Fluoroquinolone resistance and the associated genetic mechanisms were assessed by antimicrobial susceptibility and whole genome sequencing in 56 Pseudomonas aeruginosa strains from human, animal, food and environmental origins. P. aeruginosa PAO1, PA7 and PA14 reference strains were also included in the study. Twenty-two strains (37%) were resistant to, at least, one fluoroquinolone agent. Correlation between the number of changes in GyrA and ParC proteins and the level of fluoroquinolone resistance was observed. Mutations or absence of genes, such as mexZ, mvaT and nalD encoding efflux pumps regulators, were also found in resistant strains. The crpP gene was detected in 43 strains (72.9%; 17 of them non-clinical strains), and coded seven different CrpP variants, including a novel one (CrpP-7). The crpP gene was located in 23 different chromosomal mobile integrative and conjugative elements (ICEs), inserted in two tRNAs integration sites. A great variety of structures was detected in the crpP-ICEs elements, e.g., the fimbriae related cup clusters, the mercury resistance mer operon, the pyocin S5 or S8 bacteriocin encoding genes, and mobilization genes. The location of crpP-like genes in mobilizable ICEs and linked to heavy metal resistance and virulence factors is of significant concern in P. aeruginosa. This work provides a genetic explanation of the fluoroquinolone resistance and crpP-associated pathogenesis of P. aeruginosa from a One-Health approach.

中文翻译：

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人类、动物、食物和环境来源的铜绿假单胞菌对氟喹诺酮类药物的耐药性：CrpP 和可动员 ICE 的作用

通过对来自人类、动物、食物和环境来源的 56 种铜绿假单胞菌菌株的抗菌敏感性和全基因组测序评估了氟喹诺酮类药物耐药性和相关遗传机制。铜绿假单胞菌PAO1、PA7 和 PA14 参考菌株也包括在研究中。22 株 (37%) 至少对一种氟喹诺酮类药物具有抗药性。观察到 GyrA 和 ParC 蛋白的变化数量与氟喹诺酮类药物耐药水平之间的相关性。在耐药菌株中也发现了基因突变或缺失，例如编码外排泵调节剂的mexZ、mvaT和nalD 。crpP _基因在 43 株（72.9%；其中 17 株为非临床株）中检测到，并编码了 7 种不同的 CrpP 变体，包括一种新的 CrpP 变体（CrpP-7）。crpP基因位于 23 个不同的染色体移动整合和接合元件 (ICE) 中，插入两个 tRNA 整合位点。在crpP- ICEs元件中检测到多种结构，例如菌毛相关杯簇、耐汞mer操纵子、pyocin S5或S8细菌素编码基因和动员基因。crpP样基因在可动员 ICE 中的位置并与重金属抗性和毒力因子相关，这在铜绿假单胞菌中是一个重要问题。. 这项工作从 One-Health 方法提供了对铜绿假单胞菌的氟喹诺酮耐药性和crpP相关发病机制的遗传解释。