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Research Note: Evaluation of quinine as a chemoprophylactic candidate against histomoniasis in turkeys

Histomoniasis, also commonly referred to as blackhead disease, is caused by the protozoan parasite Histomonas meleagridis. Since the removal of nitarsone in 2015, no approved prophylactics are available for mitigating histomoniasis. Disease incidence and high mortalities are frequently associated wi...

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Detalles Bibliográficos
Autores principales: Beer, L.C., Hargis, B.M., Vuong, C.N.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8531845/
https://www.ncbi.nlm.nih.gov/pubmed/34601438
http://dx.doi.org/10.1016/j.psj.2021.101469
Descripción
Sumario:Histomoniasis, also commonly referred to as blackhead disease, is caused by the protozoan parasite Histomonas meleagridis. Since the removal of nitarsone in 2015, no approved prophylactics are available for mitigating histomoniasis. Disease incidence and high mortalities are frequently associated with turkey flocks, although infection of broiler breeders also occurs. Quinine is a naturally occurring alkaloid with antimalarial properties. In vitro assays have shown strong antihistomonal properties of quinine, leading to our hypothesis that quinine inclusion within the feed could prevent histomoniasis in turkeys. Selected concentrations of quinine were included within a turkey starter diet to evaluate effects on body weight gain (BWG), liver lesions, cecal lesions, and mortality of H. meleagridis-challenged turkeys. On day-of-hatch, poults were randomly assigned to either the basal diet or a quinine diet. Groups consisted of a non-challenged control (NC; basal diet), 0.022% quinine + challenge, 0.067% quinine + challenge, 0.2% quinine + challenge, or a positive-challenged control (PC; basal diet). On d 10, challenged groups were intracloacally inoculated with 10(5)H. meleagridis cells/turkey, and lesions were evaluated on d 21 post-infection. Individual body weights were recorded on d 0, d 10, and d 31 to calculate the pre-challenge and post-challenge BWG. No significant differences (P > 0.05) were observed between the d 0 to 10 pre-challenged BWG between quinine treatment diets and the basal diet. Similarly, no differences (P > 0.05) were observed in post-challenge d10-31 BWG of the quinine dietary treatments as compared to the PC. Cumulative mortalities, liver lesions, and cecal lesions related to histomoniasis were not reduced (P > 0.05) in any of the quinine treatment groups as compared to the PC. Although quinine successfully reduced H. meleagridis cells in vitro, results from the in vivo experiment indicated no reduction in histomoniasis severity as evidenced by similar lesions and mortality as the PC. Taken together, these data indicate that quinine inclusion within the feed at these concentrations and under these experimental conditions was not efficacious in the prevention or treatment of histomoniasis.