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Efficacy of Malaria Intermittent Preventive Treatment in Angolan Endemic Areas
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P. falciparum
parasites are responsible for severe morbidity and its chemoresistance is notorious. Thus, is necessary to evaluate the effectiveness of intermittent preventive treatment (IPT). For this purpose, 107 malaria patient samples were DNA sequenced against
pfdhps
and
pfdhfr
genes. The results showed: 46% with double mutant haplotypes ACNRNVI in codons 59 and 108; 27% with double mutations in codons 51 and 108 with haplotype ACICNVI, 17% triple mutant at codons 51, 59 and 108 with haplotypes ACIRNVI; 2% triple mutant at codons 50, 51, 108 and 59, 108, and 164 with haplotypes ARICNVI ACNRNVL; 6% with a single mutation at codon 108, showing ACNCNVI haplotype and; only wild type sample ‐ ACNCSVI (2%). The 108N mutation (change of serine for asparagine ‐ S108N) in
pfdhfr
gene ‐ a mutation described as the predecessor for all resistant emergence strains ‐ was the most prevalent (98%) followed by 59R (65%) and 51I (47% ). Regarding
pfdhps
gene, a total prevalence of 437G mutation, with the exception of one sample (4%) with wild haplotype SAKAA were noted. Among the mutant samples, 88% had a single mutation presenting haplotype SGKAA; 6% showed double mutants at codons 437 and 540 with haplotype SGEAA and; 6% with double mutant at codons 436 and 437 (AGKAA). Quadruple (triple
pfdhfr
+ single
pfdhps
) and triple mutants (double
pfdhfr
+ single
pfdhps
) were recorded. Considering the significant percentage of
P. falciparum
parasites circulating in Lubango with a resistance profile associated with pyrimethamine and sulphadoxine tolerance, we conclude that the IPT should not be effective in Angola.
Title: Efficacy of Malaria Intermittent Preventive Treatment in Angolan Endemic Areas
Description:
P.
falciparum
parasites are responsible for severe morbidity and its chemoresistance is notorious.
Thus, is necessary to evaluate the effectiveness of intermittent preventive treatment (IPT).
For this purpose, 107 malaria patient samples were DNA sequenced against
pfdhps
and
pfdhfr
genes.
The results showed: 46% with double mutant haplotypes ACNRNVI in codons 59 and 108; 27% with double mutations in codons 51 and 108 with haplotype ACICNVI, 17% triple mutant at codons 51, 59 and 108 with haplotypes ACIRNVI; 2% triple mutant at codons 50, 51, 108 and 59, 108, and 164 with haplotypes ARICNVI ACNRNVL; 6% with a single mutation at codon 108, showing ACNCNVI haplotype and; only wild type sample ‐ ACNCSVI (2%).
The 108N mutation (change of serine for asparagine ‐ S108N) in
pfdhfr
gene ‐ a mutation described as the predecessor for all resistant emergence strains ‐ was the most prevalent (98%) followed by 59R (65%) and 51I (47% ).
Regarding
pfdhps
gene, a total prevalence of 437G mutation, with the exception of one sample (4%) with wild haplotype SAKAA were noted.
Among the mutant samples, 88% had a single mutation presenting haplotype SGKAA; 6% showed double mutants at codons 437 and 540 with haplotype SGEAA and; 6% with double mutant at codons 436 and 437 (AGKAA).
Quadruple (triple
pfdhfr
+ single
pfdhps
) and triple mutants (double
pfdhfr
+ single
pfdhps
) were recorded.
Considering the significant percentage of
P.
falciparum
parasites circulating in Lubango with a resistance profile associated with pyrimethamine and sulphadoxine tolerance, we conclude that the IPT should not be effective in Angola.
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