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Hepatitis E acquired in the UK
  1. C G TEO
  1. West Cornwall Hospital
  2. St. Clare Street, Penzance
  3. Cornwall TR18 2PF, UK
  4. Public Health Laboratory
  5. Penventinnie Lane, Truro
  6. Cornwall TR1 3LQ, UK
  7. Hepatitis and Retrovirus Laboratory
  8. PHLS Central Public Health Laboratory
  9. 61 Colindale Avenue, London NW9 5HT, UK
  1. Dr Levine.dflreens{at}

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We can confirm the finding of McCruddenet al (OpenUrlCrossRefPubMedWeb of Science) , that acute infection with hepatitis E virus (HEV) can be acquired in the UK. A 61 year old man presented in March 1999 after a two week illness with fever, malaise, and nausea, followed by cholestatic jaundice and a palpable spleen. Results of tests included alkaline phosphatase 277 IU/l, alanine aminotransferase 2118 IU/l, bilirubin 244 umol/l and INR 1.7. He had no risk factors for liver disease and did not swim in the sea. He had not travelled outside the UK for four years and had never been to an area where hepatitis E was endemic. Serology was negative for acute markers of hepatitis A and EBV and for any evidence of hepatitis B or CMV. Clinical recovery was uneventful and four months later, liver function tests had returned to normal. Serum was taken from the patient at presentation and at one, two, three, and eight months. All specimens were examined by enzyme immunoassay for total anti HEV antibody (HEVEIA, Abbott, Maidenhead, Berks, UK) and IgM anti HEV antibody (HEV IgM ELISA, Genelabs Diagnostics PTE Ltd, Singapore). The first sample was positive in the total and IgM anti HEV antibodies. Over the following months the IgM reactivity waned and then became negative while the total antibody test remained positive. Blood samples from close contacts (including a friend who had been to India four years earlier) were tested at eight months and were all negative for total anti HEV antibody.

We believe that our patient too had UK community acquired hepatitis E, although the source of his infection remains unknown. One possibility is consumption of imported food contaminated with HEV. This mechanism has been responsible for cases of hepatitis A.1It is difficult to identify a particular imported food as the source of our patient's infection as his dietary habits were not unusual and had not changed. Another hypothesis is that HEV may be a zoonotic infection. HEV has been demonstrated in pigs in several countries, including the US.2 Two human HEV cases acquired in the US involved a virus similar to porcine strains of HEV.3Furthermore, pig handlers in China and Thailand have high rates of HEV seropositivity.2 Serological evidence of HEV infection has also been found in wild rats in the US.4

Our patient reported no contact with rats or pigs but we are arranging for HEV genetic sequencing to be performed on his serum samples. We recommend that HEV serology should be more commonly applied to blood specimens from patients with acute hepatitis of obscure cause. Few laboratories in the UK test routinely for HEV and those centres that do test are usually referred specimens only from patients with a history of travel to an area where HEV is endemic. Unless more indigenous cases are detected and followed up epidemiologically, the origin of such infection will remain obscure.


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