Japanese Encephalitis is caused by Flavivirus belonging to family Flaviviridae. The family Flaviviridae includes 67 viruses of which 29 cause human illness. The virus is 40 – 60 mm diameter with RNA as a genetic material covered with a protein envelop. The envelop contains a single glycoprotein and lipid. So far, direct transmission of infection from human to human has not been reported. The clinical spectrum of flavivirus infection includes non – specific febrile illness, fever with arthralgia and rash, and central nervous system infection. (asceptic meningitis or encephalitis.) Pathogenesis is mediated by direct viral injury to infected cells and indirectly by mediators (cytokines) released from cells during the process of immunologic clearance. Because the clinical illness is non specific and not readily differentiable except in the setting of an epidemic, the physician must use epidemiological information and specific laboratory test to arrive at accurate diagnosis. All infected individuals develop antibodies to the virus. The ration between clinical & sub clinical cases ranges from 1: 200 to 1: 1000 exhibiting an iceberg phenomenon. The natural history of JE virus involves mosquito vectors and vertebrate hosts. Environmental factors ensure viral transmission in and between these groups.
The Japanese Encephalitis virus has been recovered from about 30 species of mosquitoes from 5 genera. C. Tritaeniorhynchus thrive in rice fields. They inhabit elevations below 1500 meters and usually bite at dusk, dawn and extreme hours of night. The important factors which ensure spillover of the disease to humans are density and longevity of infected mosquito populations, existence of amplifying hosts like pigs and human exposure to infected vectors. Mosquitoes are zoophilic (Feed on animals – vertebrate hosts). Female mosquitoes get infected after feeding on viraemia hosts.
Non Human Vertebrate Hosts
Pig to pig transmission ensures virus multiplication. Bovines largely attract mosquitoes but do not amplify the virus and hardly demonstrate viremia. Horses may manifest encephalitis. Ardeid birds including herons and egrets are also involved in transmission. Transovarial transmission may occur within mosquito population.
The period of viremia in the pig is 1–2 weeks. It has been shown that porcine sero conversion precedes human infections by 2–3 weeks and that vector density enhancement correlated with increased sero conversion in pigs and virus amplification in the pig occurs in the last quarter of the year. Serological studies in several vertebrates in the endemic areas using HI tests for antibody demonstrated that Pigs exhibit highest sero conversion rate and titres. This is substantiated by the fact that outbreaks are evident during and after the monsoons, in the North from June to November and from September to January in the south.