Molecular monitoring of the Leu-164 mutation of dihydrofolate reductase in a highly sulfadoxine/pyrimethamine-resistant area in Africa

Edwin Ochong¹ , Alexis Nzila¹^,2 , Serah Kimani¹ , Gilbert Kokwaro¹ , Theonest Mutabingwa³^,4 , William Watkins² and Kevin Marsh⁵^,6

¹Kenya Medical Research Institute (KEMRI)/Wellcome Trust Collaborative Research Programme, Wellcome Trust Research Laboratories P.O Box 43640 Nairobi, Kenya

²Department of Pharmacology and Therapeutics, University of Liverpool, Liverpool L69 3BX, UK

³National Institute for Medical Research, Amani, Tanzania

⁴London School of Tropical Medicine and Hygiene, Gates Malaria Partnership, London, UK

⁵KEMRI/Wellcome Trust Collaborative Research Programme, Centre for Geographical Medicine Research KEMRI PO Box 230, Kilifi, Kenya

⁶Nuffield Department of Medicine, John Radcliffe Hospital, Oxford, UK

author email corresponding author email

Malaria Journal 2003, 2:46doi:10.1186/1475-2875-2-46


Published:	15 December 2003

Abstract

The selection of point mutation at codon 164 (from isoleucine to leucine) of the dihydrofolate reductase (DHFR) enzyme in Plasmodium falciparum is associated with high sulfadoxine /pyrimethamine (SP) resistance. Using the yeast expression system that allows the detection of dhfr allele present at low level, the presence of this mutation had previously been reported between 1998–1999 in Muheza, Tanzania, an area of high SP resistance. Eighty five P. falciparum isolates, obtained from the same area between 2002 and 2003, were analysed for the presence of Leu-164 mutation, using standard protocol based on PCR-RFLP. None of the isolates had the Leu-164 mutation.