Japanese B Encephalitis

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Japanese B encephalitis is an exotic, mosquito-borne disease affecting many animals, including wild birds, horses, swine and people. In swine, the only evidence of disease may be reproductive failure.


Japanese B encephalitis (JE) occurs in most domestic animals; also in wild birds, reptiles, perhaps chickens, and people. Swine can be infected and all ages are susceptible. Major epidemics have occurred in horses, donkeys and people.

Japanese encephalitis is confined largely to southeastern Asia, Indonesia, and major Pacific islands. At least 20 countries have reported occurrence of the disease. In many locales, epidemics correlate with the mosquito season.

Historical information

Japanese encephalitis was first described in 1933. Major epidemics in people have been reported from Japan, Korea, India and Nepal. The disease has not been reported in the western hemisphere. Abortion in women, and encephalitis in children, have been caused by JE so the virus is recognized as an important zoonosis.


The etiologic agent is a single-stranded RNA Flavivirus and is related to West Nile virus. It is unstable in the environment and easily inactivated by many disinfectants. The virus can be grown in many cell culture systems, including cells derived from embryonic or larval mosquito tissues.


Mosquitoes become infected by feeding on viremic hosts. The virus is then transmitted through the mosquitoes’ saliva when they subsequently feed on uninfected people or animals. The virus is transmitted mainly by mosquitoes of three genera (Aedes, Culex, and Anopheles) and can be transmitted vertically in some species of mosquitoes. Infected mosquitoes feed on a wide range of mammals, birds and reptiles. Infected pigs become viremic and are a major source of virus for mosquitoes. Often there is a correlation between outbreaks in people and the concurrent presence of infected mosquitoes and swine in the region. Other known or suspected reservoirs include snakes, lizards, many wild birds and chickens.


Infected pigs remain viremic for several days. On the basis of research largely in other animals, the virus is believed to induce suppressor T-cells to produce a factor that suppresses humoral and cell mediated responses. This makes animals less resistant to infection. In porcine fetuses, the virus often causes the development of anomalies in the brain as well as encephalitis and degenerative neuronal changes.

Transplacental infection in swine sometimes occurs. The effect of the virus depends on whether the fetuses are immunologically competent. When dams are infected between 40-60 days in gestation, fetuses often are killed and some are mummified. There may be no effect on fetuses if they are 85 or more days in gestation. Fetal deaths are believed to be caused by destruction of vital stem cells.

Clinical signs

Mature swine seldom show signs of infection other than those of reproductive failure. Signs may occur in fetuses or piglets if their dam was infected during pregnancy. Signs include stillborn and mummified fetuses or weak pigs that may have signs of central nervous system (CNS) disease. Subcutaneous edema and hydrocephalus may be present in stillborn pigs. Abortions seldom occur. Infected boars may have orchitis, reduced libido and disturbance of spermatogenesis. Young, susceptible pigs occasionally contract JE and show signs of CNS lesions.


Gross lesions in stillborn or weak, infected piglets include hydrocephalus, subcutaneous edema, ascites, hydrothorax, hemorrhages on serous membranes, congestion of lymph nodes and necrotic foci in the liver and spleen. Other lesions may include congested meninges, hypoplastic areas in the cerebral cortex, hypoplasia of the cerebellum or spinal hypomyelinogenesis.

Histologically, in infected fetuses or piglets there is diffuse nonsuppurative encephalitis, neuronal degeneration and necrosis in the cerebrum and cerebellum. In mature boars there is excessive fluid in the tunica vaginalis, orchitis, epididymitis, and degenerative changes in seminiferous epithelium.


A definitive diagnosis is often based on isolation and identification of the virus from fetuses or infected piglets. Virus usually is isolated from brain extracts inoculated into suckling mice or cell cultures. Virus can be identified by neutralization tests in suckling mice or cell culture. Alternatively, viral antigen in tissues from infected fetuses or stillborn pigs can be identified by fluorescent antibody (FA) or avidin-biotin staining using formalin-fixed tissues treated with trypsin. In suspected outbreaks, serial serum samples from pigs sometimes are used to show a rising titer against JE. Serologic tests that reveal antibody in fetuses also are useful in diagnosis.


It may be possible to break the cycle of infection by controlling mosquito populations, but this often is impractical. The disease can be controlled by vaccinating the breeding stock; vaccines are common in parts of Asia. Young gilts and boars are vaccinated twice at two to three week intervals prior to the mosquito season. Growing pigs are also vaccinated in endemic areas.