Evidence map›Paper›PMID 27035661›Full record

ArticlePLoS neglected tropical diseases2016

New Trypanosoma evansi Type B Isolates from Ethiopian Dromedary Camels.

Hadush Birhanu, Tadesse Gebrehiwot, Bruno Maria Goddeeris, Philippe Büscher, Nick Van Reet

Abstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

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

  1. Pooled it
  2. Molecular Characterization and Prevalence ofPathogens (Basel, Switzerland) · 2026
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  13. Drug resistance in animal trypanosomiases: Epidemiology, mechanisms and control strategies.International journal for parasitology. Drugs and drug resistance · 2024
    Review
  14. Article
  15. Article
  16. Molecular identification of new Trypanosoma evansi type non-A/B isolates from buffaloes and cattle in Indonesia.Revista brasileira de parasitologia veterinaria = Brazilian journal of veterinary parasitology : Orgao Oficial do Colegio Brasileiro de Parasitologia Veterinaria · 2024
    Article
  17. Review
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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.

Hadush BirhanuCollege of Veterinary Medicine, Mekelle University, Mekelle, Ethiopia.
Tadesse GebrehiwotCollege of Veterinary Medicine, Mekelle University, Mekelle, Ethiopia.
Bruno Maria GoddeerisKU Leuven, Faculty of Bioscience Engineering, Department of Biosystems, Leuven, Belgium.
Philippe BüscherInstitute of Tropical Medicine, Department of Biomedical Sciences, Antwerp, Belgium.
Nick Van ReetInstitute of Tropical Medicine, Department of Biomedical Sciences, Antwerp, Belgium.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTrypanosoma (T.) evansi is a dyskinetoplastic variant of T. brucei that has gained the ability to be transmitted by all sorts of biting flies. T. evansi can be divided into type A, which is the most abundant and found in Africa, Asia and Latin America and type B, which has so far been isolated only from Kenyan dromedary camels. This study aimed at the isolation and the genetic and phenotypic characterisation of type A and B T. evansi stocks from camels in Northern Ethiopia. METHODOLOGY/PRINCIPAL

findingsT. evansi was isolated in mice by inoculation with the cryopreserved buffy coat of parasitologically confirmed animals. Fourteen stocks were thus isolated and subject to genotyping with PCRs targeting type-specific variant surface glycoprotein genes, mitochondrial minicircles and maxicircles, minisatellite markers and the F1-ATP synthase γ subunit gene. Nine stocks corresponded to type A, two stocks were type B and three stocks represented mixed infections between A and B, but not hybrids. One T. evansi type A stock was completely akinetoplastic. Five stocks were adapted to in vitro culture and subjected to a drug sensitivity assay with melarsomine dihydrochloride, diminazene diaceturate, isometamidium chloride and suramin. In vitro adaptation induced some loss of kinetoplasts within 60 days. No correlation between drug sensitivity and absence of the kinetoplast was observed. Sequencing the full coding sequence of the F1-ATP synthase γ subunit revealed new type-specific single nucleotide polymorphisms and deletions. CONCLUSIONS/SIGNIFICANCE: This study addresses some limitations of current molecular markers for T. evansi genotyping. Polymorphism within the F1-ATP synthase γ subunit gene may provide new markers to identify the T. evansi type that do not rely on variant surface glycoprotein genes or kinetoplast DNA.

Indexed as

AnimalsArsenicalsCamelusDiminazeneDNA, KinetoplastDNA, ProtozoanEthiopiaGenotypeMicePhenanthridinesPhenotypePhylogenyPolymerase Chain ReactionProton-Translocating ATPasesSuraminTriazinesArsenicalsDiminazenediminazene aceturateDNA, KinetoplastDNA, Protozoanisometamidium chloridemelarsominePhenanthridinesProton-Translocating ATPasesSuraminTriazinesTrypanocidal Agents

Identifiers

PMID27035661
PMCPMC4818106

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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.