Bacterial meningitis pathophysiology: Difference between revisions
Jump to navigation
Jump to search
Aysha Aslam (talk | contribs) |
Aysha Aslam (talk | contribs) |
||
| Line 40: | Line 40: | ||
===Role of Genetics=== | ===Role of Genetics=== | ||
Genetic polymorphism in | Genetic polymorphism in individuals may determine the suscepitibity to develop bacterial meningitis, the severity of infection and ability to recover. | ||
===Gross pathology=== | ===Gross pathology=== | ||
Revision as of 19:38, 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[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.
- Bacteria seeds transcellularly to enter the intravascular space.
- Surface encapsulation may play important role in entry of bacterial pathogen across epithelium into blood stream
- Blood stream entry of bacterial pathogen may result in activation of complement pathway and infalmmatory process[3]
- Bacterial capsule helps evasion of complement system and ultimate entry into the CNS through blood brain barrier[3]
- Individual genetic susceptibilty and immune response determine the severity of infection
Meningeal infalmmation
- Meningeal inflammation follows bacterial invasion into the blood.
- Bacterial entry into brain may occur through highly vascularised areas such as leptomeningeal blood vessels or choroid plexus.
- Intracranial entry of bactrial pathogen through tight junctions of blood CSF or blood CNS barrier mayroid epitheo occur through special interaction of adhesins and proteins on the surface of choroid epithelial cells[4]
Associated conditons
Following conditions may increase the susceptibitly to develop bacterial meningitis:
- Trauma to skull
- HIV
- Diabetes mellitus
- Organ transplant
Role of Genetics
Genetic polymorphism in individuals may determine the suscepitibity to develop bacterial meningitis, the severity of infection and ability to recover.
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.
- ↑ 3.0 3.1 Joiner KA (1988). "Complement evasion by bacteria and parasites". Annu Rev Microbiol. 42: 201–30. doi:10.1146/annurev.mi.42.100188.001221. PMID 3059994.
- ↑ Brown EJ, Joiner KA, Gaither TA, Hammer CH, Frank MM (1983). "The interaction of C3b bound to pneumococci with factor H (beta 1H globulin), factor I (C3b/C4b inactivator), and properdin factor B of the human complement system". J Immunol. 131 (1): 409–15. PMID 6223077.