Japanese encephalitis (JE)

Occurrence: Asia, notifiable in many countries.
Age affected: All ages, human risk.
Causes: Japanese encephalitis virus.
Effects: Sudden death, fever, nervous signs, abortion, mummies, stillbirths, weak piglets, boar infertility.


Japanese B encephalitis is caused by a small RNA virus, a flavivirus 40 nm in diameter. It has been defined antigenically and by restriction endonuclease techniques (techniques which cut nucleic acid and demonstrate fragments). It is extremely unstable outside the body and is rapidly inactivated by disinfectants, heat and extremes of pH. It grows well in cell culture. Infection results from mosquito bites and is followed by viraemia. The central nervous system may be affected but the major effects result from infection of the testis and the development of orchitis and multiplication in the foetus between 40 and 60 days’ gestation to cause foetal death. Virus may persist in spleen macrophages and has been demonstrated by RT-PCR (a Polymerase Chain Reaction) during winter when virus cannot be isolated from the pig. Infection may be transmitted in semen. 

Mode of transmission

Infection results from mosquito bites principally Culex tritaeniorhynchus but other mosquito species may be involved (C. vishnui, India, C. annulirostris, Torres Straits). Infection may be transmitted in semen. Wild birds and the pig may be reservoirs of infection which can then be transmitted to humans.

Clinical signs

Clinical signs may follow infection in piglets but it is normally asymptomatic. The major effects are on numbers born alive which are reduced. Mummified foetuses, stillborn and weak pigs are produced. Boars lose libido, develop abnormal semen and azoospermia as a result of testicular infections.

Japanese B encephalitis should be considered as a potential cause of small litters, the birth of mummified piglets and semen abnormalities occurring in South East Asia in the mosquito season. Its presence in an area may result in human cases which stimulate investigation of nearby pig populations. Antibody can be detected in the blood of infected pigs by haemagglutination inhibition and by ELISA tests, but may not be diagnostic in vaccinated animals. Confirmation of diagnosis is by demonstration of the virus in the mummified and stillborn foetuses. Presence of the virus in an area may be confirmed from pooled mosquito material or by the use of sentinel pigs which develop the infection and seroconvert (develop rising antibody levels to the virus).

Postmortem lesions

Mummified and stillborn foetuses born to infected sows are the material usually examined. Stillborn piglets may be oedematous and neuronal changes may be present. The virus may be isolated from them or demonstrated in their tissues by serological methods. RT-PCR and nested RT-PCR (variations on the Polymerase Chain Reaction) can detect nucleic acid sequences even when the virus cannot be isolated.

Treatment and prevention

There is no treatment. The reproductive effects on productivity resulting from boar infertility may be reduced by supplementing natural mating by artificial insemination from uninfected boars and by regular screening of boars for semen quality. Live attenuated virus vaccines should be given to breeding stock twice 2-3 weeks before the start of the mosquito season. Killed, oil adjuvanted vaccines have been described. Semen from affected boars should not be used. The risk to man is such that those working with pigs in an infected area should be vaccinated.

Special note

This virus is transmissible to humans, workers in affected areas should be vaccinated and suspect material in laboratories handled in containment. This disease is notifiable and suspicion of it should be reported to the state veterinarian.