Page 171 - congress

ORAL PRESENTATION / SÖZLÜ SUNUM

Rising Benzimidazole Resistance in Ancylostoma caninum: Implications for Dog Health

Hande İrem SÖNMEZ 1,2,* Elif MADAK Mina Cansu KARAER
1
3
Hıfsı Oğuz SARIMEHMETOĞLU 2

1 Graduate School of Health Science, Ankara University, Ankara, TÜRKIYE
2 Department of Parasitology, Faculty of Veterinary Medicine, Ankara University, Ankara, TÜRKIYE
3 Institute of Preclinical Sciences, Veterinary Faculty, University of Ljubljana, SLOVENIA

*Correspound Author: hisonmez@ankara.edu.tr

Ancylostoma caninum, a hookworm species of zoonotic importance, is a significant
gastrointestinal nematode commonly seen in dogs and capable of causing serious clinical
conditions. Benzimidazole group anthelmintics, which have been widely used for many years
in the control of this parasite, act by binding to the β-tubulin protein, thereby inhibiting
microtubule polymerization and disrupting the parasite’s cellular functions, ultimately
leading to its death. However, in recent years, the increasing number of cases in which
benzimidazole treatment fails to eliminate A. caninum infections has brought the issue of
drug resistance into focus. At the molecular level, resistance is primarily associated with
point mutations in the β-tubulin isotype-1 gene, which interfere with the drug's ability to bind
to its target protein, rendering the treatment ineffective. Resistance is reported more
frequently in dog populations exposed to frequent and repeated anthelmintic treatments,
such as shelter dogs and racing dogs.
This review focuses on global cases of benzimidazole resistance in A. caninum. In the
United States of America, benzimidazole resistance was first identified through a mutation
at codon 198 of the β-tubulin isotype-1 gene; in subsequent years, mutations associated with
codons 134 and 167 were also reported. In studies conducted in Australia, mutations related
to resistance have been detected at codons 134, 167, 198, and 200 of the same gene. In
Brazil, a mutation at codon 200 has been identified, and fenbendazole treatment in infected
dogs has shown insufficient efficacy. In Canada, mutations associated with resistance have
been detected at codon 167 in samples from various dog breeds, with reports indicating a
higher frequency of this mutation in some breeds.
The spread of resistance not only compromises parasite control but also increases the
persistence of infections and the risk of reinfection in dogs, posing serious health challenges.
Infections caused by resistant A. caninum strains in immunocompromised puppies and
environments with high animal density can result in severe clinical outcomes such as
anemia, weight loss, hypoproteinemia, and even death. Moreover, frequent and ineffective
treatments can lead to chronic parasitic carriage in dogs, thereby increasing the infection
pressure both at the individual and population level.
The emergence of benzimidazole resistance in A. caninum also poses a significant
threat to public health due to its zoonotic nature and potential for transmission to humans.

168