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 Parascaris univalens, Ascaris suum and Ascaris lumbricoides. Adult Parascaris 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 Parascaris 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 Parascaris spp. These data suggest that different mechanisms lead to BZ resistance in ascarid and strongyle nematodes.