2026-04-19T11:12:16Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1015462025-12-10T00:52:57Zcom_2072_1057col_2072_478917

00925njm 22002777a 4500 dc Guggisberg, Ann M. author Sundararaman, Sesh A. author Lanaspa, Miguel author Moraleda Redecilla, Cinta author González, Raquel author Mayor Aparicio, Alfredo Gabriel author Cisteró, Pau author Hutchinson, David author Kremsner, Peter G. author Hahn, Beatrice H. author Bassat Orellana, Quique author Odom, Audrey R. author 2016-09-05T12:52:52Z 2017-07-20T22:01:24Z 2016-07-20 2016-08-03T18:01:09Z Novel antimalarial therapies are needed in the face of emerging resistance to artemisinin combination therapies. A previous study found a high cure rate in Mozambican children with uncomplicated Plasmodium falciparum malaria 7 days post treatment with a fosmidomycin-clindamycin combination. However, 28-day cure rates were low (45.9%), due to parasite recrudescence. We sought to identify any genetic changes underlying parasite recrudescence. To this end, we utilized a selective whole genome amplification method to amplify parasite genomes from blood spot DNA samples. Parasite genomes from pre-treatment and post-recrudescence samples were subjected to whole genome sequencing to identify nucleotide variants. We find that our data do not support the existence of a genetic change responsible for recrudescence following fosmidomycin-clindamycin treatment. Additionally, we find that previously described resistance alleles for these drugs do not represent biomarkers of recrudescence. Future studies should continue to optimize fosmidomycin combinations for use as antimalarial therapies. Malària Plasmodium falciparum Vacuna de la malària Malaria Plasmodium falciparum Malaria vaccine Whole genome sequencing to evaluate the resistance landscape following antimalarial treatment failure with fosmidomycin-clindamycin