A strain of Trypanosoma brucei when recently introduced into mice and imperfectly accommodated to this species of host produced infections relatively resistant to various trypanocidal drugs. On the other hand, when the strain had become highly accommodated and its pathogenicity increased to a maximum as the result of repeated passages, infected animals were readily cured. The exact mechanism on which this difference in resistance may depend has not been investigated. Attention is directed, however, to the important fact that the drugs acted poorly when the strain was in an attenuated state, as shown by the prolonged course of infection and the occurrence of marked fluctuations in the number of parasites present in the blood. Thus the chemotherapeutic response was weak at the time when the host itself was able to exercise an effective resistance. Later, when the host's resistance had become negligible, the curative action of the drugs was pronounced.