Johnson James R, Johnston Brian, Kuskowski Michael A, Sokurenko Evgeni V, Tchesnokova Veronika
Veterans Affairs Medical Center, Minneapolis, Minnesota, USA University of Minnesota, Minneapolis, Minnesota, USA
Veterans Affairs Medical Center, Minneapolis, Minnesota, USA University of Minnesota, Minneapolis, Minnesota, USA.
Antimicrob Agents Chemother. 2015 Aug;59(8):4471-80. doi: 10.1128/AAC.00673-15. Epub 2015 May 18.
The recent expansion of the H30 subclone of Escherichia coli sequence type 131 (ST131) and its CTX-M-15-associated H30Rx subset remains unexplained. Although ST131 H30 typically exhibits fluoroquinolone resistance, so do multiple other E. coli lineages that have not expanded similarly. To determine whether H30 isolates have more intense fluoroquinolone resistance than other fluoroquinolone-resistant E. coli isolates and to identify possible mechanisms, we determined the MICs for four fluoroquinolones (ciprofloxacin, levofloxacin, moxifloxacin, and norfloxacin) among 89 well-characterized, genetically diverse fluoroquinolone-resistant E. coli isolates (48 non-H30 and 41 H30 [23 H30Rx and 18 H30 non-Rx]). We compared the MICs with the H30 and H30Rx status, the presence/number of nonsynonymous mutations in gyrA, parC, and parE, the presence of aac(6')-1b-cr (an aminoglycoside/fluoroquinolone agent-modifying enzyme), and the efflux pump activity (measured as organic solvent tolerance [OST]). Among 1,518 recent E. coli clinical isolates, ST131 H30 predominated clonally, both overall and among the fluoroquinolone-resistant isolates. Among the 89 study isolates, compared with non-H30 isolates, H30 isolates exhibited categorically higher MICs for all four fluoroquinolone agents, higher absolute ciprofloxacin and norfloxacin MICs, more nonsynonymous mutations in gyrA, parC, and parE (specifically gyrA D87N, parC E84V, and parE I529L), and a numerically higher prevalence of (H30Rx-associated) aac(6')-1b-cr but lower OST scores. All putative resistance mechanisms were significantly associated with the MICs [for aac(6')-1b-cr: ciprofloxacin and norfloxacin only]. parC D87N corresponded with ST131 H30 and parE I529L with ST131 generally. Thus, more intense fluoroquinolone resistance may provide ST131 H30, especially H30Rx [if aac(6')-1b-cr positive], with subtle fitness advantages over other fluoroquinolone-resistant E. coli strains. This urges both parsimonious fluoroquinolone use and a search for other fitness-enhancing traits within ST131 H30.
大肠杆菌序列类型131(ST131)的H30亚克隆及其与CTX-M-15相关的H30Rx亚群最近的扩张原因仍不明。虽然ST131 H30通常表现出氟喹诺酮耐药性,但其他多个未类似扩张的大肠杆菌谱系也是如此。为了确定H30分离株是否比其他氟喹诺酮耐药的大肠杆菌分离株具有更强的氟喹诺酮耐药性,并确定可能的机制,我们测定了89株特征明确、基因多样的氟喹诺酮耐药大肠杆菌分离株(48株非H30和41株H30 [23株H30Rx和18株H30非Rx])对四种氟喹诺酮(环丙沙星、左氧氟沙星、莫西沙星和诺氟沙星)的最低抑菌浓度(MIC)。我们将MIC与H30和H30Rx状态、gyrA、parC和parE中非同义突变的存在/数量、aac(6')-1b-cr(一种氨基糖苷/氟喹诺酮药物修饰酶)的存在以及外排泵活性(以有机溶剂耐受性[OST]衡量)进行了比较。在1518株近期大肠杆菌临床分离株中,ST131 H30在总体上以及氟喹诺酮耐药分离株中均占克隆优势。在89株研究分离株中,与非H30分离株相比,H30分离株对所有四种氟喹诺酮药物的MIC绝对更高,环丙沙星和诺氟沙星的绝对MIC更高,gyrA、parC和parE中存在更多非同义突变(特别是gyrA D87N、parC E84V和parE I529L),并且(与H30Rx相关的)aac(6')-1b-cr的发生率在数值上更高,但OST评分更低。所有推定的耐药机制均与MIC显著相关[对于aac(6')-1b-cr:仅与环丙沙星和诺氟沙星相关]。parC D87N与ST131 H30相对应,parE I529L一般与ST131相对应。因此,更强的氟喹诺酮耐药性可能使ST131 H30,尤其是H30Rx [如果aac(6')-1b-cr呈阳性],相对于其他氟喹诺酮耐药的大肠杆菌菌株具有细微的适应性优势。这促使我们既要谨慎使用氟喹诺酮,又要在ST131 H30中寻找其他增强适应性的特征。