Japanese encephalitis

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By Medifit Education



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Japanese encephalitis: A mosquito-borne flavi virus infection that is the leading cause of viral encephalitis in Asia. Japanese encephalitis virus cannot be transmitted from person-to-person. The Japanese encephalitis virus is related to the viruses of St. Louis encephalitis and Murray Valley encephalitis and to the West Nile virus. Infection leads to overt encephalitis in only 1 of 20 to 1,000 cases, and a vaccine is available. Travelers to Asia from non-endemic countries have a very low risk of infection (less than 1 case per million travelers).


Japanese encephalitis is caused by a flavivirus, which can affect both humans and animals. The virus is passed from animals to humans through the bite of an infected mosquito.

Pigs and wading birds are the main carriers of the Japanese encephalitis virus. A mosquito becomes infected after sucking the blood from an infected animal or bird. If you get bitten by an infected mosquito, it can pass on the virus.

The mosquitoes that carry Japanese encephalitis usually breed in rural areas, particularly where there are flooded rice fields or marshes, although infected mosquitoes have also been found in urban areas. They usually feed between sunset and sunrise.

Japanese encephalitis cannot be passed from person to person.

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On a cellular level, after attachment of the Japanese encephalitis virus (JEV) to a host cell membrane, local membrane disruption may lead to entry of the virus into the cell itself. Subsequently, viremia develops, leading to inflammatory changes in the heart, lungs, liver, and reticuloendothelial system. Most infections are cleared before the virus can invade the central nervous system (CNS), leading to subclinical disease.

Subclinical or mild forms of Japanese encephalitis resolve in a few days if the CNS is not involved. In such cases, the infection may not produce symptoms and therefore remains undetected. However, given the neurotropic character of JEV, neurologic invasion can develop, possibly by growth of the virus across vascular endothelial cells, leading to involvement of large areas of the brain, including the thalamus, basal ganglia, brain stem, cerebellum (especially the destruction of the cerebellar Purkinje cells), hippocampus, and cerebral cortex. Persistent infection and congenital transmission may occur. The levels of varying immune response (intrinsic, cellular, humoral) have been characterized. Higher levels of certain cytokines (interferon-alpha, interleukins 6 and 8) have been associated with an increased mortality risk. The types of response implicate impaired T-helper-cell immunity in patients with severe advanced disease.

Overall, JEV is believed to result in increased CNS pathology because of its direct neurotoxic effects in brain cells and its ability to prevent the development of new cells from neural stem/progenitor cells (NPCs). JEV likely represents the first mosquito-transmitted viral pathogen to affect neural stem cells. These cells can serve important roles in injury recovery; consequently, Japanese encephalitis–induced disruption of neural stem cell growth may be particularly important to further morbidity and mortality.

Recent studies indicate that other CNS cells besides neurons, such as astrocytes and microglial cells, may have replicative viral infection due to JEV, resulting in potential damage to the blood-brain barrier as well.

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In most people, the Japanese encephalitis virus causes either no symptoms or mild, short-lived symptoms, which are often mistaken for flu.

Only around 1 in every 250 people who become infected develops more obvious symptoms of Japanese encephalitis. This usually happens between 5 and 15 days after infection.

Initial symptoms of infection can include:

  • a high temperature (fever)
  • headache
  • feeling and being sick
  • diarrhoea
  • muscle pain

In some cases, these initial symptoms may be followed a few days later by more serious problems, as the infection spreads to the brain. This is known as encephalitis and it can cause more wide-ranging symptoms, such as:

  • seizures (fits)
  • stiff neck
  • muscle weakness
  • changes in mental state – which can range from mild confusion to being very agitated or slipping into a coma
  • uncontrollable shaking of body parts (tremor)
  • inability to speak
  • paralysis (inability to move certain body parts)

Up to one in every three people who develop these more serious symptoms will die as a result of the infection.

In those who survive, these symptoms tend to slowly improve. However, it can take several months to make a full recovery and up to half of those who do survive are left with permanent brain damage. This can lead to long-term problems such as tremors and muscle twitches, personality changes, muscle weakness, learning difficulties and paralysis in one or more limbs.

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Japanese encephalitis (JE) should be considered in a patient with evidence of a neurologic infection (e.g., meningitis, encephalitis, or acute flaccid paralysis) who has recently traveled to or resided in an endemic country in Asia or the western Pacific.

Laboratory diagnosis of JE is generally accomplished by testing of serum or cerebrospinal fluid (CSF) to detect virus-specific IgM antibodies. JE virus IgM antibodies are usually detectable 3 to 8 days after onset of illness and persist for 30 to 90 days, but longer persistence has been documented. Therefore, positive IgM antibodies occasionally may reflect a past infection or vaccination. Serum collected within 10 days of illness onset may not have detectable IgM, and the test should be repeated on a convalescent sample. For patients with JE virus IgM antibodies, confirmatory neutralizing antibody testing should be performed. In fatal cases, nucleic acid amplification, histopathology with immunohistochemistry, and virus culture of autopsy tissues can also be useful.


If you have any of the symptoms of Japanese encephalitis and have recently visited, or are still in, an area where the infection is found, you should seek immediate medical advice.



By Medifit Education