We characterized 100 Escherichia coli urosepsis isolates from adult patients according to host compromise status by means of ribotyping, PCR phylogenetic grouping, and PCR detection of papG alleles and the virulence-related genes sfa/foc, fyuA, irp-2, aer, hly, cnf-1 and hra. We also tested these strains for copies of pap and hly and their direct physical linkage with other virulence genes in an attempt to look for pathogenicity islands (PAIs) described for the archetypal uropathogenic strains J96, CFT073, and 536. Most of the isolates belonged to E. coli phylogenetic groups B2 and D and bore papG allele II, aer, and fyuA/irp-2. papG allele II-bearing strains were more common in noncompromised patients, while papG allele-negative strains were significantly more frequent in compromised patients. Fifteen ribotypes were identified. The three archetypal strains harbored different ribotypes, and only one-third of our urosepsis strains were genetically related to one of the archetypal strains. Three and 18 strains harbored three and two copies of pap, respectively, and 5 strains harbored two copies of hly. papGIII was physically linked to hly, cnf-1, and hra (reported to be PAI II J96 -like genetic elements) in 14% of the strains. The PAI II J96 -like domain was inserted within pheR tRNA in 11 strains and near leuX tRNA in 3 strains. Moreover, the colocalized genes cnf-1, hra, and hly were physically linked to papGII in four strains and to no pap gene in three strains. Escherichia coli is the most frequent cause of gram-negative bacterial extraintestinal infections, such as cystitis, prostatitis, pyelonephritis, bacteremia, and neonatal meningitis, in humans. Several virulence factors enhance the capacity of E. coli to cause systemic infections; unlike most commensal E. coli strains, extraintestinal isolates possess genes encoding various combinations of adhesins (P and S fimbriae), iron acquisition systems (e.g., aerobactin and yersiniabactin), host defense avoidance mechanisms (capsule or O-specific antigen), and toxins (e.g., hemolysin and cytonecrotizing factor) (13,14,17,42). Genes coding for multiple virulence factors are located together on large blocks of chromosomal DNA known as pathogenicity islands (PAIs) (18).Recent studies suggest that extraintestinal pathogenic E. coli strains belong mostly to phylogenetic group B2 and, to a lesser extent, group D (5, 8, 39). In contrast, commensal E. coli strains generally belong to phylogenetic groups A and B1 (12).In this study, we determined the phylogenetic group, genetic diversity, and virulence gene distribution of 100 well-characterized E. coli blood isolates from adults with communityacquired urosepsis, according to host compromise status. We also sought copies of pap and hly and their direct physical linkage with certain virulence genes, consistent with their colocalization on PAIs described for archetypal uropathogenic E. coli strains. MATERIALS AND METHODSBacterial strains. One hundred E. coli strains were recovered by blood culture from 100 consecutive adult...

We studied 100 well-characterized E. coli blood isolates from patients with urosepsis for their susceptibility to nalidixic acid, ampicillin and trimethoprim-sulfamethoxazole, according to prevalence of virulence factors, phylogenetic groups and subgroups, PAI II(J96)-like domains (determined by physical linkage of cnf1, hly and hra) and PAI I(CFT073)-like domains (determined by physical linkage of papGII to the hly locus). Nalidixic acid resistance was associated with a lower prevalence of sfa/foc, K1 antigen, pathogenicity island II(J96)-like domains, subgroup B2/I and a shift towards group A.