Abstract
BackgroundPlasmodium falciparum is the predominant human malaria species in Mozambique and a lead cause of mortality among children and pregnant women nationwide. Sulphadoxine/pyrimethamine (S/P) is used as first line antimalarial treatment as a partner drug in combination with artesunate.MethodsA total of 92 P. falciparum-infected blood samples, from children with uncomplicated malaria attending the Centro de Saude de Bagamoyo in the Province of Maputo-Mozambique, were screened for S/P resistance-conferring mutations in the pfdhfr and pfdhps genes using a nested mutation-specific polymerase chain reaction and restriction digestion (PCR-RFLP). The panel of genetic polymorphisms analysed included the pfdhfr 164L mutation, previously reported to be absent or rare in Africa.ResultsThe frequency of the S/P resistance-associated pfdhfr triple mutants (51I/59R/108N) and of pfdhfr/pfdhps quintuple mutants (51I/59R/108N + 437G/540E) was 93% and 47%, respectively. However, no pfdhfr 164L mutants were detected.ConclusionThe observation that a considerably high percentage of P. falciparum parasites contained S/P resistance-associated mutations raises concerns about the validity of this drug as first-choice treatment in Mozambique. On the other hand, no pfdhfr 164L mutant was disclosed, corroborating the view that that this allele is still rare in Africa.
Highlights
Plasmodium falciparum is the predominant human malaria species in Mozambique and a lead cause of mortality among children and pregnant women nationwide
As the intensity of chloroquine resistance increased, the country implemented a change of first-line antimalarial treatment in 2002 to a combination of sulphadoxine/pyrimethamine (S/P) + amodiaquine
In 2004, this has been further altered to Sulphadoxine/ pyrimethamine (S/P) + artesunate, in line with current WHO recommendations for the use of Artemisinin Combination Therapies (ACTs) [1]
Summary
Plasmodium falciparum is the predominant human malaria species in Mozambique and a lead cause of mortality among children and pregnant women nationwide. Sulphadoxine and pyrimethamine (S/P) act as synergistic inhibitors of folate biosynthesis which, in malaria parasites, is an obligatory requirement for the production of nucleotides and DNA synthesis. Because both compounds act synergistically, any loss of efficiency in either component results in the reduction of the effectiveness of the combination as whole. In this context, the occurrence of certain molecular polymorphisms in the dihydrofolate reductase (pfdhfr) and dihydropteroate synthase (pfdhps) genes have been associated to in vivo S/P treatment outcome [2,3]. In East Africa, the occurrence of the so-called pfdhfr/pfdhps quintuple mutant parasites (dhfr 51I/59R/108N + dhps 437G/540E) appears to be a good predictor of S/P treatment failure [4,5]
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