Swiss mice with chronicTrypanosoma bruceiinfections become refractory to subsequent infection withBabesia microtiandB. rodhaini. Infection withB. microti7 days afterT. bruceiresulted 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 establishedT. bruceiinfections also showed reduced susceptibility toB. rodhaini. In mice similarly infected withT. bruceiand the malaria parasitesPlasmodium chabaudi chabaudiandP. c. adamithe pre-patent periods were noticeably prolonged but the subsequent parasitaemias were unaffected. Infections withP. yoeliiwere unaffected.Trypanosoma bruceiinfections 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.
