Changes in the pathogenicity of relapsed diminazene aceturate (DA)-resistant Trypanosoma brucei brucei as the trypanosomes are transmitted from DA-treated hosts to another set of animals

This study investigated the changes in pathogenicity of relapsed diminazene aceturate (DA)-resistant Trypanosoma brucei brucei (TBB) as the trypanosomes are transmitted from DA-treated hosts to another set of animals. The Federe strain of T. brucei brucei which was known to be DA resistant was used to infect two groups of rats, one of which was treated at the peak of infection. There was temporary clearance of the trypanosomes from blood of the treated group and subsequent relapse of the infection. The relapsed trypanosomes were used to infect a group of rats (group A1), and the pathogenicity of the relapsed T. brucei brucei in this rat group was compared to that of a group infected with primary T. brucei brucei stock that was not treated with DA (group B1). Results showed that when compared with the B1 rats, the A1 group had a slower onset of parasitaemia, significantly lower (p < 0.01) level of parasitaemia all through the study, significantly longer (p < 0.01) time period to reach peak parasitaemia, significantly longer (p < 0.01) post-infection survival time and significantly higher (p < 0.05) packed cell volume from day 6 post-infection. Further sequential transmission of this same T. brucei brucei infection to another group of rats (A2 and B2) produced the same effects on the above parameters used to assess pathogenicity. It was concluded that beyond temporarily clearing trypanosomes from blood of treated animals, treatment with DA reduces the pathogenicity of DA-resistant T. brucei brucei, and this reduced pathogenicity is carried on as the T. brucei brucei is further sequentially transmitted to another set of animals.