Bacterial strategies for surviving antibiotics during urinary tract infection: could uropathogenic Escherichia coli be persisters?
Abstract
Treating bacterial infections, such as urinary tract infection (UTI), with antibiotics does not always resolve the infection and often results in subsequent re-infection. Treatment failure can be driven by bacterial mechanisms of resistance, tolerance or persistence, collectively known as the antibiotic non-response. Antibiotic resistance is well characterized across various bacterial species and implicated in poor clinical outcomes in various infection settings. In the instance of resistance, bacteria harbour genetic determinants to evade antibiotics and continue to grow during treatment. Notably, bacteria can escape antibiotic killing in the absence of resistance genes. In response to the environment, an entire bacterial population can slow its growth rate, becoming tolerant to bactericidal antibiotic exposure. Alternatively, a subpopulation of bacteria, known as persister cells, survive whereas the remainder of the population is eliminated by bactericidal antibiotics. Both mechanisms enable bacteria to survive treatment, with the capacity to regrow following cessation of antibiotic treatment. However, our understanding of tolerance and persistence in the context of UTI is limited. Thus, two bacterial phenotypes that might contribute to poor outcomes are overlooked both in the clinic and in research, which could add to the challenges of treatment failure and recurrent UTI.
Related
- Phenotypic Characterization of OXA-439, an OXA-163 variant, isolated from uropathogenic Escherichia coli
- Isolation and phenotypic characterization of bacteriophages targeting multidrug-resistant biofilm-forming uropathogenic Escherichia coli from hospital sewage
- Cross-species convergence of surface polysaccharides shapes the virulence of an atypical carbapenem resistant uropathogenic Escherichia coli clone
- Antibacterial activity of a newly identified phage-derived endolysin and its parental bacteriophage against clinical uropathogenic Escherichia coli
- High Sensitivity of the rpiAB Escherichia coli Mutants to Antibiotics Is Associated with the Participation of the deo-Operon in a Hypothetical Ribose-5-Phosphate Futile Cycle
BibTeX
@article{costas2026bacterial,
title = {{Bacterial strategies for surviving antibiotics during urinary tract infection: could uropathogenic Escherichia coli be persisters?}},
author = {Ariana Costas and Bill Söderström and Molly Ingersoll},
journal = {Nature Reviews Urology},
year = {2026},
month = oct,
doi = {10.1038/s41585-026-01191-2},
url = {https://pasteur.hal.science/pasteur-05836005v1},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Bacterial strategies for surviving antibiotics during urinary tract infection: could uropathogenic Escherichia coli be persisters?
AU - Ariana Costas
AU - Bill Söderström
AU - Molly Ingersoll
PY - 2026
DA - 2026/10/14
JO - Nature Reviews Urology
DO - 10.1038/s41585-026-01191-2
UR - https://pasteur.hal.science/pasteur-05836005v1
AB - Treating bacterial infections, such as urinary tract infection (UTI), with antibiotics does not always resolve the infection and often results in subsequent re-infection. Treatment failure can be driven by bacterial mechanisms of resistance, tolerance or persistence, collectively known as the antibiotic non-response. Antibiotic resistance is well characterized across various bacterial species and implicated in poor clinical outcomes in various infection settings. In the instance of resistance, bacteria harbour genetic determinants to evade antibiotics and continue to grow during treatment. Notably, bacteria can escape antibiotic killing in the absence of resistance genes. In response to the environment, an entire bacterial population can slow its growth rate, becoming tolerant to bactericidal antibiotic exposure. Alternatively, a subpopulation of bacteria, known as persister cells, survive whereas the remainder of the population is eliminated by bactericidal antibiotics. Both mechanisms enable bacteria to survive treatment, with the capacity to regrow following cessation of antibiotic treatment. However, our understanding of tolerance and persistence in the context of UTI is limited. Thus, two bacterial phenotypes that might contribute to poor outcomes are overlooked both in the clinic and in research, which could add to the challenges of treatment failure and recurrent UTI.
SN - 1759-4812
SN - 1759-4820
ER -