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Antimicrobial Agents and Chemotherapy, May 2009, p. 1898-1906, Vol. 53, No. 5
0066-4804/09/$08.00+0     doi:10.1128/AAC.01293-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Surfactants, Aromatic and Isoprenoid Compounds, and Fatty Acid Biosynthesis Inhibitors Suppress Staphylococcus aureus Production of Toxic Shock Syndrome Toxin 1{triangledown}

Peter J. McNamara,* Rae Ellen Syverson, Kathy Milligan-Myhre, Olga Frolova, Sarah Schroeder, Joshua Kidder, Thanh Hoang, and Richard A. Proctor

Department of Medical Microbiology and Immunology, University of Wisconsin School of Medicine, Madison, Wisconsin 53706

Received 26 September 2008/ Returned for modification 29 October 2008/ Accepted 6 February 2009

Menstrual toxic shock syndrome is a rare but potentially life-threatening illness manifest through the actions of Staphylococcus aureus toxic shock syndrome toxin 1 (TSST-1). Previous studies have shown that tampon additives can influence staphylococcal TSST-1 production. We report here on the TSST-1-suppressing activity of 34 compounds that are commonly used additives in the pharmaceutical, food, and perfume industries. Many of the tested chemicals had a minimal impact on the growth of S. aureus and yet were potent inhibitors of TSST-1 production. The TSST-1-reducing compounds included surfactants with an ether, amide, or amine linkage to their fatty acid moiety (e.g., myreth-3-myristate, Laureth-3, disodium lauroamphodiacetate, disodium lauramido monoethanolamido, sodium lauriminodipropionic acid, and triethanolamine laureth sulfate); aromatic compounds (e.g. phenylethyl and benzyl alcohols); and several isoprenoids and related compounds (e.g., terpineol and menthol). The membrane-targeting and -altering effects of the TSST-1-suppressing compounds led us to assess the activity of molecules that are known to inhibit fatty acid biosynthesis (e.g., cerulenin, triclosan, and hexachlorophene). These compounds also reduced S. aureus TSST-1 production. This study suggests that more additives than previously recognized inhibit the production of TSST-1.

* Corresponding author. Mailing address: University of Wisconsin-Madison, Department of Medical Microbiology and Immunology, 1550 Linden Dr., Madison, WI 53706. Phone: (608) 262-3067. Fax: (608) 262-8418. E-mail: pjmcnamara{at}wisc.edu

{triangledown} Published ahead of print on 17 February 2009.

Antimicrobial Agents and Chemotherapy, May 2009, p. 1898-1906, Vol. 53, No. 5
0066-4804/09/$08.00+0     doi:10.1128/AAC.01293-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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