Travel Health Information Sheets
- Introduction
- Epidemiology
- Risk for travellers
- Transmission
- Signs and symptoms
- Treatment
- Prevention
- References
- Reading list
- Links
Hepatitis E is a non-enveloped spherical RNA virus that has been recently classified in the Hepevirus genus. The virus is transmitted by the faecal-oral route. Although humans are considered to be the natural host, antibodies to hepatitis E virus or closely related viruses, have been found in several animal species, suggesting that hepatitis E may be a zoonosis [1].
Hepatitis E was first recognised as a clinical entity in the 1980s in India [1], having previously been referred to as enterically transmitted non-A, non-B hepatitis (ET-NANB). Outbreaks have now been recorded from many areas of the world.
(Data from the Travel and Migrant Health Section of the Health Protection Agency)
Global epidemiology
Hepatitis E is endemic in regions of the world where sanitation is poor, particularly in parts of Asia, Mexico and Central America, and Africa. Since the 1950s, epidemics of ET-NANB have frequently been documented in the Indian sub-continent, in particular India. An outbreak occurred in Delhi in 1955-56 when around 29,300 people were affected [2]. The largest outbreak was however, reported in Kanpur city in Uttar Pradesh in 1991 where over 79,000 clinical cases were reported [3]. This outbreak was due to the faecal contamination of drinking water supplied from the river Ganges. Nepal, Pakistan, Bangladesh, and Myanmar have also reported outbreaks up to 1999 [4]. More recently, hepatitis E has been reported in north and west Africa, and Mexico; in 2004 and 2005, outbreaks involving over 100 deaths were reported in Goz Amer and Goz Beida, Sudanese refugee camps in eastern Chad [5, 6].
While hepatitis E is recognised as causing epidemics in resource-poor countries, sporadic cases also occur in richer countries, and are generally associated with travel to endemic regions. However, cases in which the patient has not reported recent foreign travel have been reported in resource-rich countries such as New Zealand, Australia, United States, Netherlands, Japan, Taiwan, Germany, France, Spain, Greece, and Austria as well as the United Kingdom [7]. The route of transmission for these sporadic cases is not always determined. Some studies have suggested a zoonotic source; in particular pigs may be an important reservoir [8] but more investigation is needed.
Hepatitis E in travellers from England, Wales and Northern Ireland
Source of data
Laboratory reports from the Immunisation Department at the Health Protection Agency (HPA) Centre for Infections. Laboratory reports are based on reports from the routine laboratory reporting system (Co-Surv and Labbase 2), with supplementary information from yellow forms sent to the Department by the reporting laboratory.
Figure 1: Laboratory reports of hepatitis E by travel history, England, Wales, and Northern Ireland: 1994 - 2003
From routine laboratory reporting, there were 33 cases of hepatitis E reported on average annually. Of those, since 1997, an average of 38% was associated with recent foreign travel (figure 1). Travel history reporting has however, decreased since 1994, which makes interpretation of the data difficult. Of those cases that had reported recent foreign travel, the majority had travelled to the Indian sub-continent, in particular, Bangladesh. [In March 2003, there was a cluster of 15 acute cases of hepatitis E in north east London associated with travel to the Sylhet region of Bangladesh [9].]
In 1996, the Central Public Health Laboratory (now the HPA Centre for Infections) introduced a serodiagnostic service for cases of hepatitis E and a survey of cases between 1996 and 2003 has been completed [7]. The survey found that during the study period, there were 186 cases, of which 129 (69%) reported recent travel to endemic countries. The most reported region of travel was the Indian sub-continent, over half (66/129) to Bangladesh. The 17 cases that were not associated with recent foreign travel may have been related to exposure to pigs. Enhanced surveillance of hepatitis E in England and Wales is currently being conducted by the HPA, and will examine risk factors for non travel-associated cases. This may in turn identify more travel-associated cases in the future.
Travellers to hepatitis E endemic regions who visit areas with poor sanitation are at risk of the disease [10]. Outbreaks are more common following heavy rain and flooding which results in contamination of water supplies with untreated sewage.
The primary source of infection with hepatitis E virus appears to be from faecally contaminated water. Food borne transmission also occurs. Direct person-to-person transmission is uncommon with secondary cases among household contacts unusual.
It is suspected that hepatitis E has animal reservoirs as closely related virus has been isolated from non-human primates and other animals such as pigs, cows, sheep, goats, deer and rodents [1, 11, 12].
