Evidence map›Paper›PMID 24989984›Full record

ArticleMalaria journal2014

Trends in drug resistance codons in Plasmodium falciparum dihydrofolate reductase and dihydropteroate synthase genes in Kenyan parasites from 2008 to 2012.

Dennis W Juma, Angela A Omondi, Luiser Ingasia, Benjamin Opot, Agnes Cheruiyot, Redemptah Yeda, Charles Okudo, Jelagat Cheruiyot, Peninnah Muiruri, Bidii Ngalah and 7 more

Open access · goldAbstract read
In one paragraph

Article in Malaria journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

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  7. Polymorphism of Drug Resistance GenesTropical medicine and infectious disease · 2023
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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

17 authors at 2 institutions in 1 country.

Dennis W Juma
Angela A Omondi
Luiser Ingasia
Benjamin Opot
Agnes Cheruiyot
Redemptah Yeda
Charles Okudo
Jelagat Cheruiyot
Peninnah Muiruri
Bidii Ngalah
Lorna J Chebon
Fredrick Eyase
Jacob Johnson
Wallace D Bulimo
Hoseah M Akala
Ben Andagalu
Edwin KamauGlobal Emerging Infections Surveillance (GEIS) Program, United States Army Medical Research Unit-Kenya (USAMRU-K), Kenya Medical Research Institute (KEMRI) - Walter Reed Project, Kisumu and Nairobi, Kenya. edwin.kamau@us.army.mil.
United States Army Medical Research Directorate - Africa · KEKenya Medical Research Institute · KE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSulphadoxine-pyrimethamine (SP), an antifolate, was replaced by artemether-lumefantrine as the first-line malaria drug treatment in Kenya in 2004 due to the wide spread of resistance. However, SP still remains the recommended drug for intermittent preventive treatment in pregnant women and infants (IPTP/I) owing to its safety profile. This study assessed the prevalence of mutations in dihydrofolate reductase (Pfdhfr) and dihydropteroate synthase (Pfdhps) genes associated with SP resistance in samples collected in Kenya between 2008 and 2012.

methodsField isolates collected from Kisumu, Kisii, Kericho and Malindi district hospitals were assessed for genetic polymorphism at various loci within Pfdhfr and Pfdhps genes by sequencing.

resultsAmong the Pfdhfr mutations, codons N51I, C59R, S108N showed highest prevalence in all the field sites at 95.5%, 84.1% and 98.6% respectively. Pfdhfr S108N prevalence was highest in Kisii at 100%. A temporal trend analysis showed steady prevalence of mutations over time except for codon Pfdhps 581 which showed an increase in mixed genotypes. Triple Pfdhfr N51I/C59R/S108N and double Pfdhps A437G/ K540E had high prevalence rates of 86.6% and 87.9% respectively. The Pfdhfr/Pfdhps quintuple, N51I/C59R/S108N/A437G/K540E mutant which has been shown to be the most clinically relevant marker for SP resistance was observed in 75.7% of the samples.

conclusionSP resistance is still persistently high in western Kenya, which is likely due to fixation of key mutations in the Pfdhfr and Pfdhps genes as well as drug pressure from other antifolate drugs being used for the treatment of malaria and other infections. In addition, there is emergence and increasing prevalence of new mutations in Kenyan parasite population. Since SP is used for IPTP/I, molecular surveillance and in vitro susceptibility assays must be sustained to provide information on the emergence and spread of SP resistance.

Indexed as

Drug ResistanceAdolescentAdultAgedAntimalarialsChildChild, PreschoolDihydropteroate SynthaseFemaleHumansInfantKenyaMaleMiddle AgedPlasmodium falciparumPolymorphism, GeneticAntimalarialsDihydropteroate SynthaseTetrahydrofolate Dehydrogenase

Identifiers

PMID24989984
PMCPMC4094641
OpenAlexW2124270158

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.