<p>Detection of Chromosomal and Plasmid-Mediated Quinolone Resistance Among <em>Escherichia coli</em> Isolated from Urinary Tract Infection Cases; Zagazig University Hospitals, Egypt</p>

Abstract

Introduction: Resistance to fluoroquinolones (FQ) in uropathogenic Escherichia coli (UPEC) has emerged as a growing problem. Chromosomal mutations and plasmidmediated quinolone resistance (PMQR) determinants have been implicated. Data concerning the prevalence of these determinants in UPEC in our hospital are quite limited. Purpose: To investigate the occurrence and genetic determinants of FQ resistance in UPEC isolated from urinary tract infection (UTI) cases in Zagazig University Hospitals. Patients and Methods: Following their isolation, the identification and susceptibility of UPEC isolates were performed by matrix-assisted laser desorption/ionization-time-of-flight mass spectrometer (MALDI-TOF MS). FQ resistance was detected by the disc diffusion method. Ciprofloxacin minimal inhibitory concentration (MIC) was determined using E-test. Chromosomal mutations in the gyrA gene were detected using polymerase chain reactionrestriction fragment length polymorphism (PCR-RFLP), and for detection of PMQR, a couple of multiplex PCR reactions were used. Results: Among a total of 192 UPEC isolates, 46.9% (n=90) were FQ resistant. More than half of the isolates (57.8%) exhibited high-level ciprofloxacin resistance (MIC > 32 µg/mL). Mutations in gyrA were detected in 76.7% of isolates, with 34.4% having mutations at more than one site. PMQR determinants were detected in 80.1% of UPEC isolates, with aac(6ʹ)-Ibcr gene being the most frequent found in 61.1% of isolates. Conclusion: There is a high prevalence of both gyrA mutations and PMQR determinants among UPEC isolates in our hospital which contribute to high-level ciprofloxacin resistance, a finding that may require the revision of the antibiotics used for empirical treatment of UTI.

Characterization of Integrons and Quinolone Resistance in Clinical Escherichia coli Isolates in Mansoura City, Egypt

“…Among the detected qnr genes, qnrS International Journal of Microbiology showed the highest prevalence, which agrees with previous studies [47][48][49]. Although detected in only 4.65% of our isolates, qnrB gene was reported as one of the most abundant genes in other studies [39,45,50]. qnrC gene was absent in all tested isolates, which agrees with other studies [45,51,52].…”

“…PMQR was detected in 36/43 (83.72%) phenotypically fluoroquinolone-resistant isolates. Several studies showed similar results [ 39 , 40 ]. Other studies that investigated PMQR genes recorded variations in their prevalence rate even in the same country [ 41 – 44 ].…”

“…In previous studies, integron I was more frequent among Gram-negative bacteria [36][37][38]. [39,40]. Other studies that investigated PMQR genes recorded variations in their prevalence rate even in the same country [41][42][43][44].…”

Clinical Impact of Revised Ciprofloxacin Breakpoint in Patients with Urinary Tract Infections by Enterobacteriaceae

“…However, the acquisition of plasmid-mediated quinolone resistance (PMQR) genes has been increasingly reported in Enterobacteriaceae species in most parts of the world [ 22 , 23 ]. The co-existence of mutations in QRDR and PMQR genes could occur, and the accumulation of these different mutations was associated with high level quinolone resistance [ 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 ]. There were also several reports that Enterobacteriaceae isolates, which are susceptible to quinolone, also had carried mutations in QRDR or PMQR genes [ 14 , 22 , 28 , 29 , 30 ].…”

“…The co-existence of mutations in QRDR and PMQR genes could occur, and the accumulation of these different mutations was associated with high level quinolone resistance [ 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 ]. There were also several reports that Enterobacteriaceae isolates, which are susceptible to quinolone, also had carried mutations in QRDR or PMQR genes [ 14 , 22 , 28 , 29 , 30 ]. There was a report that this led to them showing no clinical response when CIP resistance was acquired by the quinolone resistance gene, even when CIP MIC was about 0.25–0.5 μg/mL [ 30 ].…”