In vitro testing of drug susceptibility was performed by the standard 42-hour 3H-hypoxanthine uptake inhibition method [5 (link)]. Susceptibility to dihydroartemisinin, artesunate, and ten standard or new anti-malarial drugs, ie chloroquine, quinine, mefloquine, lumefantrine, monodesethylamodiaquine (biologically active metabolite of amodiaquine), pyronaridine, piperaquine, atovaquone, doxycycline and pyrimethamine, was assessed. The laboratory-adapted clone W2, tested on the same day, was used as a reference. Isolates from imported malaria, tested on the same batch of plates, were used as comparators.
Polymorphisms of pfcrt, pfmdr1, pfmrp and pfnhe-1, involved in quinoline resistance, and in pfATPase6, postulated to be involved in artemisinin resistance, and the copy number of pfmdr1 were assessed [6 ].
The French malaria consensus [7 (link)] and the WHO [8 ] recommend to clinically examine patient and control parasitaemia at D0, D3, D7 and D28 to evaluate anti-malarial efficacy. Blood controls were performed at D0, D4, D7 and D43. The genotyping of parasites was assessed at D0, D4 and D7 using six microsatellite loci (microsatellites 7A11, pf2689, pf2802, C4M79, TRAP, C4M69) [9 (link)], msp1 and msp2 [10 (link)].
Polymorphisms of pfcrt, pfmdr1, pfmrp and pfnhe-1, involved in quinoline resistance, and in pfATPase6, postulated to be involved in artemisinin resistance, and the copy number of pfmdr1 were assessed [6 ].
The French malaria consensus [7 (link)] and the WHO [8 ] recommend to clinically examine patient and control parasitaemia at D0, D3, D7 and D28 to evaluate anti-malarial efficacy. Blood controls were performed at D0, D4, D7 and D43. The genotyping of parasites was assessed at D0, D4 and D7 using six microsatellite loci (microsatellites 7A11, pf2689, pf2802, C4M79, TRAP, C4M69) [9 (link)], msp1 and msp2 [10 (link)].
Free full text: Click here
