Japanese encephalitis

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Japanese B encephalitis
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Japanese encephalitis
Other namesJapanese B encephalitis
Supportive care[1]
PrognosisPermanent neurological problems occur in up to half of survivors[2]
Frequency68,000[2]
Deaths17,000[2]

Japanese encephalitis (JE) is an infection of the brain caused by the Japanese encephalitis virus (JEV).[3] While most infections result in little or no symptoms, occasional inflammation of the brain occurs.[3] In these cases, symptoms may include headache, vomiting, fever, confusion and seizures.[1] This occurs about 5 to 15 days after infection.[1]

JEV is generally spread by

Pigs and wild birds serve as a reservoir for the virus.[2] The disease occurs mostly outside of cities.[2] Diagnosis is based on blood or cerebrospinal fluid testing.[2]

Prevention is generally achieved with the

care being supportive.[1] This is generally carried out in a hospital.[1] Permanent problems occur in up to half of people who recover from JE.[2]

The disease primarily occurs in

outbreaks.[2] The disease was first described in Japan in 1871.[2][4]

Signs and symptoms

The Japanese encephalitis virus (JEV) has an incubation period of 2 to 26 days.[5] The vast majority of infections are asymptomatic: only 1 in 250 infections develop into encephalitis.[6]

Severe rigors may mark the onset of this disease in humans. Fever, headache and

non-specific symptoms of this disease which may last for a period of between 1 and 6 days. Signs which develop during the acute encephalitic stage include neck rigidity, cachexia, hemiparesis, convulsions and a raised body temperature between 38–41 °C (100.4–105.8 °F). The mortality rate of the disease is around 25% and is generally higher in children under five, the immuno-suppressed and the elderly. Transplacental spread has been noted. Neurological disorders develop in 40% of those who survive with lifelong neurological defects such as deafness, emotional lability and hemiparesis occurring in those who had central nervous system involvement.[7]

Japanese encephalitis virus enters the brain through two ways and leads to infection of neurons and encephalitis

Increased

excitatory neurotransmitters, prostaglandin, reactive oxygen, and nitrogen species are secreted by activated microglia.[citation needed
]

In a

chemokines from different brain regions during a progressive Japanese encephalitis infection was also observed.[citation needed
]

Although the net effect of the proinflammatory mediators is to kill infectious organisms and infected cells as well as to stimulate the production of molecules that amplify the mounting response to damage, it is also evident that in a nonregenerating organ such as the brain, a dysregulated innate immune response would be deleterious. In JE the tight regulation of microglial activation appears to be disturbed, resulting in an autotoxic loop of microglial activation that possibly leads to bystander neuronal damage.[8] In animals, key signs include infertility and abortion in pigs, neurological disease in horses, and systemic signs including fever, lethargy and anorexia.[9]

Cause

It is a disease caused by the

Japanese encephalitis virus (JEV).[10]

Virology

Japanese encephalitis virus
Flavivirus structure and genome
Virus classification Edit this classification
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Kitrinoviricota
Class: Flasuviricetes
Order: Amarillovirales
Family: Flaviviridae
Genus: Flavivirus
Species:
Japanese encephalitis virus

JEV is a virus from the family

St. Louis encephalitis virus. The positive sense single-stranded RNA genome is packaged in the capsid which is formed by the capsid protein. The outer envelope is formed by envelope protein and is the protective antigen. It aids in entry of the virus into the cell. The genome also encodes several nonstructural proteins (NS1, NS2a, NS2b, NS3, N4a, NS4b, NS5). NS1 is produced as a secretory form also. NS3 is a putative helicase, and NS5 is the viral polymerase. It has been noted that Japanese encephalitis infects the lumen of the endoplasmic reticulum (ER)[12][13]
and rapidly accumulates substantial amounts of viral proteins.

Based on the envelope gene, there are five genotypes (I–V). The Muar strain, isolated from a patient in Malaya in 1952, is the prototype strain of genotype V. Genotype V is the earliest recognized ancestral strain.[14] The first clinical reports date from 1870, but the virus appears to have evolved in the mid-16th century. Over sixty complete genomes of this virus had been sequenced by 2010.[citation needed]

Diagnosis

Japanese encephalitis is diagnosed by commercially available tests detecting JE virus-specific IgM antibodies in serum and/or cerebrospinal fluid, for example by IgM capture ELISA.[15]

JE virus IgM antibodies are usually detectable 3 to 8 days after onset of illness and persist for 30 to 90 days, but longer persistence has been documented. Therefore, positive IgM antibodies occasionally may reflect a past infection or vaccination. Serum collected within 10 days of illness onset may not have detectable IgM, and the test should be repeated on a convalescent sample. For patients with JE virus IgM antibodies, confirmatory neutralizing antibody testing should be performed.[16] Confirmatory testing in the US is available only at the CDC and a few specialized reference laboratories. In fatal cases, nucleic acid amplification and virus culture of autopsy tissues can be useful. Viral antigen can be shown in tissues by indirect fluorescent antibody staining.[9]

Prevention

Japanese encephalitis vaccine "ENCEVAC" in the Japanese language

Infection with Japanese encephalitis confers lifelong

vaccines available: SA14-14-2, IXIARO (IC51, also marketed in Australia, New Zealand as JESPECT and India as JEEV[17]) and ChimeriVax-JE (marketed as IMOJEV).[18] All current vaccines are based on the genotype III virus.[citation needed
]

A

formalin-inactivated mouse-brain-derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s. The widespread use of vaccine and urbanization has led to control of the disease in Japan and Singapore. The high cost of this vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunization program.[10]

The most common adverse effects are redness and pain at the injection site. Uncommonly, an

autoimmune neurological complications of around 1 per million vaccinations.[19] However where the vaccine is not produced in mouse brains but in vitro using cell culture there are few adverse effects compared to placebo, the main side effects being headache and myalgia.[20]

