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Escherichia coli (E. coli) causes most urinary tract infections in children, while antimicrobial-resistance patterns vary across settings and have worsened for several clinically important agents. Conventional urine culture identifies organisms recovered from urine, and standard susceptibility testing characterizes planktonic antimicrobial activity; neither establishes the in situ organization or reservoir of the recovered bacteria. Pediatric studies have demonstrated variable biofilm-forming capacity among urinary E. coli isolates and have identified intracellular bacteria or intracellular bacterial communities in exfoliated urothelial cells, although the full developmental cycle and the contribution of quiescent intracellular reservoirs to recurrence remain incompletely established in children. This narrative review critically evaluates pediatric evidence concerning surface-associated biofilm, intracellular localization, clonal background, antimicrobial resistance, and potential intestinal or community sources of resistant E. coli. Infant studies support the intestine as a potential reservoir for some urinary and other extraintestinal infections, while community studies document mobile resistance determinants and possible food-animal, environmental, and maternal acquisition routes; these findings do not establish a continuous within-child pathway from acquisition to urinary infection. Current clinical measures remain guideline-based diagnosis, antimicrobial stewardship, individualized treatment selection, and minimization of unnecessary catheter exposure. Candidate anti-biofilm, bacteriophage, microbiome-directed, and vaccine strategies lack controlled pediatric efficacy evidence. The review distinguishes direct pediatric clinical observations from studies of pediatric-origin isolates and from adult, animal, and in vitro evidence.
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Goroftei et al. (2026) studied this question.
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