Department of Biochemistry and Medical Biotechnology, School of Tropical Medicine, 108 C.R Avenue, Kolkata 700073, India.
Department of Biochemistry and Medical Biotechnology, School of Tropical Medicine, 108 C.R Avenue, Kolkata 700073, India.
J Glob Antimicrob Resist. 2018 Sep;14:217-223. doi: 10.1016/j.jgar.2018.03.009. Epub 2018 Mar 31.
Co-resistance to fluoroquinolones and β-lactams results in treatment complications for uropathogenic Escherichia coli (UPEC) infections. This study aimed to detect the coexistence and co-transmission of plasmid-mediated quinolone resistance (PMQR) and extended-spectrum β-lactamase (ESBL) genes in UPEC from Kolkata, India.
Escherichia coli was detected biochemically from culture-positive urine samples. Antimicrobial resistance and ESBL production were confirmed by disk diffusion assay. Transfer of PMQR and ESBL genes was performed using azide-resistant E. coli J53 as recipient. PCR was conducted to identify PMQR and ESBL genes, plasmid incompatibility types, insertion sequences, integrons and ERIC-PCR patterns.
PMQR determinants were detected in 50.0% (35/70) of ciprofloxacin-resistant isolates, with ESBL production in 42.9% (15/35) and a β-lactamase inhibitor-resistant phenotype in 51.4% (18/35). The highest co-occurrence (37.1%; 13/35) and co-transmission of aac(6')-Ib-cr with bla, bla and bla was observed. Among the conjugal plasmids, replicon types FrepB/FrepB+F1B were predominant, with rare incidences of A/C, N, X, I1, FIIS, L/M and H1. Distribution of integrons and ISEcp1 and IS26, either alone or in combination, irrespective of PMQR and ESBL gene types was observed. Discrete ERIC-PCR profiles indicated that acquisition of PMQR and ESBLs and their dissemination may be attributed to horizontal gene transfer.
This study demonstrates for the first time the risk of co-transmission of fluoroquinolone and β-lactam resistance amongst UPEC from Kolkata, posing a major public-health threat and limiting treatment options. Monitoring at the molecular level is necessary to design appropriate prescription policies to combat the alarming rise in drug resistance amongst these uropathogens.
氟喹诺酮类药物和β-内酰胺类药物的共同耐药导致尿路致病性大肠杆菌（UPEC）感染的治疗复杂化。本研究旨在检测来自印度加尔各答的 UPEC 中质粒介导的喹诺酮耐药（PMQR）和超广谱β-内酰胺酶（ESBL）基因的共存和共传播。
从培养阳性的尿液样本中通过生化方法检测大肠杆菌。通过纸片扩散法确认抗生素耐药性和 ESBL 产生。使用叠氮化钠抗性大肠杆菌 J53 作为受体进行 PMQR 和 ESBL 基因的转移。通过 PCR 检测 PMQR 和 ESBL 基因、质粒不相容类型、插入序列、整合子和 ERIC-PCR 模式。
在 50.0%（35/70）的环丙沙星耐药分离株中检测到 PMQR 决定因素，其中 42.9%（15/35）产生 ESBL，51.4%（18/35）表现出β-内酰胺酶抑制剂耐药表型。观察到最高的共存（37.1%；13/35）和共转移 aac(6')-Ib-cr 与 bla、bla 和 bla。在共轭质粒中，FreprepB/FreprepB+F1B 型为主，A/C、N、X、I1、FIIS、L/M 和 H1 型罕见。观察到整合子和 ISEcp1 和 IS26 的分布，无论是单独存在还是组合存在，无论 PMQR 和 ESBL 基因类型如何。离散的 ERIC-PCR 图谱表明，PMQR 和 ESBL 耐药的获得和传播可能归因于水平基因转移。
本研究首次证明了来自加尔各答的 UPEC 中氟喹诺酮类药物和β-内酰胺类药物耐药性的共传播风险，对公共健康构成重大威胁，并限制了治疗选择。在分子水平上进行监测对于制定适当的处方政策以对抗这些尿路病原体中令人震惊的耐药性上升是必要的。
