The long-term effects of selective pressure from conjugate pneumococcal vaccine on the serotype distribution and antimicrobial resistance of carriage and invasive isolates of Streptococcus pneumoniae are unknown. Early changes demonstrate a reduction in vaccine serotypes and an increase in nonvaccine serotypes (NVT) among both carriage and invasive isolates. Ongoing surveillance is necessary to identify emerging invasive serotypes and antimicrobial susceptibilities.
Enhanced surveillance of invasive pneumococcal disease in Massachusetts began in October 2001 and remains ongoing. Isolates from children less than 5 are sent to the Massachusetts Department of Public Health and subsequently to the Maxwell Finland laboratory for serotyping and determination of antimicrobial susceptibility. Annual incidence rates for vaccine serotype and NVT disease are calculated using 2000 census data.
NVT caused 72%–91% of invasive pneumococcal disease annually in children less than 5 years of age between 2002 and 2005. Serotype 19A has emerged as the most frequent cause of IPD in Massachusetts. A multidrug-resistant clone (ceftriaxone, amoxicillin, azithromycin and trimethoprim-sulfamethoxazole) (MLST 320) was first identified in Massachusetts in 2005.
Three years after the introduction of pneumococcal conjugate vaccine for universal administration to children less than 2 in Massachusetts, a significant increase in invasive disease due to serotype 19A was observed. Although MLST 199 remains the most frequent sequence type among invasive isolates (of 19A), a multidrug-resistant sequence type, not previously identified in Massachusetts, has become an important cause of invasive disease. Further surveillance of the changing ecology of S. pneumoniae is necessary as a 4-year time period is not sufficient to fully evaluate the impact of PCV of pneumococcal infections.
From the *Maxwell Finland Laboratory for Infectious Diseases; †Department of Pediatrics, Boston University School of Medicine; Boston, MA; ‡Department of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim Health Care; §Division of General Pediatrics, Children's Hospital Boston, Boston, MA; and ∥Department of Infectious Disease Epidemiology, St. Mary's Hospital, Imperial College London, London, UK.
Accepted for publication January 25, 2007.
Address for correspondence: Stephen I. Pelton, MD, Maxwell Finland Laboratory for Infectious Disease, Boston Medical Center, Boston, MA, 617-414-7408; E-mail: email@example.com.