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Nature of the Genetic Determinant Controlling Exfoliative Toxin Production in Staphylococcus aureus

¹ Department of Microbiology, College of Medicine, University of Utah, Salt Lake City, Utah 84132

ABSTRACT

Phage group II Staphylococcus aureus has been identified as the etiological agent of the staphylococcal scaleded skin syndrome. The development of an animal model system permitted fulfillment of Koch's postulates and recognition of exfoliative toxin (ET) as being responsible for some of the clinical manifestations of this syndrome. Initial studies directed toward associating a lysogenic phage with the genetic control of ET synthesis failed to support this hypothesis. Growth of two Tox⁺ strains at 44 C was more effective than growth in ethidium bromide or sodium dodecyl sulfate in eliminating the ability to produce ET. The early and rapid accumulation of ET-negative (Tox^–) variants during growth of strain UT 0007 at 44 C, the lack of any selective advantage of the Tox^– variants over Tox⁺ cells during growth at 44 C, and an enhanced elimination frequency at 44 C of 97.9% over the spontaneous frequency of loss strongly suggest that the gene for ET synthesis is extrachromosomal. Additional evidence suggests that this gene is located on a plasmid which is not associated with genes for penicillinase synthesis and cadmium resistance. Two Tox⁺ strains harbored lysogenic phage capable of transducing cadmium resistance, but not penicillin resistance, to specific Tox^– recipients.

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• Koblenzer, P. J. (1976). Toxic Epidermal Necrolysis (TEN; Ritter's Disease) and Staphylococcal Scalded Skin Syndrome (SSSS): A Description and Review. CLIN PEDIATR 15: 724-730