Fungal meningitis pathophysiology: Difference between revisions
Prince Djan (talk | contribs) |
Prince Djan (talk | contribs) |
||
Line 36: | 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> | ||
===Genetics=== | |||
Homozygous neutrophil dependent mutation of caspase recruitment domain 9 (CARD9) have been discovered to predispose to invasive chronic Candida infections, especially of the central nervous system.<ref name="pmid25933095">{{cite journal| author=Herbst M, Gazendam R, Reimnitz D, Sawalle-Belohradsky J, Groll A, Schlegel PG et al.| title=Chronic Candida albicans Meningitis in a 4-Year-Old Girl with a Homozygous Mutation in the CARD9 Gene (Q295X). | journal=Pediatr Infect Dis J | year= 2015 | volume= 34 | issue= 9 | pages= 999-1002 | pmid=25933095 | doi=10.1097/INF.0000000000000736 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25933095 }} </ref> | |||
===Gross pathology=== | ===Gross pathology=== |
Revision as of 17:36, 1 February 2017
Fungal meningitis Microchapters |
Diagnosis |
Treatment |
Case Studies |
Fungal meningitis pathophysiology On the Web |
American Roentgen Ray Society Images of Fungal meningitis pathophysiology |
Risk calculators and risk factors for Fungal meningitis pathophysiology |
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]
Genetics
Homozygous neutrophil dependent mutation of caspase recruitment domain 9 (CARD9) have been discovered to predispose to invasive chronic Candida infections, especially of the central nervous system.[3]
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.
- ↑ Herbst M, Gazendam R, Reimnitz D, Sawalle-Belohradsky J, Groll A, Schlegel PG; et al. (2015). "Chronic Candida albicans Meningitis in a 4-Year-Old Girl with a Homozygous Mutation in the CARD9 Gene (Q295X)". Pediatr Infect Dis J. 34 (9): 999–1002. doi:10.1097/INF.0000000000000736. PMID 25933095.