Contributing factors to reduced ecdysteroid titers in Heliothis virescens parasitized by Microplitis croceipes

Heliothis virescens parasitized by Microplitis croceipes stop development at a predictable point prior to parasite emergence. The objectives of this study were to examine several factors which might contribute to the syndrome by comparing parasitized and nonparasitized larvae at specific and correspondingly similar physiological points in their development. Fifth stadium nonparasitized larvae experience a small pupal commitment burst of ecdysone followed by a large burst. In contrast, ecdysteroid titers in parasitized larvae remained at the pupal commitment level during the entire 5th stadium. Data shows that ecdysone 20-monooxygenase and sterol precursors are not limiting factors, with the possible exception of limited hemolymph sterol at the end of parasitoid development. In addition, isolated prothoracic glands from parasitized larvae produce amounts of ecdysteroid comparable to controls when stimulated with a crude Manduca sexta prothoracicotropic hormone preparation. Juvenile hormone esterase titers in parasitized larvae are low throughout the 5th stadium. They do not show the major rapid increase in activity normally associated with the latter part of the active feeding period in the nonparasitized 5th instar. Possible explanations for the low ecdysteroid titers in parasitized larvae include failure to synthesize and release prothoracic gland stimulatory factor by the poorly developed fat body, insufficient sterol precursors at the critical time of ecdysteroid synthesis, inhibition of the release of PTTH, failure of the prothoracic gland to respond to PTTH, and the consequences of abnormally high juvenile hormone titers.