Detection of possible resistance mechanisms in uropathogenic escherichia coli strains isolated from kidney transplant recipients based on whole genome sequencing

Background: Urinarytract infections are a global health concern, with uropathogenic Escherichia coli (UPEC) accounting for 80–90% of cases. Given the rise in antimicrobial re sistance, our aim was to elucidate the genetic mechanisms behind low-level resistance to ciprofloxacin and fosfomycin (LLCR a...

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Detalles Bibliográficos
Autores: Herrera-Espejo, Soraya, Rubio, Alejandro, Ceballos-Romero, Lucía, Pachón Díaz, Jerónimo, Pérez-Pulido, Antonio J, Cordero Matia, María Elisa, Pachón Ibáñez, María Eugenia
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2025
País:España
Institución:Universidad de Sevilla (US)
Repositorio:idUS. Depósito de Investigación de la Universidad de Sevilla
OAI Identifier:oai:idus.us.es:11441/169865
Acceso en línea:https://hdl.handle.net/11441/169865
https://doi.org/10.3390/biom15020260
Access Level:acceso abierto
Palabra clave:Whole-genome sequencing
Antimicrobial resistance
Uropathogenic escherichia coli
Descripción
Sumario:Background: Urinarytract infections are a global health concern, with uropathogenic Escherichia coli (UPEC) accounting for 80–90% of cases. Given the rise in antimicrobial re sistance, our aim was to elucidate the genetic mechanisms behind low-level resistance to ciprofloxacin and fosfomycin (LLCR and LLFR) in UPEC strains, using whole-genome se quencing (WGS) to identify point mutations in chromosomal and plasmid genes cohort UPEC wascollected from kidney transplant recipients at the Virgen del Rocío Univer sity Hospital, Spain. Minimum inhibitory concentrations were determined for ciprofloxacin and fosfomycin to categorize strains into LLCR and LLFR. Twenty strains were selected for WGS, with genome annotations. Point mutations were identified and analyzed using alignment tools, and protein stability changes were predicted. Results: LLCR strains exhibited mutations in key quinolone resistance-determining regions of the gyrA gene, in 83% of cases. The qnrS1 plasmid gene was found in 17% of LLCRstrains. LLFR strains showed mutations in the glpT and cyaA genes. Mutations in the uhp gene family were linked to the fosfomycin resistant phenotype, suggesting a multi-step resistance evolution mechanism. Conclusions: This study highlights the complex interplay between chromosomal and plasmid genes in UPEC’s resistance to ciprofloxacin and fosfomycin. The findings contribute to understand ing low-level resistance mechanisms and may guide the development of novel therapeutic strategies to combat multidrug-resistant strains.