Invasion and translocation of uropathogenic Escherichia coli isolated from urosepsis and patients with community-acquired urinary tract infection.

Uropathogenic Escherichia coli (UPEC) strains are found in high numbers in the gut of patients with urinary tract infections (UTIs). We hypothesised that in hospitalised patients, UPEC strains might translocate from the gut to the blood stream and that this could be due to the presence of virulence genes (VGs) that are not commonly found in UPEC strains that cause UTI only. To test this, E. coli strains representing 75 dominant clonal groups of UPEC isolated from the blood of hospitalised patients with UTI (urosepsis) (n = 22), hospital-acquired (HA) UTI without blood infection (n = 24) and strains isolated from patients with community-acquired (CA)-UTIs (n = 29) were tested for their adhesion to, invasion and translocation through Caco-2 cells, in addition to the presence of 34 VGs associated with UPEC. Although there were no differences in the rate and degree of translocation among the groups, urosepsis and HA-UTI strains showed significantly higher abilities to adhere (P = 0.0095 and P < 0.0001 respectively) and invade Caco-2 cells than CA-UTI isolates (P = 0.0044, P = 0.0048 respectively). Urosepsis strains also carried significantly more VGs than strains isolated from patients with only UTI and/or CA-UTI isolates. In contrast, the antigen 43 allele RS218 was found more commonly among CA-UTI strains than in the other two groups. These data indicate that UPEC strains, irrespective of their source, are capable of translocating through gut epithelium. However, urosepsis and HA-UTI strains have a much better ability to interact with gut epithelia and have a greater virulence potential than CA-UPEC, which allows them to cause blood infection.

Comparison between virulence characteristics of dominant and non-dominant Escherichia coli strains of the gut and their interaction with Caco-2 cells.

Escherichia coli strains are normal inhabitants of the gut and are normally found in the faeces of the host at different population sizes. We characterised faecal E. coli of 45 healthy male (n = 17) and female (n = 28) volunteers by testing 28 isolates from each individual. These isolates were typed and divided into dominant (if constituted >50% of the population tested) and non-dominant types in each individual. Representative strains of each dominant and non-dominant type were tested for their virulence gene profiles, their ability to form biofilm, adhere to, invade and translocate through a gut epithelial cell line (Caco-2 cells). Strains belonging to dominant types adhered significantly more to Caco-2 cells than non-dominant strains (5.7 ± 0.3 versus 4.3.± 0.13 CFU/cell mean ± SEM, P = 0.0003). They also invaded (135 ± 6 versus 63 ± 13 CFU) and translocated through Caco-2 cells (84 ± 5 versus 32 ± 9 CFU) significantly more than non-dominant strains (P < 0.0001 and P = 0.0002, respectively). Moreover, dominant strains showed the ability to form significantly more biofilm than non-dominant strains (1.1 ± 0.01 versus 0.5 ± 0.1 OD600, P < 0.0001). Majority (51%) of the strains belonged to phylogroup D followed by B2 (23%). Furthermore, out of 25 virulence genes tested, kpsMTII, papC and papG allele III were found to be significantly higher among dominant than non-dominant strains. Our results suggest that E. coli strains dominating the gut may have virulence properties that enable them to efficiently interact with the gut epithelium and translocate under predisposing conditions of the host.