Bacterial meningitis pathophysiology: Difference between revisions

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===Meningeal infalmmation===
===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
===Associated conditons===
===Associated conditons===
===Role of Genetics===
===Role of Genetics===

Revision as of 19:24, 10 January 2017

Meningitis main page

Bacterial meningitis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Meningitis from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

CT

MRI

Lumbar Puncture

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

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

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

Associated conditons

Role of Genetics

Gross pathology

Microscopic pathology

References

  1. https://www.cdc.gov/meningitis/bacterial.html Accessed on 10th Jan, 2017
  2. 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.


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