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Nature 305, 709 - 712 (20 October 1983); doi:10.1038/305709a0

The toxic shock syndrome exotoxin structural gene is not detectably transmitted by a prophage

Barry N. Kreiswirth, Sven Löfdahl*, Marsha J. Betley, Mary O'Reilly, Patrick M. Schlievert, Merlin S. Bergdoll & Richard P. Novick

Public Health Research Institute of the City of New York, New York, New York 10016, USA
Food Research Institute, University of Wisconsin, Madison, Wisconsin 53706, USA
Department of Microbiology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
*Present address: Department of Bacteriology, National Bacteriological Laboratory, Stockholm, Sweden.

Toxic shock syndrome (TSS) is a complex of generalized symptoms caused by a local staphylococcal infection, and a circulating toxin is thought to be involved. Indeed, nearly 100% of TSS isolates produce an exoprotein, TSSE, that is thought to have an aetiological role on the basis of positive animal tests (refs 1,2 and F. Quimby, personal communication) and human serological data3. Although the precise role of TSSE in TSS remains unclear (E. Kass, personal communication), no other staphylococcal factor has been implicated. Our preliminary studies of the genetics of TSSE production failed to demonstrate plasmid or phage involvement or linkage with known chromosomal genes (ref. 4 and B.N.K. et al., unpublished data); however, Schutzer et al. have found that most TSS strains harbour prophages with common plating characteristics and suggest that the toxin(s) involved in TSS are transmitted by lysogenic conversion5. We show here that TSSE is not demonstrably transferred by lysogeny; moreover, we have cloned the gene and found that the cloned product is serologically and biologically indistinguishable from the native protein, and that the TSSE determinant is associated with a larger DNA segment that is absent or rearranged in TSSE- strains.

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