The Role of Cell Wall Mutations in Antimicrobial Resistance by Escherichia coli O157:H7: A Molecular Evolution Study

The E. coli O157:H7 strain has been the subject of many studies. In addition to producing severe abdominal illness in humans and animals, the E. coli O157:H7 strain is characterized by the production of Shiga toxins and demonstrates resistance to multiple antibiotics.

In this study, 20 fecal samples from patients with typical symptoms of E. coli O157:H7 infection and 20 from animals that tested positive for the same pathogen were analyzed. The bacterium was isolated, identified, and classified using both culture-based and molecular methods, employing the rpoB, stx, waa, and waaO genes.

The E. coli O157:H7 strain classification was highly similar to the E. coli O157:H7 strain Sakai. The rpoB, stx, waa, and waaO genes were deposited on the NCBI website under accession numbers PP059841, OR939814, PP059843, and PP059842, respectively. The mutant sequences at the waa sites K, L, and Y were analyzed to determine the alterations in the associated gene function, cell wall formation, and the ability of the mutant E. coli O157:H7 to develop antibiotic resistance compared to the wild-type.

Antibiotic resistance in the mutant E. coli O157:H7 increased significantly regarding some type of theses antimicrobial agents, while in some cases it decreased. This depends on the type of antibiotics and its mode of action and target. This may be explained by the waaK and waaL genes, which prevent the entry of antimicrobial agents into the bacterial cell.