| Abstrakt: |
Experiments were conducted with a clone ofTrypanosoma congolense, IL 3580, which exhibited a low level of resistance to isometanidium chloride. Five cattle were treated intramuscularly with isometamidium chloride at a dose rate of 0·5mgkg−1body weight (BW) and challenged 28 days later with 5Glossina morsitans centralisinfected withT. congolenseIL 3580. All 5 cattle and 15 untreated steers challenged on the same day became parasitaemic by day 15 post-infection. Thus, at a dose of 0·5 mg kg−1BW, the prophylactic action of isometamidium chloride did not extend to 28 days following treatment. Subsequently, the 20 steers were divided into 4 groups of 5 animals each and treated with isometamidium chloride at one of the following dose rates; 0·5 or 1·0 mg kg−1BW intramuscularly and 0·5 or 1·0 mg kg−1BW intravenously (Groups A, B, C and D, respectively). Group A consisted of the 5 animals that had previously been treated with isometamidium chloride. Animals relapsed in all groups except those in Group B, treated intramuscularly with isometamidium chloride at a dose of 1·0 mg kg−1BW. Four of the 5 animals in Group A, treated intramuscularly with isometamidium chloride at a dose of 0·5 mg kg−1BW relapsed following a mean interval of 16 days post-treatment. Similarly, infections in all animals in Groups C and D, given intravenous injections of isometamidium chloride at a dose of 0·5 and 1·0mg kg−1BW, respectively, were not eliminated as a result of treatment. The mean intervals to first detection of parasitaemia in these 2 groups following treatment were 14 and 20 days, respectively. The results therefore indicate that intravenous administration of isometamidium chloride does not enhance the drug’s therapeutic efficacy in the treatment of aT. congolenseclone which expresses a low, but significant, level of resistance to isometamidium. |
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