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Am. J. Trop. Med. Hyg., 80(4), 2009, pp. 523-527
Copyright © 2009 by The American Society of Tropical Medicine and Hygiene

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SHORT REPORT


Five-Year Surveillance of Molecular Markers of Plasmodium falciparum Antimalarial Drug Resistance in Korogwe District, Tanzania: Accumulation of the 581G Mutation in the P. falciparum Dihydropteroate Synthase Gene

Michael Alifrangis*, John P. Lusingu, Bruno Mmbando, Michael B. Dalgaard, Lasse S. Vestergaard, Deus Ishengoma, Insaf F. Khalil, Thor G. Theander, Martha M. Lemnge, AND Ib C. Bygbjerg
Centre for Medical Parasitology, Department of International Health, Immunology and Microbiology, University of Copenhagen, Copenhagem, Denmark; Department of Infectious Diseases, Copenhagen University Hospital, Copenhagen, Denmark; National Institute for Medical Research, Tanga Centre, Tanga, Tanzania

 

ABSTRACT

In January 2007, Tanzania replaced sulfadoxine-pyrimethamine (SP) with artemether-lumefantrine for treatment of uncomplicated malaria. This study examined the impact of widespread SP use on molecular markers of Plasmodium falciparum drug resistance in blood samples from persons living in two villages in Korogwe District, Tanzania, from 2003 through 2007. The prevalence of the P. falciparum dihydropteroate synthase (Pfdhps) gene 581G mutation increased from 12% in 2003 to 56% in 2007 (P < 0.001), resulting in an increase in the triple mutant Pfdhps haplotype SGEGA from 8% to 32% (P < 0.001). In contrast, the chloroquine-sensitive P. falciparum chloroquine resistance transporter (Pfcrt) CVMNK haplotype increased from 6% to 30% (P < 0.001). The dramatic increase of the triple Pfdhps mutant SGEGA haplotype may endanger the continued use of SP for intermittent presumptive treatment of pregnant women (IPTp). Further studies are needed to determine the importance of Pfdhps SGEGA haplotype parasites on the efficacy of SP for IPTp.

Received July 9, 2008. Accepted for publication December 4, 2008.

Acknowledgments: All study participants, including their parents or guardians, are kindly acknowledged. We thank Ulla Abildtrup and Charles Brown (Noguchi Memorial Institute for Medical Research, University of Ghana, Accra, Ghana) for excellent technical assistance. The study was conducted under the auspices of the Joint Malaria Programme, a collaborative research initiative between Centre for Medical Parasitology at the University of Copenhagen and Copenhagen University Hospital, Kilimanjaro Christian Medical College, London School of Hygiene and Tropical Medicine and the Tanzania National Institute for Medical Research.

Financial support: The field study was supported by the Tanzania-Denmark ENRECA programme (104.Dan.8.L.312) and project 91106 by the Danish International Development Agency.

* Address correspondence to Michael Alifrangis, Centre for Medical Parasitology, Institute for International Health, Immunology and Microbiology, CSS, Øster Farimagsgade 5, Building 22+23, PO Box 2099, 1014 Copenhagen K, Denmark. E-mail: micali{at}sund.ku.dk

Authors’ addresses: Michael Alifrangis, Michael B. Dalgaard, Lasse S. Vestergaard, Insaf F. Khalil, Thor G. Theander, and Ib C. Bygbjerg, Centre for Medical Parasitology, Institute for International Health, Immunology and Microbiology, CSS, Øster Farimagsgade 5, Building 22+23, PO Box 2099, 1014 Copenhagen K, Denmark, E-mails: micali{at}sund.ku.dk, michael.dalgaard{at}cmp.dk, l.vestergaard{at}cmp.dk, insafk{at}sund.ku.dk, thor{at}sund.ku.dk, and iby{at}sund.ku.dk. John P. Lusingu, Bruno Mmbando, Deus Ishengoma, and Martha M. Lemnge, National Institute for Medical Research, Tanga Medical Research Centre, PO Box 5004, Tanga, Tanzania, E-mails: jlusingu{at}tanga.mimcom.net, b.mmbando{at}biostat.ku.dk, dishengoma{at}tanga.mimcom.net, and lemnge{at}tanga.mimcom.net.






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