Fecal Carriage of Colibactin-Encoding Escherichia coli Associated With Colorectal Cancer Among a Student Populace.

Fecal carriage of the colibactin ( clb ) gene in Escherichia coli is described as a source that could promote carcinogenesis, progressing to colorectal cancer. The present study investigated the demographic, dietary, and antibiotic consumption variables as correlates for fecal carriage of clb +/ E coli among the student populace. In a randomized cross-sectional survey, E coli (N = 136) from the fecal samples of eligible students were characterized and evaluated for antibiotic resistance, β-lactamase (blm), biofilm, virulence factor production, and strain tryptophan reverse mutagenic activity. The encoded clb +/ E coli were analyzed for correlates with principal component analysis. Of all the E coli strains, a low rate of 2 clb+/E coli (1.5%) and higher rates of biofilm (13.2%) and blm producers (11.8%) were recorded among the mutant strains as compared with the nonmutant types. All the clb+ / E coli showed complete resistance to amoxicillin, Augmentin (amoxicillin and clavulanate), gentamicin, and trimethoprim/sulfamethoxazole. The fecal clb -encoded E coli (1.5%) were not associated with demographic status, fiber-based food (odds ratio [OR], 1.03; 95% CI, 56.74-138.7; P = .213), alcohol (OR, 1.27; 95% CI, 61.74-147.1; P = .221), antibiotic consumptions (OR, 1.11; 95% CI, 61.29-145.3; P = .222), and handwashing (OR, 1.17; 95% CI, 60.19-145.5; P = .216). The hierarchical cluster of blm+/ E coli revealed high-level resistance with a multiantibiotic resistance index ≥0.2 ( P < .05). Only 12% of all strains were tryptophan mutant/ blm +, and 1.5% of clb +/EC blm+ were observed in fecal samples with a 452-base pair size. Trimethoprim/sulfamethoxazole and biofilm production positively regressed with clb expression ( P > .05). Principal component analysis score plot indicated an association of clb +/EC blm+ with dietary pattern, alcohol, blm, and hemolysin production. The combined activity of blm and biofilm production in the gut microbiota could promote clb +/ E coli colonization, facilitating genotoxin production and possible colorectal cancer induction.