Infectious encephalitis is typically caused by a viral infection. Vaccines for measeles mumps, rubella and chcken pox have reduced the rate of encephalitis from these diseases, but other viruses can cause encephalitis. The most common causes of viral encephalitis are herpes simplex virus 1 and 2 varicella zoster virus and enteroviruses, which cause gastrointestinal illness.
Encephalitis can also result from certain viruses carried by mosquitoes, ticks and other insects or animals such as:
Japanese encephalitis virus
West nile fever
La Crosse virus
St. Louis virus
Other infectious microorganism include:
The American Equine Encephalitides
The alphavirus genus contains 4 viruses which produce encephalitis; EEE, WEE, VEE and Everglades. The Everglades virus is related to EEE but is restricted to the state of Florida in the U.S.A. EEE and WEE plays an important role in the transmission of the diseas between mosquitoes and birds, similarly VEE between mosquitoes and rodents.
The disease manifestation include flu like symptoms in the earlier stages. The probability of developing encephalitis vary widely between the different viruses; it is highest for the EEE and lowest for the VEE.
No specific therapy is available against these viruses. Although inactivated vaccines have been prepared by the U.S. army against these viruses, they are not available for issue to the public at large and their efficacy had yet to be proven. Public warnings should be issued when these viruses are prevalent.In cities with highest amount of population vector control is indicated.
The family of arbovirus include toga virus,
Autoimmune encephalitis occurs when a person’s own antibodies or immune cells attack the brain. Antibodies may target specific proteins or receptors in the brain, which determine the type of autoimmune encephalitis:
In anti-NMDA receptor encephalitis, the immune system targets the NMDA receptors in the brain.
In VGKC-complex antibody encephalitis, the immune system targets the VGKC brain protein complex that includes subtypes LGI-1 and CASPR2.
GABA-A and GABA-B receptors may also be targeted.