RUI: Effects of the Antimicrobial Agent Triclosan on the Emergence of Antibiotic Resistant Staphylococcus Aureus

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Triclosan is a broad spectrum antimicrobial agent that is currently found in many consumer goods. Triclosan inhibits the bacterial enzyme enoyl acyl carrier protein (ACP) reductase. This enzyme catalyzes the last step in fatty acid biosynthesis in microorganisms. Several studies have indicated that decreased susceptibility to triclosan correlates with quinolone antibiotic resistance. The quinolones inhibit the bacterial DNA metabolic enzymes, DNA gyrase and topoisomerase IV. Resistance to the quinolone antibiotics maps to the genes encoding DNA gyrase, topoisomerase IV, or to genes encoding multi-drug efflux pumps. Triclosan resistance also maps to genes encoding multi-drug efflux pumps or to genes encoding regulatory proteins that control the expression of these pumps. The primary focus of this project is to determine whether triclosan resistance contributes to antibiotic resistance in Staphylococcus aureus. S. aureus is a human pathogen for which therapeutic options for the treatment of infections caused by this organism have become limited. Preliminary studies by this laboratory have demonstrated the triclosan susceptibility profiles of 12 S. aureus clinical and laboratory strains. Triclosan resistance was detected in 10 of these strains. Among the 10 triclosan resistant strains, 4 are also resistant to the quinolone antibiotics. This project will use molecular biological and biochemical experiments to further characterize the nature of these triclosan resistant strains. The emergence of antibiotic resistance is a growing problem among pathogenic bacteria. The results of this project will lead to a deeper understanding of the impact of antimicrobial product usage by consumers on the emergence of antibiotic resistant bacteria.