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Escherichia coli is a major human pathogen, and it can develop antimicrobial resistance (AMR) and produce biofilm, both contribute to therapeutic failure. We investigated the relationship between AMR, biofilm formation and genomic background in clinical E. coli isolates. Biofilm formation and minimum inhibitory concentrations (MICs) were determined phenotypically in 86 isolates, and 39 isolates with extreme biofilm phenotypes were selected for whole-genome sequencing; 33 were retained after quality control. Acquired AMR genes, AMR-associated mutations, plasmid replicons and biofilm- and adherence-associated genes were identified, and population structure was characterized by multilocus sequence typing and phylogroup analysis. The 33 sequenced isolates represented 20 sequence types (STs), including ST12, ST69, ST73, ST127, ST131, ST141 and ST1993. Acquired AMR genes were detected in 16/33 isolates, including blaCTX-M-1, blaCTX-M-15, blaCTX-M-27 and qnrS1. Biofilm formation was not significantly associated with MIC values, acquired AMR gene count or AMR-associated mutation count. In contrast, the number of biofilm- and adherence-associated genes correlated positively with quantitative biofilm formation (Spearman ρ = 0.564, p = 0.00064). In this study, virulence determinant genes of fimbriae, curli, adhesins, motility, autotransporters and biofilm regulation were tested. The phylogroup B2 was the predominant (21/33) in our E. coli isolates. Four E. coli isolates belonged to ST131 and showed variable biofilm formations; exploratory analysis identified five missense and one upstream qseC variant shared by the two low-biofilm isolates. QseC is a two-component sensor kinase implicated in motility and biofilm regulation. Our findings suggest that biofilm formation and AMR are not necessarily linked phenotypes in clinical E. coli isolates. However, the genome sequencing demonstrated positive correlation with number of biofilm- and adherence-associated genes and their association with quantitative biofilm formation in diverse E. coli clones obtained in a clinical center.
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Falus et al. (2026) studied this question.
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