Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Antimicrob Agents Chemother. 2012 Feb;56(2):743-50. doi: 10.1128/AAC.05122-11. Epub 2011 Nov 28.
We conducted population-based surveillance for pneumococcal bacteremia within a 5-county region surrounding Philadelphia from October 2001 through September 2008, the period following introduction of the seven-valent pneumococcal conjugate vaccine. Erythromycin resistance increased from 14.7% in 2001-2002 to 20.3% in 2007-2008, while the resistance rate to penicillin (MIC, ≥2 μg/ml) decreased from 7.2% to 4.2% during the same period. The most predominant serotypes associated with erythromycin resistance in 2007-2008 included 19A (29.7%), 15A (29.2%), 6C (10.1%), 3 (5.6%), and 6A (4.5%). The molecular mechanisms for the increasing erythromycin resistance were mainly due to the growing presence of mef(A) negative erm(B)(+) and mef(A)(+) erm(B)(+) genotypes, which increased from 20.0% to 46.1% and from 1.8% to 19.1%, respectively, from 2001-2002 to 2007-2008. However, mef(A)-mediated erythromycin resistance decreased from 72.7% in 2001-2002 to 34.8% in 2007-2008. Serotypes related to the erm(B) gene were 15A (45.6%), 19A (20.9%), 3 (10.1%), and 6B (6.3%); serotypes related to the mef(A) gene were 6A (18.6%), 19A (15.0%), 6C (9.3%), and 14(8.4%); serotypes associated with the presence of both erm(B) and mef(A) were 19A (81.5%), 15A (7.7%), and 19F (6.2%). Pulsed-field gel electrophoresis analysis demonstrated that erythromycin-resistant isolates within the 19A serotype were genetically diverse and related to several circulating international clones. In contrast, erythromycin-resistant isolates within the 15A serotype consisted of clonally identical or closely related isolates.
我们在费城周边的 5 个县进行了基于人群的肺炎球菌菌血症监测,监测时间为 2001 年 10 月至 2008 年 9 月,这段时间正值 7 价肺炎球菌结合疫苗推出之后。红霉素耐药率从 2001-2002 年的 14.7%上升到 2007-2008 年的 20.3%,而同期青霉素(MIC≥2μg/ml)耐药率从 7.2%下降到 4.2%。2007-2008 年与红霉素耐药相关的最主要血清型包括 19A(29.7%)、15A(29.2%)、6C(10.1%)、3(5.6%)和 6A(4.5%)。红霉素耐药性增加的主要分子机制是由于 mef(A)阴性 erm(B)(+)和 mef(A)(+) erm(B)(+)基因型的出现增加,这两种基因型的比例分别从 2001-2002 年的 20.0%和 1.8%增加到 2007-2008 年的 46.1%和 19.1%。然而,mef(A)介导的红霉素耐药性从 2001-2002 年的 72.7%下降到 2007-2008 年的 34.8%。与 erm(B)基因相关的血清型为 15A(45.6%)、19A(20.9%)、3(10.1%)和 6B(6.3%);与 mef(A)基因相关的血清型为 6A(18.6%)、19A(15.0%)、6C(9.3%)和 14(8.4%);同时携带 erm(B)和 mef(A)基因的血清型为 19A(81.5%)、15A(7.7%)和 19F(6.2%)。脉冲场凝胶电泳分析表明,19A 血清型中的红霉素耐药分离株具有遗传多样性,并与几个流行的国际克隆株有关。相比之下,15A 血清型中的红霉素耐药分离株由克隆相同或密切相关的分离株组成。