Japanese encephalitis

Japanese encephalitis

Japanese encephalitis

Japanese encephalitis virus JEV is the most important cause of viral encephalitis in Asia. It is a mosquito-borne flavivirus, and belongs to the same genus as dengue, yellow fever and West Nile viruses.

The first case of Japanese encephalitis viral disease (JE) was documented in 1871 in Japan.

The annual incidence of clinical disease varies both across and within endemic countries, ranging from 10 per 100 000 population or higher during outbreaks.

A literature review estimates nearly 68 000 clinical cases of JE globally each year, with approximately 13 600 to 20 400 deaths. JE primarily affects children.

Most adults in endemic countries have natural immunity after childhood infection, but individuals of any age may be affected.

Most JEV infections are mild (fever and headache) or without apparent symptoms, but approximately 1 in 250 infections results in severe clinical illness. The incubation period is between 4-14 days.

In children, gastrointestinal pain and vomiting may be the dominant initial symptoms. Severe disease is characterized by rapid onset of high fever, headache, neck stiffness, disorientation, coma, seizures, spastic paralysis and ultimately death.

The case-fatality rate can be as high as 30% among those with disease symptoms.

Of those who survive, 20%–30% suffer permanent intellectual, behavioural or neurological sequelae such as paralysis, recurrent seizures or the inability to speak.

24 countries in the WHO South-East Asia and Western Pacific regions have JEV transmission risk, which includes more than 3 billion people.

JEV is transmitted to humans through bites from infected mosquitoes of the Culex species (mainly Culex tritaeniorhynchus). Humans, once infected, do not develop sufficient viraemia to infect feeding mosquitoes.

The virus exists in a transmission cycle between mosquitoes, pigs and/or water birds (enzootic cycle).

The disease is predominantly found in rural and periurban settings, where humans live in closer proximity to these vertebrate hosts.

In most temperate areas of Asia, JEV is transmitted mainly during the warm season, when large epidemics can occur. In the tropics and subtropics, transmission can occur year-round but often intensifies during the rainy season and pre-harvest period in rice-cultivating regions.

Individuals who live in or have travelled to a JE-endemic area and experience encephalitis are considered a suspected JE case. A laboratory test is required in order to confirm JEV infection and to rule out other causes of encephalitis.

WHO recommends testing for JEV-specific IgM antibody in a single sample of cerebrospinal fluid (CSF) or serum, using an IgM-capture ELISA.

Testing of CSF sample is preferred to reduce false-positivity rates from previous infection or vaccination
Surveillance of the disease is mostly syndromic for acute encephalitis syndrome.

Confirmatory laboratory testing is often conducted in dedicated sentinel sites, and efforts are undertaken to expand laboratory-based surveillance. Case-based surveillance is established in countries that effectively control JE through vaccination.

There is no antiviral treatment for patients with JE. Treatment is supportive to relieve symptoms and stabilize the patient.

Safe and effective JE vaccines are available to prevent disease. WHO recommends having strong JE prevention and control activities, including JE immunization in all regions where the disease is a recognized public health priority, along with strengthening surveillance and reporting mechanisms.

Even if the number of JE-confirmed cases is low, vaccination should be considered where there is a suitable environment for JE virus transmission. There is little evidence to support a reduction in JE disease burden from interventions other than the vaccination of humans.

Thus, vaccination of humans should be prioritized over vaccination of pigs and mosquito control measures.

There are 4 main types of JE vaccines currently in use: inactivated mouse brain-derived vaccines, inactivated Vero cell-derived vaccines, live attenuated vaccines, and live recombinant (chimeric) vaccines.

Over the past years, the live attenuated SA14-14-2 vaccine manufactured in China has become the most widely used vaccine in endemic countries, and it was prequalified by WHO in October 2013.

Cell-culture based inactivated vaccines and the live recombinant vaccine the yellow fever vaccine strain have also been licensed and WHO-prequalified.

In November 2013, Gavi opened a funding window to support JE vaccination campaigns in eligible countries.

To reduce the risk for JE, all travellers to Japanese encephalitis-endemic areas should take precautions to avoid mosquito bites. Personal preventive measures include the use of mosquito repellents, long-sleeved clothes, coils and vaporizers. Travellers spending extensive time in JE endemic areas are recommended to get vaccinated before travel.

