We sought to measure trends in Streptococcus pneumoniae carriage and antibiotic resistance in young children in Massachusetts communities after widespread adoption of heptavalent 7-valent pneumococcal conjugate vaccine (PCV7) and before the introduction of the 13-valent PCV (PCV13).
We conducted a cross-sectional study including collection of questionnaire data and nasopharyngeal specimens among children aged <7 years in primary care practices from 8 Massachusetts communities during the winter season of 2008–2009 and compared with similar studies performed in 2001, 2003–2004, and 2006–2007. Antimicrobial susceptibility testing and serotyping were performed on pneumococcal isolates, and risk factors for colonization in recent seasons (2006–2007 and 2008–2009) were evaluated.
We collected nasopharyngeal specimens from 1011 children, 290 (29%) of whom were colonized with pneumococcus. Non-PCV7 serotypes accounted for 98% of pneumococcal isolates, most commonly 19A (14%), 6C (11%), and 15B/C (11%). In 2008–2009, newly targeted PCV13 serotypes accounted for 20% of carriage isolates and 41% of penicillin-nonsusceptible S. pneumoniae. In multivariate models, younger age, child care, young siblings, and upper respiratory illness remained predictors of pneumococcal carriage, despite near-complete serotype replacement. Only young age and child care were significantly associated with penicillin-nonsusceptible S. pneumoniae carriage.
Serotype replacement post-PCV7 is essentially complete and has been sustained in young children, with the relatively virulent 19A being the most common serotype. Predictors of carriage remained similar despite serotype replacement. PCV13 may reduce 19A and decrease antibiotic-resistant strains, but monitoring for new serotype replacement is warranted.
From the *Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA; †Division of Infectious Diseases, Department of Medicine, and Department of Laboratory; Medicine, Children's Hospital Boston, Boston, MA; ‡Division of General Pediatrics, Department of Medicine, Children's Hospital Boston, Boston, MA; §Maxwell Finland Laboratories, Boston University School of Medicine, Boston, MA; ¶Department of Infectious Disease Epidemiology, Imperial College, London, England; ‖Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA; and **Division of Infectious Diseases and Health Policy Research Institute, University of California Irvine School of Medicine, Irvine, CA.
Accepted for publication October 24, 2011.
P.C.W. and G.M.L. are co-first authors.
Conflicts of interest and source of funding: Supported by the National Institutes of Health (R01 AI066304, Finkelstein). Dr. Hanage (WPH) was funded as a Royal Society Research Fellow during this study. Dr. Pelton receives research support from Novartis, Intercell, Glaxo Smith Kline, and Pfizer, Inc. He has also received honoraria for participation in advisory board meetings on conjugate vaccines from Novartis, GSK and Pfizer, Inc. Dr. Lipsitch has received consulting support from AIR Worldwide, Pfizer, Novartis, and the Avian/Pandemic Flu Registry (Outcome Sciences), supported by Roche. The authors have no other funding or conflicts of interest to disclose.
Address for correspondence: Susan Huang, MD, MPH, Division of Infectious Diseases, University of California Irvine School of Medicine, 101 The City Drive South, City Tower, Suite 400, Zot Code 4081, Orange, CA 92868. E-mail: firstname.lastname@example.org.
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