Rotavirus (RV) antigenemia and RNAemia are common findings in rotavirus-infected children. Sporadic associations between RV antigenemia and extraintestinal manifestations of RV infection have been observed. We examined the clinical severity of RV gastroenteritis in patients with and without RV antigenemia or RNAemia.
Stool, serum and whole blood samples were collected from children seen with acute gastroenteritis in Tampere University Hospital and studied for RV using reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. Only exclusively RV-positive specimens were included into this study. The patients were divided into groups according to RV findings from stool, serum and blood specimens. Clinical manifestations were graded according to 20-point Vesikari scoring system.
Of 374 children, 155 (41%) had RV in their stools. Of these 155 children, 105 (67%) were found to have RV RNA in the serum; of those, 94 (90%) had also RV enzyme-linked immunosorbent assay antigen. Thus antigenemia occurred in 61% (94 cases) of RV-infected children all of whom had concomitant RNAemia. Neither antigenemia nor RNAemia were detected in 85 patients with non-RV gastroenteritis. Patients who had RV RNA and RV antigen in both serum and stools were more likely to have a higher level of fever and more severe vomiting than patients who had RV only in stools. G1 genogroup RV was more often associated with RNAemia and antigenemia than other genogroups combined.
Rotavirus antigenemia and viremia are commonly detected in children hospitalized for RV gastroenteritis and may be associated with increased severity of fever and vomiting.
From the *Vaccine Research Center, University of Tampere; and †Department of Pediatrics, Tampere University Hospital, Tampere, Finland.
Accepted for publication October 8, 2013.
T. Vesikari has been Principal Investigator of clinical trials of rotavirus vaccines produced by Merck and GlaxoSmithKline, and is a member of advisory boards of SanofiPasteur-MSD, Merck and Pfizer. Funding was provided by University of Tampere. The authors have no other funding or conflicts of interest to disclose.
Address for correspondence: Maria Hemming, BM, Biokatu 10, 33520 Tampere, Finland. E-mail: firstname.lastname@example.org.