Major outbreaks of JE occur every 2-15 years. JE transmission intensifies during the rainy season, during which vector populations increase.

However, there has not yet been evidence of increased JEV transmission following major floods or tsunamis.

The spread of JEV in new areas has been correlated with agricultural development and intensive rice cultivation supported by irrigation programmes.

WHO responds to JE by:

  • providing global recommendations for JE control, including the use of vaccines. WHO recommends JE immunization in all regions where the disease is a recognized public health priority and supports implementation.
  • providing technical support for JE surveillance, JE vaccine introduction and large-scale JE vaccination campaigns, and evaluation of JE vaccine effectiveness and programmatic impact. 

Source: https://www.who.int/news-room/fact-sheets/detail/japanese-encephalitis

Japanese B encephalitis disease and vaccine information

Japanese encephalitis

********** The use of Japanese B Encephalitis Vaccine **************

Background:

Japanese B Encephalitis is a viral disease transmitted by mosquitoes. Over 50,000 cases are reported to occur each year. The disease is found in over 25 countries throughout the world. These are mainly in South East Asia as can be seen from the following list of endemic countries;

Australia, Bangladesh, Bhutan, Brunei, Cambodia, China, Hong Kong, India, Indonesia, Japan, Korea, Laos, Malaysia, Mynamar (Burma), Nepal, Pakistan, Philippines, Russia, Singapore, Sri Lanka, Taiwan, Thailand, Trust Territory, Vietnam, Pacific Islands.

Transmission Profile:

The disease is transmitted through the bite of an infected female culex mosquito. In the majority of cases these may occur within rural areas of the endemic countries and especially in regions where pig farming is found. Transmission can occur in urban areas but this is uncommon.

Disease Profile:

Patients with the disease usually present within the first week or two of having been bitten by an infected mosquito. They will usually develop distinct symptoms of a ‘flu illness with muscle pains and headache. Following this initial phase patients frequently present with vomiting and diarrhoea.

These early gastrointestinal symptoms are then followed by more severe neurological signs as the virus effects the patients brain tissue. Seizures and paralysis are then seen and the condition carries a mortality rate of between 10% to 40%.

In up to 80% of those who survive there may be residual neurological findings.

Risk of Disease:

It is reported that the risk of Japanese B Encephalitis is approximately 1/1,000,000 for normal short term travellers to some of the endemic countries.

This risk rises to approximately 1/5,000 for those living in rural areas for more than one month in the endemic countries.

This is particularly the case between May to September in South East Asia or between July to December in North India/Pakistan/Bangladesh.

Outcome:

There is no specific form of therapy against Japanese B Encephalitis and so it is essential that those at risk are as well protected against the disease as possible. This protection takes two forms; general protection against mosquito bites and specific vaccination against the disease.

Protection against Mosquitoes:

As with many arboviral (arthropod borne viral) diseases the main protection rests in taking all possible care against being bitten. The mosquitoes which transmit Japanese B Encephalitis tend to bite mainly in the evening time though day biting in shady areas may also occur.

Vaccination:

There is a killed vaccine against the disease which can be used in those at high risk. The vaccine is given on three occasions (days 0, 7-14, 28). This should give a 2 to 3 year protection against the disease. Cover for up to 3 months can usually be achieved by giving the vaccine on two occasions (day 0, 7-14)

Contraindications to the Vaccine:

Patients with a previous history of reaction to this vaccine should not be revaccinated. Also the vaccine should not be given to those with a history of allergy to rodents. Those pregnant should also not be vaccinated unless the risk of the disease is felt to be considerable.

Reactions:

Unfortunately in the early 1990’s a number of reactions were associated with the use of Japanese B Encephalitis vaccine.

From these figures it was estimated that significant reactions could occur with this particular vaccine in 4 to 8 of every 10,000 doses. This frequency of reaction would limit the widespread use of the vaccine.

Since this time it appears that there are now very few reactions occurring to the vaccine. The vaccine is now available in the US following extensive monitoring.

Who should be Vaccinated:

Nevertheless, this figure of possible vaccine related reactions makes the vaccine unacceptable for wide spread use in the short term traveller and so it is only recommended for those felt to be at significant risk.

