It has been shown previously that infection with Plasmodium yoelii nigeriensis reduces the number of eggs produced by female Anopheles stephensi. Here we examine the mechanism underlying fecundity reduction. Ovaries from infected and uninfected (control) female mosquitoes were examined 12, 24 or 36 h after blood-feeding during the first gonotrophic cycle (replicated) or the second gonotrophic cycle (unreplicated). Follicular development was assessed according to Christophers' stages and the proportions of developing and resorbing follicles per ovary were determined. Resorption of some follicles commenced within 12 h of blood-feeding, affecting significantly more follicles in the infected females: 1.1% v. 3.2%. The difference was greatest 36 h after blood-feeding: 25% reduction (10 v. 35%) in the first cycle; 16% reduction (9 v. 25%) in the second gonotrophic cycle. The mean speed of oogenesis was also found to be significantly retarded in infected mosquitoes. During the second gonotrophic cycle, for example, only 92-94% of follicles reached stage III by 24 h and stage IV by 36 h in infected females, whereas all the developing follicles of uninfected females reached these stages more or less synchronously in the time specified.

Both anopheline and culicine mosquitoes have been shown to incur a reduction in reproductive fitness when infected with malaria parasites. The agent of rodent malaria, Plasmodium yoelii nigeriensis, was used as a laboratory model to investigate changes in the accumulation of protein in the ovaries of Anopheles stephensi when infected with oocysts or when feeding on mice with heavy asexual parasitaemia but no mature gametocytes. Herein we report that during the early phases of the gonotrophic cycle the ovarian protein content increased normally; however, after 16 h post-blood-feeding there was a significant reduction in the total protein content in ovaries from infected mosquitoes. The development of ovaries from mosquitoes undergoing a second gonotrophic cycle and containing maturing oocysts was similarly affected. Ovarian protein profiles produced by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed a depletion of the yolk protein vitellin. Ovaries from mosquitoes feeding on a mouse with 31% parasitaemia, no detectable gametocytes and a low haematocrit (29% packed cell volume) also exhibited a reduction in protein content, although this did not occur until much later in the gonotrophic cycle. The role of blood-meal quality and malaria infection in the reduction in egg production is discussed.