Abstract
The aim of this study was to identify and compare the plasmid replicons of clinical uropathogenic Escherichia coli (UPEC) isolates, involving extended spectrum β-lactamase (ESBL)-positive and ESBL-negative, E. coli ST131 and non-ST131 and various ST131 subclones. Plasmid replicon typing on 24 clinical UPEC isolates was carried out using polymerase chain reaction-based replicon typing. A statistical analysis was performed to assess the associations between plasmid replicon types and ESBL carriage, and to evaluate the link between ST131 isolates and high replicon carriage. Eight replicons, I1α, N2, Iγ, X1, FIIS, K, FIA, and FII were detected. The FII was the most common replicon identified here. ESBL-positive E. coli isolates were highly associated with I1α, N2, Iγ, X1, and FIIS replicons, while FIA was present only in ESBL-negative group. ST131 isolates were highly associated with I1α and N2 replicons compared to non-ST131. No link was found between replicon carriage and the number or type of ESBLs in E. coli isolates. The diversity observed in replicon patterns of our clinical E. coli isolates indicates that they might be originated from different sources. The presence of replicons reported previously in animal sources suggests a possible transfer of antimicrobial resistance between animal and human bacterial isolates.
Highlights
The diversity observed in replicon patterns of our clinical E. coli isolates indicates that they might be originated from different sources
Urinary tract infections (UTIs) are commonly caused by Escherichia coli (E. coli),[1] and it is shown that uropathogenic E. coli (UPEC) subset are responsible for approximately 80% of UTIs.[2]
FII replicons were found alone in 11 isolates and combined with FIA in two isolates. This is concordant with several reports showing that IncF plasmids are limited to Enterobacteriaceae and mainly present in E. coli,[22] and is in agreement with many reports describing the epidemiology of Isolate No of Replicon replicons type(s)
Summary
Urinary tract infections (UTIs) are commonly caused by Escherichia coli (E. coli),[1] and it is shown that uropathogenic E. coli (UPEC) subset are responsible for approximately 80% of UTIs.[2]. ESBLs are enzymes capable of degrading β-lactams antibiotics, rendering these agents inactive.[5] ESBL genes have evolved into several hundreds of variants, complicating the fight against ESBL-producing bacterial isolates causing UTIs.[6] For instance, blaCTX-M gene has nearly 170 gene variants so far.[7] Among CTX-M gene variants, blaCTX-M-15 is the most common and it belongs to the CTX-M-1 phylogroup.[8] Plasmids carry the vast majority of ESBL genes, and they are major players in the transfer and dissemination of ESBL-mediated resistance among clinical bacterial strains.[9] There has been a link between particular plasmid types and ESBL-encoding genes. IncFII plasmids frequently carry blaCTX-M-15, while IncK plasmids commonly harbor blaCTX-M-14.10
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