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PO 8269 SELECTION OF SEVEN-MUTATION PFCRT-PFMDR1 GENOTYPE AFTER SCALING-UP SEASONAL MALARIA CHEMOPREVENTION WITH SULPHADOXINE-PYRIMETHAMINE AND AMODIAQUINE IN MALI
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  1. Hamma Maiga1,
  2. Amadou Bamadio2,
  3. Aliou Traore2,
  4. Nouhoum Diallo2,
  5. Modibo Diarra2,
  6. Issaka Sagara2,
  7. Hamidou Niangaly2,
  8. Samba Coumare2,
  9. Boubou Sangare2,
  10. Djibril Traore2,
  11. Michel Vaillant3,
  12. Alassane Dicko2,
  13. Ogobara K Doumbo, †2,
  14. Abdoulaye Djimde2
  1. 1National Institute of Public Health Research, Bamako, Mali
  2. 2Malaria Research and Training Center, University of Bamako, Mali
  3. 3Luxembourg Institute of Health

Abstract

Background WHO recommended seasonal malaria chemoprevention (SMC) in 2012 for Sahel countries in Africa with the aim to reduce malaria among children under 5 years old by using sulphadoxine-pyrimethamine and amodiaquine (SP+AQ). This strategy was scaled up in Mali from 2012. The use of millions of doses of SP+AQ could generate potential Plasmodium falciparum resistance in mutant parasites. The aim of this study was to monitor the prevalence of Pfdhfr +Pfdhps +pfcrt + pfmdr 1 mutations in parasites infecting the target population.

Methods Two cross-sectional surveys were conducted before (August 2012, n=662) and after (June 2014, n=670) a pilot implementation of SMC in the health district of Koutiala. Children aged 3–59 months received 3 and 4 rounds of curative doses of SP+AQ over two malaria seasons in 2012 and 2013, respectively. Genotypes of P. falciparum Pfdhfr codons 51, 59, 108 and 164; Pfdhps codons 437 and 540, Pfcrt codon 76 and Pfmdr1 codon 86 were analysed by PCR on DNA of parasites from SMC population blood samples (after and before) and non-SMC patients aged 7 years or above (November 2014, n=500).

Results In the SMC population 191 and 85 children before and after SMC implementation, respectively, were included in’the molecular analysis. In the non-SMC patients, 220 were’successfully PCR analysed. In the SMC population, the’prevalence of the six-mutation Pfcrt [Pfdhfr-dhps quintuple +Pfcrt-76T] genotype increased significantly after SMC implementation, from 0.0% to 7.1% (p=0.0008). The post-intervention prevalence of the six-mutation Pfmdr1 [Pfdhfr-dhps quintuple +Pfmdr1–86Y] and the seven-mutation Pfcrt +Pfmdr 1 [Pfdhfr-dhps quintuple +Pfmdr1–86Y+Pfcrt-76T] genotypes were both 1.2% among the SMC population. No six-mutation and seven-mutation genotypes were observed among SMC population at baseline nor in the non-SMC patient population (p=0.30).

Conclusion SMC increased the prevalence of the six-mutation Pfcrt genotype of P. falciparum that can lead to resistance in a population exposed to SMC with SP+AQ.

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