Malaria is one the world’s most widespread lethal diseases. Plasmodium falciparum, P. vivax, P. ovale, P. malariae and P. knowlesi induce human pathology. These species could be differentially diagnosed using the genotyping of cytochrome b, Pfdhfr and RNA 18S. The persistence of P. falciparum, the most lethal parasite, is mainly due to antimalarial drug resistance. Indeed, a few years after the start of the ambitious malaria eradication program in 1960, chloroquine resistance emerged in Asia and spread widely in all the endemic areas. It was associated with genotypes in P. falciparum chloroquine resistance transporter (CVIET, SVMNT, CVMNT, CVIDT, SVIET and CVMET). The use of new drugs such as sulfadoxine-pyrimethamine (SP) leads quickly to SP-resistant parasites associated with genotypes on P. falciparum DiHydroFolate reductase (I51-R59-N108-I164) and P. falciparum DiHydroPteroate synthetase (436-437-580-613). Recently, the delay of parasite clearance has been described with artemisinine (the most efficacious antimalarial drug). This resistance was associated with the K13 propeller genotype. Since malaria species and antimalarial drug resistance markers could be characterized using nucleic acid sequences, genotyping is needed for malarial monitoring of species distribution and antimalarial drug resistance.
Part of the book: Genotyping