Health & Medical Health & Medicine Journal & Academic

Preventive Treatment and Anti-malarial Drug Resistance

Preventive Treatment and Anti-malarial Drug Resistance

Conclusions and Recommendations


In conclusion, when human movement frequently occurs between areas with different malaria transmission intensities:

  • the expected role of low and high transmission areas in the spread of anti-malarial parasite resistance may be inverted, with resistance consistently spreading more quickly in high transmission areas for all rates of IPTi dosing and in both the RS vs R1 and R1 vs R2 competition;

  • the demography of infection in low transmission areas tends to change to reflect the demography of high transmission areas when regions are connected by movement;

  • fast movement rates lead to strong interaction between the interacting populations and the rate of spread of R1 relative to RS and R2 relative to R1 parasites tend to behave the same in both populations, as should be expected.

Results from this model have important public health applications for the monitoring/surveillance policies looking for the speed of spread of resistant parasites. If regions are connected with each other by human movement, monitoring in high malaria transmission areas is likely to detect the fastest spread of drug resistance, regardless of the rate of IPTi dose applied and independent of which level of resistance is being detected. On the other hand, if regions are assumed to be, or in fact are, unconnected, then the best place to monitor in order to detect the rapid spread of resistance depends on both the rate/frequency of IPT dose and the level of resistance that is to be detected. Overall, these results indicate that different public health policies are needed when the area in question is an isolated high or low malaria transmission area, or whether it is close and interacting with a neighbouring low or high transmission area via human movement.

Furthermore, the same drug is sometimes utilized for IPTi and for symptomatic drug treatment of malaria. Thus it may be difficult to use experiments to distinguish the individual roles of either IPTi or symptomatic drug treatment on the acceleration of the spread of drug resistant malaria, with or without human movement. A theoretical framework, as presented here, is thus relevant as the effect of IPTi in accelerating the spread of drug resistance can be isolated as demonstrated in this study.

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