Abstract

The hemolymph juvenile hormone (JH) titers of Manduca sexta larvae parasitized by Apanteles congregatus were determined using the black Manduca bioassay and found to be significantly higher than titers of normally fed or starved unparasitized fifth instar larvae. In vitro measurements of hemolymph esterase activity indicated that JH-specific esterase activity was reduced in parasitized larvae, contributing to the high JH titer. Analysis of host ecdysteroid titers by radioimmunoassay showed the presence of an ecdysteroid peak during parasite emergence from the host that was similar to the prewandering peak seen in unparasitized larvae. Host prothoracic gland activity is apparently necessary for emergence, as indicated by the failure of parasites to emerge from hosts that were neck or abdomen ligatured early in the fifth instar. The onset of emergence in intact hosts was accelerated by the infusion of ecdysone prior to the normal expected time of emergence. In addition to causing in vivo endocrinological changes, parasitism also markedly affected host epidermal responsiveness to exogenous 20-hydroxyecdysone (20-HE). When terminal stage fourth instar larvae were neck ligatured and injected with 20-HE prior to parasite emergence, the host epidermis failed to synthesize new cuticle. Sensitivity increased after the onset of emergence, and larval molting was elicited with large doses of 20-HE similar to molting of preterminal stage hosts with first instar parasites. These findings were interpreted as indicating that parasitism interferes with the normal molting response to exogenous ecdysteroids.

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