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INCREASING PREVALENCE OF WILDTYPES IN THE DIHYDROFOLATE REDUCTASE GENE OF PLASMODIUM FALCIPARUM IN AN AREA WITH HIGH LEVELS OF SULFADOXINE/PYRIMETHAMINE RESISTANCE AFTER INTRODUCTION OF TREATED BED NETS

In Magoda and Mpapayu villages in Tanzania, we have previously found comparable high prevalence of Plasmodium falciparum resistance to sulfadoxine/pyrimethamine (S/P) in vivo and of mutations in the dihydrofolate reductase (dhfr) and dihydropteroate synthetase (dhps) genes of P. falciparum responsible for resistance to S/P. In December 1998, Magoda received insecticide-treated nets (ITNs), whereas ITNs were introduced in Mpapayu in March 2001. We have studied the effect of ITNs on P. falciparum resistance genes by monitoring the prevalence of dhfr and dhps genotypes in children less than five years old living in the villages from 1998 to 2000. In 2000, after two years of bed net use, the prevalence of wild types in codon 51, 59, and 108 of dhfr increased significantly in Magoda compared with previous years. Furthermore, the prevalence of dhfr wild types was significantly higher in Magoda than in Mpapayu in 2000. The impact of ITNs on the transmission intensity seems not only to affect the overall malaria morbidity, but may even facilitate restoration of susceptibility to antimalarial drugs.

Received April 2, 2003. Accepted for publication July 5, 2003.

Acknowledgments: We are grateful to the people of Magoda and Mpapayu villages, the village helpers and the technicians, Julius Mhina and Jumaa Akida (National Institute for Medical Research, Amani, Tanzania) for assisting with the fieldwork in Tanzania. We thank laboratory technicians Jimmy Weng and Gitte Hoff Jensen for excellent technical assistance in performing the polymerase chain reaction–restriction fragment length polymorphism. We also thank Theophil Rwegohora (National Institute for Medical Research, Bombo Field Station, Tanga, Tanzania) for providing annual rainfall data for the neighboring village of Masaika, Tanzania, and Thor G. Theander, Lars Hviid (Centre for Medical Parasitology, Copenhagen, Denmark), and Anders Björkman (Karolinska Institute, Stockholm, Sweden) for helpful comments on this manuscript.

Financial support: This study was supported by a grant from the Research Council of the Danish International Development Agency (DANIDA RUF, grant no. 90892). The study in Tanzania was supported by DANIDA grant no. 104.Dan.8L as part of a Tanzanian-Danish collaboration under the Enhancement of Research Capacity (ENRECA) program.

Authors’ addresses: Michael Alifrangis and Insaf F. Khalil, Panum Institute, Institute of Medical Microbiology and Immunology, Building 24.2, Blegdamsvej 3, 2200 Copenhagen N, Denmark. Martha M. Lemnge, Method D. Segeja, and Stephen M. Magesa, National Institute for Medical Research, Amani Research Centre, PO Box 4, Amani, Tanga, Tanzania. Anita M. Rønn and Ib C. Bygbjerg, Institute of Public Health, University of Copenhagen, Nørre Alle 4-6, 2200 Copenhagen N, Denmark.

Reprint requests: Michael Alifrangis, Panum Institute, Institue of Medical Microbiology and Immunology, Building 24.2, Blegdamsvej 3, 2200 Copenhagen N, Denmark, Telephone: 45-3532-7676, Fax: 45-3532-7851, E-mail: malif{at}biobase.dk.

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