Shifting Genetic Structure of Invasive Serotype 19A Pneumococci in the United States

Abstract

(See the editorial commentary by Tyrrell, on pages 1345–7. ) Background. Following 7-valent conjugate vaccine introduction in the United States in 2000, invasive serotype (sero19A) pneumococcal disease (IPD) emerged rapidly. Sero19A IPD incidence increased slightly during 2005–2008 (from 2.3 cases to 2.5 cases per 100,000 population), whereas sero19A penicillin resistance (defined as a minimum inhibitor concentration [MIC] ≥2 μg/mL) increased significantly (from 28.7% to 43.7%). To better understand changes, we characterized sero19A isolates recovered during 2004–2008. Methods. We performed antimicrobial susceptibility testing on all 2767 sero19A IPD isolates identified through the Centers for Disease Control Active Bacterial Core surveillance during 2004–2008. We genotyped 1804 (96.3%) of 1874 sero19A isolates recovered during 2005–2007 and all 148 year 2008 sero19A isolates from children Results. Resistant clonal complex (CC) 320/271^19A increased from 20.9% (115 of 550) to 32.9% (208 of 633; P < .001) of IPD isolates during 2005–2007, which paralleled increased sero19A penicillin resistance (from 28.7% [163 of 567 isolates] to 39.5% [261 of 661 isolates]; P < .001). Total IPD due to 320/271^19A increased during 2005–2007 and increased from 2.1 to 3.6 cases per 100,000 population during 2005–2008 in children 19A increased from 7.5% (41 of 550) to 13.6% (85 of 633) of sero19A isolates during 2005–2007 (P = .002). Conclusions. Sero19A rates may have plateaued; however, clonal shifts are increasing resistance. Increased IPD caused by CC320/271^19A and CC695^19A could reflect additional selective advantages in addition to resistance.