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

**Authors:** Paul A Akinduti, Ovbiosa O Izevbigie, Omobolanle A Akinduti, Ezekiel O Enwose, Emmanuel O Amoo

PMC · DOI: 10.1093/ofid/ofae106 · Open Forum Infectious Diseases · 2024-02-26

## TL;DR

This study found a low presence of a specific type of E. coli linked to colorectal cancer in student fecal samples, with no clear connection to diet, alcohol, or antibiotic use.

## Contribution

The study identifies fecal carriage of clb+/E. coli in students and explores its potential role in colorectal cancer without finding demographic or dietary correlations.

## Key findings

- Only 1.5% of E. coli strains carried the colibactin gene linked to colorectal cancer.
- Clb+/E. coli showed complete resistance to several antibiotics like amoxicillin and trimethoprim/sulfamethoxazole.
- Biofilm and blm production were more common in mutant E. coli strains and may promote clb+/E. coli colonization.

## Abstract

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+/ECblm+ 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+/ECblm+ 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.

## Linked entities

- **Genes:** CLYBL (citramalyl-CoA lyase) [NCBI Gene 171425], BLM (BLM RecQ like helicase) [NCBI Gene 641]
- **Chemicals:** amoxicillin (PubChem CID 33613), Augmentin (PubChem CID 23665637), gentamicin (PubChem CID 3467), trimethoprim/sulfamethoxazole (PubChem CID 358641)
- **Diseases:** colorectal cancer (MONDO:0005575)
- **Species:** Escherichia coli (taxon 562)

## Full-text entities

- **Genes:** beta-lactamase [NCBI Gene 7872529]
- **Diseases:** Colorectal Cancer (MESH:D015179), carcinogenesis (MESH:D063646)
- **Chemicals:** alcohol (MESH:D000438), Trimethoprim/sulfamethoxazole (MESH:D015662), gentamicin (MESH:D005839), Augmentin (MESH:D019980), tryptophan (MESH:D014364), amoxicillin (MESH:D000658)
- **Species:** Escherichia coli (E. coli, species) [taxon 562]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC10981395/full.md

## References

53 references — full list in the complete paper: https://tomesphere.com/paper/PMC10981395/full.md

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Source: https://tomesphere.com/paper/PMC10981395