Prevalence of silent plasmid-mediated fosfomycin-resistance genes among clinical isolates of fosfomycin-susceptible Escherichia coli
DOI:
https://doi.org/10.3855/jidc.21476Keywords:
clinical samples, silent genes, E. coli, fosfomycinAbstract
Introduction: Infections caused by Escherichia coli place a considerable burden on both patients and healthcare facilities. This study aims to investigate the prevalence and molecular detection of silent plasmid-mediated fosfomycin-resistance (PMFR) genes among fosfomycin-sensitive, extended-spectrum β-lactamase (ESβL)- producing E. coli isolates.
Methodology: Clinical samples of E. coli were collected from various sources and hospitals in Duhok‚ Iraq‚ from December 2020 to April 2021. Standard microbiological techniques and the Vitek II system were used to identify E. coli, which was further confirmed through species-specific genes. The Kirby-Bauer method was employed for antimicrobial sensitivity testing, followed by the detection of targeted PMFR and genes using conventional polymerase chain reaction (PCR).
Results: High resistance levels were observed against ampicillin, ceftriaxone, tetracycline, and ciprofloxacin, whereas a lower resistance rate was detected for carbapenems. Notably, all the isolates were susceptible to fosfomycin. Four isolates tested positive for fosA3, four were positive for fosA, and 16 were positive for the blaCTX-M9 gene. Within the isolates, three co-harbored fosA3, fosA, and blaCTX-M9 genes, while one isolate co-expressed fosA3 and blaCTX-M9 genes. The distribution of these genes, both individually and co-harbored, was observed across all clinical samples analyzed, except those derived from blood and sputum.
Conclusions: The dissemination of silent PMFR genes could pose a future risk for public health under the selective pressure of antibiotics, especially extended-spectrum beta-lactams, for a long time, or transfer to other bacteria, potentially leading to the activation of these genes.
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Copyright (c) 2026 Rojan Albazaz, Haliz Saddeq Hasan, Najim A. Yassin

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