Bacterial meningitis pathophysiology
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Bacterial meningitis Microchapters |
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Diagnosis |
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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[1]
- 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. [2]
- Once host immune response is evaded, bacteria attach themselves to the mucosa via fimbriae or pilli which facilitate colonization process.
Invasion and seeding
- Once colonized, the invasion of bacteria occurs via special adhesion proteins called adhesins.[2]
- Adhesins may help bacteria to cross epithelial barrier intracellularly or intercellularly.
Meningeal infalmmation
Associated conditons
Role of Genetics
Gross pathology
Microscopic pathology
References
- ↑ https://www.cdc.gov/meningitis/bacterial.html Accessed on 10th Jan, 2017
- ↑ 2.0 2.1 Stephens DS, Farley MM (1991). "Pathogenic events during infection of the human nasopharynx with Neisseria meningitidis and Haemophilus influenzae". Rev Infect Dis. 13 (1): 22–33. PMID 1901998.