Hospital Clínic, Cellex Laboratory, CIBERES (Center for net Biomedical Research Respiratory diseases, 06/06/0028) - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), School of Medicine, University of Barcelona, Spain.
Respiratory Intensive Care Unit, Pneumology Department, Hospital Clínic, Barcelona, Spain.
J Antimicrob Chemother. 2022 May 29;77(6):1600-1610. doi: 10.1093/jac/dkac084.
Non-cystic fibrosis bronchiectasis (BE) is a chronic structural lung condition that facilitates chronic colonization by different microorganisms and courses with recurrent respiratory infections and frequent exacerbations. One of the main pathogens involved in BE is Pseudomonas aeruginosa.
To determine the molecular mechanisms of resistance and the molecular epidemiology of P. aeruginosa strains isolated from patients with BE.
A total of 43 strains of P. aeruginosa were isolated from the sputum of BE patients. Susceptibility to the following antimicrobials was analysed: ciprofloxacin, meropenem, imipenem, amikacin, tobramycin, aztreonam, piperacillin/tazobactam, ceftazidime, ceftazidime/avibactam, ceftolozane/tazobactam, cefepime and colistin. The resistance mechanisms present in each strain were assessed by PCR, sequencing and quantitative RT-PCR. Molecular epidemiology was determined by MLST. Phylogenetic analysis was carried out using the eBURST algorithm.
High levels of resistance to ciprofloxacin (44.19%) were found. Mutations in the gyrA, gyrB, parC and parE genes were detected in ciprofloxacin-resistant P. aeruginosa strains. The number of mutated QRDR genes was related to increased MIC. Different β-lactamases were detected: blaOXA50, blaGES-2, blaIMI-2 and blaGIM-1. The aac(3)-Ia, aac(3)-Ic, aac(6″)-Ib and ant(2″)-Ia genes were associated with aminoglycoside-resistant strains. The gene expression analysis showed overproduction of the MexAB-OprM efflux system (46.5%) over the other efflux system. The most frequently detected clones were ST619, ST676, ST532 and ST109.
Resistance to first-line antimicrobials recommended in BE guidelines could threaten the treatment of BE and the eradication of P. aeruginosa, contributing to chronic infection.
非囊性纤维化支气管扩张症（BE）是一种慢性结构性肺病，易导致不同微生物的慢性定植，并伴有反复呼吸道感染和频繁恶化。参与 BE 的主要病原体之一是铜绿假单胞菌。
确定 BE 患者分离的铜绿假单胞菌菌株的耐药分子机制和分子流行病学。
从 BE 患者的痰中分离出 43 株铜绿假单胞菌。分析以下抗菌药物的敏感性：环丙沙星、美罗培南、亚胺培南、阿米卡星、妥布霉素、氨曲南、哌拉西林/他唑巴坦、头孢他啶、头孢他啶/阿维巴坦、头孢洛扎/他唑巴坦、头孢吡肟和多粘菌素。通过 PCR、测序和定量 RT-PCR 评估每种菌株的耐药机制。通过 MLST 确定分子流行病学。使用 eBURST 算法进行系统发育分析。
发现对环丙沙星（44.19%）的耐药水平较高。在耐环丙沙星的铜绿假单胞菌菌株中检测到 gyrA、gyrB、parC 和 parE 基因突变。QRDR 基因突变数量与 MIC 增加有关。检测到不同的β-内酰胺酶：blaOXA50、blaGES-2、blaIMI-2 和 blaGIM-1。aac(3)-Ia、aac(3)-Ic、aac(6″)-Ib 和 ant(2″)-Ia 基因与氨基糖苷类耐药株有关。基因表达分析显示 MexAB-OprM 外排系统（46.5%）过度表达，而其他外排系统表达不足。最常检测到的克隆是 ST619、ST676、ST532 和 ST109。
对 BE 指南推荐的一线抗菌药物的耐药性可能威胁 BE 的治疗和铜绿假单胞菌的清除，导致慢性感染。
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