High frequency of Plasmodium falciparum CICNI/SGEAA and CVIET haplotypes without association with resistance to sulfadoxine/pyrimethamine and chloroquine combination in the Daraweesh area, in Sudan
- 29 March 2008
- journal article
- Published by Springer Nature in European Journal of Clinical Microbiology & Infectious Diseases
- Vol. 27 (8) , 725-732
- https://doi.org/10.1007/s10096-008-0499-1
Abstract
Estimation of the prevalence of the molecular markers of sulfadoxine/pyrimethamine (SP) and chloroquine (CQ) resistance and validation of the association of mutations with resistance in different settings is needed for local policy guidance and for contributing to a global map for anti-malarial drug resistance. In this study, malaria patients treated with SP alone (60) and SP with CQ (194) had a total treatment failure (TF) of 35.4%, with no difference between the two arms. The polymerase chain reaction–enzyme-linked immunosorbent assay (PCR-ELISA) method was used to identify polymorphisms in 15 loci in the dhfr, dhps and pfcrt genes in a subset of 168 infections. The results revealed a similar frequency of all single nucleotide polymorphisms (SNPs) in the two arms, except dhps 581G, which was over-represented in infections that failed to respond to SP alone (TF). In all infections, a high frequency of dhfr CICNI haplotype (51I and 108N) was found, but without discrimination between the adequate clinical and parasitological response (ACPR, 75.6%) and TF (82.9%). Similarly, the dhps SGEAA haplotype (437G and 540E) (ACPR, 60.5%; TF, 65.9%) and the combined CICNI/SGEAA haplotype (ACPR, 50%; TF 55%) were not associated with TF. In contrast to other studies in Africa, the triple 51I/59R/108N mutation was rare (0.6%). In addition, the pfcrt CVIET haplotype (93%) was found to be associated with the CICNI/SGEAA haplotype. Finally, these data represent a baseline for SP resistance molecular markers needed before the deployment of SP/artesunate combination therapy in the SudanKeywords
This publication has 31 references indexed in Scilit:
- The implication of dihydrofolate reductase and dihydropteroate synthetase gene mutations in modification of Plasmodium falciparum characteristicsMalaria Journal, 2007
- Antifolate Resistance inPlasmodium falciparum:Multiple Origins and Identification of NoveldhfrAllelesThe Journal of Infectious Diseases, 2006
- Occurrence of the Southeast Asian/South American SVMNT Haplotype of the Chloroquine‐Resistance Transporter Gene inPlasmodium falciparumin TanzaniaThe Journal of Infectious Diseases, 2006
- The efficacy of sulfadoxine–pyrimethamine alone and in combination with chloroquine for malaria treatment in rural Eastern Sudan: the interrelation between resistance, age and gametocytogenesisTropical Medicine & International Health, 2006
- Evolution of Drug‐Resistance Genes inPlasmodium falciparumin an Area of Seasonal Malaria Transmission in Eastern SudanThe Journal of Infectious Diseases, 2004
- Molecular Determination of Point Mutation Haplotypes in the Dihydrofolate Reductase and Dihydropteroate Synthase of Plasmodium falciparum in Three Districts of Northern TanzaniaAntimicrobial Agents and Chemotherapy, 2003
- Malaria in 2002Nature, 2002
- High‐Level Chloroquine Resistance in Sudanese Isolates ofPlasmodium falciparumIs Associated with Mutations in the Chloroquine Resistance Transporter Genepfcrtand the Multidrug Resistance Genepfmdr1The Journal of Infectious Diseases, 2001
- Polymorphisms in thePlasmodium falciparum pfcrtandpfmdr‐1Genes and Clinical Response to Chloroquine in Kampala, UgandaThe Journal of Infectious Diseases, 2001
- Sequence Variation of the Hydroxymethyldihydropterin Pyrophosphokinase: Dihydropteroate Synthase Gene in Lines of the Human Malaria Parasite, Plasmodium falciparum, with Differing Resistance to SulfadoxineEuropean Journal of Biochemistry, 1994