Pupae and pharate adults of Saucophaga bullata parasitized by the ectoparasitoid, Nasonia vitvipennis, either died immediately or entered a developmental arrest. Death was the dominant response in young pupae (2 days after pupariation) and late pharate adults(>9 days after pupariation): death occurred within 48 h after envenomation, even in the absence of parasitoid larvae. The dominant response of intermediate aged hosts (3-9 days after pupariation) was an arrested or retarded development, the duration of which was age-dependent. Hosts envenomated as pupae remained arrested as pupae. Development progressed slowly in hosts envenomated as pharate adults, but none succeeded in completing pharate adult development. Likewise, diapausing hosts were developmentally suppressed following envenomation and appeared to be ''preserved'' for up to 40 days before death occurred. Host arrestment was induced by injection of wasp venom and was independent of the presence of parasitoid larvae. Envenomation in the anterior half of the body was more deleterious to the host than envenomation in the posterior half: with anterior injection, death was more rapid and far fewer hosts succeeded in depositing eye pigment or forming body bristles. Host arrestment could not be countered with injection of 20-hydroxyecdysone, thus suggesting the developmental suppression is not the consequence of an ecdysteroid deficiency. Progeny production by N. vitvipennis was nearly the same on an intact host as on an isolated thorax-abdomen of the host, but far fewer progeny were produced on an isolated head-thorax preparation of the host. This suggests that either a factor in the head region is detrimental to parasitoid development or some aspect of the abdomen promotes parasitoid development.