Background: Invasive pneumococcal disease (IPD) rates decreased after 7-valent pneumococcal conjugate vaccine (PCV) introduction in 2000. We assessed whether previously described decreases were sustained.
Methods: Active laboratory-based surveillance identified IPD cases in 5 Tennessee Counties. For each case, clinical data were collected, and antibiotic susceptibility testing and serotyping were performed. Penicillin resistance was defined as intermediate- or high-level resistance to penicillin. Serotypes were classified as PCV7, PCV13 (6 additional serotypes not in PCV7), pneumococcal polysaccharide vaccine (PPV23, 11 additional serotypes not in PCV13 and nonvaccine serotypes. Total and penicillin-resistant IPD rates were calculated for persons <2, 2–14 and ≥15 years of age before (1998 to 1999) and after (2001 to 2008) PCV7 introduction.
Results: Annual IPD rates in children <2 years of age declined by 75% after PCV7 introduction (P < 0.001). Annual IPD rates in children 2–14 years of age declined by 51% after PCV7 introduction (P < 0.001). IPD rates in persons ≥15 of age years initially decreased 40% from 22 to 13 per 100,000 person-years (from 1998 through 2004), and then increased to 18 per 100,000 person-years in 2008. Both IPD and penicillin-resistant IPD PCV7 serotypes were almost completely eliminated in all age groups by 2008. During 2005 to 2008, 52.5%, 58% and 38% of IPD serotypes in children <2, 2–14 and ≥15 years of age, respectively, were the additional 6 serotypes in PCV13.
Conclusions: Overall, 9 years after PCV7 introduction both penicillin-susceptible and resistant IPD rates PCV7 serotypes have been nearly eliminated in Tennessee in all age groups. Total IPD rates remain reduced in children <15 years of age, whereas total IPD rates in persons ≥15 years of age have approached pre-PCV7 rates due to modest increases in nonvaccine serotypes.
From the *Departments of Pediatrics, ‡Preventive Medicine, §Medicine, ¶Biostatistics, and ‖Center for Education and Research on Therapeutics, Vanderbilt University School of Medicine; **Tennessee Department of Health; and ‡‡Geriatric Research Education and Clinical Center and Clinical Research Center of Excellence, Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN.
Accepted for publication January 15, 2013.
We would like to dedicate this article to our late friend and colleague Patrick Arbogast, PhD, a brilliant statistician who was integral to our research and teaching mission at Vanderbilt. He is missed (August 2012).
Supported in part by ATPM/CDC Cooperative Agreement TS-0825 and CDC Emerging Infections Program Cooperative Agreement U50/CCU416123. N.B.H. received support from NIH Vanderbilt Mentored Clinical Research Scholar Program K12 RR-017697.
N.B.H. receives grant support from Sanofi Pasteur and Pfizer and served on the data safety monitoring board for Novartis; C.G.G. has received research support from Pfizer and served as consultant for GSK; T.R.T. received research support from Sanofi Pasteur; P.G.A. received grant support from Pfizer and W.S. has received consulting fees from Merck, Pfizer, Dynavax, GlaxoSmithKline and Novartis. The authors have no other funding or conflicts of interest to disclose.
Address for correspondence: Natasha Halasa, MD, MPH, Associate Professor of Pediatrics, Pediatric Infectious Diseases, Vanderbilt University Medical Center, D7232 MCN, 1161 21st Ave South, Nashville, TN 37232. E-mail: firstname.lastname@example.org.