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Acute hepatitis E infection in a visitor to Louisiana.

Abstract: A man from Africa had been visiting Mississippi and Louisiana when he had development of acute hepatitis. Although hepatitis E is endemic to many parts of the world and has been associated with large outbreaks, it has remained relatively uncommon in this country. With growing foreign travel and an ever-increasing number of cases reported nationally, hepatitis E infection should be considered more frequently in the differential diagnosis of acute hepatitis.

Key Words: acute hepatitis, hepatitis E virus, travel medicine

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Acute hepatitis E (HEV) infection is endemic in Asia, Africa, and Central America (1-5) and is becoming more frequent in Japan. (6) In the past few years, a number of cases have been reported in Americans returning from abroad as well as in visitors from endemic areas traveling to the United States. (7-12) We report a recent case of an African man visiting Louisiana and Mississippi. Although HEV antibody has been found in rats from Louisiana, (13) this is believed to be the first active human case reported in the state.

Case Report

A 31-year-old man from Cameroon was visiting southern Mississippi for about 3 weeks before the sudden onset of nausea, vomiting, and abdominal and lower back pain. Upon physical examination, the patient was deeply jaundiced and had marked right upper quadrant and lower back tenderness. The metabolic panel and complete blood count were normal, but the total bilirubin was 20.4 mg/dL (<1.3 mg/dL), alanine aminotransferase was 2,899 U/L (<46 U/L), and aspartate aminotransferase was 2,815 U/L (<45 U/L). Except for his country of origin, he reported no risk factors for viral hepatitis. Hepatitis A (HAV) total antibody was positive, but the HAV IgM antibody was negative. Hepatitis B core total antibody was positive, whereas the core IgM antibody and surface antigen were negative. Hepatitis C antibody was negative. The ceruloplasmin was 35 mg/dL (16 to 35.6 mg/dL). There were undetectable serum levels of acetaminophen and ethanol, and the antinuclear antibody titer was less than 1:40. Abdominal ultrasound showed normal liver size and flow patterns within the hepatic veins, portal veins, and inferior vena cava. Liver biopsy revealed diffuse areas of inflammation with minimal iron deposits and without fibrosis. Supportive treatment was given, and the hospital course was uneventful, with a rapid improvement in both symptoms and liver enzymes. Given his country of origin, HEV was suspected and a serum sample was sent to the National Center for Infectious Diseases. HEV IgM antibody was positive, and on follow-up several weeks later the patient was asymptomatic with normal liver enzymes.

Discussion

Hepatitis E is an icosahedral nonenveloped single-stranded RNA virus that is spread fecal-orally. Infections occur in endemic areas and sporadically in nonendemic areas. Epidemiology differs from HAV infection primarily by age group. Although both are spread fecal-orally, HAV typically occurs in children, whereas HEV patients tend to be older. This patient is typical in that there is evidence of past HAV infection, but HEV infection occurred in the adult. Epidemics have been associated with contaminated water supplies, (14) and sporadic cases may have animal intermediates. Although the reservoir is unknown and several animals have been linked to contact transmission, (15-18) person-to-person transmission is thought to be rare. (19) The incubation period has been reported to be as little as 2 weeks, with continued virus excretion in stool for up to 2 weeks after the onset of illness. The disease course is typically mild to moderate in severity and lasts only a few weeks. No evidence of chronic infection has been reported. (20,21) The overall case fatality rate is less than 3%, (22) with the main exception being pregnant women, in which mortality rates are as high as 20% during the third trimester. (23)

Although hepatitis E is endemic to many parts of the world and has been associated with large outbreaks, it has remained relatively uncommon in this country. Although the two most common genotypes are Asian/Burmese (genotype 1) and Mexican (genotype 2), at least one genotype (genotype 3) has been isolated that is unique to the United States, (24) suggesting that endemic infection in this country is possible.

With growing foreign travel and an ever-increasing number of cases reported nationally, the prevalence may begin to rise; therefore, hepatitis E infection should be considered more frequently in the differential diagnosis of acute hepatitis.

Conclusion

Prevention is the same for any enterically transmitted infection. This includes good hygiene, sanitary handling of food and water, and only eating cooked food. Immunoglobulin from endemic areas has not been shown to confer protection, (25) and supportive measures remain standard of care with therapy.

References

1. Tandon BN, Joshi YK, Jain SK, et al. An epidemic of non-A, non-B hepatitis in North India. Indian J Med Res 1982;75:739-744.

2. Belabbes EH, Bouguermouh A, Benatallah A, et al. Epidemic non-A, non-B hepatitis in Algeria: strong evidence for its spreading by water. J Med Virol 1985;16:257-263.