This is usually only those who will be living for more than 1 month in the endemic countries mentioned earlier in this leaflet. An exception to this general rule may be for those travellers who will be highly exposed to mosquito bites in rural regions during exploration trips or extensive trekking holidays.

NOTE:

The information contained in this leaflet is of a very general nature. Specific health care information should be sought by every individual traveller and this information must only be used as an information guideline.

Source: https://www.tmb.ie/vaccinations/japanese-b-encephalitis

Origin and Evolution of Japanese Encephalitis Virus in Southeast Asia

Japanese encephalitis

1. Ali, A., and A. Igarashi. 1997. Antigenic and genetic variations among Japanese encephalitis virus strains belonging to genotype 1. Microbiol. Immunol. 41:241-252. [PubMed] [Google Scholar]

2. Briese, T., X.-Y. Jia, C. Huang, L. J. Grady, and W. I. Lipkin. 1999. Identification of a Kunjin/West Nile- flavivirus in brains of patients with New York encephalitis. Lancet 354:1261-1262. [PubMed] [Google Scholar]

3. Chambers, T. J., C. S. Hahn, R. Galler, and C. M. Rice. 1990. Flavivirus genome organisation, expression and replication. Annu. Rev. Microbiol. 44:649-688. [PubMed] [Google Scholar]

4. Chen, B. Q., and B. J. Beaty. 1982. Japanese encephalitis vaccine (2-8 strain) and parent (SA 14 strain) viruses in Culex tritaeniorhynchus mosquitoes. Am. J. Trop. Med. Hyg. 31:403-407. [PubMed] [Google Scholar]

5. Chen, W. R., R. Ricco-Hesse, and R. B. Tesh. 1992. A new genotype of Japanese virus from Indonesia. Am. J. Trop. Med. Hyg. 47:61-69. [PubMed] [Google Scholar]

6. Chen, W. R., R. B. Tesh, and R. Ricco-Hesse. 1990. Genetic variation of Japanese encephalitis virus in nature. J. Gen. Virol. 71:2915-2922. [PubMed] [Google Scholar]

7. Chua, K. B., W. J. Bellini, P. A. Rota, B. H. Harcourt, A. Tamin, S. K. Lam, T. G. Ksiazek, P. E. Rollin, S. R. Zaki, W.-J. Shieh, C. S. Goldsmith, D. J. Gubler, J. T. Roehrig, B. Eaton, A. R. Gould, J.

Olson, H. Field, P. Daniels, A. E. Ling, C. J. Peters, L. J. Anderson, and B. W. J. Mahy. 2000. Nipah virus: a recently emergent deadly paramyxovirus. Science 288:1432-1435.

[PubMed] [Google Scholar]

8. Gaunt, M. W., A. A. Sall, X. Lamballerie, A. K. Falconar, T. I. Dzhivanian, and E. A. Gould. 2001. Phylogenetic relationships of flaviviruses correlate with their epidemiology, disease association and biogeography. J. Gen. Virol. 82:1867-1876. [PubMed] [Google Scholar]

9. Gould, E. A. 2002. Evolution of the Japanese serological group viruses, p. 391-404. In J. S. Mackenzie, A. D. Barrett, and V. Deubel (ed.), Current topics in microbiology and immunology: Japanese encephalitis and West Nile virus infections, vol. 267. Springer-Verlag, Berlin, Germany.

10. Gould, E. A., P. M. Zanotto, and E. C. Holmes. 1997. The genetic evolution of flaviviruses, p. 51-63. In J. F. Saluzzo and B. Dodet (ed.), Factors in the emergence of arbovirus diseases. Elselvier, Paris, France.

11. Hancock, J., and J. Kushlan. 1984. The herons handbook. Harper and Row, New York, N.Y.

12. Hanna, J., S. Ritchie, D. A. Phillips, J. Shield, M. C. Bailey, J. S. Mackenzie, M. Poidinger, B. J. McCall, and P. J. Mills. 1996. An outbreak of Japanese encephalitis in the Torres Trait, Australia, 1995. Med. J. Aust. 165:256-260. [PubMed] [Google Scholar]

13. Hasegawa, H., M. Yoshida, S. Fujita, and Y. Kobayashi. 1994. Comparison of structural proteins among antigenically different Japanese encephalitis virus strains. Vaccine 12:841-844. [PubMed] [Google Scholar]

14. Huong, V. T. Q., D. Q. Ha, and V. Deubel. 1993. Genetic study of Japanese encephalitis viruses from Vietnam. Am. J. Trop. Med. Hyg. 49:538-544. [PubMed] [Google Scholar]

15. Innis, B. L. 1995. Japanese encephalitis, p. 147-174. In J. S. Porterfield (ed.), Exotic viral infections. Chapman & Hall, London, United Kingdom.

