Evidence map›Paper›PMID 34709520›Full record

ArticleInternational microbiology : the official journal of the Spanish Society for Microbiology2022

Fluoroquinolone resistance contributing mechanisms and genotypes of ciprofloxacin- unsusceptible Pseudomonas aeruginosa strains in Iran: emergence of isolates carrying qnr/aac(6)-Ib genes.

Mahsa Nabilou, Laleh Babaeekhou, Maryam Ghane

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Article in International microbiology : the official journal of the Spanish Society for Microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 57% of its field
1 · What the graph read from it

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3 · Its place in the literature

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4 citing papers in PubMed, 5 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Mahsa NabilouDepartment of Biology, Islamshahr Branch, Islamic Azad University, Islamshahr, Iran.
Laleh BabaeekhouDepartment of Biology, Islamshahr Branch, Islamic Azad University, Islamshahr, Iran. babaeekhou@iiau.ac.ir.ORCID http://orcid.org/0000-0002-5127-3813
Maryam GhaneDepartment of Biology, Islamshahr Branch, Islamic Azad University, Islamshahr, Iran.
Islamic Azad University Islamshahr Branch · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFluoroquinolones (FQs) including ciprofloxacin (CIP) are key antibiotics for the treatment of Pseudomonas aeruginosa infections, but resistance to FQs is developing as a result of chromosomal mutations or efflux pump effects. Plasmid-mediated quinolone resistance (PMQR) has been recently reported in the Enterobacteriaceae family. This study aimed to investigate the mechanisms of CIP insusceptibility in P. aeruginosa isolates from ICU patients and to characterize their genotypes.

methodsA total of 40 ciprofloxacin unsusceptible (CIP-US) P. aeruginosa isolates from Tehran hospitals were recruited in this study. A broth microdilution assay was performed to find acquired resistance profiles of the isolates. All isolates were screened for target-site mutations (gyrA and parC), PMQR genes, and efflux pumps (mexB, D, Y, and E) expression. Clonality was determined by random amplified polymorphic DNA (RAPD)-PCR, and genotyping was performed on 5 selected isolates by analyzing 7 loci in the existing multilocus sequence typing scheme.

resultsThirty-eight out of 40 CIP-US isolates (95%) were categorized as MDR. Seven (17.5%) had gyrA mutation in codons 83, and no mutation was detected in parC; 77.5% of the isolates were positive for PMQR genes. Among PMQR genes, qnrB (30%), qnrC (35%), and qnrD (30%) predominated, while qnrA, qnrS, and aac(6)-Ib genes were harbored by 20.5%, 12.5%, and 15% of the isolates respectively. Efflux pump protein expression was observed in 35% of the isolates. After RAPD-PCR, 19 different genotypes were yielded, and 5 of them were classified into sequence types (STs): 773, 1160, 2011, 2386, and 359.

conclusionIn this first-time study on P. aeruginosa CIP-US strains from Iranian ICU patients, three main CIP unsusceptibility mechanisms were investigated. A single mutation in one CIP target enzyme could explain high CIP resistance. qnr genes in the isolates can be considered as a CIP-unsusceptibility mechanism among studied isolates. Efflux pumps have more contribution in multidrug resistance than CIP susceptibility. CIP-US isolates of this study have not spread from distinct clonal strains and probably emerged from different sources. STs identified for the first time in this study in Iran should be considered as emerging MDR strains.

Indexed as

CiprofloxacinQuinolonesAnti-Bacterial AgentsDrug Resistance, BacterialFluoroquinolonesGenotypeHumansIranMicrobial Sensitivity TestsPlasmidsPseudomonas aeruginosaRandom Amplified Polymorphic DNA TechniqueAnti-Bacterial AgentsCiprofloxacinFluoroquinolonesQuinolonesCIP-USFQMexMLSTPMQRPseudomonas aeruginosa

Identifiers

PMID34709520
OpenAlexW3210327665

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.