Emergence of 19A as virulent and multidrug resistant Pneumococcus in Massachusetts following universal immunization of infants with pneumococcal conjugate vaccine.
BACKGROUND
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.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Pelton
Stephen I
SI
Maxwell Finland Laboratory for Infectious Diseases, Boston University School of Medicine, Boston, MA, USA. spelton@bu.edu
Huot
Heather
H
Finkelstein
Jonathan A
JA
Bishop
C J
CJ
Hsu
Katherine K
KK
Kellenberg
Joan
J
Huang
Susan S
SS
Goldstein
Richard
R
Hanage
William P
WP
D000900:Anti-Bacterial Agents / Q000494:pharmacology; D002353:Carrier State; D002675:Child, Preschool; D016000:Cluster Analysis; D004269:DNA, Bacterial / Q000737:chemistry / Q000235:genetics; D024901:Drug Resistance, Multiple, Bacterial; D000069443:Heptavalent Pneumococcal Conjugate Vaccine; D006801:Humans; D015994:Incidence; D007223:Infant; D008404:Massachusetts / Q000453:epidemiology; D022401:Meningococcal Vaccines / Q000276:immunology*; D008826:Microbial Sensitivity Tests; D011008:Pneumococcal Infections / Q000453:epidemiology / Q000276:immunology* / Q000382:microbiology*; D022242:Pneumococcal Vaccines / Q000276:immunology*; D017422:Sequence Analysis, DNA; D012703:Serotyping; D013296:Streptococcus pneumoniae / Q000145:classification* / Q000187:drug effects* / Q000276:immunology / Q000472:pathogenicity
D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial; D000069443:Heptavalent Pneumococcal Conjugate Vaccine; D022401:Meningococcal Vaccines; D022242:Pneumococcal Vaccines