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10.1186/s12936-017-1747-6

http://scihub22266oqcxt.onion/10.1186/s12936-017-1747-6
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suck abstract from ncbi


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pmid28288632
      Malar+J 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.
  • |*Drug Resistance [MESH]
  • |*Polymorphism, Genetic [MESH]
  • |Antimalarials/*administration & dosage [MESH]
  • |Child [MESH]
  • |Child, Preschool [MESH]
  • |Chloroquine/*administration & dosage [MESH]
  • |Humans [MESH]
  • |Liberia [MESH]
  • |Malaria, Falciparum/drug therapy [MESH]
  • |Plasmodium falciparum/*drug effects/genetics [MESH]
  • |Polymerase Chain Reaction [MESH]
  • |Proguanil/administration & dosage/*analogs & derivatives [MESH]
  • |Protozoan Proteins/genetics/metabolism [MESH]
  • |Pyrimethamine/*administration & dosage [MESH]


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