Autochthonous Hepatitis E Co-Infection Causing More Severe Acute Hepatitis B Infection

Abstract

Introduction: Acute hepatitis E is caused by an RNA virus (HEV) endemic in many parts of the developing world usually producing a brief icteric illness, similar to Hepatitis A. In Western countries, acute HEV is rare and usually seen in subjects that have recently traveled to endemic areas (Central and Southeast Asia, North and West Africa and Mexico). However, there have been multiple case reports of autochthonous (locally acquired) HEV in the United Kingdom, Japan, Holland, and France of unknown sources. Hepatitis B Virus (HBV) is transmitted by percutaneous and mucous membrane exposure to infectious body fluids and in adults it is likely to cause clinically apparent acute HBV infection. Less than 1% of the cases of acute HBV progress to fulminant liver failure although the disease may be more severe in patients with other hepatitis viruses. We describe a rare case of dual acute HBV and HEV in the USA with severe clinical manifestations. Case Presentation: A 70-year-old male developed generalized myalgias, headache, nausea, and fatigue. Six weeks prior while in Florida, he had a sexual encounter with a sex worker. The patient had no history of previous hepatic disease and was found to have icteric hepatitis with ALT/AST >1500 U/L and bilirubin of 4.1 mg/dl. He had detectable HBV surface antigen (HBsAg) and anti-HBc IgM consistent with acute HBV with a HBV viral load of >1.1x108 IU/ml. Further laboratory work-up at that time for other etiologies was negative and the patient denied any new medications or recent acetaminophen intake. Supportive care was initiated but the patient began to show evidence of hepatic synthetic dysfunction with prolonged prothrombin time and continued worsening of aminotransferases and bilirubin. Further laboratory analysis revealed detectable anti-HEV IgM consistent with acute HEV infection. Biopsy showed marked hepatitis (Scheuer Grade 4) and early bridging fibrosis (Scheuer Stage 3) and with bile ductular proliferation characteristic of HEV supporting the impression of co-infection by both HBV and HEV. Antiviral therapy with entecavir was initiated and the patient slowly improved. One year later, the patient is negative for HBs Ag, anti-HBc IgM, HBV DNA and anti-HEV. He is asymptomatic. Discussion: This is a unique case of acute HEV in a patient without travel to an endemic area consistent with an autochthonous infection in the United States. This case is also unique due to the severity of the acute co-infection with HBV and HEV. Practitioners should be aware of this viral hepatitis that can worsen other hepatitides and consider screening for HEV in cases of acute hepatitis.