Intrinsic Mechanism Decreases Susceptibility ofEscherichia coli O157:H7 to Multiple Antibiotics

Abstract

Chloramphenicol-resistant mutants ofEscherichia coli O157:H7 (n = 52) demonstrated multiple resistance to tetracycline, nalidixic acid, and ciprofloxacin. Approximately half of the mutants approached the clinical level of resistance to the antibiotic tetracycline. Mutants demonstrated a wide range of sensitivity to each antibiotic; for tetracycline, some isolates demonstrated a twofold increase, whereas others demonstrated a 15-fold increase in resistance. Continuous exposure to chloramphenicol did not affect the growth of mutants, suggesting that mutation does not have a negative effect on cell survival. Complementation experiments with a functional marR restored antibiotic susceptibility of selected mutants to levels similar to wild-type strains, suggesting that mar mutation was responsible for the decrease in sensitivity. The multiple antibiotic resistance (mar) operon is a global regulator controlling intrinsic resistance toward structurally and functionally unrelated antibiotics and other noxious agents. Antimicrobial use in both human and agricultural practice should be administered in a manner to prevent selection of resistant mutants.