Suramin-resistance was experimentally induced in cloned or uncloned T. evansi populations using both immunosuppressed and immunocompetent mice by administration of subcurative doses of the drug. The highest level of resistance achieved was 3,000 fold using cloned trypanosomes in immunosuppressed mice. In the absence of suramin, suramin-resistance in T. evansi was observed to be stable for ten passages in mice. The results obtained in this study imply that induction of suramin resistance is by a mutational event followed by selection of resistant mutants by the presence of the drug. Immunosuppression of animals by heavy parasite burden or stressful conditions in conjunction with underdosing may therefore play an important role in the development of drug resistance under field conditions.