TY - JOUR
T1 - Population snapshot of emergent Streptococcus pneumoniae serotype 19A in the United States, 2005
AU - Moore, Matthew R.
AU - Gertz, Robert E.
AU - Woodbury, Robyn L.
AU - Barkocy-Gallagher, Genevieve A.
AU - Schaffner, William
AU - Lexau, Catherine
AU - Gershman, Kenneth
AU - Reingold, Arthur
AU - Farley, Monica
AU - Harrison, Lee H.
AU - Hadler, James L.
AU - Bennett, Nancy M.
AU - Thomas, Ann R.
AU - McGee, Lesley
AU - Pilishvili, Tamara
AU - Brueggemann, Angela B.
AU - Whitney, Cynthia G.
AU - Jorgensen, James H.
AU - Beall, Bernard
N1 - Funding Information:
We acknowledge the use of the pneumococcal MLST database (Imperial College London), which is funded by the Wellcome Trust. We thank the pneumococcal MLST database curator, Cynthia Bishop, for designation of new alleles and allelic profiles.
Funding Information:
Received 3 September 2007; accepted 26 October 2007; electronically published 5 March 2008. Potential conflicts of interest: none reported. Presented in part: 47th Annual Interscience Conference on Antimicrobial Agents and Chemotherapy, Chicago, IL, 17 September 2007 (abstract S401A-633). Financial support: Emerging Infections Program and Antimicrobial Working Group, Centers for Disease Control and Prevention, and National Vaccine Program Office; and Division of Minority Opportunities in Research, National Institute of General Medical Science, National Institutes of Health (FIRST Institutional Research and Academic Career Development Award [K12] to R.L.W.). Reprints or correspondence: Prof. Bernard Beall, 1600 Clifton Rd., Mailstop C02, Atlanta, GA 30333 (bbeall@cdc.gov).
PY - 2008/4/1
Y1 - 2008/4/1
N2 - Background. Serotype 19A invasive pneumococcal disease (IPD) increased annually in the United States after the introduction of the 7-valent conjugate vaccine (PCV7). To understand this increase, we characterized serotype 19A isolates recovered during 2005. Methods. IPD cases during 1998-2005 were identified through population-based surveillance. We performed susceptibility testing and multilocus sequence typing on 528 (95%) of 554 serotype 19A isolates reported in 2005. Results. The incidence of IPD due to serotype 19A increased from 0.8 to 2.5 cases per 100,000 population between 1998 and 2005 (P < .05), whereas the overall incidence of IPD decreased from 24.4 to 13.8 cases per 100,000 population (P < .05). Simultaneously, the incidence of IPD due to penicillin-resistant 19A isolates increased from 6.7% to 35% (P < .0001). Of 151 penicillin-resistant 19A isolates, 111 (73.5%) belonged to the rapidly emerging clonal complex 320, which is related to multidrug-resistant Taiwan 19F-14. The remaining penicillin-resistant strains were highly related to other clones of PCV7 serotypes or to isolates within major 19A clonal complex 199 (CC199). In 1999, only CC199 and 3 minor clones were apparent among serotype 19A isolates. During 2005, 11 multiple-isolate clonal sets were detected, including capsular switch variants of a serotype 4 clone. Conclusions. PCV7 ineffectiveness against serotype 19A, antibiotic resistance, clonal expansion and emergence, and capsular switching have contributed to the genetic diversity of 19A and to its emergence as the predominant invasive pneumococcal serotype in the United States.
AB - Background. Serotype 19A invasive pneumococcal disease (IPD) increased annually in the United States after the introduction of the 7-valent conjugate vaccine (PCV7). To understand this increase, we characterized serotype 19A isolates recovered during 2005. Methods. IPD cases during 1998-2005 were identified through population-based surveillance. We performed susceptibility testing and multilocus sequence typing on 528 (95%) of 554 serotype 19A isolates reported in 2005. Results. The incidence of IPD due to serotype 19A increased from 0.8 to 2.5 cases per 100,000 population between 1998 and 2005 (P < .05), whereas the overall incidence of IPD decreased from 24.4 to 13.8 cases per 100,000 population (P < .05). Simultaneously, the incidence of IPD due to penicillin-resistant 19A isolates increased from 6.7% to 35% (P < .0001). Of 151 penicillin-resistant 19A isolates, 111 (73.5%) belonged to the rapidly emerging clonal complex 320, which is related to multidrug-resistant Taiwan 19F-14. The remaining penicillin-resistant strains were highly related to other clones of PCV7 serotypes or to isolates within major 19A clonal complex 199 (CC199). In 1999, only CC199 and 3 minor clones were apparent among serotype 19A isolates. During 2005, 11 multiple-isolate clonal sets were detected, including capsular switch variants of a serotype 4 clone. Conclusions. PCV7 ineffectiveness against serotype 19A, antibiotic resistance, clonal expansion and emergence, and capsular switching have contributed to the genetic diversity of 19A and to its emergence as the predominant invasive pneumococcal serotype in the United States.
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U2 - 10.1086/528996
DO - 10.1086/528996
M3 - Article
C2 - 18419539
AN - SCOPUS:42549136536
VL - 197
SP - 1016
EP - 1027
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
SN - 0022-1899
IS - 7
ER -