In 2000, a 7-valent pneumococcal conjugate vaccine (PCV7) was licensed for use among US children. Many sites have since reported changes in invasive pneumococcal disease (IPD). We recognized an opportunity to describe the changes in epidemiology, clinical syndromes, and serotype distribution during a 14-year period including 4 years before vaccine introduction and spanning the entire PCV7 era.
Cases were defined as children <18 years of age who were cared for at Primary Children's Medical Center for culture-confirmed IPD. We defined the prevaccine period as the time frame spanning from 1997 to 2000 and the postvaccine period from 2001 to 2010. Demographics, clinical data, and outcomes were collected through electronic query and chart review. Streptococcus pneumoniae serotyping was performed using the capsular swelling method.
The median age of children with IPD increased from 19 months during the prevaccine period to 27 months during postvaccine period (P = 0.02), with a larger proportion of IPD among children older than 5 years. The proportion of IPD associated with pneumonia increased substantially from 29% to 50% (P < 0.001). This increase was primarily attributable to an increase in complicated pneumonia (17% to 33%, P < 0.001). Nonvaccine serotypes 7F, 19A, 22F, and 3 emerged as the dominant serotypes in the postvaccine period. In children with IPD who were younger than 5 years, for whom vaccine is recommended, 67% of the cases were caused by serotypes in 13-valent PCV during 2005 to 2010.
After PCV7 was introduced, significant changes in IPD were noted. One-third of IPD occurred in children older than 5 years, who were outside the age-group for which PCV is recommended. Continued surveillance is warranted to identify further evolution of the epidemiology, clinical syndromes, and serotype distribution of S. pneumoniae after 13-valent PCV licensure.
From the *Division of Pediatric Infectious Diseases, Department of Pediatrics, University of Utah Health Sciences Center, Salt Lake City, UT; †Pediatrics, Kaiser Permanente, Los Angeles, CA; ‡Primary Children's Medical Center, Intermountain Health Care, Salt Lake City, UT; and §Section of Infectious Diseases, Department of Pediatrics, Baylor College of Medicine, Houston, TX.
Accepted for publication October 18, 2011.
Supported by grants from the National Institute of Allergy and Infectious Diseases (U01A1082482) (to K.A., C.L.B.), (U01 AI074419-01) (to C.L.B., A.J.B., A.T.P.), (U01AI082184-01) (to A.T.P., A.J.B.), 1K23-AI079401-01A1 (to A.J.B.); National Institute of Child Health and Human Development (K-24 HD047249-01A1) (to C.L.B.); and the Centers for Disease Control Prevention (U18-IP000303-01) (to K.A., C.L.B., A.T.P., A.J.B.). This project was further supported by the University of Utah, Department of Pediatrics through the Children's Health Research Center and the Pediatric Clinical and Translational Research Scholars Program, the H. A. and Edna Benning Presidential Endowment, and the Primary Children's Medical Center Foundation. The authors have no other funding or conflicts of interest to disclose.
Address for correspondence: Krow Ampofo, MB, ChB, Division of Pediatric Infectious Disease and Geographic Medicine, University of Utah Health Sciences Center, 295 Chipeta Way, 2S010, Salt Lake City, UT 84108. E-mail: Krow.Ampofo@hsc.utah.edu.