Viral meningitis pathophysiology differs from virus to another and depends on many factors like age, immune status and gene expression. Invasion into the meninges by a pathogen can set up a local inflammatory response. The clinical signs are due to this meningeal irritation – for example, Kernig’s sign is due to pain produced by stretching of the inflamed meninges.

• 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.^[1]

• Enteroviruses:
  • They include coxsackievirus A&B, echovirus, hepatitis A, and poliovirus.
  • Infection can be started in the nasal mucosa and after that it can be ingested in the stomach. It attaches to the enterocytes then the viruses reach the peyer’s patches of the lamina propria where the replication takes place.
  • The replication which occurs at this site causes viremia to further organs like the lung, brain and liver at which another replication takes place at these organs causing more viremia. Infection of the nervous system can occur via this viremia which is responsible for the clinical manifestaions of the disease.

• Arboviruses:
  • Common arvboviruses in the United States^[2]:
    • St. louis encephalitis virus (Flavivirus)
    • Western equine encephalitis virus (Alphavirus)
    • Colorado tick fever virus (Coltivirus)
  • They commonly cause encephalitis. However, they are responsible for causing viral meningitis.
  • Pathogenesis is similar to the enteroviruses pathogenesis. The difference between them is in the start process of the infection. The infection starts by the arthropod bite to the skin then virus replication takes place in the lymph nodes then viremia occurs in the distant organs and finally the virus reaches the brain.

• Mumps:
  • Infection occurs through respiratory droplet that infects first the parotid gland causing parotitis.
  • After the infection, viremia takes place and the virus reaches the brain causing meningitis.

• Human herpes viruses:^[3]
  • They include: Herpes simplex virus 1, Herpes simplex virus 2, human herpes virus 1, Cytomegalovirus, epstein barr virus and human herpes virus 8.
  • Primary infection by the herpes viruses is like the other viral infections by invasion through the respiratory and gastric mucosa and the replication followed by the viremia till reaching the brain causing meningitis.
  • Latent infection may occur when the virus is stimulated again by tissue damage or exposure to ultraviolet light.

Infectious transmission is different among the viruses causing viral meningitis:

• Enteroviruses: Feco-oral transmission and may be transmitted by the respiratory droplet
• Herpes simplex virus: Inter-human transmission
• Arboviruses, such as West nile virus : Transmitted through mosquitoes bite
• Mumps: Transmitted via the blood
• Influenza: Postinfections – airborne transmission
• Lymphocytic choriomeningitis virus: Transmitted from the rodents

There is no genetic inheritance correlated with the viral meningitis.

Microscopic pathological findings in viral meningitis may include the following:

• Pleocytosis (10-1000 cells/µl)
• Polymorphous population of lymphocytes
• Activated lymphocytes
• Plasma cells may be binuclear or multinuclear
• Activated monocytes