Swiss mice with chronic Trypanosoma brucei infections become refractory to subsequent infection with Babesia microti and B. rodhaini. Infection with B. microti 7 days after T. brucei resulted in an obvious inhibition of the babesia parasitaemias and this inhibition became more profound as the time interval between the infections increased, until at 17-20 days the parasitaemias were totally abolished. Even after intravenous injection of large numbers of parasites parasitaemias were inhibited. Similar inhibition was obtained in BALB/c mice but not in C57BL/6 mice. Mice with established T. brucei infections also showed reduced susceptibility to B. rodhaini. In mice similarly infected with T. brucei and the malaria parasites Plasmodium chabaudi chabaudi and P. c. adami the pre-patent periods were noticeably prolonged but the subsequent parasitaemias were unaffected. Infections with P. yoelii were unaffected. Trypanosoma brucei infections were not affected by the intracellular parasites. Among the mechanisms investigated to explain these findings were changes in red blood cell populations, cross-reacting antigens, the release of toxic factors and the generation of activated oxygen species. None of these could account for the inhibition observed.