Escherichia coli is a human commensal and faecal indicator bacteria which is also the etiologic agent of several nosocomial- and community-acquired infections. Amoxicillin-clavulanate (AMC) is a widely prescribed β-lactam/β-lactamase inhibitor which is used against E. coli infections. Resistance to AMC in E. coli has been primarily attributed to point mutations in blaTEM-1 resulting in inhibitor-resistant TEM (IRT) β-lactamases. In this study, we have explored the reasons underlying AMC-resistance in waterborne E. coli. Most of the studies regarding IRT-producing E. coli have been conducted on clinical samples and studies exploring genetic mechanisms underlying AMC-resistance in aquatic E. coli are scarce. Since, blaTEM-1 and several antimicrobial resistance determinants are located on mobile genetic elements they can easily disseminate among other microbes inhabiting urban waterbodies. Thus, it is important to understand the underlying mechanisms to check the dissemination of AMC-resistance in other waterborne pathogens. Our results indicated that AMC-resistant E. coli were susceptible to other β-lactam/β-lactamase inhibitors like, ampicillin/sulbactam and piperacillin/tazobactam. Though, blaTEM-1 was present, none of the strains harbored point mutations which could qualify as IRT and only one strain harbored both blaTEM-1 and blaOXA-1. Hyperproduction of blaTEM-1, presence of plasimd-mediated ampC or promoter/attenuator mutations in the chromososmal ampC might not be related to IRT-like phenotype or AMC-resistance. This suggests that other mechanisms like, increased plasmid copy numbers or gene amplification or deficiency in the expression/function of porins might be responsible for AMC-resistance in waterborne E. coli.
Keywords: Amoxicillin-clavulanate; Escherichia coli; Inhibitor-resistant TEM; β-lactam/β-lactamase inhibitors.
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