No abstract

Injection of the insect growth regulator (IGR) azadirachtin into Manduca sexta larvae that were parasitized by Cotesia congregata adversely affected subsequent endoparasite development when the compound was administered prior to the first larval ecdysis of the wasps. Injection of 2.5–10 μg of azadirachtin into newly ecdysed fourth or fifth instar hosts partially inhibited or totally suppressed the first larval ecdysis of the parasites. Instead of initiating rapid growth similar to parasites developing in hosts injected with the solvent carrier (ethanol) only, parasites in azadirachtin‐treated hosts never grew beyond the size normally attained in early terminal stage hosts. The host larvae survived for 2 weeks or longer following injection of azadirachtin, but their parasites never recovered and died encased within one or two exuvial cuticles. The parasitism‐specific hemolymph polypeptides previously shown to be characteristic of terminal stage hosts were undetectable in larvae in which the parasites failed to ecdyse to the second instar. The observed effects of azadirachtin on development of C. congregata differ significantly from those induced by other IGRs in parasitized M. sexta, suggesting azadirachtin has a unique, though as yet undefined, mode of action. Compared to other IGRs, this compound is extremely potent in terms of the minimum doses required to prevent emergence, but affects only the L1‐L2 ecdysis and not the L2‐L3 transition. In contrast, other compounds such as juvenoids and the JH esterase inhibitor BEPAT (S‐benzyl‐0‐ethyl phosphoramidothiolate) permit the parasite to grow and develop normally until the wasps become pharate third instar larvae, then inhibit the second larval ecdysis and emergence from the host.