EFFECTS OF A NONSTEROIDAL ECDYSONE AGONIST, TEBUFENOZIDE ON HOST PARASITOID INTERACTIONS

Tebufenozide (RH-5992), a nonsteroidal ecdysone agonist, stimulated significant (P less than or equal to 0.05) growth in both testes of post-diapausing codling moth larvae and a dormant Ascogaster larva in its overwintering host's hemocoel. Tebufenozide elicited the same responses in post-diapausing testes and Ascogaster larvae as were reported earlier in insects treated with 20-hydroxyecdysone (20-OHE) [Friedlander, J Insect Physiol 35:29 (1989); Brown et al., Endocrinological Frontiers in Physiological Insect Ecology, Wroclaw: Wroclaw Technical University Press, pp 443-447 (1988)]. Only a trace (less than or equal to 1%) of C-14-tebufenozide was recovered from gonads and exuviae of healthy larvae, or from Ascogaster larvae removed from parasitized hosts; however, the renewed growth of testes and Ascogaster larvae and apolysis of codling moth integument were an obvious response to the hormone agonist. Most of the injected C-14-tebufenozide was recovered from host fat body, while the alimentary canal retained approximately 40% of the C-14-tebufenozide fed in an artificial diet. Host exposure to tebufenozide did not cause apolysis in endo- or ectoparasitic hymenopterans feeding on treated codling moth larvae; however, the endoparasitold trapped in the host's hemocoel died as its host's tissue deteriorated. Different results were observed on ectoparasitoids developing on treated hosts. Ectoparasitic Hyssopus sp. (Eulophidae) larvae feeding on tebufenozide treated hosts pupated in the normal length of time. Hyssopus adults which developed from larvae fed tebufenozide treated hosts were fertile and produced as many progeny as adults reared from solvent fed controls. There was no evidence of secondary poisoning to Hyssopus sp. and codling moth exposure to tebufenozide may actually benefit the rearing of this eulophid by maintaining the host in the susceptible larval stage and preventing the host larva from spinning a cocoon. (C) 1994 Wiley-Liss, inc.