Abstract
Escherichia coli is a common pathogen in both humans and animals. Quinolones are used to treat infections caused by Gram-negative bacteria, but resistance genes emerged. Only scarce studies investigated the association between plasmid-mediated quinolone resistance (PMQR) genes and integrons in clinical isolates of E. coli. The current study investigated the prevalence of quinolone resistance and integrons among 134 clinical E. coli isolates. Eighty (59.70%) isolates were quinolone-resistant, and 60/134 (44.77%) isolates were integron positive with the predominance of class I integrons (98.33%). There was a significant association between quinolone resistance and the presence of integrons (P < 0.0001). Isolates from Urology and Nephrology Center and Gastroenterology Hospital were significantly quinolone-resistant and integron positive (P ≤ 0.0005). Detection of PMQR genes on plasmids of integron-positive isolates showed that the active efflux pump genes oqxAB and qepA had the highest prevalence (72.22%), followed by the aminoglycoside acetyltransferase gene (aac(6′)-Ib-cr, 66.67%) and the quinolone resistance genes (qnr, 61.11%). Amplification and sequencing of integrons' variable regions illustrated that no quinolone resistance genes were detected, and the most predominant gene cassettes were for trimethoprim and aminoglycoside resistance including dfrA17, dfrB4, and dfrA17-aadA5. In conclusion, this study reported the high prevalence of PMQR genes and integrons among clinical E. coli isolates. Although PMQR genes are not cassette-born, they were associated with integrons' presence, which contributes to the widespread of quinolone resistance in Egypt.
Highlights
IntroductionE severity of infections can vary from mild to life-threatening conditions based on the virulence capacity and antimicrobial resistance of the bacterium
Despite being a well-known member of the normal flora for both humans and animals [1], the pathogenic strains of Escherichia coli cause a wide variety of infections including the skin and soft tissue, urinary tract, gastrointestinal tract, and central nervous system [2]. e severity of infections can vary from mild to life-threatening conditions based on the virulence capacity and antimicrobial resistance of the bacterium.Fluoroquinolones are broad-spectrum synthetic antibiotics that can successfully treat infections caused by Enterobacteriaceae
The association between Plasmid-mediated quinolone resistance (PMQR) and integrons among environmental isolates has been reported in several studies [8, 11,12,13], only few studies investigated the association between them in clinical E. coli isolates, and the investigations of the location of these genes on the variable region gene cassettes were scarce. erefore, our study aimed to investigate the prevalence and association of quinolone resistance and integrons among clinical E. coli isolates
Summary
E severity of infections can vary from mild to life-threatening conditions based on the virulence capacity and antimicrobial resistance of the bacterium. Fluoroquinolones are broad-spectrum synthetic antibiotics that can successfully treat infections caused by Enterobacteriaceae. Resistance to fluoroquinolones is increasing that is mediated chromosomally by modifications in their targets such as DNA gyrase and topoisomerase. Plasmid-mediated quinolone resistance (PMQR) is spreading among Gram-negative bacteria. Ree main mechanisms are employed for PMQR resistance. E first is the modification of quinolones’ targets by qnr proteins [encoded by quinolone resistance genes (qnr genes)]. Fluoroquinolones are modified through acetylation by the aminoglycoside acetyltransferase enzyme (encoded by the aac(6′)-Ib-cr gene). Excretion of hydrophobic fluoroquinolones by active efflux pumps such as QepA and OqxAB (encoded by qep, oqxA, and oqxB genes) [4]
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