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Artemisinin-based combination therapies (ACTs) play a key role in malaria treatment and control. However, (partial) artemisinin resistance emerged in the mid-2010s in East Africa, defined by delayed parasite clearance in vivo and/or parasite survival in vitro or ex vivo despite a pulse-exposure to the active metabolite dihydroartemisinin (by ring stage survival assay, RSA). Associated mutations in the P. falciparum Kelch13 (pfK13) propeller domain are considered validated resistance markers. In East Africa, these markers are spreading.1 ACT efficacy is largely maintained as long as the non-artemisinin partner drug is effective. Once both compounds are compromised, treatment failures increase, as seen in Southeast Asia.1 In Uganda, decreased in vitro susceptibility of P. falciparum to dihydroartemisinin and lumefantrine has been observed.2 Although ACT efficacy remains predominantly good in Africa,1 treatment failures of artemether-lumefantrine (AL) have recently been reported among travellers returning from Africa.3–6 Here, we report a case of two consecutive AL treatment failures in a non-immune traveller returning from Uganda, supported by in vitro and molecular data.
Oliveira et al. (Tue,) studied this question.
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