A study was undertaken to evaluate and compare the effectiveness of three anthelmintics, ivermectin, fenbendazole, and a combination of ivermectin and pyrantel pamoate, on fecal egg count reductions of cyathostomes and Parascaris equorum in 30 foals at the Texas A&M Horse Center. The foals were reared under standard horse center practices and were naturally infected with both cyathostomes and Parascaris. The foals were randomized into three treatment groups with individuals being rerandomized after each eight week observation period. The treatments of ivermectin and fenbendazole were given at the manufacturer's recommended doses and the pyrantel treatment was given at two times the manufacturer's recommended dose. All doses were based on weights taken prior to treatment. Fecal egg counts were performed at the time of treatment and at two week intervals after treatment for a total of eight weeks. Each foal received a total of three treatments during the course of the study along with the most effective treatment at the conclusion of the study. Fecal egg counts were performed by a modified McMaster's test with a sensitivity of 25 eggs per gram of feces and by the modified Wisconsin double centrifugal floatation with a sensitivity of 0.2 eggs per gram of feces. Fecal egg reduction percentages were calculated for each two week interval. Analysis of the results showed that ivermectin, either used alone or with pyrantel was a more effective anthelmintic for cyathostome (small strongyle) control than fenbendazole. Fenbendazole and pyrantel showed a higher initial reduction in Parascasris eggs when compared to the ivermectin only treated group, but ivermectin showed improved egg reduction over time. At the conclusion of this study, a primary treatment of ivermectin at the manufacturer's recommended dose and treatment of pyrantel at two times the manufacturer's recommended dose was recommended to control cyathostome egg production and severely reduce the initial number of Parascaris adults in the foals at this facility. Subsequent monthly does of ivermectin at the manufacturer's recommended dose was also recommended to continue to control both parasites. Follow up fecal examinations were also recommended to test the continued effectiveness of the recommended treatment protocol.

A scaris is a genus of parasitic worms (helminths) found in the small intestine of various mammalian hosts, including Ascaris lumbricoides in humans, Parascaris equorum and P univalens in horses, Ascaris suum in pigs, Toxocara cati in cats and Toxocara canis in dogs. To date, Parascaris spp. are the only Ascaris worms that have developed resistance to anthelmintic drugs. The mechanisms of resistance in Parascaris spp are incompletely understood, partly due to the absence of robust in-vitro models. Further complicating in-vitro studies, Parascaris spp lack a free-living larval stage as their larva only hatch within the host. The aim of this study was to develop in-vitro methods for hatching, scoring the viability of Parascaris L3 larvae and exposing them to the anthelmintic drugs ivermectin, pyrantel, thiabendazole, and the herbal extract carvacrol. This study shows that mechanical Ascaris egg breaking using a homogenizer resulted in a hatching rate of 98%. Our viability scoring system could distinguish an ivermectin resistant larvae from an ivermectin susceptible larvae derived from different farms. This indicates that this method may have utility for the screening of larvae ivermectin resistance on the level of farm populations. Interestingly, a highly paralytic effect observed after carvacrol exposure. Carvacrol shows direct paralytic effects on Parascaris larvae in a dose-dependent manner, as higher concentrations were lethal to all exposed larvae. This result presents a potential future opportunity for carvacrol used in the treatment of Ascaris infections. To conclude our results, we have successfully developed an in-vitro model as well as a scoring system for the viability of Parascaris L3 stage larvae, which can be used for assaying the effect on larvae after drug exposure