The neutralizing antibody persists in the circulation for at least two to three years, and perhaps longer.[21][22] The total duration of protection is unknown, but because there is no firm evidence for protection beyond three years, boosters are recommended every three years for people who remain at risk.[23] Furthermore, there are no data available regarding the interchangeability of other JE vaccines and IXIARO.[citation needed]

Treatment

There is no specific treatment for Japanese encephalitis and treatment is supportive,

transmission from person to person and therefore patients do not need to be isolated.[citation needed
]

A breakthrough in the field of Japanese encephalitis therapeutics is the identification of

transcriptomic study provides a hypothesis of neuroinflammation and a new lead in development of appropriate therapies for Japanese encephalitis.[26][27]

The effectiveness of

intravenous immunoglobulin for the management of encephalitis is unclear due to a lack of evidence.[28] Intravenous immunoglobulin for Japanese encephalitis appeared to have no benefit.[28]

Epidemiology

Disability-adjusted life year for Japanese encephalitis per 100,000 inhabitants in 2002
  no data
  less than 1
  1–5
  5–10
  10–15
  15–20
  20–25
  25–30
  30–35
  35–40
  40–45
  45–50
  more than 50

Japanese encephalitis (JE) is the leading cause of viral encephalitis in Asia, with up to 70,000 cases reported annually.[29] Case-fatality rates range from 0.3% to 60% and depend on the population and age. Rare outbreaks in U.S. territories in the Western Pacific have also occurred. Residents of rural areas in endemic locations are at highest risk; Japanese encephalitis does not usually occur in urban areas.[citation needed]

Countries which have had major epidemics in the past, but which have controlled the disease primarily by vaccination, include China, South Korea, Singapore, Japan, Taiwan and Thailand. Other countries that still have periodic epidemics include Vietnam, Cambodia, Myanmar, India, Nepal, and Malaysia. Japanese encephalitis has been reported in the Torres Strait Islands, and two fatal cases were reported in mainland northern Australia in 1998. There were reported cases in Kachin State, Myanmar in 2013. There were 116 deaths reported in Odisha's Malkangiri district of India in 2016.[citation needed]

In 2022, the notable increase in distribution of the virus in Australia due to climate change became a concern to health officials as the population has limited immunity to the disease and the presence of large numbers of farmed and feral pigs could act as reservoirs for the virus.[7] In February 2022, Japanese encephalitis was detected and confirmed in piggeries in Victoria, Queensland and New South Wales. On 4 March, cases were detected in South Australia. By October 2022, the outbreak in eastern mainland Australia had caused 42 symptomatic human cases of the disease, resulting in seven deaths.[30][31]

Humans, cattle, and horses are dead-end hosts as the disease manifests as fatal encephalitis. Pigs act as an amplifying host and have a very important role in the epidemiology of the disease. Infection in swine is asymptomatic, except in pregnant sows, when abortion and fetal abnormalities are common sequelae. The most important vector is Culex tritaeniorhynchus, which feeds on cattle in preference to humans. The natural hosts of the Japanese encephalitis virus are birds, not humans, and many believe the virus will therefore never be eliminated.[32] In November 2011, the Japanese encephalitis virus was reported in Culex bitaeniorhynchus in South Korea.[33]

Recently, whole genome

neurons infected with the Japanese encephalitis virus has shown that neurons play an important role in their own defense against Japanese encephalitis infection. Although this challenges the long-held belief that neurons are immunologically quiescent, an improved understanding of the proinflammatory effects responsible for immune-mediated control of viral infection and neuronal injury during Japanese encephalitis infection is an essential step for developing strategies for limiting the severity of CNS disease.[34]

A number of drugs have been investigated to either reduce viral replication or provide neuroprotection in cell lines or studies upon mice. None are currently advocated in treating human patients.

Evolution

It is theorized that the virus may have originated from an ancestral virus in the mid-1500s in the Malay Archipelago region and evolved there into five different genotypes which spread across Asia.[41] The mean evolutionary rate has been estimated to be 4.35×10−4 (range: 3.49×10−4 to 5.30×10−4) nucleotide substitutions per site per year.[41]

References

  1. ^ a b c d e f g "Symptoms and Treatment". CDC. August 2015. Archived from the original on 17 June 2017. Retrieved 29 October 2017.
  2. ^ a b c d e f g h i j k l m n o p q "Japanese encephalitis". World Health Organization. December 2015. Archived from the original on 13 July 2017. Retrieved 29 October 2017.
  3. ^ a b "Japanese Encephalitis". CDC. August 2015. Archived from the original on 24 May 2017. Retrieved 29 October 2017.
  4. ^ "Japanese encephalitis - Causes". 6 February 2019.
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  7. ^ a b Davey, Melissa (8 March 2022). "What is Japanese encephalitis and why is it spreading in Australia?". The Guardian Australia. Retrieved 20 October 2022.
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  9. ^ a b Japanese Encephalitis Virus Archived 18 July 2013 at the Wayback Machine reviewed and published by WikiVet, accessed 11 October 2011.
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  17. ^ "Jeev an inactivated Japanese Encephalitis vaccine launched in Hyderabad". pharmabiz.com. 15 September 2012. Archived from the original on 23 October 2012. Retrieved 11 January 2013.
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  25. ^ Japanese encephalitis~treatment at eMedicine
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  30. ^ Australian Government Department of National pest & disease outbreaks (March 2022). "Japanese encephalitis". {{cite journal}}: Cite journal requires |journal= (help)
  31. ^ "Japanese encephalitis virus". Australian Government Department of Health and Aged Care. Retrieved 20 October 2022.
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External links