16. Jan, L. R., K. L. Chen, C. F. Lu, Y. C. Wu, and C. B. Horng. 1996. Complete nucleotide sequence of the genome of Japanese encephalitis virus ling strain: the presence of a 25-nucleotide deletion in the 3′-nontranslated region. Am. J. Trop. Med. Hyg. 55:603-609. [PubMed] [Google Scholar]

17. Kuno, G., G. J. Chang, K. R. Tsuchiya, N. Karabatsos, and C. B. Cropp. 1998. Phylogeny of the genus Flavivirus. J. Virol. 72:73-83. [PMC free article] [PubMed] [Google Scholar]

18. Lanciotti, R. S., J. T. Roehrig, V. Deubel, J. Smith, M. Parker, K. Steele, B. Crise, K. E. Volpe, M. B. Crabtree, J. H. Scherret, R. A. Hall, J. S. MacKenzie, C. B. Cropp, B. Panigrahy, E. Ostlund, B. Schmitt, M. Malkinson, C. Banet, J.

Weissman, N. Komar, H. M. Savage, W. Stone, T. McNamara, and D. J. Gubler. 1999. Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States. Science 286:2333-2337.

[PubMed] [Google Scholar]

19. Lobigs, M., I. D. Marshall, R. C. Weir, and L. Dalgarno. 1988. Murray Valley encephalitis virus field strains from Australia and Papua New Guinea: studies on the sequence of the major envelope protein gene and virulence for mice. Virology 165:245-255. [PubMed] [Google Scholar]

20. Mackenzie, J. S., C. A. Johansen, S. A. Ritchie, A. F. van den Hurk, and R. A. Hall. 2002.

Japanese encephalitis virus as an emerging virus: the emergence and spread of Japanese encephalitis virus in Australasia, p. 49-73. In J. S. Mackenzie, A. D. Barrett, and V. Deubel (ed.

), Current topics in microbiology and immunology: Japanese encephalitis and West Nile virus infections, vol. 267. Springer-Verlag, Berlin, Germany. [PubMed]

21. Monath, T. P., and F. X. Heinz. 1996. Flaviviruses, p. 961-1034. In B. N. Fields, D. M. Knipe, and P. M. Howley (ed.), Fields virology, 3rd ed. Lippincott-Raven, Philadelphia, Pa.

22. Ni, H., and A. D. Barrett. 1998. Attenuation of Japanese encephalitis virus by selection of its mouse brain membrane receptor preparation escape variants. Virology 241:30-36. [PubMed] [Google Scholar]

23. Ni, H., and A. D. Barrett. 1995. Nucleotide and deduced amino acid sequence of the structural protein genes of Japanese encephalitis viruses from different geographical locations. J. Gen. Virol. 76:401-407. [PubMed] [Google Scholar]

24. Ni, H., N. J. Burns, G. J. Chang, M. J. Zhang, M. R. Wills, D. W. Trent, P. G. Sanders, and A. D. Barrett. 1994.

Comparison of nucleotide and deduced amino acid sequence of the 5′ noncoding region and structural protein genes of the wild-type Japanese encephalitis virus strain SA14 and its attenuated vaccine derivatives.

J. Gen. Virol. 75:1505-1510. [PubMed] [Google Scholar]

25. Poidinger, M., R. A. Hall, and J. S. Mackenzie. 1996. Molecular characterization of the Japanese encephalitis serocomplex of the flavivirus genus. Virology 218:417-421. [PubMed] [Google Scholar]

26. Pyke, A. T., D. T. Williams, D. J. Nisbet, A. F. van den Hurk, C. T. Taylor, C. A. Johansen, J. Macdonald, R. A. Hall, R. J. Simmons, R. J. Mason, J. M. Lee, S. A. Ritchie, G. A. Smith, and J.

S. Mackenzie. 2001. The appearance of a second genotype of Japanese encephalitis virus in the Australasian region. Am. J. Trop. Med. Hyg. 65:747-753.

