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Viral Etiologies of Infant Bronchiolitis, Croup and Upper Respiratory Illness During 4 Consecutive Years

Miller, E. Kathryn MD, MPH*; Gebretsadik, Tebeb MPH; Carroll, Kecia N. MD, MPH*; Dupont, William D. PhD; Mohamed, Yassir A. MS*; Morin, Laura-Lee MA*; Heil, Luke BS*; Minton, Patricia A. RN; Woodward, Kimberly BSN; Liu, Zhouwen MS; Hartert, Tina V. MD, MPH; Williams, John V. MD

Pediatric Infectious Disease Journal: September 2013 - Volume 32 - Issue 9 - p 950–955
doi: 10.1097/INF.0b013e31829b7e43
Original Studies

Background: Prospective data on viral etiology and clinical characteristics of bronchiolitis and upper respiratory illness (URI) in infants are limited.

Methods: This prospective cohort enrolled previously healthy term infants during inpatient or outpatient visits for acute URI or bronchiolitis during September to May 2004 to 2008. Illness severity was determined using an ordinal bronchiolitis severity score. Common respiratory viruses were identified by real-time reverse-transcriptase polymerase chain reaction.

Results: Of 648 infants, 67% were enrolled during inpatient visits and 33% during outpatient visits. Seventy percent had bronchiolitis, 3% croup and 27% URI. Among infants with bronchiolitis, 76% had respiratory syncytial virus (RSV), 18% human rhinovirus (HRV), 10% influenza, 2% coronavirus, 3% human metapneumovirus and 1% parainfluenza virus. Among infants with croup, 39% had HRV, 28% parainfluenza virus, 28% RSV, 11% influenza, 6% coronavirus and none human metapneumovirus. Among infants with URI, 46% had HRV, 14% RSV, 12% influenza, 7% coronavirus, 6% parainfluenza virus and 4% human metapneumovirus. Individual viruses exhibited distinct seasonal, demographic and clinical expression.

Conclusions: The most common infections among infants seeking care in unscheduled medical visits for URI or bronchiolitis were RSV and HRV. Demographic differences were observed between patients with different viruses, suggesting that host and viral factors play a role in phenotypic expression of viral illness.

From the Departments of *Pediatrics, Biostatistics, Medicine, and §Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN.

Accepted for publication May 8, 2013.

Supported by KL2 RR24977-03 (E.K.M.), Thrasher New Investigator Award (E.K.M.), Thrasher Research Fund Clinical Research Grant (T.V.H.), NIH mid-career investigator award K24 AI 077930 (T.V.H.), UL1 RR024975 (Vanderbilt CTSA), NIH K01 AI070808 mentored clinical science award (K.N.C.) and NIH AI085062 (J.V.W.). E.K.M. is supported by NIH K23 AI091691-02 and March of Dimes Basil O’Conner Award. T.V.H. is supported by NIH U19 AI 095227, R01 HS018454, R01 HS019669 and NIH K12 ES 015855. J.V.W. serves on the Scientific Advisory Board for Quidel. T.V.H. has received grant support from MedImmune. E.K.M. has received grant support from MedImmune. The authors have no other funding or conflicts of interest to disclose.

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Address for correspondence: E. Kathryn Miller, MD, MPH, Department of Pediatrics, Division of Allergy, Immunology, and Pulmonary Medicine, Vanderbilt University School of Medicine, 1161 21st Ave S, Nashville, TN 37232. E-mail: Eva.k.miller@vanderbilt.edu.

© 2013 by Lippincott Williams & Wilkins, Inc.