Bacterial meningitis pathophysiology: Difference between revisions
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===Colonization and evasion of host immune response=== | ===Colonization and evasion of host immune response=== | ||
*Colonization of pathogenic organism involves evasion of host immune response mechanism. | |||
*IgA protease produced by bacterial pathogen cleave mucosal IgA antibodies which prevent the bacteria from attachment to the mucosal surface. | |||
*Once host immune response is evaded, bacteria attach themselves to the mucosa via fimbriae or pilli which facilitate colonization process. | |||
* | |||
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===Invasion and seeding=== | ===Invasion and seeding=== | ||
===Meningeal infalmmation=== | ===Meningeal infalmmation=== |
Revision as of 17:59, 10 January 2017
Bacterial meningitis Microchapters |
Diagnosis |
Treatment |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]
Overview
Pathophysiology
Pathogenensis of bacterial meningitis is a complex process which may occur due to imbalance between the host immune response and virulence factors of pathogen causing infection. Following steps may explain the underlying process in a comprehensive way:
Transmission
- H. influenza type b and N. meningitides may be transmitted by close contact or prolong contact with patient suffering from meningitis
- It may also spread by exchanging throat and respiratory secretions (couging and kissing)
- Listeria monocytogenes may spread by eating contaminated food.
- Most people are carriers and do not develop the disease.
Colonization and evasion of host immune response
- Colonization of pathogenic organism involves evasion of host immune response mechanism.
- IgA protease produced by bacterial pathogen cleave mucosal IgA antibodies which prevent the bacteria from attachment to the mucosal surface.
- Once host immune response is evaded, bacteria attach themselves to the mucosa via fimbriae or pilli which facilitate colonization process.
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