Resistance to drug by different isolates Trypanosoma evansi in China
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Trypanosoma evansi
IC50
Cross-resistance
Trypanosoma evansi
Cloning (programming)
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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.
Trypanosoma evansi
Immunosuppression
Chagas Disease
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ABSTRAK : To study drug efficiency and strain resistancy in Indonesia the drugs Suramin, Isometamedium chloride and Diminazene aceturate were tested in mice. Mice were inoculated with the fresh blood from animals infected with various T. evansi isolates and treatment was carried out 24 hours later. Suramin has been found to be an effective drug against surra at a dose rate of 5 mg/kg and there are some indications that a smaller dose is still effective. At dose rates of 3.5 to 7 mg/kg Diminazene aceturate appeared to be an effective drug for certain isolates, but was not effective against others. Isometamidium chloride at the dose rates of 0.25 to 3 mg/kg was generally ineffective.
Trypanosoma evansi
Diminazene
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The first reported human case of trypanosomiasis caused by Trypanosoma evansi was treated using suramin. Patient follow-up indicates that the drug and specific regimen used were well tolerated. Clinical, serological and parasitological investigations at 6 months indicate complete cure of the patient. Suramin should be considered in the treatment of other cases of human T. evansi infection, if they occur.
Trypanosoma evansi
Nifurtimox
Regimen
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Trypanosoma evansi
Hypoxanthine
Diminazene
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Trypanosoma evansi
Diminazene
Cross-resistance
Minicircle
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The kinetic pattern of suramin was studied in uninfected and experimental Trypanosoma evansi infected (4.06 x 107 trypanosomes calf) in buffalo calves. The course of infection was chronic in experimental Tevansi infected buffalo calves and the infection was diagnosed by mice sub-inoculation test. The plasma level of suramin was 103.8± 1.63 and 160.5 ± 3.60 flg/ml at 1 min which declined to 8.29 ± 0.19 and 10.9 ± 0.88 Ilg/ml at 7 day in infected and uninfected buffalo calves, respectively, when suramin was administered @0.5 g/45 kg body weight. However, no concentration of the drug was found in plasma after 7 days post treatment. The pharmacokinetics ofsuramin following ilv administration was calculated by 3-compartmental open model. There was significant lower plasma levels up to 6 h and lower values of oc2' t'h ee2' AVC and Cpo in infected than uninfected buffalo calves.
Trypanosoma evansi
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Trypanosoma evansi
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Trypanosoma evansi
IC50
Cross-resistance
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Trypanosoma evansi
Wet season
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