To analyze whether Escherichia coli strains that cause urinary tract infections (UPEC) share virulence characteristics with the diarrheagenic E. coli (DEC) pathotypes and to recognize their genetic diversity, 225 UPEC strains were examined for the presence of various properties of DEC and UPEC (type of interaction with HeLa cells, serogroups and presence of 30 virulence genes). No correlation between adherence patterns and serogroups was observed. Forty-five serogroups were found, but 64% of the strains belonged to one of the 12 serogroups (O1, O2, O4, O6, O7, O14, O15, O18, O21, O25, O75, and O175) and carried UPEC virulence genes (pap, hly, aer, sfa, cnf). The DEC genes found were: aap, aatA, aggC, agg3C, aggR, astA, eae, ehly, iha, irp2, lpfA O113 , pet, pic, pilS, and shf. Sixteen strains presented aggregative adherence and/or the aatA sequence, which are characteristics of enteroaggregative E. coli (EAEC), one of the DEC pathotypes. In summary, certain UPEC strains may carry DEC virulence properties, mostly associated to the EAEC pathotype. This finding raises the possibility that at least some faecal EAEC strains might represent potential uropathogens. Alternatively, certain UPEC strains may have acquired EAEC properties, becoming a potential cause of diarrhoea.

Urinary tract infections (UTI) affect community and healthcare patients worldwide and may have different clinical outcomes. We assessed the phylogenetic origin, the presence of 43 virulence factors (VFs) of diarrheagenic and extraintestinal pathogenic Escherichia coli, and the occurrence of hybrid strains among E. coli isolates from 172 outpatients with different types of UTI. Isolates from phylogroup B2 (46%) prevailed, followed by phylogroups A (15.7%) and B1 (12.2%), with similar phylogenetic distribution in symptomatic and asymptomatic patients. The most frequent VFs according to their functional category were fimA (94.8%), ompA (83.1%), ompT (63.3%), chuA (57.6%), and vat (22%). Using published molecular criteria, 34.3% and 18.0% of the isolates showed intrinsic virulence and uropathogenic potential, respectively. Two strains carried the eae and escV genes and one the aggR gene, which classified them as hybrid strains. These hybrid strains interacted with renal and bladder cells, reinforcing their uropathogenic potential. The frequency of UPEC strains bearing a more pathogenic potential in the outpatients studied was smaller than reported in other regions. Our data contribute to deepening current knowledge about the mechanisms involved in UTI pathogenesis, especially among hybrid UPEC strains, as these could colonize the host’s intestine, leading to intestinal infections followed by UTI.

Extra-intestinal pathogenic Escherichia coli (ExPEC) may inhabit the human gut microbiota without causing disease. However, if they reach extra-intestinal sites, common cystitis to bloodstream infections may occur, putting patients at risk. To examine the human gut as a source of endogenous infections, we evaluated the E. coli clonal diversity of 18 inpatients’ guts and their relationship with strains isolated from urinary tract infection (UTI) in the same hospital. Random amplified polymorphic DNA evaluated the clonal diversity, and the antimicrobial susceptibility was determined by disk diffusion. One isolate of each clone detected was sequenced, and their virulome and resistome were determined. Overall, 177 isolates were screened, among which 32 clones were identified (mean of two clones per patient), with ExPEC strains found in over 75% of the inpatients’ guts. Endogenous infection was confirmed in 75% of the cases. ST10, ST59, ST69, ST131, and ST1193 clones and critical mobile drug-resistance encoding genes (blaCTX-M-15, blaOXA-1, blaDHA-1, aac(6′)-lb-cr, mcr-1.26, qnrB4, and qnrB19) were identified in the gut of inpatients. The genomic analysis highlighted the diversity of the fecal strains, colonization by lactose-negative E. coli, the high frequency of ExPEC in the gut of inpatients without infections, and the presence of β-lactamase producing E. coli in the gut of inpatients regardless of the previous antibiotics’ usage. Considering that we found more than one ExPEC clone in the gut of several inpatients, surveillance of inpatients’ fecal pathogens may prevent UTI caused by E. coli in the hospital and dissemination of risk clones.