3. Arankalle VA, Chadha MS, Mehendale SM, et al. Outbreak of enterically transmitted non-A, non-B hepatitis among school children. Lancet 1988;2:1199-1200.

4. Velazquez O, Stetler HC, Avila C, et al. Epidemic transmission of enterically transmitted non-A, non-B hepatitis in Mexico, 1986-1987. JAMA 1990;263:3281-3285.

5. Tsega E, Krawczynski K, Hansson BG, et al. Outbreak of acute hepatitis E virus infection among military personnel in northern Ethiopia. J Med Virol 1991;34:232-236.

6. Yatsuhashi H. Epidemiological and clinical features of hepatitis E in Japan. J Gastroenterol 2004;39:702-703.

7. Hepatitis E among US travelers, 1989-1992. MMWR 1993;42:1-4.

8. Fortier D, Treadwell TL, Koff RS, et al. Enterically transmitted non-A, non-B hepatitis: importation from Mexico to Massachusetts. N Engl J Med 1989;320:1281-1282.

9. Dawson GJ, Mushahwar IK, Chan KH, et al. Detection of long-lasting antibody to hepatitis E virus in a US traveler to Pakistan. Lancet 1992;34:426-427.

10. Tsang TH, Denison EK, Williams HV, et al. Acute hepatitis E infection acquired in California. CID 2000;30:618-619.

11. Herrera JL. Hepatitis E as a cause of non-A, non-B hepatitis. Arch Intern Med 1993;153:773-775.

12. Bader TF, Krawczynski K, Polish LB, et al. Hepatitis E in a US traveler to Mexico. N Engl J Med 1991;325:1659.

13. Kabrane-Lazizi Y, Fine JB, Elm J, et al. Evidence for widespread infection of wild rats with hepatitis E virus in the United States. Am J Trop Med Hyg 1999;61:331-335.

14. Viswanath R. Infectious hepatitis in Delhi (1955-1965): a critical study. Indian J Med Res 1957;45:1-29.

15. Arankalle VA, Chobe LP, Joshi MV, et al. Human and swine hepatitis E viruses from Western India belong to different genotypes. J Hepatol 2002;36:417-425.

16. Tei S, Kitajima N, Takahashi K, et al. Zoonotic transmission of hepatitis E virus from deer to human beings. Lancet 2003;362:371-373.

17. Banks M, Bendall R, Grierson S, et al. Human and porcine hepatitis E strains, United Kingdom. Emerg Infect Dis 2004;10:953-955.

18. Okamoto H, Takahashi M, Nishizawa T, et al. Presence of antibodies to hepatitis E virus in Japanese pet cats. Infection 2004;32:57-58.

19. Zuckerman AJ. Hepatitis E virus: the main cause of enterically transmitted non-A, non-B hepatitis. BMJ 1990;300:1475-1476.

20. Khuroo MS, Saleem M, Teli MR, et al. Failure to detect chronic liver disease after epidemic non-A, non-B hepatitis. Lancet 1980;2:97-98.

21. Krawczynski K. Hepatitis E. Hepatology 1993;17:932-941.

22. Enterically transmitted non-A, non-B hepatitis, East Africa. MMWR 1987;36:241-244.

23. World Health Organization, Hepatitis E. <http://www.who.int/media-centre/factsheets/fs280/en/> (accessed September 2004).

24. Kwo PY, Schlauder GG, Carpenter HA, et al. Acute hepatitis E by a new isolate acquired in the United States. Mayo Clin Proc 1997;72:1133-1136.

25. Khuroo MS, Dar MY. Hepatitis E. Evidence for person-to-person transmission and inability of low dose immune serum globulin from an Indian source to prevent it. Indian J Gastroenterol 1992;11:113-116.

James Edward Walker, Jr., MD, PHD, Todd Martin Brown, MD, Thomas Lanier Hagood, MD, and William Morgan Cassidy, MD

From the Department of Internal Medicine, Louisiana State University Health Sciences Center, Earl K. Long Memorial Hospital, 5825 Airline Highway, Baton Rouge, LA.

Reprint requests to Dr. William M. Cassidy, Earl K. Long Memorial Hospital, 5825 Airline Highway, Baton Rouge, LA 70805. Email: wcassi@lsuhsc.edu

Accepted November 22, 2004.

RELATED ARTICLE: Key Points

* Hepatitis E virus infection is usually benign and self-limited.

* There is a higher fatality rate in pregnant women.

* Hepatitis E virus should be considered in the differential diagnosis of acute viral hepatitis with negative serology for hepatitis A, B, and C viruses.

* Person-to-person transmission is rare.
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Title Annotation:Case Report
Author:Cassidy, William Morgan
Publication:Southern Medical Journal
Date:Jul 1, 2005
Words:1455
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