The Role of Cell Wall Mutation in the Pathogenicity of E. coli H7:O157: A Molecular Evolution Study

E. coli H7:O157 was the subject of many studies. It was the cause of many outbreaks and food poisoning. The bacterium's pathogenicity is highly associated with cell wall modification and change. A total of 20 fecal samples tested positive for E. coli H7:O157 from patients who showed the typical symptoms of the infection, and another 20 from animals were collected. The bacterium was isolated and identified by cultural and molecular methods. The waa K, waa L, and waa Y sites were subjected to directed mutagenesis, and the effect of these mutations was studied and analyzed compared to the wild type. We found that the pathogenicity of mutant E. coli H7:O157 increased significantly when ingested by the lab. Animals. The explanation for this may be attributed to the waa K and waa L, since there is a significant change in transmembrane helix ratio compared to the wild type, allowing uncontrolled release of Shiga toxin to the infected animals, causing their death in 6 hours. Specific sites in the waa operon, namely waa K and waa L, play the leading role in controlling the progress of pathogenicity. When these sites are mutated, it may cause an increase in the virulence of this bacterium.