Background: Uropathogenic Escherichia coli (UPEC) has increased the incidence of urinary tract infection (UTI). It is the cause of more than 80% of community-acquired cystitis cases and more than 70% of uncomplicated acute pyelonephritis cases. Aim: The present study describes the molecular epidemiology of UPEC O25b clinical strains based on their resistance profiles, virulence genes, and genetic diversity. Methods: Resistance profiles were identified using the Kirby–Bauer method, including the phenotypic production of extended-spectrum β-lactamases (ESBLs) and metallo-β-lactamases (MBLs). The UPEC serogroups, phylogenetic groups, virulence genes, and integrons were determined via multiplex PCR. Genetic diversity was established using pulsed-field gel electrophoresis (PFGE), and sequence type (ST) was determined via multilocus sequence typing (MLST). Results: UPEC strains (n = 126) from hospitalized children with complicated UTIs (cUTIs) were identified as O25b, of which 41.27% were multidrug resistant (MDR) and 15.87% were extensively drug resistant (XDR). The O25b strains harbored the fimH (95.23%), csgA (91.26%), papGII (80.95%), chuA (95.23%), iutD (88.09%), satA (84.92%), and intl1 (47.61%) genes. Moreover, 64.28% were producers of ESBLs and had high genetic diversity. ST131 (63.63%) was associated primarily with phylogenetic group B2, and ST69 (100%) was associated primarily with phylogenetic group D. Conclusion: UPEC O25b/ST131 harbors a wide genetic diversity of virulence and resistance genes, which contribute to cUTIs in pediatrics.

Urinary tract infections (UTIs) are a leading cause of illness in children and adults of all ages, with uropathogenic Escherichia coli (UPEC) being the primary agent responsible. During colonization and subsequent infection of the urinary tract (UT), UPEC requires the expression of genes associated with virulence, such as those that encode the fimbrial adhesins FimH, PapG, and CsgA, as well as the presence of the TosA protein and the flagellar appendages of the bacteria. However, for colonization and infection to be successful, UPEC must overcome the host’s immunological barriers, such as physical barriers, expressed peptides and proteins, and immune cells found in the UT. In this context, the UT functions as an integral system where these factors act to prevent the colonization of uropathogens. Significant genetic diversity exists among UPEC strains, and the clonal complex ST131 represents one of the key lineages. This lineage has a high content of virulence genes, multiple mechanisms of antibiotic resistance, and a high frequency of extended-spectrum β-lactamases (ESBLs). New knowledge regarding protein structures known as adhesins and their role in the infection process can help identify therapeutic targets and aid in the design of vaccines. These vaccines could be based on the development of chimeric fusion proteins (FimH + CsgA + PapG), which may significantly reduce the incidence of UTIs in pediatric and adult patients.