Evidence map›Paper›PMID 40598187›Full record

ArticleMalaria journal2025

Artemisinin and partner drug resistance markers in Plasmodium falciparum from Tanzanian paediatric malaria patients, 2016-2022.

Aveline Assey, Silvia Scialabba, Maria Mgella Zinga, Philip Koliopoulos, Welmoed van Loon, Caroline A Minja, Britta Groendahl, Johannes Plett, Stephan Gehring, Mariam M Mirambo and 3 more

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Article in Malaria journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Aveline Assey *Department of Parasitology and Entomology, Catholic University of Health and Allied Sciences, P.O. Box 1464, Mwanza, Tanzania.
Silvia Scialabba *Centre of Paediatric and Adolescent Medicine, University Medical Center, 55131, Mainz, Germany.
Maria Mgella ZingaDepartment of Parasitology and Entomology, Catholic University of Health and Allied Sciences, P.O. Box 1464, Mwanza, Tanzania. mariazinga@gmail.com.
Philip KoliopoulosCentre of Paediatric and Adolescent Medicine, University Medical Center, 55131, Mainz, Germany.
Welmoed van LoonCharité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität Zu Berlin, Charité Center for Global Health, Institute of International Health, 13353, Berlin, Germany.
Caroline A MinjaDepartment of Biochemistry and Molecular Biology, Catholic University of Health and Allied Sciences, P. O. Box 1464, Mwanza, Tanzania.
Britta GroendahlCentre of Paediatric and Adolescent Medicine, University Medical Center, 55131, Mainz, Germany.
Johannes PlettCentre of Paediatric and Adolescent Medicine, University Medical Center, 55131, Mainz, Germany.
Stephan GehringCentre of Paediatric and Adolescent Medicine, University Medical Center, 55131, Mainz, Germany.
Mariam M MiramboDepartment of Microbiology and Immunology, Catholic University of Health and Allied Sciences, P.O. Box 1464, Mwanza, Tanzania.
Neema KayangeDepartment of Paediatrics, Catholic University of Health and Allied Sciences, P.O. Box 1464, Mwanza, Tanzania.
Frank P MockenhauptCharité-Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt-Universität Zu Berlin, Charité Center for Global Health, Institute of International Health, 13353, Berlin, Germany.
Stephen E MshanaDepartment of Microbiology and Immunology, Catholic University of Health and Allied Sciences, P.O. Box 1464, Mwanza, Tanzania.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlasmodium falciparum malaria remains a significant public health concern in Tanzania, particularly among children under 5 years of age. The emergence and spread of partial artemisinin resistance in East Africa add to this concern. Specific mutations in the P. falciparum kelch-13 (Pfk13) and multidrug drug resistance 1 (Pfmdr1) genes are associated with artemisinin resistance and lumefantrine tolerance, respectively. The emergence of antimalarial drug resistance may be associated with unstable transmission in sub-Saharan Africa (SSA). Time-trends of Pfk13 and Pfmdr1 mutations as well as the multiplicity of infection (MOI) as a proxy for transmission intensity were investigated.

methodsBetween 2016 and 2022, 173 P. falciparum PCR-positive samples were collected from febrile inpatient and outpatient children aged 3 months to 18 years at selected health facilities in Mwanza, Tanzania. Pfk13 and Pfmdr1 were amplified by PCR and Sanger-sequenced. Polymorphic Pfmsp1 and Pfmsp2 allelic markers were genotyped by nested PCR in 168 samples to assess MOI.

resultsAmong 143 samples successfully sequenced for Pfk13, 7.0% (10/143) exhibited non-synonymous mutations including the WHO-validated artemisinin resistance marker R561H in 1.4% (2 patients, 2022). As for Pfmdr1, the wild-type N86 allele was observed in 100% (97/97) of isolates, and about half (55/97) carried the wild-type Y184 allele. The mean multiplicity of infection (MOI) was 1.5, and did not change significantly over time. Single-genotype and polyclonal infections were observed in 59.3% (80/135), and 40.7% (55/135) respectively.

conclusionThis study from Mwanza, Tanzania demonstrates the presence of a validated artemisinin resistance marker Pfk13 R561H in 2022 and suggests increased lumefantrine tolerance. MOI as a proxy marker of endemicity was low and stable over the six years of observation. The detection of these resistance markers reinforces the need for continuous genetic surveillance to sustain the efficacy of antimalarial therapies in paediatric patients.

Indexed as

AntimalarialsArtemisininsDrug ResistanceMalaria, FalciparumPlasmodium falciparumAdolescentATP-Binding Cassette, Sub-Family C ProteinsChildChild, PreschoolFemaleHumansInfantMaleMutationProtozoan ProteinsTanzaniaAntimalarialsartemisininArtemisininsATP-Binding Cassette, Sub-Family C ProteinsMdr1 protein, Plasmodium falciparumProtozoan ProteinsArtemisinin resistanceGenetic diversityMultiplicity of infectionPfk13Pfmdr1Pfmsp1Pfmsp2Plasmodium falciparum

Identifiers

PMID40598187
PMCPMC12217380

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