We compared the effectiveness of two extinction interventions, extinction by omission and noncontingent delivery of reinforcement, to treat aggressive behavior with a 10-year-old boy. Before the intervention, a functional analysis revealed that aggression was maintained by positive reinforcement in the form of attention. The extinction by omission intervention consisted of ignoring aggressive behavior. Noncontingent reinforcement involved delivering attention to the boy on a fixed-time schedule. Both treatments were compared using a multielement research design. Noncontingent reinforcement produced a more rapid elimination of aggression. Additionally, the schedule of noncontingent reinforcement was gradually thinned during the intervention. Finally, both parents successfully implemented the noncontingent schedule of reinforcement independently for up to 5 weeks after treatment.

Aggression↗

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

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failed to demonstrate plasmid or phage involvement or linkage with known chromosomal genes (ref. 4 and B.N.K. et al., unpublished data); however, Schutzer et al.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

Animals↗

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