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{{Viral meningitis}}
{{CMG}} {{AE}} {{AEL}}


==Overview==
Viral meningitis pathophysiology differs from virus to another and depends on many factors like age, immune status and gene expression.
==Pathogenesis==
*The causative viral agents can reach the nervous system via the blood or the nerves themselves. There is a difference in both pathways pathogenesis. Viral spreading through the blood (viremia) is more common in viral meningitis pathogenesis. The viruses enter to the pulmonary and intestinal mucosa at which they spread into the blood to reach the lymph nodes where viral replication takes place and this is called primary viremia. At this point, the host cells try to prevent further replication from happening and if they fail to stop the replication, secondary viremia will take place and the viruses can spread to the nervous system causing many clinical manifestations. <ref name="pmid11051293">{{cite journal| author=Rotbart HA| title=Viral meningitis. | journal=Semin Neurol | year= 2000 | volume= 20 | issue= 3 | pages= 277-92 | pmid=11051293 | doi=10.1055/s-2000-9427 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11051293  }} </ref>
==Transmission==
Infectious transmission is different among the viruses causing viral meningitis:
*Enteroviruses: Feco-oral transmission
*Mumps: Transmitted via the blood
*Influenza: Postinfections - airborne transmission
*Lymphocytic choriomeningitis virus: Transmitted by the rodents.
==Genetics==
==Associated conditions==
==Gross pathology==
==Microscopic pathology==
==References==
{{Reflist|2}}

Latest revision as of 18:06, 1 May 2017