Japanese encephalitis

Ravindra Kumar Garg MD (Dr. Garg of King George's Medical University in Lucknow, India, has no relevant financial relationships to disclose.)
John E Greenlee MD, editor. (Dr. Greenlee of the University of Utah School of Medicine received an honorarium from Merck for authorship.)
Originally released August 17, 2000; last updated July 21, 2016; expires July 21, 2019

This article includes discussion of Japanese encephalitis, Japanese B encephalitis, and Japanese encephalitis virus myelitis. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

The Japanese encephalitis virus is a flavivirus and a mosquito-borne human pathogen. It is the most important cause of viral encephalitis. Japanese encephalitis may cause diffuse encephalitis. Japanese encephalitis is the most important cause of viral encephalitis in many countries of Asia, with nearly 68,000 clinical cases every year. The case-fatality rate can be as high as 30%. Permanent neurologic or psychiatric sequelae can occur in 30% to 50% of patients. Children are more frequently and severely affected. Several reports describe increasing numbers of cases of Japanese encephalitis among Western travelers returning from Asia. A observation noted that TLR3 gene polymorphism might confer host genetic susceptibility to Japanese encephalitis in Indian population. The clinical features of Japanese encephalitis virus infection range from a nonspecific flu-like illness to a severe and often fatal meningoencephalomyelitis. MRI characteristically shows high-signal lesions in the thalamus and substantia nigra. In endemic countries, positivity of serological tests in cerebrospinal fluid, both for dengue virus and Japanese encephalitis, has been described. No specific antiviral therapy is available for Japanese encephalitis. Treatment is mainly supportive and symptomatic. Intravenous immunoglobulin has been shown to augment the development of neutralizing antibodies in Japanese encephalitis patients, and it may be used as therapeutic agent in the future. Vaccination of the population at risk is the method of choice for prevention. The inactivated mouse brain-derived (IMB) vaccines have now been replaced by cell culture-based vaccines. In this article, the author has reviewed in detail the various aspects of Japanese encephalitis.

Key points

 

• Japanese encephalitis virus is a neurotropic flavivirus that is the causative agent of the major mosquito-borne encephalitis in the world.

 

• Among 68,000 annual cases of Japanese encephalitis, approximately 30% die, and up to 50% of survivors may have sequelae.

 

• Japanese encephalitis, in the endemic areas, is regarded as a disease of children.

 

• Japanese encephalitis dominantly affects the thalamus, corpus striatum, brainstem, and spinal cord.

 

• Japanese encephalitis manifests with altered sensorium, seizures, and focal neurologic deficit.

 

• In the absence of effective antiviral therapy, Japanese encephalitis treatment is symptomatic and supportive.

 

• The main measure for Japanese encephalitis prevention is the use of a live attenuated vaccine for humans.

Historical note and terminology

Since the end of the 19th century, Japanese encephalitis has been recognized as a scourge of the orient. Epidemics of encephalitis have been described in Japanese literature since 1870, with thousands of cases recorded in some years. In 1933 a filterable agent was transferred from the brain of a fatal case and used to cause encephalitis in monkeys; the virus was then isolated in 1935. The term “Japanese B encephalitis” was used originally to distinguish these summer epidemics from Von Economo's “encephalitis lethargica” (labeled type A) (Innis 1995). The term “B” has since been dropped. The virus was subsequently classed as a member of the genus flavivirus (family Flaviviridae), named after the prototype Yellow fever virus (in Latin, flavus means yellow). Although of no taxonomic significance, the ecological term “arbovirus” is often used to describe the fact that Japanese encephalitis virus is arthropod (insect) borne. A vaccine developed by Albert Sabin (later of poliomyelitis fame) and others during World War II has been available for 30 years. Despite the existence of this vaccine, Japanese encephalitis has grown as a problem in the last 50 years because of its geographical spread and increased incidence.

Image: CDC Health Information for International Travel 2012 - Japanese encephalitis
The disease threatens both residents and travelers in endemic areas and is one of the most important emerging arboviruses (Solomon and Cardosa 2000).

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