Triclosan: a widely used biocide and its link to antibiotics.

@article{Schweizer2001TriclosanAW,
  title={Triclosan: a widely used biocide and its link to antibiotics.},
  author={Herbert P. Schweizer},
  journal={FEMS microbiology letters},
  year={2001},
  volume={202 1},
  pages={
          1-7
        }
}
  • H. Schweizer
  • Published 2001
  • Biology, Medicine
  • FEMS microbiology letters
Triclosan is the active ingredient in a multitude of health care and consumer products with germicidal properties, which have flooded the market in recent years in response to the public's fear of communicable bacteria. Although originally thought to kill bacteria by attacking multiple cellular targets, triclosan was recently shown to target a specific bacterial fatty acid biosynthetic enzyme, enoyl-[acyl-carrier protein] reductase, in Gram-negative and Gram-positive bacteria, as well as in the… Expand
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The data provide a molecular mechanism for the antibacterial activity of triclosan and substantiate the hypothesis that its activity results from inhibition of a specific cellular target rather than non-specific disruption of the bacterial cell membrane. Expand
Cross-Resistance between Triclosan and Antibiotics inPseudomonas aeruginosa Is Mediated by Multidrug Efflux Pumps: Exposure of a Susceptible Mutant Strain to Triclosan Selects nfxB Mutants Overexpressing MexCD-OprJ
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Exposure of a susceptible Δ(mexAB-oprM) strain to triclosan selected multidrug-resistant bacteria at high frequencies exposed them to the MexCD-OprJ efflux system due to mutations in its regulatory gene, nfxB, and the MICs of several drugs for these mutants were increased up to 500-fold. Expand
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Triclosan targets lipid synthesis
TLDR
It is shown that triclosan blocks lipid synthesis in Escherichia coli, and that mutations in, or overexpression of, the gene fabI (which encodes enoyl reductase, involved in fatty acid synthesis) prevents this blockage. Expand
Mechanism of Triclosan Inhibition of Bacterial Fatty Acid Synthesis*
TLDR
Formation of a noncovalent “bi-substrate” complex accounts for the effectiveness of triclosan as a FabI inhibitor and illustrates that mutations in the FabI active site that interfere with the formation of a stable FabI-NAD+-triclosan ternary complex acquire resistance to the drug. Expand
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TLDR
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Results contradict the view that these compounds directly disrupt membranes and suggest that their widespread use will select for resistant bacterial populations. Expand
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It is shown that triclosan specifically inhibits InhA, the enoyl reductase from Mycobacterium tuberculosis and a target for the antitubercular drug isoniazid. Expand
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