Plasmodium falciparum, responsible for lethal cases of malaria, is treated with artemisinin-based combination therapy including dihydroartemisinin–piperaquine. The emergence of resistant parasites against dihydroartemisinin–piperaquine was reported in southeast Asia in 2008 and.
In this work, French Guiana field isolates, 40 (47%) of 86 (95% CI 35·9–57·1) were shown to be resistant to piperaquine in vitro principally due to pfCRTC350R (ie, Cys350Arg), also associated with dihydroartemisinin–piperaquine treatment failure (n=3 [50%] of 6). A high prevalence of piperaquine resistance markers was also observed in Suriname in 19 (83%) of 35 isolates and in Guyana in 579 (73%) of 791 isolates.
The pfCRTC350R mutation emerged before pfpm2 and pfpm3 amplification in a temporal sequence different from southeast Asia, and in the absence of artemisinin partial resistance, suggesting a geographically distinctive epistatic relationship between these genetic markers.
