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2017 ; 16
(1
): 113
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Unexpected selections of Plasmodium falciparum polymorphisms in previously
treatment-naïve areas after monthly presumptive administration of three different
anti-malarial drugs in Liberia 1976-78
#MMPMID28288632
Jovel IT
; Björkman A
; Roper C
; Mårtensson A
; Ursing J
Malar J
2017[Mar]; 16
(1
): 113
PMID28288632
show ga
BACKGROUND: To assess the effect on malaria prevalence, village specific monthly
administrations of pyrimethamine, chlorproguanil, chloroquine or placebo were
given to children in four previously treatment-naïve Liberian villages, 1976-78.
Plasmodium falciparum in vivo resistance developed to pyrimethamine only.
Selection of molecular markers of P. falciparum resistance after 2 years of
treatment are reported. METHODS: Blood samples were collected from 191 study
children in a survey in 1978. Polymorphisms in pfcrt, pfmdr1, pfdhfr, pfdhps,
pfmrp1 and pfnhe1 genes were determined using PCR-based methods. RESULTS: Pfcrt
72-76 CVIET was found in one chloroquine village sample, all remaining samples
had pfcrt CVMNK. Pfmdr1 N86 prevalence was 100%. A pfmdr1 T1069(ACT?ACG)
synonymous polymorphism was found in 30% of chloroquine village samples and 3% of
other samples (P = 0.008). Variations in pfnhe1 block I were found in all except
the chloroquine treated village (P < 0.001). Resistance associated pfdhfr 108N
prevalence was 2% in the pyrimethamine village compared to 45-65% elsewhere,
including the placebo village (P = 0.001). CONCLUSIONS: Chloroquine treatment
possibly resulted in the development of pfcrt 72-76 CVIET. Selection of pfmdr1
T1069(ACG) and a pfnhe1 block 1 genotypes indicates that chloroquine treatment
exerted a selective pressure on P. falciparum. Pyrimethamine resistance
associated pfdhfr 108N was present prior to the introduction of any drug.
Decreased pfdhfr 108N frequency concurrent with development of pyrimethamine
resistance suggests a non-pfdhfr polymorphisms mediated resistance mechanism.