JAPANESE ENCEPHALITIS

 AGENT

Japanese encephalitis (JE) virus is a single-stranded RNA virus that belongs to the genusFlavivirus and is closely related to West Nile and Saint Louis encephalitis viruses.

TRANSMISSION

JE virus is transmitted to humans through the bite of an infected mosquito, primarily Culexspecies. The virus is maintained in an enzootic cycle between mosquitoes and amplifying vertebrate hosts, primarily pigs and wading birds. Humans are incidental or dead-end hosts, because they usually do not develop a level or duration of viremia sufficient to infect mosquitoes.

Japanese encephalitis (JE) virus, a flavivirus, is closely related to West Nile and St. Louis encephalitis viruses. JE virus is transmitted to humans through the bite of infected Culex species mosquitoes, particularly Culex tritaeniorhynchus.

The virus is maintained in a cycle between mosquitoes and vertebrate hosts, primarily pigs and wading birds. Humans are incidental or dead-end hosts, because they usually do not develop high enough concentrations of JE virus in their bloodstreams to infect feeding mosquitoes.

JE virus transmission occurs primarily in rural agricultural areas, often associated with rice production and flooding irrigation. In some areas of Asia, these conditions can occur near urban centers.

EPIDEMIOLOGY

JE virus is the most common vaccine-preventable cause of encephalitis in Asia, occurring throughout most of Asia and parts of the western Pacific (Map 3-08). Local transmission of JE virus has not been detected in Africa, Europe, or the Americas. Transmission principally occurs in rural agricultural areas, often associated with rice cultivation and flood irrigation. In some areas of Asia, these ecologic conditions may occur near, or occasionally within, urban centers. In temperate areas of Asia, transmission is seasonal, and human disease usually peaks in summer and fall. In the subtropics and tropics, seasonal transmission varies with monsoon rains and irrigation practices and may be prolonged or even occur year-round.

In endemic countries, where adults have acquired immunity through natural infection, JE is primarily a disease of children. However, travel-associated JE can occur among people of any age. For most travelers to Asia, the risk for JE is extremely low but varies based on destination, duration, season, and activities.

From 1973 through 2011, there were 58 published reports of travel-associated JE among travelers from nonendemic countries. From the time of licensure of a JE vaccine in the United States in 1992 through 2011, only 7 JE cases among US travelers have been reported to CDC.

The overall incidence of JE among people from nonendemic countries traveling to Asia is estimated to be <1 case per 1 million travelers. However, expatriates and travelers who stay for prolonged periods in rural areas with active JE virus transmission are likely at similar risk as the susceptible resident population (5–50 cases per 100,000 children per year). Travelers on even brief trips might be at increased risk if they have extensive outdoor or nighttime exposure in rural areas during periods of active transmission. Short-term (<1 month) travelers whose visits are restricted to major urban areas are at minimal risk for JE. In some endemic areas there are few human cases among residents because of natural immunity among older people or vaccination; however, JE virus is usually still maintained in these areas in an enzootic cycle between animals and mosquitoes. Therefore, susceptible visitors may be at risk for infection.

CLINICAL PRESENTATION

Most human infections with JE virus are asymptomatic; <1% of people infected with JE virus develop clinical disease. Acute encephalitis is the most commonly recognized clinical manifestation of JE virus infection. Milder forms of disease, such as aseptic meningitis or undifferentiated febrile illness, can also occur. The incubation period is 5–15 days. Illness usually begins with sudden onset of fever, headache, and vomiting. Mental status changes, focal neurologic deficits, generalized weakness, and movement disorders may develop over the next few days.

• The classical description of JE includes a parkinsonian syndrome with masklike facies, tremor, cogwheel rigidity, and choreoathetoid movements.
• Acute flaccid paralysis, with clinical and pathological features similar to those of poliomyelitis, has also been associated with JE virus infection.
• Seizures are common, especially among children.
• Common clinical laboratory findings include moderate leukocytosis, mild anemia, and hyponatremia. Cerebrospinal fluid (CSF) typically has a mild to moderate pleocytosis with a lymphocytic predominance, slightly elevated protein, and normal ratio of CSF to plasma glucose.

The case-fatality ratio is approximately 20%–30%. Among survivors, 30%–50% have serious neurologic, cognitive, or psychiatric sequelae.

DIAGNOSIS

JE should be suspected in a patient with evidence of a neurologic infection (such as encephalitis, meningitis, 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 virus infection should be performed by using a JE virus–specific IgM-capture ELISA on CSF or serum. JE virus–specific IgM can be measured in the CSF of most patients by 4 days after onset of symptoms and in serum by 7 days after onset. A ≥4-fold rise in JE virus–specific neutralizing antibodies between acute- and convalescent-phase serum specimens may be used to confirm the diagnosis. Vaccination history, date of onset of symptoms, and information regarding other flaviviruses known to circulate in the geographic area that may cross-react in serologic assays need to be considered when interpreting results.

Humans have low levels of transient viremia and usually have neutralizing antibodies by the time distinctive clinical symptoms are recognized. Virus isolation and nucleic-acid amplification tests are insensitive in detecting JE virus or viral RNA in blood or CSF and should not be used for ruling out a diagnosis of JE.

TREATMENT----There is no specific antiviral treatment forJE; therapy consists of supportive care and management of complications.

PREVENTION------The best way to prevent mosquito borne diseases, including JE, is to avoid mosquito bites.The natural transmission cycle involves Culex tritaeniorhynchus and other Culex mosquitoes, such as Cx. gelidus and Cx. Vishnui, which breed primarily in ricefields and feed on humans in the early evenings.The infected mosquito transmits the virus to humans and animals during biting. The mosquitoes breed where there is abundant water such as rice paddies and become infected by feeding on pigs and wild birds infected with the Japanese encephalitis virus. The disease is not directly transmitted from person to person.Fogging operations with malathion technical is advised to be conducted in these areas where suspected JE cases were occurred to interrupt any further transmission. Technical malathion thermal fogging itself becomes an unavoidable part of vector control in JE outbreak.

Vaccine---There is a vaccine for Japanese encephalitis but it is usually not recommended for members of the general public. The vaccine is only recommended for endemic areas in Asia and Western Pacific Region, particularly in rural areas.