Transfusion-associated Hepatitis E, France

Systematic molecular characterization of multidrug-resistant Mycobacterium tuberculosis complex isolates from Spain. To the Editor: Hepatitis E virus (HEV) is a leading cause of acute and fulminant hepatitis in developing countries (1). In industrialized countries , HEV seroprevalence rates of 0.4%–3% are common, and evidence is mounting that autochthonous transmission might account for a substantial proportion of infections (1–3). Whereas fecal-oral HEV transmission is preponderant in developing countries , other routes have been demonstrated in industrialized countries, among them consumption of pork or boar meat (1,4). Parenteral transmission was first suggested but not demonstrated (5,6). Because viruses cannot be fully inactivated in blood products, HEV recently emerged as a transfusion-transmitted pathogen, with 6 reported cases, including 3 in which comparative analysis of HEV sequences from blood donor and recipient was performed (7). We describe what is, to our knowledge, the first case in France and the first case worldwide involving a child as blood recipient. A 7-year-old boy was examined in June 2006; he had erythematous-papulous skin and an increased level of alanine aminotransferase (ALT, 796 IU/L) of 1 week's duration. From October 2005 to May 2006, he had received several courses of combined chemotherapy for a rhabdoid tumor in his kidney. Therapy included carbo-platin, cyclophosphamide, etoposide, adriamycin, and vincristine, and, because of the chemotherapy's hema-totoxicity, the patient required 22 transfusions of concentrated erythro-cytes or platelets. Peak levels of ALT and bilirubin were reached 4 weeks after onset of hepatitis (2,001 IU/L and 49 µmol/L, respectively), and ALT levels returned to normal range (8–45 IU/L) 6 weeks later. During a follow-up examination, the boy's prothrom-bin index remained >80%, and clinical signs mostly consisted of clinical jaundice. HEV diagnosis was established by detection in serum of HEV antibod-ies (EIAgen Kits, Adaltis Develop-and HEV RNA with in-house assays. Other infectious or noninfectious causes of acute hepatitis were excluded. HEV immunoglobulin M (IgM) was weakly positive in June 2006 (optical density ratio = 1.6), then strongly positive the next month (ratio = 10.8); IgG remained negative. HEV RNA was detected from serum samples collected in June 2006 by an in-house real-time PCR that targeted the open reading frame 2 region of the HEV genome. Sequences of primers/ probe are as follows: HevMrsRT fwd: 5′-AATTRATTTCGTCGGCY GG-3′; HevMrsRTRev: 5′-ACW G T C G G C T C G C C AT T G-3 ′ ; HevMrsFam: 5′-FAM-ACTCYCGC CASGTYGTCTCA-TAMRA-3′. Serum samples taken from 12 U of blood …