As with the other hepatitis viruses, hepatitis E infection can cause sub-clinical illness, or acute, symptomatic hepatitis with jaundice and fulminant hepatitis. Hepatitis E is not associated with chronic infection.
Following an incubation period of 4 to 6 weeks (range 3 to 8 weeks), fatigue, loss of appetite, nausea, abdominal pain and hepatomegaly may occur. The majority of hepatitis E infections are self-limited followed by complete recovery; sub-clinical illness is most common in children. Symptomatic hepatitis E infection is more common in young adults aged 15-40 years and in pregnant women [1].
Overall the mortality rate ranges from 1-4%, however pregnancy can be associated with fulminant hepatitis and a mortality rate of 20% and increased foetal wastage [10, 13].
There is no specific treatment for hepatitis E infection, but rather supportive intervention.
As most infections are contracted through the faecal-oral route, the risk of acquiring hepatitis E can be reduced by following food and water hygiene guidelines and by ensuring good personal hygiene.
Pregnant women should be advised about the importance of strict food, water and personal hygiene practices.
Although several studies are currently in progress, there is no vaccine available to protect against hepatitis E.
1. World Health Organization. Hepatitis E fact sheet No. 280 [online] [cited 1 December 2005]. Available online at http://www.who.int/mediacentre/factsheets/fs280/en/.
2. Vishwanathan R. Infectious hepatitis in Delhi (1955-56): a critical study; epidemiology. Ind J Med Res (suppl.) 1957; 45: 1-30.
3. Naik SR, Aggarwal R, Salunke PN, Mehrotra NN. A large waterborne viral hepatitis E epidemic in Kanpur, India. Bull World Health Organ 1992; 70 (5): 597-604.
4. Labrique AB, Thomas DL, Stoszek SK, Nelson KE. Hepatitis E: an emerging infectious disease. Epidemiol Rev 1999; 21 (2): 162-79.
5. World Health Organization. Hepatitis E, Chad - update. Wkly Epid Rec 2004; 79 (37): 329. Available online at http://www.who.int/wer/2004/en/wer7937.pdf.
6. ProMED-mail. Hepatitis E - Chad (Eastern) ProMED-mail 2005 [online]; 22 Aug [cited 2 December 2005] Archive no: 20050822.2477. Available at http://www.promedmail.org.
7. Ijaz S, Arnold E, Banks M, Bendall RP, Cramp ME, Cunningham R et al. Non-travel-associated hepatitis E in England and Wales: demographic, clinical, and molecular epidemiological characteristics. J Inf Dis 2005; 192: 1166-72.
8. Yazaki Y, Mizuo H, Takahashi M, et al. Sporadic acute or fulminant hepatitis E in Hokkaido, Japan, may be food-borne, as suggested by the presence of hepatitis E virus in pig liver as food. J Gen Virol 2003; 84: 2351-7.
9. Turbitt D, Nixon G. Cluster of cases of hepatitis E in north east London. In: Health Protection Agency Annual Conference; 2004 Sep 13-15; Warwick, United Kingdom. London: HPA; p 29.
10. Zuckerman JN. Hepatitis E and the traveller. Travel Med Infect Dis 2003; 1: 73-76
11. Tei S, Kitajima N, Takahashi K, Mishiro S. Zoonotic transmission of hepatitis E virus from deer to human beings. Lancet 2003; 362: 371-373.
12. Wu JC, Chen CM, Chiang TY et al. Clinical and epidemiological implications of swine hepatitis E virus infection. J Med Virol 2000; 60: 166-171.
13. Tsega E, Hansson BG, Krawczynski K and Nordenfelt E. Acute sporadic viral hepatitis in Ethiopia: causes, risk factors, and effects on pregnancy. Clin Infect Dis 1992; 14: 961-965.
DuPont H, Steffen R. Textbook of Travel Medicine and Health 2nd edition 2001 BC Decker Inc. Ontario
Khuroo MS. Viral hepatitis in international travellers: risks and prevention. Int J Antimicrobial Agents 2003; 21: 143-52
Skidmore SJ. Tropical aspects of viral hepatitis. Hepatitis E. Trans Roy Soc Trop Med Hyg. 1997; 91: 125-126
World Health Organization
www.who.int/mediacentre/factsheets/fs280/en/
Centres for Disease Control and Prevention http://wwwn.cdc.gov/travel/contentYellowBook.aspx
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