Isolation, identification, and slow-growth phenotype characterization of a clinically derived Escherichia coli from urinary tract infection
4 affiliations
- 1Department of Clinical Laboratory, University-Town Hospital of Chongqing Medical University, Chongqing, China.
- 2College of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
- 3Department of Laboratory Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
- 4Second Clinical College, Chongqing Medical University, Chongqing, China.
Abstract
A slow-growth Escherichia coli isolate, designated E. coli 105X, was recovered from a patient with urinary-tract infection. Initial biochemical profiling misidentified it as Shigella boydii; however, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and average nucleotide identity analysis (98.67% relative to uropathogenic E. coli CFT073) unequivocally reclassified the strain as E. coli. Antimicrobial susceptibility testing revealed broad-spectrum resistance to β-lactams, aminoglycosides and fluoroquinolones, which was mediated by 53 acquired resistance determinants, including the extended-spectrum β-lactamase genes blaCTX-M-55 and blaTEM-1, together with an expanded repertoire of efflux pump systems. Whole-genome sequencing (WGS) disclosed 45399 single-nucleotide polymorphisms and 1736 insertions/deletions relative to E. coli CFT073. Functional enrichment analyses demonstrated that non-synonymous mutations in 11 flagellar biosynthesis genes (e.g., flgA, fliK), the peptidoglycan synthase-encoding mrcB, and 29 growth-associated loci collectively perturb energy allocation and compromise biofilm formation, resulting in a markedly prolonged doubling time. Concurrently, E. coli 105X lacks canonical virulence factors such as the siderophore enterobactin and P fimbriae, but has acquired temperature-sensitive hemagglutinin and type IV pili. Taken together, E. coli 105X exemplifies a distinctive adaptive strategy in which metabolic bottlenecks synergize with structural mutations to establish a “slow-growth, high-resistance, re-engineered virulence” phenotype. These findings underscore the critical necessity of molecular diagnostic tools for accurate identification of morphologically atypical clinical E. coli isolates, and provide a theoretical rationale for developing targeted combination therapies that interfere with core bacterial energy-metabolism pathways.
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BibTeX
@article{yu2026isolation,
title = {{Isolation, identification, and slow-growth phenotype characterization of a clinically derived Escherichia coli from urinary tract infection}},
author = {Wenqiang Yu and Yao Ou and Shanshan Dong and Xiangyu Deng and Siqiang Niu and Xiongyu Jiang and Ranran Tang and Shuqi Zhang and Qiongyuan Zhang and Dinghua Liu and Chunhong Zou and Jiangling Wu and Yumei Zhao},
journal = {PLOS One},
year = {2026},
month = oct,
doi = {10.1371/journal.pone.0358948},
url = {https://doi.org/10.1371/journal.pone.0358948},
note = {CC BY},
}
RIS
TY - JOUR
TI - Isolation, identification, and slow-growth phenotype characterization of a clinically derived Escherichia coli from urinary tract infection
AU - Wenqiang Yu
AU - Yao Ou
AU - Shanshan Dong
AU - Xiangyu Deng
AU - Siqiang Niu
AU - Xiongyu Jiang
AU - Ranran Tang
AU - Shuqi Zhang
AU - Qiongyuan Zhang
AU - Dinghua Liu
AU - Chunhong Zou
AU - Jiangling Wu
AU - Yumei Zhao
PY - 2026
DA - 2026/10/29
JO - PLOS One
DO - 10.1371/journal.pone.0358948
UR - https://doi.org/10.1371/journal.pone.0358948
AB - A slow-growth Escherichia coli isolate, designated E. coli 105X, was recovered from a patient with urinary-tract infection. Initial biochemical profiling misidentified it as Shigella boydii; however, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and average nucleotide identity analysis (98.67% relative to uropathogenic E. coli CFT073) unequivocally reclassified the strain as E. coli. Antimicrobial susceptibility testing revealed broad-spectrum resistance to β-lactams, aminoglycosides and fluoroquinolones, which was mediated by 53 acquired resistance determinants, including the extended-spectrum β-lactamase genes blaCTX-M-55 and blaTEM-1, together with an expanded repertoire of efflux pump systems. Whole-genome sequencing (WGS) disclosed 45399 single-nucleotide polymorphisms and 1736 insertions/deletions relative to E. coli CFT073. Functional enrichment analyses demonstrated that non-synonymous mutations in 11 flagellar biosynthesis genes (e.g., flgA, fliK), the peptidoglycan synthase-encoding mrcB, and 29 growth-associated loci collectively perturb energy allocation and compromise biofilm formation, resulting in a markedly prolonged doubling time. Concurrently, E. coli 105X lacks canonical virulence factors such as the siderophore enterobactin and P fimbriae, but has acquired temperature-sensitive hemagglutinin and type IV pili. Taken together, E. coli 105X exemplifies a distinctive adaptive strategy in which metabolic bottlenecks synergize with structural mutations to establish a “slow-growth, high-resistance, re-engineered virulence” phenotype. These findings underscore the critical necessity of molecular diagnostic tools for accurate identification of morphologically atypical clinical E. coli isolates, and provide a theoretical rationale for developing targeted combination therapies that interfere with core bacterial energy-metabolism pathways.
SN - 1932-6203
ER -