Japanese encephalitis

Japanese encephalitis: Description, Causes and Risk Factors:

Japanese encephalitisJapanese encephalitis is a mosquito-borne viral disease that affects horses, donkeys, pigs and humans. In countries where it is endemic, this virus causes reproductive losses in swine and encephalitis in horses. Birds, which are infected asymptomatically, serve as important reservoir hosts. In humans, Japanese encephalitis can be a very serious disease: although most infections are asymptomatic, clinical cases tend to manifest as severe, often fatal encephalitis. Epidemics, which occur periodically in endemic regions, can cause significant morbidity and mortality in unvaccinated humans and animals. Approximately 4,000 people died during the 1924 epidemic in Japan, and nearly 2500 died in South Korea in 1949. In Japan, close to 3700 horses died in 1949. Sporadic cases also occur in susceptible humans and animals throughout the mosquito season.

During the last fifty years, Japanese encephalitis virus has gradually expanded its geographic range within Asia. It has also become endemic in parts of Australia and Indonesia. When this virus becomes established in a new region, major epidemics can occur. There is a possibility that Japanese encephalitis could become endemic in the United States. The West Nile virus, a closely related Flavivirus, was introduced to the U.S. in the late 1990s and has become endemic in wild birds and native mosquitoes.

Japanese encephalitis virus is an arbovirus (arthropod-transmitted virus) in the genus Flavivirus and family Flaviviridae. There is only one serotype but there are two subtypes of the virus (Nakayama and JaGar-01). Viral strains can also be grouped into four or perhaps five genotypes.

Japanese encephalitis virus is closely related to St. Louis encephalitis virus, Murray Valley encephalitis virus and West Nile virus; these viruses and a few others comprise the Japanese encephalitis serogroup of the Flaviviruses.

Japanese encephalitis virus is usually transmitted by mosquitoes in the genus Culex. The specific mosquito vectors vary with the region; however, Culex tritaeniorhynchus is important in spreading this virus to humans and domesticated animals across a wide geographic range. C. tritaeniorhynchus breeds in rice paddies and connecting canals, and is active at twilight. Many other species of Culex including C. vishnui and C. fuscocephala can also transmit Japanese encephalitis virus. In some regions, Aedes mosquitoes have been implicated in transmission. The virus has also been isolated from mosquitoes in the genera Anopheles and Mansonia; however, their role in transmission has not been confirmed.

Humans are usually infected when they are bitten by a mosquito. Some cases are acquired in the laboratory or during tissue sample collection; Japanese encephalitis virus can be transmitted through mucous membranes or broken skin, inhaled in aerosols, or acquired by needle-stick injuries. Although this virus is occasionally recovered from human blood, people are generally thought to be dead-end hosts.


Less than 1% of people infected with Japanese encephalitis (JE) virus develop clinical illness.

  • In persons who develop symptoms, the incubation period is typically 5-15 days.
  • Initial symptoms often include fever, headache, and vomiting.
  • Mental status changes, neurologic symptoms, weakness, and movement disorders might develop over the next few days.
  • Seizures are common, especially among children.


A definitive diagnosis can be made by virus isolation. Japanese encephalitis virus can be isolated in chicken embryo, porcine or hamster kidney cells, African green monkey kidney (Vero) cells, the MDBK cell line or mosquito cell lines (e.g. C3/36). Tissue samples are also inoculated into 2-4 day old mice. The isolated virus can be recognized as a Flavivirus by hemagglutination inhibition or enzyme-linked immunosorbent assays (ELISAs). It can be confirmed as Japanese encephalitis virus by virus neutralization, reverse transcription polymerase chain reaction (RT-PCR) assays, or immunofluorescence for viralantigens. Virus isolation from sick or dead horses is often unsuccessful.

RT-PCR can also detect viral nucleic acids directly in tissues or blood. Immunohistochemistry has been used to identify viral antigens in the central nervous system (CNS). Histopathology is also helpful.

Serologic tests include virus neutralization, hemagglutination inhibition, ELISAs and immunofluorescence. Complement fixation is also used occasionally. A latex agglutination test has been described in swine. In endemic regions, serologic diagnosis usually depends on a significant rise in titer with paired acute and convalescent samples. A presumptive diagnosis may be made if a high titer is found in a single serum sample, but supportive evidence should be collected if possible. In horses, the detection of specific IgM and IgG in cerebrospinal fluid (CSF) is also good evidence of infection. In regions where other viruses in the Japanese encephalitis serogroup are present, cross-reactions can occur in serologic tests. These reactions can be differentiated by virus neutralization or with epitope-blocking ELISAs.


There is no specific treatment for Japanese encephalitis and treatment is supportive; with assistance given for feeding, breathing or seizure control as required. Raised intracranial pressure may be managed with mannitol (ResectisolSM). Rest, fluids, and use of pain relievers and medication to reduce fever may relieve some symptoms.

Preventative measures include the use of insect repellents, insecticide-impregnated bed nets, and long-sleeved shirts and pants to discourage mosquito bites. Environmental modifications to decrease mosquito populations, including insecticide spraying, may be used in some areas. Several vaccines are available for humans. These vaccines are protective for all genotypes. In some countries, vaccination is routine in children. In non-endemic areas, laboratory workers at risk of infection should be vaccinated. Travelers should also be vaccinated before traveling to endemic areas, if they will be in danger of infection. Travelers to rural areas are at higher risk than those who visit only urban regions. The risk also varies with the season, duration of travel, activities and lodgings. There is no treatment other than supportive therapy.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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