Adam Heather J, Schurek Kristen N, Nichol Kimberly A, Hoban Chris J, Baudry Trish J, Laing Nancy M, Hoban Daryl J, Zhanel George G
Clinical Microbiology, Health Sciences Centre, MS673-820 Sherbrook St., Winnipeg, Manitoba R3A 1R9, Canada.
Antimicrob Agents Chemother. 2007 Jan;51(1):198-207. doi: 10.1128/AAC.00609-06. Epub 2006 Nov 6.
Molecular characterization of fluoroquinolone-resistant Streptococcus pneumoniae in Canada was conducted from 1997 to 2005. Over the course of the study, 205 ciprofloxacin-resistant isolates were evaluated for ParC and GyrA quinolone resistance-determining region (QRDR) substitutions, substitutions in the full genes of ParC, ParE, and GyrA, reserpine sensitivity, and serotype and by pulsed-field gel electrophoresis. Rates of ciprofloxacin resistance of S. pneumoniae increased significantly, from less than 1% in 1997 to 4.2% in 2005. Ciprofloxacin resistance was greatest in people >64 years of age and least in those <16 years of age. Significant increases were also noted in rates of resistance to gatifloxacin, gemifloxacin, levofloxacin, and moxifloxacin, to the current rates of 1.6%, 1.0%, 1.1%, and 1.0%, respectively. The most common genotype observed consisted of QRDR substitutions in GyrA (Ser81Phe) and ParC (Ser79Phe). Substitutions outside the QRDR of GyrA, ParC, and ParE were not associated with fluoroquinolone resistance in this study. Overall, 21% of isolates were reserpine-sensitive and were thus assumed to be efflux positive. The ciprofloxacin-resistant isolates belonged to 35 different serotypes, but 10 (19F, 11A, 23F, 6B, 22F, 12F, 6A, 14, 9V, and 19A) accounted for 72% of all isolates. The majority of the isolates were found to be genetically unrelated by pulsed-field gel electrophoresis. Within the observed clusters, there was considerable genetic heterogeneity with regard to fluoroquinolone resistance mechanisms and serotypes. Continued surveillance and molecular analysis of fluoroquinolone-resistant S. pneumoniae in Canada are essential for appropriate empirical treatment of infections and early detection of novel resistance mechanisms.
1997年至2005年期间,对加拿大耐氟喹诺酮类肺炎链球菌进行了分子特征分析。在研究过程中,对205株耐环丙沙星菌株进行了ParC和GyrA喹诺酮耐药决定区(QRDR)替代、ParC、ParE和GyrA全基因替代、利血平敏感性、血清型以及脉冲场凝胶电泳分析。肺炎链球菌对环丙沙星的耐药率显著上升,从1997年的不到1%升至2005年的4.2%。环丙沙星耐药率在64岁以上人群中最高,在16岁以下人群中最低。加替沙星、吉米沙星、左氧氟沙星和莫西沙星的耐药率也显著上升,目前分别为1.6%、1.0%、1.1%和1.0%。观察到的最常见基因型包括GyrA(Ser81Phe)和ParC(Ser79Phe)中的QRDR替代。在本研究中,GyrA、ParC和ParE的QRDR外的替代与氟喹诺酮耐药性无关。总体而言,21%的分离株对利血平敏感,因此被认为是外排阳性。耐环丙沙星分离株属于35种不同血清型,但10种(19F、11A、23F、6B、22F、12F、6A、14、9V和19A)占所有分离株的72%。通过脉冲场凝胶电泳发现,大多数分离株在基因上不相关。在观察到的簇中,氟喹诺酮耐药机制和血清型方面存在相当大的基因异质性。对加拿大耐氟喹诺酮类肺炎链球菌进行持续监测和分子分析对于感染的适当经验性治疗和新耐药机制的早期发现至关重要。