[PubMed] [Google Scholar]

27. Rey, F. A., F. X. Heinz, C. Mandl, C. Kunz, and C. Harrison. 1995. The envelope glycoprotein from tick-borne encephalitis virus at 2 Å resolution. Nature 375:291-298. [PubMed] [Google Scholar]

28. Scherret, J. H., J. S. Mackenzie, R. A. Hall, V. Deubel, and E. A. Gould. 2002. Phylogeny and molecular epidemiology of West Nile and Kunjin viruses. Curr. Top. Microbiol. Immunol. 267:373-390. [PubMed] [Google Scholar]

29. Solomon, T., and M. J. Cardosa. 2000. Emerging arboviral encephalitis. Br. Med. J. 321:1484-1485. [PMC free article] [PubMed] [Google Scholar]

30. Solomon, T., N. M. Dung, R. Kneen, M. Gainsborough, D. W. Vaughn, and V. T. Khanh. 2000. Japanese encephalitis. J. Neurol. Neurosurg. Psychiatry 68:405-415. [PMC free article] [PubMed] [Google Scholar]

31. Solomon, T., N. M. Dung, R. Kneen, L. T. Thao, M. Gainsborough, A. Nisalak, N. P. Day, F. J. Kirkham, D. W. Vaughn, S. Smith, and N. J. White. 2002. Seizures and raised intracranial pressure in Vietnamese patients with Japanese encephalitis. Brain 125:1084-1093. [PubMed] [Google Scholar]

32. Solomon, T., R. Kneen, N. M. Dung, V. C. Khanh, T. T. N. Thuy, D. Q. Ha, N. P. J. Day, A. Nisalak, D. W. Vaughn, and N. J. White. 1998. Poliomyelitis- illness due to Japanese encephalitis virus. Lancet 351:1094-1097. [PubMed] [Google Scholar]

33. Solomon, T., and D. W. Vaughn. 2002. Clinical features and pathophysiology of Japanese encephalitis and West Nile virus infections, p. 171-194. In J. S. Mackenzie, A. D. Barrett, and V. Deubel (ed.), Current topics in microbiology and immunology: Japanese encephalitis and West Nile virus infections, vol. 267. Springer-Verlag, Berlin, Germany. [PubMed]

34. Sumiyoshi, H., C. Mori, I. Fuke, K. Morita, S. Kuhara, J. Kondou, Y. Kikuchi, H. Nagamtu, and A. Igarashi. 1987. Complete nucleotide sequence of the Japanese encephalitis virus genome RNA. Virology 161:497-510. [PubMed] [Google Scholar]

35. Tsai, T. F. 1997. Factors in the changing epidemiology of Japanese encephalitis and West Nile fever, p. 179-189. In J. F. Saluzzo and B. Dodet (ed.), Factors in the emergence of arbovirus diseases. Elselvier, Paris, France.

36. Tsai, T. F. 2000. New initiatives for the control of Japanese encephalitis by vaccination: minutes of a W. H. O./CVI meeting, Bangkok, Thailand, 13-15 October 1998. Vaccine 18(Suppl. 2):1-25. [PubMed] [Google Scholar]

37. Tsai, T. F., F. Popovici, C. Carnescu, G. L. Campbell, and N. I. Nedlelcu. 1998. West Nile encephalitis epidemic in Southeastern Romania. Lancet 352:767-771. [PubMed] [Google Scholar]

38. Uchil, P. D., and V. Satchidanandam. 2001. Phylogenetic analysis of Japanese encephalitis virus: envelope gene based analysis reveals a fifth genotype, geographic clustering, and multiple introductions of the virus into the Indian subcontinent. Am. J. Trop. Med. Hyg. 65:242-251. [PubMed] [Google Scholar]

39. Vaughn, D. W., and C. H. Hoke. 1992. The epidemiology of Japanese encephalitis: prospects for prevention. Epidemiol. Rev. 14:197-221. [PubMed] [Google Scholar]

40. Wallace, A. R. 1869. The Malay Archipelago. The land of the Orang-utan and the bird of paradise. A narrative of travel, with studies of man and nature, vol. I. MacMillan and Co., London, United Kingdom.

