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A strategic model for the simulation of drug resistance in African animal trypanosomiasis
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A strategic model for the simulation of drug resistance in African animal trypanosomiasis

  1. A strategic model for the simulation of drug resistance in African Animal Trypanosomiasis Frank Hansen, Bernard Bett, Erick Ouma Mungube, Tom Randolph The problem: African Animal Trypanosomiasis (AAT) is a major constraint for the productivity of African agricultural systems. Tsetse flies of the genus Glossina act as vectors that transport the parasitic protozoan Trypanosoma spp. between hosts. The strategy most widely used to manage the disease is the application of trypanocidal drugs, but the emergence of resistance has put into question the long-term viability of their use. In certain areas of West Africa, drug resistant and drug susceptible strains of trypanosomes co-exist. When in such an area the disease prevalence is successfully reduced by removal of the majority of the tsetse vectors, the remaining numbers of diseased animals is so small that it becomes difficult to measure the impact of vector control on the development of drug resistance. Moreover, little is known about how drug resistance is likely to evolve if vector control is subsequently discontinued. The solution: Dynamic system models can simulate the processes that drive the dynamics of vector, host and parasite populations. Such models can increase our understanding of the diseases dynamics even in situations where empirical measurement is problematic. The model: Cattle as individuals Both vector and host can be in one of 4 states • Susceptible • infected with a drug sensitive strain • infected with a drug resistant strain • infected with a mix of both strains Vectors as pools in different infection states Treatment: • every 30 days on animals with visible infection • removes drug sensitive parasites • no effect on drug resistant parasites Infection: • homogenous mixing • Tsetse feed every 3 days • infections mix upon contact Population: • 125 cows (25 not treated, serve as wildlife reservoir) • 1000 tsetse, reduced to 100 by vector control 0 20 40 60 80 100 120 n u m b e r s healthy sensitive mixed resistant 0 5 10 15 20 25 30 35 1 70 139 208 277 346 415 484 553 622 691 760 829 898 967 1036 n u m b e r s time [days] 0 20 40 60 80 100 120 n u m b e r s healthy sensitive mixed resistant 0 5 10 15 20 25 30 35 1 74 147 220 293 366 439 512 585 658 731 804 877 950 1023 n u m b e r s time [days] Worst case scenario Best case scenario- Simulations run for 3 years - vector control applied in 2nd year - average of 100 replicates-Treatment efficiancy: 60% - Test sensitivity: 60% -Treatment efficiancy: 95% - Test sensitivity: 99% In both cases purely sensitive infections die out. There is an equilibrium between mixed and purely resistant infections. In the worst case there are less purely resistant infections. Cattle Tsetse Cattle Tsetse During vector control disease prevalence is effectively reduced. With the end of vector control the same equilibrium between mixed and resistant infections is established. Conclusions: The ratio of drug sensitive to drug resistant parasites is determined by factors other than vector abundance. Hence the reduction in vector abundance does not alter this ratio. It is likely that the presence of hosts that are not treated (wildlife reservoir or other livestock) stabilizes the ratio of drug resistance.
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