Studies of quinapyramine-resistance of Trypanosoma brucei evansi in China.
Abstract: In the present article, we summarize our studies of antrycide-resistance of Trypanosoma brucei evansi in four aspects in the last recent several years, the analysis of quinapyramine-sensitive situation of T. b. evansi in China, biological characteristics of T. b. evansi population in quinapyramine-resistance and biological materials of quinapyramine-resistance in T. b. evansi population. Firstly, the correlative assays of effective dosage of quinapyramine on T. b. evansi disease between in vivo and in vitro methods showed that their relationship was parabolic with positive correlation. On the other hand, the IC(50) and CD(100) values of 12 T. b. evansi isolates, AHB, GDB1, GDB2, HNB, JSB1, JSB2, YNB, ZJB, GDH, GXM, HBM and XJCA, collected from buffaloes, horses, mules and camels across nine provinces of China were examined using the two methods, respectively. Among them, the nine isolates, AHB, GDB1, GDB2, HNB, JSB1, JSB2, YNB, ZJB and GDH, became quinapyramine-sensitive T. b. evansi. Secondly, T. evansi populations could rapidly obtain antrycide-resistance when they were passed through immunosuppressed mice treated with low doses of the drug. But, the replication rate of trypanosomes with antrycide-resistance decreases as the level of drug-resistance increases. Thirdly, the analysis of the HK, G6PDH, ALAT and ASAT isoenzymes showed that they were not involved in the quinapyramine-resistance of T. b. evansi. But the protein bands of 15.79kDa and 19.76kDa might be involved in the antrycide-resistance of T. b. evansi population. At genetic level, the gene, TbTA1, could be amplified from the T. b. evansi isolate sensitive to quinapyramine-sensitivity but the T. b. evansi isolate with quinapyramine-resistance using not only the RT-PCR technique, but also PCR technique. We used the SSH (Suppression Subtractive Hybridization) to clone highly or low expressed cDNA fragments caused by production of antrycide-resistance in T. b. evansi. The 5 low and 9 high expressed new cDNA fragments were amplified. Among them, the 3 low expressed cDNA fragments had the same sequence of 65 amino acids and the 3 high expressed cDNA fragments were located in chromosome VI, like T. brucei. Lastly, more work needs to be done in order to elucidate the mechanism of quinapyramine-resistance of T. b. evansi.
Crown Copyright © 2010. Published by Elsevier B.V. All rights reserved.
Publication Date: 2010-09-08 PubMed ID: 20813092DOI: 10.1016/j.actatropica.2010.08.016Google Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
- Review
- Diagnosis
- Disease control
- Disease Diagnosis
- Disease Etiology
- Disease Management
- Disease Outbreaks
- Disease Prevalence
- Disease Surveillance
- Disease Transmission
- Disease Treatment
- Equine Health
- Genetics
- Horses
- In Vitro Research
- In Vivo
- Infectious Disease
- Parasites
- Veterinary Care
- Veterinary Medicine
- Veterinary Procedure
- Veterinary Research
Summary
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The research article offers a comprehensive insight into the resistance of Trypanosoma brucei evansi, a parasite causing the disease, to the drug quinapyramine in China. The study evaluates the drug’s effectiveness in treating the disease, the biological characteristics of quinapyramine-resistant parasites, and the genetic materials related to drug resistance.
Understanding Resistance to Quinapyramine
- The study involves several aspects of drug-resistance. The researchers assessed quinapyramine’s effectiveness, the biological behavior of resistant parasites, and the biological materials linked to this resistance. The central aim was to develop a comprehensive understanding of the challenge posed by drug-resistant T. b. evansi.
- Analyses were conducted, both in a controlled environment (in vitro) and with a living host (in vivo). The researchers found a positive correlation between the effectiveness of quinapyramine and how it is utilized. This suggests more variables that can be tweaked to improve effectiveness.
- The study also involved the evaluation of different T. b. evansi isolates. Some isolates developed resistance to quinapyramine, demonstrating the parasite’s evolving adaptability.
Effects of Drug Resistance on Parasite Growth
- Experiments revealed that T. b. evansi populations can quickly develop resistance when exposed to low doses of antrycide, a commonly used drug.
- However, the research also showed that as drug resistance increases, the growth rate of the parasites decreases. This implies that if a drug-resistant strain of T. b. evansi develops, it may reproduce slower than its drug-sensitive counterparts.
Investigating the Role of Proteins in Drug Resistance
- The study sought to identify which genes could be contributing to drug resistance. The researchers looked at specific enzymes but found they were not involved in resistance.
- Analysis showed that two protein bands could be associated with resistance to antrycide. The team amplified the TbTA1 gene from drug-sensitive T. b. evansi, but not from those that are resistant, using both RT-PCR and PCR techniques, highlighting its potential role in drug resistance.
Future Directions
- The research concludes by indicating that further work is required to clarify the mechanism of quinapyramine-resistance in T. b. evansi. Fully understanding this process is key for future strategies to craft effective treatments against the disease caused by the parasite.
Cite This Article
APA
Liao D, Shen J.
(2010).
Studies of quinapyramine-resistance of Trypanosoma brucei evansi in China.
Acta Trop, 116(3), 173-177.
https://doi.org/10.1016/j.actatropica.2010.08.016 Publication
Researcher Affiliations
- Sichuan Academy of Animal Science, Lane 7 Niu Sha Road, Chengdu, Sichuan, PR China. liaodjin@yahoo.com.cn
MeSH Terms
- Animals
- Animals, Domestic / parasitology
- Antiprotozoal Agents / pharmacology
- China
- Drug Resistance
- Humans
- Inhibitory Concentration 50
- Mice
- Protozoan Proteins / biosynthesis
- Protozoan Proteins / genetics
- Quinolinium Compounds / pharmacology
- Trypanosoma brucei brucei / drug effects
- Trypanosoma brucei brucei / isolation & purification
Citations
This article has been cited 4 times.- Mekonnen G, Mohammed EF, Kidane W, Nesibu A, Yohannes H, Van Reet N, Büscher P, Birhanu H. Isometamidium chloride and homidium chloride fail to cure mice infected with Ethiopian Trypanosoma evansi type A and B. PLoS Negl Trop Dis 2018 Sep;12(9):e0006790.
- Giordani F, Morrison LJ, Rowan TG, DE Koning HP, Barrett MP. The animal trypanosomiases and their chemotherapy: a review. Parasitology 2016 Dec;143(14):1862-1889.
- Seebeck T, Sterk GJ, Ke H. Phosphodiesterase inhibitors as a new generation of antiprotozoan drugs: exploiting the benefit of enzymes that are highly conserved between host and parasite. Future Med Chem 2011 Aug;3(10):1289-306.
- Suganuma K, Mochabo KM, Chemuliti JK, Kiyoshi K, Noboru I, Kawazu SI. Ascofuranone antibiotic is a promising trypanocidal drug for nagana. Onderstepoort J Vet Res 2024 Feb 8;91(1):e1-e6.
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