41. Wang, E., H. Ni, R. Xu, A. D. Barrett, S. J. Watowich, D. J. Gubler, and S. C. Weaver. 2000. Evolutionary relationships of endemic/epidemic and sylvatic dengue viruses. J. Virol. 74:3227-3234. [PMC free article] [PubMed] [Google Scholar]

42. Williams, D. T., L. F. Wang, P. W. Daniels, and J. S. Mackenzie. 2000. Molecular characterization of the first Australian isolate of Japanese encephalitis virus, the FU strain. J. Gen. Virol. 81:2471-2480. [PubMed] [Google Scholar]

43. Zanotto, P. M., E. A. Gould, G. F. Gao, P. H. Harvey, and E. C. Holmes. 1996. Population dynamics of flaviviruses revealed by molecular phylogenies. Proc. Natl. Acad. Sci. USA 93:548-553. [PMC free article] [PubMed] [Google Scholar]

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC149749/

Facts about Japanese encephalitis

Japanese encephalitis

The Japanese encephalitis virus is present in Asia, from Japan to India and Pakistan, and outbreaks are erratic and spatially and temporally limited phenomena, occurring quite unpredictably, even if all conditions appear to be present in a definite place.

 It is a leading cause of viral encephalitis in Asia, with 30-50,000 cases reported annually.

It seems that there is a decrease of incidence in Asia which has been attributed to widespread vaccination (in children) and changes in agricultural practices and human behaviours.

The pathogen

Japanese encephalitis virus is an enveloped RNA virus of the genus Flavivirus, family Flaviviridae, and in the same antigenic complex as West Nile virus.

The virus was first isolated in 1935 from the brain of a fatal encephalitis case in Japan.

Five distinct viral genotypes have been identified but it seems that there are not apparent differences in humans between diseases resulting from infection by these different viruses.

Clinical features

Most human infections are asymptomatic. On average, one person in 200 infected develops a severe neuroinvasive illness which is characterized by rapid onset of high fever, headache, neck stiffness, disorientation, coma, seizures (second to elderly, in children), spastic paralysis. Milder forms of disease, such as aseptic meningitis or undifferentiated febrile illness can also occur. 

The case fatality rate in patients with severe disease is 20- 30% and about 30% of the patients surviving the illness have significant neurological sequelae (motor paresis, spasticity, movement disorders, chronic seizures, and developmental delay).

Transmission  

 The incubation period is usually 5 to 15 days. The viremia in humans is low and of short duration. Humans do not contribute in the chain of transmission and are considered dead-end hosts. 

Japanese encephalitis virus is maintained in an enzootic cycle between Culicidae mosquitoes present in irrigated rice fields and Ardeidae water birds (e.g. egrets, heron). Environmental conditions may favour high viral amplification with passage to pigs.

When these zoophilic mosquito populations reach high numbers the biting rate increases in humans. Horses are susceptible to viral infection (some strains) and can develop encephalitis.

In Asia, Culex tritaeniorhynchus and Culex vishnui appear to be the most important maintenance vectors for Japanese encephalitis virus. However other mosquito species e.g.

Culex pipiens pipiens, Culex pipiens molestus or Culex quinquefasciatus, show a moderate efficiency for transmission, and transavarial transmission has been demonstrated in some Aedes species including Aedes albopictus.

 

Diagnostics

The diagnosis of Japanese encephalitis infection relies on the detection of specific IgM antibodies which are present in cerebrospinal fluid and serum specimens from patients after 4-7 days post onset clinical symptoms.

The test should always include other closely related flaviviruses (e.g. West Nile, Usutu, dengue, tick borne encephalitis) for comparison and interpretation including the vaccination history status (e.g. tick-borne encephalitis, yellow fever).

Confirmation of the diagnosis needs to be done by neutralisation assays. 

Viral direct detection by RT-PCR could be performed on blood or CSF in early stage of the disease and on cerebral biopsies from deceased patients. The viremia is very short and limited to the early phase of the disease. There are only very few commercial diagnostic assays for serology available.

Case management and treatment

There is no specific treatment for Japanese encephalitis virus infection. In more severe cases, patients usually need to be hospitalised for supportive treatment and management of complications.
 

Geographic distribution

The geographic distribution of Japanese encephalitis (JE) virus extends from the East the Western Pacific islands (Japan, The Philippines) to India and Pakistan on the Westand from northern China (up to Tibet region) to Papua New Guinea and northern Australia where the virus expanded in the 90’s.

