Background: A dramatic diminution in the number of rotavirus gastroenteritis cases during the 2007 to 2008 rotavirus season in the United States was likely attributable to the availability of an effective rotavirus vaccine for infants since February 2006. To exclude the possibility that factors other than vaccination accounted for the declining case frequency, we examined the 2008 to 2009 experience at the Children's Hospital of Philadelphia (CHOP).
Methods: Infants with acute gastroenteritis presenting to CHOP have been monitored for the presence of rotavirus antigen in the stool by enzyme-linked immunosorbent assay (followed by serotyping if enzyme-linked immunosorbent assay-positive) since the 1994 to 1995 epidemic season.
Results: The number of community-acquired cases during the last full rotavirus season before licensure of a vaccine was 271 in 2005 to 2006, followed by 167 cases in 2006 to 2007 and 36 in 2007 to 2008. Between 2008 and 2009, 73 community-acquired cases were identified. Almost half of the cases were seen among children older than 2 years. Unlike the late-appearing 2007 to 2008 season, the 2008 to 2009 season paralleled the typical time course observed in the prevaccine era. G9P strains caused 64% of the cases.
Conclusion: The sustained decline in the frequency of community-acquired rotavirus gastroenteritis has likely resulted from the use of the new rotavirus vaccines. The age distribution of children hospitalized for rotavirus gastroenteritis has shifted toward older children with the introduction of effective vaccines. The G9 serotype (not included in either vaccine) emerged as the most common cause of rotavirus gastroenteritis at CHOP during the 2008 to 2009 season.
From the *Division of Infectious Diseases, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, PA; †Laboratory of Clinical and Epidemiological Virology, Department of Microbiology and Immunology, Rega Institute for Medical Research, University of Leuven, Leuven, Belgium; ‡Department of Medical Communications, Merck Research Laboratories, Upper Gwynedd, PA; and §Clinical Virology Laboratory, Division of Infectious Diseases, Departments of Pediatrics and Pathology, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, PA.
Accepted for publication February 2, 2010.
Supported in part by Merck & Co., Inc. Supported by a Fonds voor Wetenschappelijk Onderzoek postdoctoral fellowship (to J.M.).
Address for correspondence: H. Fred Clark, DVM, PhD, Division of Infectious Diseases, Abramson Research Center Room 1202, The Children's Hospital of Philadelphia, 3516 Civic Center Blvd., Philadelphia, PA 19104. E-mail: firstname.lastname@example.org.