The global fight against malaria has, over the decades, repeatedly been compromised by multidrug-resistant Plasmodium falciparum strains that first emerged in southeast Asia.1 Successively, these parasites have acquired resistance to chloroquine, sulphadoxine-pyrimethamine, mefloquine, and more recently the artemisinins through point mutations or amplification in genes (crt, dhps, dhfr, mdr1, and kelch13).2–6 Following increased resistance to artesunate plus mefloquine,7,8 an early artemisinin-based combined therapy, regional authorities turned increasingly to dihydroartemisinin plus piperaquine.
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Ménard et al. (2019) studied this question.
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