Evidence map›Paper›PMID 26296743›Full record

ArticleMalaria journal2015

Chloroquine sensitivity: diminished prevalence of chloroquine-resistant gene marker pfcrt-76 13 years after cessation of chloroquine use in Msambweni, Kenya.

William Chege Kiarie, Laura Wangai, Eric Agola, Francis T Kimani, Charity Hungu

Abstract read
In one paragraph

Article in Malaria journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

21 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
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  12. Gametocyte Development and Carriage in Ghanaian Individuals with UncomplicatedThe American journal of tropical medicine and hygiene · 2018
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  13. Surveillance of Antimalarial Resistance Molecular Markers in ImportedThe American journal of tropical medicine and hygiene · 2018
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  14. Impacts of Antimalarial Drugs onThe American journal of tropical medicine and hygiene · 2018
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  16. SustainedAntimicrobial agents and chemotherapy · 2017
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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

5 authors.

William Chege KiarieInstitute of Tropical Medicine and Infectious Diseases (ITROMID), PO Box 54840-00200, Nairobi, Kenya. chege.william@gmail.com.
Laura WangaiSchool of Health Sciences, Kirinyaga University College (Constituent College of JKUAT), P.O. Box 143-10300, Kerugoya, Kenya. lauranyawira@yahoo.com.
Eric AgolaKenya Medical Research Institute, Centre for Biotechnology Research and Development (KEMRI, CBRD), PO Box 54840-00200, Nairobi, Kenya. elelo@kemri.org.
Francis T KimaniKenya Medical Research Institute, Centre for Biotechnology Research and Development (KEMRI, CBRD), PO Box 54840-00200, Nairobi, Kenya. fkimani@kemri.org.
Charity HunguKenya Medical Research Institute, Centre for Biotechnology Research and Development (KEMRI, CBRD), PO Box 54840-00200, Nairobi, Kenya. charityhungu@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlasmodium falciparum resistance to chloroquine (CQ) denied healthcare providers access to a cheap and effective anti-malarial drug. Resistance has been proven to be due to point mutations on the parasite's pfcrt gene, particularly on codon 76, resulting in an amino acid change from lysine to threonine. This study sought to determine the prevalence of the pfcrt K76T mutation 13 years after CQ cessation in Msambweni, Kenya.

methodsFinger-prick whole blood was collected on 3MM Whatman(®) filter paper from 99 falciparum malaria patients. Parasite DNA was extracted via the Chelex method from individual blood spots and used as template in nested PCR amplification of pfcrt. Apo1 restriction enzyme was used to digest the amplified DNA to identify the samples as wild type or sensitive at codon 76. Prevalence figures of the mutant pfcrt 76T gene were calculated by dividing the number of samples bearing the mutant gene with the total number of samples multiplied by 100 %. Chi square tests were used to test the significance of the findings against previous prevalence figures.

resultsOut of 99 clinical samples collected in 2013, prevalence of the mutant pfcrt 76T gene stood at 41 %.

conclusionThe results indicate a significant [χ(2) test, P ≤ 0.05 (2006 vs 2013)] reversal to sensitivity by the P. falciparum population in the study site compared to the situation reported in 2006 at the same study site. This could primarily be driven by diminished use of CQ in the study area in line with the official policy. Studies to establish prevalence of the pfcrt 76T gene could be expanded countrywide to establish the CQ sensitivity status and predict a date when CQ may be re-introduced as part of malaria chemotherapy.

Indexed as

Drug ResistanceAntimalarialsChildChild, PreschoolChloroquineCodonFemaleGenetic MarkersHumansKenyaMalaria, FalciparumMaleMembrane Transport ProteinsMolecular EpidemiologyPlasmodium falciparumPrevalenceAntimalarialsChloroquineCodonGenetic MarkersMembrane Transport ProteinsPfCRT protein, Plasmodium falciparumProtozoan Proteins

Identifiers

PMID26296743
PMCPMC4546357

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Registered trials

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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.