The transmission of Plasmodium berghei-infected mice to Anopheles stephensi mosquitoes showed a peak number of oocysts early in the infection prior to the peak of gametocytaemia. This was followed by a precipitous decline on Days 4 and 5 (see also Dearsley et al., Parasitology, 100, 359-368, 1990). By measuring percentage relative infectivity (using membrane feeds with viable gametocytes), we have shown that serum collected daily during the course of a blood-induced infection blocked infectivity from Day 6 postinfection onward. Although there was a correlation between anti-blood stage antibody levels and the loss of infectivity, a comparison of the infectivity pattern of P. berghei-infected BALB/c and SCID mice (the latter being incapable of antibody production) revealed the same pattern of inhibition in both mouse strains, suggesting that antibody alone is not responsible for this suppression. Sera taken from SCID mice late in the infection tested in vitro demonstrated a decline in infectivity similar to that observed in vivo, suggesting that a non-antibody serum factor(s) is responsible for the sustained decline in infectivity of P. berghei to A. stephensi mosquitoes.