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伤寒血清型和副伤寒血清型沙门氏菌中缺乏外排介导的喹诺酮耐药性。

Lack of efflux mediated quinolone resistance in Salmonella enterica serovars Typhi and Paratyphi A.

机构信息

UMR1282 Infectiologie et Santé Publique, Institut National de la Recherche Agronomique Nouzilly, France ; UMR1282 Infectiologie et Santé Publique, Université François Rabelais de Tours Tours, France.

Unité des Bactéries Pathogènes Entériques, Centre National de Référence des Escherichia coli, Institut Pasteur, Shigella et Salmonella Paris, France.

出版信息

Front Microbiol. 2014 Jan 27;5:12. doi: 10.3389/fmicb.2014.00012. eCollection 2014.

DOI:10.3389/fmicb.2014.00012
PMID:24478769
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3902205/
Abstract

Salmonella enterica serovars Typhi and Paratyphi A isolates from human patients in France displaying different levels of resistance to quinolones or fluoroquinolones were studied for resistance mechanisms to these antimicrobial agents. All resistant isolates carried either single or multiple target gene mutations (i.e., in gyrA, gyrB, or parC) correlating with the resistance levels observed. Active efflux, through upregulation of multipartite efflux systems, has also been previously reported as contributing mechanism for other serovars. Therefore, we investigated also the occurrence of non-target gene mutations in regulatory regions affecting efflux pump expression. However, no mutation was detected in these regions in both Typhi and Paratyphi isolates of this study. Besides, no overexpression of the major efflux systems was observed for these isolates. Nevertheless, a large deletion of 2334 bp was identified in the acrS-acrE region of all S. Typhi strains but which did not affect the resistance phenotype. As being specific to S. Typhi, this deletion could be used for specific molecular detection purposes. In conclusion, the different levels of quinolone or FQ resistance in both S. Typhi and S. Paratyphi A seem to rely only on target modifications.

摘要

对来自法国人类患者的具有不同程度抗喹诺酮类或氟喹诺酮类药物耐药性的伤寒沙门氏菌血清型 Typhi 和 Paratyphi A 分离株进行了研究,以了解其对这些抗菌药物的耐药机制。所有耐药分离株均携带与观察到的耐药水平相关的单个或多个靶基因突变(即在 gyrA、gyrB 或 parC 中)。先前也有报道称,通过上调多组分外排系统的主动外排作用也是其他血清型的一种耐药机制。因此,我们还研究了影响外排泵表达的非靶基因调控区突变的发生情况。然而,在本研究的伤寒和副伤寒分离株的这些区域均未检测到突变。此外,这些分离株中未观察到主要外排系统的过度表达。尽管如此,在所有伤寒沙门氏菌菌株的 acrS-acrE 区域发现了 2334bp 的大片段缺失,但这并未影响耐药表型。由于该缺失仅存在于伤寒沙门氏菌中,因此可用于特定的分子检测目的。总之,伤寒沙门氏菌和副伤寒沙门氏菌 A 中不同程度的喹诺酮类或氟喹诺酮类药物耐药性似乎仅依赖于靶位修饰。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/215a/3902205/6e4d0f8b1d6b/fmicb-05-00012-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/215a/3902205/6e4d0f8b1d6b/fmicb-05-00012-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/215a/3902205/6e4d0f8b1d6b/fmicb-05-00012-g0001.jpg

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