Japanese encephalitis

Preferred Scientific Name

• Japanese encephalitis

Other Scientific Names

• Japanese B encephalitis

International Common Names

• English: hydranencephaly with or without cerebellar lesions in ruminants; japanese b encephalitis in pigs- exotic

English acronym

• JE

Japanese encephalitis (JE) is a re-emerging mosquito-borne viral disease in animals and humans. Many domestic and wild animals are susceptible to the JE virus. The virus causes various forms of reproductive failures in pregnant sows, and lesions in the central nervous system (CNS) in horses. In other animals, infection is usually subclinical. Japanese encephalitis is one of the most common mosquito-borne diseases of the human central nervous system, epidemics having been recorded in Japan, South Korea, and India. Pigs are considered the most important natural amplifying animal for the virus. Episodes of human infection occur annually during the mosquito season. Disease in most people is subclinical or mild, but fatal encephalitis develops in some children.

This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. For further information on this disease from OIE, see the website: www.oie.int.

Major pathologic lesions have not been found in pigs infected with JEV. However, various abnormalities have been observed in litters from dams infected with the virus during pregnancy. Gross pathologic lesions noted in stillborn or weak neonatal piglets include hydrocephalus, subcutaneous oedema, hydrothorax, ascites, petechial haemorrhages on serous membranes, congestion of lymph nodes, necrotic foci in liver and spleen, and congested meninges or spinal cord (Burns, 1950). Cerebellar hypoplasia and spinal hypomyelinogenesis have also been described (Morimoto, 1969).

Histopathologically, significant lesions in affected piglets or stillborn pigs are restricted to the central nervous system (CNS). Most CNS lesions, mainly involving the cortex, basal ganglion, brain stem, and spinal cord, occur in pigs up to 6 months of age. Perivascular cuffing and scattered neuronal degeneration and necrosis are found in the cerebrum and cerebellum in pigs. Neuronal degeneration is prominent in the grey matter and Purkinje layers.

Pathologic changes in the testes in association with JEV infection are described (Hashimura et al., 1976; Ogasa et al., 1977). In naturally affected pigs, a large amount of mucous fluid is observed in the cavity tunica vaginalis, as well as fibrous thickening along the edge of the epididymis and the visceral layer of the tunica vaginalis. Microscopically, such testicles show oedema and inflammatory changes, with cellular infiltrations in the interstitial tissue of the epididymis and tunica vaginalis. Cell infiltration and haemorrhage are also evident in the interstitial tissue of the testes.

Pigs become infected with JEV via the bites of mosquitoes carrying the virus. Infected pigs develop viremia, which persists for approximately 12 hours to a few days. After the initial viremia, the virus disseminates to vascular tissues such as the liver, spleen, and muscle, where further replication augments the viremia. The virus enters the central nervous system via: cerebral spinal fluid; endothelial cell-, macrophage-, or lymphocyte infection; or a haematogenous route. In humans and mice, JEV infects and destroys neurons selectively, mostly in the areas of brain stem, thalamus, basal ganglion, and lower layer of cortex. In mosquitoes, JEV infection is noncytopathic.

Transplacental infection of JEV has been reported in pigs (Shimizu et al., 1954). In pregnant pigs, foetuses may become infected during the viremic period. Experimentally, after intravenous infection of pregnant pigs with JEV, virus is recoverable from foetuses as early as 7 days post-infection. In some animals, the virus fails to cross the placenta. Successful transplacental infection may depend on the time of gestation at which the dam was infected or on the strain of virus. When infection of pregnant dams takes place in the mid-third of gestation, transplacental infection and pathogenic effects are more obvious. Field observations show that fetal death and mummification are associated with JEV infection of dams between 40 and 60 days of gestation; fetuses from the gilts infected after 85 days gestation were little affected.

In nature, infection with JEV is maintained cyclically, involving vector mosquitoes (principally Culex spp. mosquitoes; Culex tritaeniorhynchus is important as it has a wide host range), birds, and mammals. Pigs are central in JE epidemiology, not only for virus maintenance and amplification, but also in transmission to humans (Ladreyt et al., 2019). A correlation between infection in pigs and infection in humans is apparent, with evidence indicating that swine play an important role in the build-up of the virus within a population. In enzootic zones, pigs are favoured feeding sources for mosquitoes. Consistent development of viremia in susceptible pigs ensures a continued supply of infected mosquitoes. Epidemiologic patterns may differ among areas of South-East Asia, as the activity of the vector mosquitoes is modified by differing climatic conditions.

Other animals and many different mosquito species (mainly Culex spp., but others have been implicated) could alter infection cycles and are factors involved in the transmission of JEV (Chang and Kim, 1966; Sazawa, 1968; Hasegawa et al., 1975). Wild birds, especially herons and egrets, are able to maintain the virus (Mansfield et al., 2017).

Vector-free transmission of JEV between pigs has been described (Ricklin et al., 2016). Under experimental conditions, needle-infected pigs shed virus in oronasal emissions and transmitted virus to co-housed uninfected pigs. This has not been demonstrated under natural conditions but could provide a mechanism for rapid spread of JEV through intensively farmed pig herds and enable transmission of disease during vector-free periods (Mansfield et al., 2017).

Japanese encephalitis virus is primarily a cause of human encephalitis. However, livestock losses in the form of fetal abnormalities and death can reduce the productivity of pig farms (Mansfield et al., 2017). Reproductive losses in pigs can reach 50-70%, with abortions in sows (stillbirths or mummified fetuses, usually at term) and reduced number and motility of sperm in boars. Mortality in non-immune, infected piglets can approach 100%, but the mortality is near zero in adult swine (OIE, 2019). Prevention of disease in livestock, particularly pigs, is primarily through vaccination although this imposes a cost on farmers that prevent its application in many parts of Asia (Mansfield et al., 2017).

JEV is the main cause of viral encephalitis in many countries of Asia with an estimated 68,000 clinical cases every year. JE primarily affects children. Most adults in endemic countries have natural immunity after childhood infection, but individuals of any age may be affected. Although most JEV infections are mild (fever and headache) or without apparent symptoms, approximately 1 in 250 infections results in severe clinical illness. The case-fatality rate among those with encephalitis can be as high as 30%. Permanent neurologic or psychiatric sequelae can occur in 30-50% of those with encephalitis (WHO, 2019). Safe and effective JE vaccines are available to prevent disease in endemic countries (WHO, 2019).

Only palliative care is available to treat affected animals (Mansfield et al., 2017).

There is no antiviral treatment for human patients with JE. Treatment is supportive to relieve symptoms and stabilize the patient (WHO, 2019).