Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations in quinolone-resistant Escherichia coli isolated from humans and swine in Denmark
Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations in quinolone-resistant Escherichia coli isolated from humans and swine in Denmark
复制标题
DOI：
10.1089/mdr.2008.0821
复制
发表时间：
2008-06-01
影响因子：
2.6
通讯作者：
Aarestrup, Frank Moller
中科院分区：
文献类型：
--
作者：
Cavaco, Lina Maria;Frimodt-Moller, Niels;Aarestrup, Frank Moller
在丹麦从人（n = 85）和猪（n = 39）分离的124株大肠杆菌中，研究了喹诺酮类耐药机制的流行率以及与萘啶酸（NAL）和环丙沙星（CIP）最低抑菌浓度（MIC）的相关性。收集物包括来自人（n = 51）和猪（n = 8）的59个高水平CIP抗性分离物（MIC >= 4）和来自人（n = 34）和猪（n = 31）的65个低水平CIP抗性分离物（MIC >= 0.125）。通过gyrA、gyrB、parC和帕雷的喹诺酮类耐药决定区（QRDRs）的PCR扩增和测序筛选靶向修饰的耐药性。除两株（98%）外，所有菌株均发生QRDR突变。所有高水平CIP抗性E.大肠杆菌中gyrA基因有一个或两个突变，并伴有parC或帕雷突变。parC和帕雷的突变仅与gyrA突变结合发现，在gyrB中未观察到突变。通过外排泵抑制剂（EPI）琼脂稀释试验，在10例人（11.8%）和29例猪（74.4%）分离株中检测到外排泵机制。在12株CIP高水平耐药的人分离株中发现了aac（6 '）-Ib-cr基因通过酶修饰介导耐药。qnrA和qnrS基因赋予喹诺酮类药物耐药的目标保护中检测到两个人类低水平CIP耐药株，不显示NAL耐药。正如预期的那样，QRDRs中的靶点突变是喹诺酮类药物耐药的最普遍机制。在大多数猪分离株中，这种机制得到了外排机制的补充。通过靶点保护或酶修饰的可转移耐药性不太常见（10%），仅限于人分离株。
Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations (MICs) of nalidixic acid (NAL) and ciprofloxacin (CIP) were investigated in 124 Escherichia coli isolated from humans (n = 85) and swine (n = 39) in Denmark. The collection included 59 high-level CIP-resistant isolates (MIC >= 4) from human (n = 51) and pig origin (n = 8) and 65 low-level CIP-resistant isolates (MIC >= 0.125) from human (n = 34) and pig origin (n = 31). Resistance by target modification was screened by PCR amplification and sequencing, of the quinolone resistance determining regions (QRDRs) of gyrA, gyrB, parC, and parE. QRDR mutations occurred in all except two isolates (98%). All high-level CIP-resistant E. coli had one or two mutations in gyrA in combination with mutations in parC or parE. Mutations in parC and parE were only found in combination with gyrA mutations, and no mutations were observed in gyrB. Efflux pump mechanisms were detected in 10 human (11.8%) and 29 porcine (74.4%) isolates by an efflux pump inhibitor (EPI) agar dilution assay. The aac(6')-Ib-cr gene mediating resistance by enzymatic modification was found in 12 high-level CIP-resistant human isolates. The qnrA and qnrS genes conferring quinolone resistance by target protection were detected in two human low-level CIP-resistant isolates that did not display NAL resistance. As expected, target mutation in QRDRs was the most prevalent mechanism of quinolone resistance. This mechanism was complemented by efflux mechanisms in most porcine isolates. Transferable resistance by target protection or enzymatic modification was less common (10%) and restricted to human isolates.