The distribution of JE is linked to irrigated rice fields combined to pig breeding.

In some locations, the virus may be transmitted year round, in other tropical areas, the timing of seasonal epidemics corresponds to the appearance of annual monsoons or rainy seasons and generally in areas with a temperate climate, the transmission prevails during the summer season.

The overall global incidence of Japanese encephalitis is unknown, but estimates suggest approximately 14,000 to 20,000 fatal cases of acute illness and 14,000 to 27,000 JE survivors with long-term neuropsychological sequelae.

Risk groups

Risk groups of Japanese encephalitis include:

  • Residents of rural areas in endemic locations, particularly children
  • Expatriates or travellers with long time exposure in rural endemic areas
  • Travellers in areas where irrigation flooding is used and lasting night in the open without a mosquito net, e.g. camping and trekking.

The disease risk is extremely low in travellers and evaluated to 1 case/1 million.

However, one should consider vaccinating travellers to JE-endemic countries that spend more than 1-2 months in risk areas during mosquito season.

The risk of Japanese encephalitis in children travellers but beyond the morbidity of the acute illness extends to potentially chronic or persistent neuropsychological deficits.

Areas of uncertainties

There is a possible risk of introduction of Japanese encephalitis virus (JEV) in EU countries via international travel and commerce with Asia, potentially allowing the introduction of mosquitoes infected with JEV.

If JEV is introduced, the virus might become established due to the significant number of susceptible mosquito vectors and vertebrate hosts.

The identification of risk factors for progression to symptomatic encephalitis and viral persistence need further investigation. 

The recent identification of a Japanese encephalitis viral RNA fragment in one Culex mosquito pool in Northern Italy might demonstrate a wider range of distribution of the virus and a potential public health threat in Europe. Additional studies are required to confirm this preliminary result.

Personal protective measures

Different kinds of vaccines (inactivated, attenuated and chimeric) are available and used in several Asiatic countries. In Europe an inactivated vaccine is currently available.

Several inactivated and live attenuated Japanese encephalitis vaccines are manufactured and used in Asia, mostly in children. One inactivated vaccine produced on Vero-cells is available in Europe for use in > 18 years adults. Paediatric clinical trials are being conducted to enable licensure this vaccine for use in children.

The implementation of attenuated vaccine in unvaccinated populations will continue to decrease the incidence of the disease in endemic areas.

Another way to prevent Japanese encephalitis infection is to avoid mosquito bites in endemic rural areas more specifically close to irrigated rice fields and pig farms. Many mosquitoes are most active at dusk and dawn. People can use insect repellents when they are outdoors and wear long sleeves and trousers at these times, or consider staying indoors during these hours.

As there is no specific treatment, the best way to prevent Japanese encephalitis infection is to avoid mosquito bites. Inactivated vaccine is available under restrictive regulations for adults with potential risk of exposure (e.g. travel for more than 1-2 months in rural areas).

Public health measures

It seems that the change of agricultural practices has substantially decreased the risk of transmission to humans. Measures aiming to control adult mosquito vectors can be applied in an outbreak situation but its impact is not well known. – See more at: http://ecdc.europa.eu/en/healthtopics/Japanese-encephalitis/public-heal…

References

 Rosen L, Tesh RB, Lien JC, Cross JH Transovarial transmission of Japanese encephalitis virus by mosquitoes. Science. 1978 Feb 24;199(4331):909-11.Solomon T. Flavivirus encephalitis. N Engl J Med. 2004 Jul 22;351(4):370–8. Petersen LR, Marfin AA. Shifting Epidemiology of Flaviviridae.

J Travel Medicine 2005; 12:S3–S11 Burchard GD et al, Expert Opinion on Vaccination of Travelers Against Japanese Encephalitis. J Travel Med 2009; 16: 204–216 DOI: 10.1111/j.1708-8305.2009.00330.x Hills SL, Griggs AC, Fischer M. Japanese encephalitis in travelers from non-endemic countries, 1973–2008. Am J Trop Med Hyg.

2010 May;82(5):930–6. Fischer M, Lindsey N, Staples JE, Hills S. Japanese encephalitis vaccines: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2010 Mar 12;59(RR-1):1–27. Fulmali PV, Sapkal GN, Athawale S, Gore MM, Mishra AC, Bondre VP.

