious so they do not spread from one person to another.
- 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]
Gross pathology
Microscopic pathology
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.