Isolation, identification, and slow-growth phenotype characterization of a clinically derived Escherichia coli from urinary tract infection

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 bla CTX-M-55 and bla TEM-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.