Introduction of Japanese encephalitis virus genotype I, India. Emerg Infect Dis. 2011 Feb;17(2):319-21

Litzba N, S. Christoph S. Klade, S. Lederer, M. Niedrig (2010) Evaluation of serological diagnostic assays in detecting the immune answer after Japanese Encephalitis vaccination., PLoS Negl Trop Dis.

2010 Nov 16;4(11):e883 Ravanini P, Huhtamo E, Ilaria V, Crobu MG, Nicosia AM, Servino L, Rivasi F, Allegrini S, Miglio U, Magri A, Minisini R, Vapalahti O, Boldorini R.

Japanese encephalitis virus RNA detected in Culex pipiens mosquitoes in Italy. Euro Surveill. 2012;17(28):pii=20221.

  • Japanese encephalitis virus

Source: https://www.ecdc.europa.eu/en/japanese-encephalitis/facts

Japanese Encephalitis

Japanese encephalitis

Japanese encephalitis (JE) is a disease spread through mosquito bites. Symptoms usually take 5-15 days to develop and include fever, headache, vomiting, confusion, and difficulty moving. Symptoms that develop later include swelling around the brain and coma. JE is a serious disease that may cause death.

Travelers who go to Asia are at risk for getting Japanese encephalitis (See map). For most travelers the risk is extremely low but depends on where you are going, the time of year, your planned activities, and the length of the trip.

You are at higher risk if you are traveling to rural areas, will be outside frequently, or will be traveling for a long period of time.  In mild climates in northern Asia the risk for JE is greater in the summer and fall.

In tropical and subtropical areas, there is a risk year-round.

Travelers can protect themselves from JE by getting JE vaccine and preventing mosquito bites.

  • Talk to your doctor about your travel plans:
    • Your doctor can help you decide if you need the JE vaccine the length of your trip, the areas where you will be traveling, and your planned activities.
  • See your doctor at least 6 weeks before your trip:
    • JE vaccine is given as two doses spaced at least 28 days apart.
    • Adults age 18–65 can get the second dose as early as 7 days after the first dose.
    • The last dose should be given at least 1 week before travel.

Prevent mosquito bites:

  • Cover exposed skin by wearing long-sleeved shirts, long pants, and hats.
  • Use an appropriate insect repellent as directed.
  • Higher percentages of active ingredient provide longer protection.

    Use products with the following active ingredients:

    • DEET (Products containing DEET include Off!, Cutter, Sawyer, and Ultrathon)
    • Picaridin (also known as KBR 3023, Bayrepel, and icaridin products containing picaridin include Cutter Advanced, Skin So Soft Bug Guard Plus, and Autan [outside the US])
    • Oil of lemon eucalyptus (OLE) or PMD (Products containing OLE include Repel and Off! Botanicals)
    • IR3535  (Products containing IR3535 include Skin So Soft Bug Guard Plus Expedition and SkinSmart)
  • Always follow product directions and reapply as directed:
    • If you are also using sunscreen, apply sunscreen first and insect repellent second.
    • Follow package directions when applying repellent on children. Avoid applying repellent to their hands, eyes, and mouth.
  • Use permethrin-treated clothing and gear (such as boots, pants, socks, and tents). You can buy pre-treated clothing and gear or treat them yourself:
    • Treated clothing remains protective after multiple washings. See the product information to find out how long the protection will last.
    • If treating items yourself, follow the product instructions carefully.
    • Do not use permethrin directly on skin.
  • Stay and sleep in screened or air conditioned rooms.
  • Use a bed net if the area where you are sleeping is exposed to the outdoors.

If you are bitten by mosquitoes:

  • Avoid scratching mosquito bites.
  • Apply hydrocortisone cream or calamine lotion to reduce itching.
  • Talk to your doctor or nurse if you feel seriously ill, especially if you have a fever.
  • Use acetaminophen.

    Do not take pain relievers that contain aspirin and ibuprofen (Advil), it may lead to a greater tendency to bleed.

  • Get lots of rest, and drink plenty of liquids.
  • Avoid spreading the disease by preventing more mosquito bites.

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Source: https://wwwnc.cdc.gov/travel/diseases/japanese-encephalitis

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