Torres-Acosta JF, Villarroel-Álvarez MS, Rodríguez-Arévalo F, Gutiérrez-Segura I, Alonso-Díaz MA

Language: Spanish
References: 0
Page: 75-81
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ABSTRACT

Introduction. The use of anthelmintics (AH) for the control of gastrointestinal nematodes (GIN) in goats is threatened by the emergence of resistant strains of GIN. No information is available on the presence of resistant nematodes in goat herds of Mexico and Yucatan. The objective was to determine the presence of GIN resistant to bencimidazols (BZ), imidazothiazols (LEV), and macrocyclic lactones (ML) in a goat herd of Yucatan, Mexico by means of the faecal egg count reduction test.
Materials and methods. Presence of GIN resistant to BZ, LEV and ML was determined through the Faecal Egg Count Reduction Test. A modified McMaster technique was used to select sixty adult goats with faecal egg counts above 150 eggs per gram of faeces (EPG). These animals were randomly distributed in four groups of 14 to 15 animals. Group 1 remained without AH treatment (T). Group 2 was treated with BZ (7.6mg/kg liveweight of albendazol per os). Group 3 with LEV (12mg/kg liveweight of levamisol subcutaneously) and group 4 with ML ((0.2mg/kg liveweight of moxidectin, subcutaneously). Animals were individually weighed and drugs administered according to weight. Animals were refrained of feed during 16 hours before AH treatment. All the animals were sampled again on day 12 post-treatment. Results of the second sampling were used to determine percentage reduction of EPG (%R) and the 95% confidence interval (IC95%). A bulk faecal culture was made for each treatment group to identify the genus of larvae in a sample of fifty infective larvae in each group.
Results. No resistance against ML was found in the herd. There were GIN resistant to BZ (%R=89, IC95%=77-94) and LEV (%R=82, IC95%=59-92). The genus of GIN resistant to BZ was Haemonchus spp. The genera of GIN resistant to LEV were Trichostrongylus spp. (96%) and Oesophagostomun spp. (4%).
Discusion. Presence of GIN resistant to LEV and BZ may have been caused by several years of subtherapeutic dosing of both AH in the herd. These subtherapeutic doses were obtained from the label of the drugs used. The lack of yearly drug rotation in the herd may have contributed towards the development of resistance.