The Prevalence of Microcin B17 and Colibactin Genes in Escherichia coli Isolated from Patients with Inflammatory Bowel Disease

Abstract Background: Escherichia coli ( E. coli ) is the most prevalent bacterial species in inflammatory bowel disease (IBD) patients stool, these isolates have been shown to differ from E. coli isolated from healthy individuals by owning many virulence factors including the production of toxins such as microcin B17 and coliba. Objective: The purpose of our study to demonstrate the prevalence of microcin B17 and colibactin genes in E. coli isolated from IBD patients stool in Karbala governorate hospitals. Materials and Methods: Sixty stool samples were collected from patients with IBD (30 from Crohn’s patients and 30 from ulcerative colitis) aged from 5 to 70 years old, of both sexes, who visited the Center of Digestive Tract and Liver Diseases in Karbala from August 2021 to September 2022. All patients were in active IBD, which is confirmed by testing fecal calprotectin production. Besides, 30 stool samples from healthy individuals were collected as control. E. coli was isolated from all samples and analyzed to detect the presence of toxin microcin B17 gene ( McbA ) and colibactin gene ( clbB ) by polymerase chain reaction using amplification of these genes. Results: The result is high prevalence of microcin B17 gene in E. coli isolates in both Crohn’s (27 [90%]) and ulcerative colitis (25 [83%]) isolates, compared with fecal commensal E. coli from control (5 [16.6%]) isolates only. While the prevalence of colibactin gene less than the micricinB17 gene with 10 isolates only from all sixty patients of IBD. Fecal calprotectin was between 50 and 200 μg/mg for most patients, which mean they had active gastrointestinal inflammation, whereas in 14 of them, their results were more than 200 μg/mg, which mean they were in acute inflammation condition. Conclusion: microcinB17-producing E. coli may have a greater role in the pathogenesis of inflammatory bowel disease due to high prevalence of its gene in IBD patients.