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Hepatitis E in India

B S Tomar1

  • 1Department of Pediatric Gastroenterology, S.M.S. Medical College, Jaipur, India. tomar-dr@jpl.vsnl.net.in

Zhonghua Minguo Xiao Er Ke Yi Xue Hui Za Zhi [Journal]. Zhonghua Minguo Xiao Er Ke Yi Xue Hui
|July 31, 1998
PubMed

Insights

Hepatitis E virus (HEV) causes over 70% of acute hepatitis in children in the subcontinent, primarily spread through contaminated water and food. HEV can be found in various bodily fluids and even insects, with potential for maternal-neonatal transmission.

Area of Science:

  • Virology
  • Hepatology
  • Public Health

Background:

  • Hepatitis E virus (HEV) is a significant cause of acute hepatitis in pediatric populations, particularly in the Indian subcontinent.
  • HEV strains in India show high genetic similarity to Chinese strains but differ from Mexican strains.
  • Over 70% of acute hepatitis cases in children in this region are attributed to HEV, with 80% occurring sporadically.

Purpose of the Study:

  • To analyze the characteristics and transmission routes of Hepatitis E virus (HEV) in a large pediatric cohort.
  • To investigate the presence of HEV in various environmental sources and bodily fluids.
  • To understand the clinical presentation, shedding patterns, and potential treatment options for HEV infection in children.

Main Methods:

  • Retrospective analysis of 10,500 pediatric cases with proven HEV infection.
  • Detection of HEV in patient samples (urine, respiratory secretions, breast milk) and environmental sources (insects, shellfish).
  • Clinical observation of HEV-infected volunteers and patients, including serological and virological assessments.

Main Results:

  • Enteric transmission via contaminated water (70%) and food (20%) accounted for 90% of cases; person-to-person spread occurred in 9.5%.
  • HEV was detected in urine, respiratory secretions, insects (flies, cockroaches, mosquitoes), and partially cooked seafood.
  • Maternal-neonatal transmission was observed in third-trimester infections; HEV was found in breast milk in 5 cases.
  • Anicteric HEV forms occurred in 40% of volunteers; virus shedding preceded icteric phases.
  • Hepatitis IgG anti-HEV persisted up to 4 years; transfusion-associated hepatitis (TAH) was documented in 5 cases.
  • Fulminant/Sub-fulminant Viral Hepatitis (FVH/SVH) occurred in 5% of cases, with alpha-interferon (IFN) and intravenous prostaglandin E1 (PGEl) showing potential benefit.
  • Inadequate water chlorination was linked to epidemics; adequate disinfection requires ≥0.5 mg/l residual chlorine for 30 minutes.

Conclusions:

  • HEV is a major etiological agent of acute hepatitis in children in the subcontinent, with diverse transmission routes including environmental and potential vectors.
  • Understanding HEV shedding patterns and persistence of anti-HEV antibodies is crucial for diagnosis and management.
  • Effective public health measures, including adequate water disinfection, are essential for controlling HEV epidemics.

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