2026-04-19T11:33:26Zhttps://recercat.cat/oai/requestoai:recercat.cat:2445/1015462025-12-10T00:52:57Zcom_2072_1057col_2072_478917
RECERCAT
author
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.
2016-09-05T12:52:52Z2017-07-20T22:01:24Z2016-07-202016-08-03T18:01:09Z
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.
(c) Guggisberg et al., 2016 info:eu-repo/semantics/openAccess
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
info:eu-repo/semantics/article info:eu-repo/semantics/acceptedVersion