Importation of macrocyclic lactone resistant cyathostomins on a US thoroughbred farm.

Anthelmintic resistance in equine cyathostomins is both widespread and highly prevalent in the benzimidazole and tetrahydropyrimidine classes; however, reports of resistance to macrocyclic lactone (ML) drugs are sparse and sporadic. This study reports a case of clear ML resistance in a group of Thoroughbred yearlings imported from Ireland to the US in 2019. Fecal egg count reduction (FECR) following ivermectin administered in February 2020 demonstrated 100% reduction in the US bred yearlings, but 93.5%, 70.5%, and 74.5% reduction in three groups of the imported yearlings. The two former groups were then retreated with ivermectin, yielding FECRs of 33.8% and 23.5%, respectively. Horses from these two groups were then assigned randomly to two possible treatments; moxidectin or a triple combination of moxidectin, oxibendazole, and pyrantel pamoate. The groups treated with moxidectin had FECRs of 90.2%, 57.3%, and 50.0%, while the triple combination had a 100% FECR in all treated groups. Subsequently, the efficacy of ivermectin was reassessed in June 2020 yielding FECRs of 99.8%, 87.7%, and 62.0% in the three imported groups. The FECRs of the US bred yearlings all remained in the 99-100% range. This is the first study to clearly demonstrate ML resistance in cyathostomins and to confirm the suspicion through reassessment. These data demonstrate that ML-resistant cyathostomins were imported from Ireland and serve to illustrate that the global movement of horses has the potential to quickly spread ML-resistant parasite isolates around the world. The equine industry is strongly encouraged to routinely monitor anthelmintic efficacy, so occurrence of ML resistant cyathostomins can be detected and appropriate interventions implemented as early as possible.

Atrophy of the sphincters of continence in an experimental model.

BACKGROUND: Pudendal nerve injury during childbirth may result in external anal sphincter (EAS) atrophy. Recently, balloon compression of the pelvic side wall has been shown to result in EAS atrophy in an experimental model. The aim of this study was to determine whether other sphincters of continence are similarly affected. METHOD: Sixteen adult female virgin Wistar rats (eight controls) were studied 4 weeks after surgery. Anal and urethral canals were dissected, snap frozen and sectioned using a cryostat (100 microm thickness). Masses of EAS, internal anal sphincter (IAS) and external urethral sphincter (EUS) were calculated stereologically and stained with succinate dehydrogenase histochemistry to differentiate striated from smooth muscle. Sphincter length was determined and total sphincter mass calculated. Data were analysed with an unpaired Student's t-test. RESULTS: Atrophy of EAS (30.9 +/- 1.7 to 21.3 +/- 1.7 mg/ kg, P = 0.001), IAS (98.1 +/- 11.3 to 67.1 +/- 5.0 mg/kg, P = 0.01) and EUS (9.6 +/- 0.98 to 7.4 +/- 0.8 mg/kg, P = 0.05) was found 4 weeks after the injury. CONCLUSION: In an experimental model of obstetric pudendal nerve injury, significant atrophy of striated and smooth muscle sphincters of continence occurs and may contribute to altered continence following vaginal childbirth.