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BACKGROUND AND OBJECTIVE   Brazil is responsible for a large number of  Plasmodium vivax  cases in America. Given the emergence of  P. vivax  parasites resistant to chloroquine and the effectiveness of antifolates in vivax malaria treatment together with a correlation between mutations in  P. vivax dhfr  and  dhps  genes and SP treatment failure, the point mutations in these genes were investigated.    METHODS   Blood samples from 54 patients experiencing vivax malaria symptomatic episodes in the Amazonian Region were investigated. Genomic DNA was extracted using a DNA extraction kit (QIAGEN TM ). Nested polymerase chain reaction (PCR) amplification was carried out followed by Sanger sequencing to detect single nucleotide polymorphisms (SNPs).    FINDINGS   All tested isolates showed non-synonymous mutations in  pvdhfr  gene: 117 N  (54/54, 100%) and 58 R  (25/54, 46%). Double mutant allele 58 R /117 N  (F  R  T  N  I, 28%) was the most frequent followed by triple mutant alleles (58 R /117 N /173 L , F  R  T  NL  , 11%; 58 R /61 M /117 N , F  RMN  I, 5% 117 N /173 L , FST  NL  , 4%) and quadruple mutant allele (58 R /61 M /117 N /173 L , F  RMNL  , 2%). A single mutation was observed at codon C383 G  in  pvdhps  gene (S  G  KAV, 48%).    CONCLUSION   No evidence of molecular signatures associated with  P. vivax  resistance to SP was observed in the Brazilian samples.

memórias do instituto oswaldo cruz

Lack of quadruple and quintuple mutant alleles associated with sulfadoxine-pyrimethamine resistance in Plasmodium vivax isolates from Brazilian endemic areas