0
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

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

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          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 data. 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failed to demonstrate plasmid or phage involvement or linkage with known chromosomal genes (ref. 4 and B.N.K. et al., unpublished data); however, Schutzer et al.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 conversion. 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.

          Related collections

          Most cited references5

          • Record: found
          • Abstract: found
          • Article: not found

          Identification and characterization of an exotoxin from Staphylococcus aureus associated with toxic-shock syndrome.

          Toxic-shock syndrome (TSS) is believed to be caused by a toxin produced by Staphylococcus aureus. An exotoxin has been identified that is associated with strains of S. aureus isolated from patients with TSS. Coded strains of S. aureus were tested for the presence of the exotoxin by polyacrylamide gel isoelectric focusing. Sixty isolates of S. aureus were tested; 28 (100%) of 28 isolates from patients with TSS but only five (16%) of 32 control isolates produced the toxin (P much less than 0.001). This protein exotoxin, which was purified by differential precipitation with ethanol and thin-layer isoelectric focusing, had an isoelectric point of 7.2. When tested by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the toxin migrated as a homogeneous protein with a molecular weight of 22,000. The exotoxin produced fever in rabbits and enhanced susceptibility to lethal shock caused by endotoxin. Other biologic properties of the exotoxin included lymphocyte mitogenicity and the capacity to suppress synthesis of IgM antibody to sheep erythrocytes.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Alteration of immune function by staphylococcal pyrogenic exotoxin type C: possible role in toxic-shock syndrome.

            Staphylococcal pyrogenic exotoxin type C (PE-C) suppressed synthesis of IgM antibodies to sheep erythrocytes by in vitro cultures of murine and rabbit splenocytes. Maximal suppression was observed on day 4 of culture and at PE-C doses of 0.1 and 0.01 microgram per 10(7) splenocytes. Endotoxin, added to cell cultures containing PE-C, caused further suppression of IgM synthesis. Endotoxin alone added to cultures was not immunosuppressive. Sublethal doses of PE-C plus endotoxin also suppressed complement-fixing antibody responses in rabbits to sheep erythrocytes; neither agent alone was suppressive. Further, the combination of PE-C and endotoxin blocked reticuloendothelial clearance of colloidal carbon by 50% during a 20-min period. PE-C enhanced the skin reactivity of rabbits previously sensitized to purified protein derivative. One-half of rabbits immunized with PE-C emulsified in adjuvant failed to make antibody to PE-C during a 112-day period. The animals that were nonresponsive to PE-C were able to make antibodies to sheep erythrocytes.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Minocycline resistance in Staphylococcus aureus: effect on phage susceptibility.

              Tetracycline-resistant strains of Staphylococcus aureus are minocycline sensitive, with the exception of strains susceptible to phages of the 83A/84/85 complex and some methicillin-resistant strains of other phage types. Strains of the 83A/84/85 complex yield mutants with increased minocycline resistance. Transduction of minocycline resistance into the susceptible strain RN 450 was obtained with donor strains possessing either markers for both extrachromosomal tetracycline resistance (tet) and chromosomal tetracycline + minocycline resistance (tmn R), or only for chromosomal tmn R resistance. The chromosomal marker was differentiated from the extrachromosomal marker by the lack of detectable extrachromosomal deoxyribonucleic acid after transfer into strain RN 450, transfer into a rec(+) strain, lack of transfer into rec(-) acceptor strain, and cotransduction with chromosomal determinants for guanine biosynthesis. Both chromosomal and extrachromosomal tetracycline resistance can be induced by tetracycline. Induction by tetracycline of chromosomal tetracycline resistance resulted in simultaneous induction of minocycline resistance. The mutation toward increased minocycline resistance (tmn --> tmn R) is a regulatory mutation toward constitutivity or semiconstitutivity. Constitutive resistance is dominant in tmn R/tet diploids. Transfer of the tet marker does not affect the phage susceptibility of the acceptor strain. The tmn R marker, originating from donor strains of the 83A/84/85 complex, renders strain RN 450 resistant to several typing phages, with the exception of phages of the 83A/84/85 complex. This could possibly account for the phage typing patterns of minocycline-resistant staphylococci.
                Bookmark

                Author and article information

                Journal
                Nature
                Nature
                Springer Nature
                0028-0836
                1476-4687
                October 1983
                October 1983
                : 305
                : 5936
                : 709-712
                Article
                10.1038/305709a0
                6226876
                4609adba-de2d-48df-ad65-7fda86ec6a0d
                © 1983

                http://www.springer.com/tdm

                History

                Comments

                Comment on this article