VENOM-INDUCED ALTERATIONS IN FLY LIPID-METABOLISM AND ITS IMPACT ON LARVAL DEVELOPMENT OF THE ECTOPARASITOID NASONIA-VITRIPENNIS (WALKER) (HYMENOPTERA, PTEROMALIDAE)

Parasitism by the ectoparasitoid Nasonia vitripennis suppressed develo pment in three species of carrion-feeding flies (Sarcophaga bullata, P hormia regina, and Sarcodexia sternodontus), but Musca domestica died quickly in response to envenomation, which made this host unsuitable f or development of N. vitripennis. More parasitoids were produced on fl ies showing arrested development than in M. domestica, and species tha t sustained the longest periods of suppressed development prior to dea th yielded the highest number of wasp progeny. Lipid levels were alter ed by envenomation in all fly species, but lipid accumulated in the fa t body only in the preferred host, S. bullata. Fat body accumulation o ccurred concurrently with a decline in the hemolymph lipid titer, sugg esting that the utilization/mobilization of fat body lipid was altered . Fat body lipid content could be elevated by parasitism, by envenomat ion (without egg deposition), or by injection of crude venom, demonstr ating that the venom alone was capable of altering fly lipid metabolis m. In the presence of feeding parasitoid larvae, the lipid content of S. bullata fat body did not reach the peak titers observed with enveno mation alone or by injection of isolated crude venom, thus suggesting that the developing wasp alters the lipid content of the host. This is consistent with the wasp larva's dependence on the timetable of host changes initiated by envenomation. Wasp larvae deposited on the host o ut of synchrony with the changes that normally follow envenomation wer e much less successful in developing to adulthood. (C) 1995 Academic P ress, Inc.