Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow-226 014, India.
Abstracts of the papers presented at the XVIII National Conference of Indian Virological Society at Post Graduate Institute of Medical Education and Research, Chandigarh, India, December 11–13, 2008.
Acute viral hepatitis and fulminant hepatic failure are usually caused by hepatitis A to E viruses and few cases are due to herpes viruses (EBV, CMV HSV) occurring either singly or in combinations; still in 10 to 30% cases of hepatitis no etiology could be found. Parvovirus B19 has been recently reported to be detected in the liver tissues and sera of patients with acute hepatitis and possibly an etiologic agent of hepatitis-associated anemia. We report a five year child presenting with decreased level of consciousness, fever and jaundice and admitted in the critical care unit of our tertiary care institute. He had highly raised serum bilirubin, liver enzymes with anemia and thrombocytopenia. U/S abdomen revealed effusions in pleura and pelvis. He was diagnosed as a case of fulminant hepatitis due to hepatitis viruses A and E. He had human parvovirus B19 (B19) specific IgM antibodies by in-house ELISA and B19 DNA in serum by nested –PCR using primers from VP1 unique region. The child later developed acute dyspnea and low oxygen saturation; was put up on ventilator. His blood culture (BACTEC 9120) had coagulase negative staphy-lococcus. He was treated with IV amoxicillin+clavulanic acid and oxygen inhalation. He had a cardiac arrest but revived. Despite all supportive treatment the child expired after 3 days of admission. To the best of our knowledge, this is the first case report from the country of mortality due to fulminant hepatitis associated with co-infection of B19 with hepatotropic viruses (Hepatitis virus A and E).
