Introduction
The widespread use of chemical anthelmintics has led to the emergence of drug resistance in zoonotic gastrointestinal helminths of pets, including Toxocara canis, Toxocara cati, Ancylostoma caninum, and Dipylidium caninum. This systematic review aims to investigate the application of bioinformatics methods to identify molecular mechanisms of resistance in domestic animal gastrointestinal helminths with a One Health approach.
Methods
This systematic review was conducted according to the PRISMA guidelines. PubMed, Scopus, Web of Science, and Google Scholar databases were searched for articles published between January 2016 and December 2025. Inclusion criteria was original studies that used bioinformatics methods to study drug resistance in gastrointestinal parasites of dogs and cats. Of the 162 articles found, 35 eligible articles were included in the final analysis.
Results
bioinformatics methods have contributed to the management of drug resistance in three main areas. First, whole genome sequencing and phylogenetic analysis have identified resistance-associated mutations in drug target genes, including the tubulin gene and the glutamate-gated chloride channel genes in various parasite species. Second, molecular docking has successfully predicted and quantified the effect of specific mutations (such as the Phe200Tyr substitution in tubulin) on reducing drug affinity for the target protein. Third, virtual screening of natural compound libraries (including flavonoids, alkaloids, and terpenoids) has led to the identification of novel molecules that are capable of binding to the mutated and defective site and can be used as alternative or auxiliary options.
Conclusion
From a One Health perspective, bioinformatics methods, including whole genome sequencing, molecular docking, virtual screening, and molecular epidemiological modeling, play a key role in the sustainable management of zoonotic parasites by reducing unnecessary use of chemical drugs, extending the lifespan of existing drugs, and preventing the spread of resistance alleles to the human population and the environment.