open access publication

Article, 2024

Lack of selection of antimalarial drug resistance markers after intermittent preventive treatment of schoolchildren (IPTsc) against malaria in northeastern Tanzania

International Journal of Infectious Diseases, ISSN 1201-9712, 1878-3511, Volume 146, Page 107102, 10.1016/j.ijid.2024.107102

Contributors

Von Wowern, Frederik [1] [2] Makenga, Geofrey 0000-0001-5681-9785 [3] [4] Wellmann Thomsen, Sarah [1] [2] Wellmann Thomsen, Louise [1] [2] Filtenborg Hocke, Emma [1] [2] Baraka, Vito 0000-0001-9694-9293 [4] Opot, Benjamin H [5] Minja, Daniel T R [4] Lusingu, John P A [4] Van Geertruyden, Jean-Pierre 0000-0001-5006-6364 [3] Hansson, Helle Holm 0000-0001-6484-1165 [1] [2] Alifrangis, Michael 0000-0002-3835-3333 (Corresponding author) [1] [2]

Affiliations

  1. [1] Copenhagen University Hospital
  2. [NORA names: Capital Region of Denmark; Hospital; Denmark; Europe, EU; Nordic; OECD];
  3. [2] University of Copenhagen
  4. [NORA names: KU University of Copenhagen; University; Denmark; Europe, EU; Nordic; OECD];
  5. [3] University of Antwerp
  6. [NORA names: Belgium; Europe, EU; OECD];
  7. [4] National Institute for Medical Research
  8. [NORA names: Tanzania; Africa];
  9. [5] Kenya Medical Research Institute
  10. [NORA names: Kenya; Africa]

Abstract

OBJECTIVE: Intermittent Preventive Treatment of schoolchildren (IPTsc) is recommended by WHO as a strategy to protect against malaria; to explore whether IPTsc with dihydroartemisinin-piperaquine (DP) or artesunate-amodiaquine (ASAQ) cause a selection of molecular markers in Plasmodium falciparum genes associated with resistance in children in seven schools in Tanga region, Tanzania. METHODS: SNPs in P. falciparum genes Pfmdr1, Pfexo, Pfkelch13, and Pfcrt and copy number variations in Pfplasmepsin-2 and Pfmdr1 were assessed in samples collected at 12 months (visit 4, n=74) and 20 months (visit 6, n=364) after initiation of IPTsc and compared with the baseline prevalence (n=379). RESULTS: The prevalence of Pfmdr1 N86 and Pfexo 415G was >99% and 0%, respectively without any temporal differences observed. The prevalence of Pfmdr1 184F changed significantly from baseline (52.2%) to visit 6 (64.6%) (χ2=6.11, P=0.013), but no differences were observed between the treatment arms (χ2=0.05, P=0.98). Finally, only minor differences in the amplification of Pfmdr1 were observed; from 10.2% at baseline to 16.7% at visit 6 (χ2=0.98, P=0.32). CONCLUSIONS: The IPTsc strategy does not seem to pose a risk for the selection of markers associated with DP or ASAQ resistance. Continuously and timely surveillance of markers of antimalarial drug resistance is recommended.

Keywords

IPTsc, N86, PfEXO, Plasmodium, Plasmodium falciparum genes, SNPs, Tanga, Tanga Region, Tanzania, WHO, amplification, amplification of pfmdr1, antimalarial drug resistance, antimalarial drug resistance markers, arm, artesunate-amodiaquine, associated with resistance, baseline, baseline prevalence, children, copy, copy number variations, differences, dihydroartemisinin-piperaquine, drug resistance, drug resistance markers, genes, initiation, intermittent preventive treatment, lack, malaria, markers, molecular markers, months, northeastern Tanzania, number variations, pfcrt, pfkelch13, pfmdr1, pfmdr1 N86, prevalence, region, resistance, resistance markers, risk, samples, school, schoolchildren, selection, selection of molecular markers, surveillance, temporal differences, treatment, treatment arms, treatment of schoolchildren, variation, visit 6, visits

Funders

  • European Commission

Data Provider: Digital Science