In October 2005, while vacationing in Paris, our 43-year-old, previously healthy patient who worked in a foreign embassy in Nepal for the past 14 months developed sudden onset of fever, anorexia, extreme chills, and sweats. She had one episode of diarrhea but denied any abdominal symptoms. She assumed that she had the “flu” and rested for several days. Seven days after the onset of her symptoms, she sought care in London, as now she had disabling myalgia and dizziness. A proper travel history was obtained, and examination at that time revealed moderate to severe tenderness on palpation of the liver. The rest of her examination was normal. Five days later, she continued having exquisite liver tenderness and developed a maculopapular eruption on the palms of her hands that was pruritic and multiple aphthous ulcers in the gingivomucosal cleft of her upper and lower lips.
Her total bilirubin was 12 μmol/L, aspartate aminotransferase was 189 IU/L, alanine aminotransferase was 102 IU/L, gamma glutamyltransferase was 94 IU/L, and lactate dehydrogenase was 1,020 IU/L. A diagnosis of viral hepatitis was made based on her clinical and laboratory findings. A complete blood count and creatinine were normal. Initial hepatitis evaluation carried out in the UK misinterpreted hepatitis C virus as the etiological agent. The patient was observed in London until her liver enzymes started falling and her liver tenderness resolved. The London physician communicated with the responsible nurse practitioner in Nepal throughout the course of the illness. On her return to Nepal, close questioning by the nurse practitioner revealed no risk factors for hepatitis C; hence, additional diagnostic tests were performed. These included hepatitis E serology, as hepatitis E is endemic in Kathmandu,1 and this agent was not tested for in the UK. Furthermore, her hepatitis C enzyme immunoassay (EIA) was negative. Both hepatitis A, which is also endemic in Nepal, and hepatitis B were ruled out. Ultimately, a diagnosis of hepatitis E was made based on a reactive hepatitis E virus IgM of 1.9 (>1.2 is positive) by EIA testing2 (Right Choice Diagnostics, Yavne, Israel). The patient’s clinical symptoms and the dermal changes improved, the liver enzymes fell to normal levels over 3 weeks, and the subject recovered uneventfully and returned to full diplomatic duties 21 days after falling ill. When we contacted her on April 16, 2007, she reported that she continues to do well.
This case emphasizes that in areas endemic for hepatitis E, even those living in the relative safety of a diplomatic environment with availability of clean water and strict food-handling techniques in the household may be at risk of contracting this illness. Hepatitis E infection that is caused by a nonenveloped RNA virus is a neglected, viral illness spread primarily by fecal–oral transmission.1,2 The clinical features commonly include a flulike illness and sometimes a transient maculopapular rash as in our patient. Unsurprisingly, Kathmandu with its unhygienic piped water supply is endemic for hepatitis E with sporadic outbreaks. The first reported epidemic outbreak of hepatitis E was in 1955 in New Delhi, India.3 An outbreak in Nepal was noted in 1983. Other epidemic outbreaks have occurred in North and West Africa, Central and Southeast Asia, and Mexico2. The illness may last from about a week to a month. Chronic infection is unknown, but rarely, fulminant hepatitis has been reported especially in people with underlying liver disease. In pregnant women, however, there may be a 25% maternal mortality, and pregnant women are an important vulnerable group in countries like Nepal.1,2 No specific treatment is available for hepatitis E. A noteworthy disease in the differential diagnosis is hepatitis A (Table 1), as both have similar route of transmission and clinical features; however, because of the effective hepatitis A vaccine, at least in the traveler population in areas of endemicity, the incidence of hepatitis A has declined. Hepatitis E has been documented in travelers but appears to be uncommon.4–6
|Incubation||14–45, mean 30 d||14–60, mean 40 d|
|Age||Children and young adults||Young adults (20–40 y)|
|Fulminant hepatitis||Rare (seen in older adults)||More common (in 25% pregnant women)|
|Lifelong immunity after infection||Present||Unknown|
|Vaccination||Effective and commercially available||Effective and not commercially available|
Despite a history of living in a country endemic for hepatitis E, testing of these patients in Western centers often neglects searching for this locally unfamiliar agent. Although the London physician correctly obtained a travel history, the hepatitis screening in the UK did not include hepatitis E.
Recently,7 several members of the Nepali parliament also came down with documented hepatitis E, presumably from drinking contaminated water in government homes and offices. In early 2007, another resident Westerner was diagnosed with this illness by one of us. Importantly, a vaccine1 for hepatitis E virus has now shown 95% efficacy in preventing clinical disease. Inexpensive and commercial availability of such a vaccine together with clean water supply and better food-handling techniques may be extremely useful in preventing this illness in local (especially pregnant women) and foreign residents alike in areas of endemicity. Otherwise, as in our case, even diplomats may be vulnerable.