期刊
INFECTION GENETICS AND EVOLUTION
卷 4, 期 4, 页码 321-327出版社
ELSEVIER
DOI: 10.1016/j.meegid.2004.04.002
关键词
Plasmodium falciparum; Dihydrofolate reductase; Dihydropteroate synthase; Point mutations; Sulphadoxime-pyrimethamine; Parasitological failure; In vivo efficacy
资金
- East Africa Network for Monitoring Antimalarial Treatment (EANMAT)
- World Health Organisation, Multilateral Initiative for Malaria (MIM) [A00028]
- Belgian Development Co-operation (BEADC-ITM)
- Prince Leopold Institute of Tropical Medicine, Antwerp, Belgium
- Fonds voor Wetenschappeljk Onderzoek-Vlanderen (FWO)
- Belgian development cooperation
The point mutations in the Plasmodium falciparum dihydrofolate reductase (dhfr) and the dihydropteroate synthase (dhps) genes that are linked to sulphadoxine-pyrimethamine (SP) resistance in vitro have been well characterised. To determine whether a few of these mutations could predict SP treatment failure in vivo, two mutations (Asn-108 and Arg-59) in the dhfr gene and one (Glu-540) in the dhps gene were analysed according to the risk of SP parasitological failure (RI-RIII) at day 28 in pre-treatment isolates in 79 Ugandan children aged 6-59 (mean = 18.4, S.D. = 8.8) months with uncomplicated falciparum malaria. Neither the dhfr-108 (P = 0.3) nor the dhps-540 (P = 0.6) or dhfr-108 + dhps-540 (P = 0.08) mutations were significantly associated with SP parasitological failure. However, the dhfr-108 + dhfr-59 (P = 0.04), the dhfr-59 + dhps-540 (P = 0.04) and the dhfr-108 + dhfr-59 + dhps-540 (P = 0.02) mutations significantly increased the risk for SP parasitological failure. Our findings confirm an earlier report that the dhfr-59 and the dhps-540 mutations could be useful genetic markers for rapid screening of populations at high risk of SP resistance. (C) 2004 Elsevier B. V. All rights reserved.
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