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Pathogens (Basel, Switzerland)2022; 11(5); 490; doi: 10.3390/pathogens11050490

Absence of Polymorphisms in Codons 167, 198 and 200 of All Seven β-Tubulin Isotypes of Benzimidazole Susceptible and Resistant Parascaris spp. Specimens from Australia.

Abstract: Benzimidazoles resistance is widespread in strongyle parasitic nematodes and associated with polym orphisms in the codons 167, 198 and 200 of isotype 1 β-tubulin (tbb-1). In ascarids, benzimidazole (BZ) resistance has rarely been reported and in none of these cases were any of these polymorphisms detected. Here, available genome and transcriptome data from WormBase ParaSite were used to compare the complete β-tubulin reservoirs of , and . Adult spp. specimens collected in Australia from horses after BZ treatment (susceptible, n = 13) or surviving BZ treatment and collected after ivermectin treatment (resistant, n = 10) were genotyped regarding codons 167, 198 and 200 using Sanger sequencing. Phylogenetic analyses clearly showed that there are no one-to-one ascarid orthologs of strongyle tbb-1 genes. In the reference genomes, as well as phenotypically susceptible and resistant spp. from Australia, six out of seven β-tubulin genes showed a BZ-susceptible genotype (F167, E198, F200). The only exception were the testis-specific β-tubulin D genes from all three ascarid species that encode tyrosine at codon 200. This was observed independently of the BZ-susceptibility phenotype of spp. These data suggest that different mechanisms lead to BZ resistance in ascarid and strongyle nematodes.
Publication Date: 2022-04-20 PubMed ID: 35631011PubMed Central: PMC9143322DOI: 10.3390/pathogens11050490Google Scholar: Lookup
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  • Journal Article

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research article explores the absence of specific genetic changes in a certain protein (-tubulin) in both benzimidazole-resistant and susceptible species of the Parascaris genus from Australia. The findings suggest that mechanisms leading to resistance to the benzimidazole class of anti-parasitic drugs vary between ascarids (Parascaris) and nematode parasites, such as strongyle worms.

Details and Methodology

A couple of key processes were used in the research:

  • Genome and transcriptome data from WormBase ParaSite, an online repository for parasitic worm draft genomes and transcriptomes, were utilised to compare the complete β-tubulin gene sequence amongst Parascaris species.
  • Adult Parascaris specimens were collected from horses in Australia after treatment with benzimidazole (susceptible group) or those surviving the benzimidazole treatment and later collected after ivermectin treatment (resistant group).
  • These specimens were then genotyped to pinpoint any potential changes at specific codon positions (167, 198 and 200) of the β-tubulin gene. These particular positions were chosen since, in the strongyle species of nematodes, mutations at these codons are linked to resistance to the benzimidazole class of drugs.

Findings

In both the data extracted from WormBase ParaSite in addition to the specimens physically collected, no polymorphisms in the identified codons were detected. Specifically:

  • Six out of seven β-tubulin genes showed a benzimidazole-susceptible genotype, indicating no deviation from the typical genetic sequence.
  • The exception was the testis-specific β-tubulin D genes, which all encoded tyrosine at codon 200, and this was witnessed across the board independent of the benzimidazole-susceptibility phenotype of the Parascaris species.

Conclusion

The absence of β-tubulin polymorphisms in the stated positions in both resistant and susceptible Parascaris spp. specimens suggests that resistance to benzimidazoles in ascarids is not correlated to these identified changes as seen in strongyles. Therefore, the study concludes that different mechanisms are in play leading to benzimidazole resistance in ascarid nematodes versus strongyle nematodes. This opens up new avenues for targeted research to understand drug resistance in different classes of parasites.

Cite This Article

APA
Özben M, von Samson-Himmelstjerna G, Freiin von Streit MKB, Wilkes EJA, Hughes KJ, Krücken J. (2022). Absence of Polymorphisms in Codons 167, 198 and 200 of All Seven β-Tubulin Isotypes of Benzimidazole Susceptible and Resistant Parascaris spp. Specimens from Australia. Pathogens, 11(5), 490. https://doi.org/10.3390/pathogens11050490

Publication

ISSN: 2076-0817
NlmUniqueID: 101596317
Country: Switzerland
Language: English
Volume: 11
Issue: 5
PII: 490

Researcher Affiliations

Özben, Murat
  • Institute for Parasitology and Tropical Veterinary Medicine, Freie Universität Berlin, 14163 Berlin, Germany.
  • Department of Parasitology (Veterinary), Ankara University Graduate School of Health Sciences, 06230 Ankara, Turkey.
von Samson-Himmelstjerna, Georg
  • Institute for Parasitology and Tropical Veterinary Medicine, Freie Universität Berlin, 14163 Berlin, Germany.
Freiin von Streit, Malene K B
  • Institute for Parasitology and Tropical Veterinary Medicine, Freie Universität Berlin, 14163 Berlin, Germany.
Wilkes, Edwina J A
  • School of Agricultural, Environmental and Veterinary Sciences, Charles Sturt University, Wagga Wagga, NSW 2678, Australia.
Hughes, Kristopher J
  • School of Agricultural, Environmental and Veterinary Sciences, Charles Sturt University, Wagga Wagga, NSW 2678, Australia.
Krücken, Jürgen
  • Institute for Parasitology and Tropical Veterinary Medicine, Freie Universität Berlin, 14163 Berlin, Germany.

Conflict of Interest Statement

The authors declare no conflict of interest.

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Citations

This article has been cited 1 times.
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