Moniliformin toxicosis in turkeys and chickens

Rachel Yvonne Reams, Purdue University

Abstract

The potential role of moniliformin and its interaction with monensin in the development of Turkey Knockdown and Sudden Death Syndromes in poultry was investigated in a series of 4-week feeding trials with poults and chicks. In vitro models of moniliformin toxicosis were used to better characterize the mechanism of action of moniliformin. Sudden death due to cardiotoxicosis was induced in chicks and poults with diets amended with F. fujikuroi, that were formulated to contain 20-330 ppm moniliformin. Gross, microscopic and ultrastructural alterations of the cardiotoxicosis were consistent with early myocardial degeneration and necrosis, followed by hypertrophy. Electrocardiographic alterations in poults and chicks fed moniliformin were consistent with ventricular hypertrophy, myocardial injury and hypoxia. Moniliformin toxicosis resulted in dose-dependent increases in serum concentrations of aspartate aminotransferase and pyruvate that were useful indicators of myocardial damage and decreased pyruvate dehydrogenase function, respectively, in the poultry in this study. Clinical signs and lesions of knockdown or monensin toxicosis were not produced and monensin did not enhance moniliformin toxicosis. A variety of models were explored for potential use in the in vitro evaluation of moniliformin toxicosis. HEPA-1 cells, chick embryos and guinea pig atria, under the conditions of these models, were not susceptible to moniliformin toxicosis. L6 myoblasts were a useful model of moniliformin toxicosis. Microscopic and ultrastructural lesions of dose-dependent cellular degeneration and necrosis were noted in L6 myoblasts exposed to ($>$0.015 $\mu$g moniliformin/$\mu$l). Supplementation of the medium with thiamine and pyruvate, or to a lesser extent with selenium, provided significant protection to cells exposed to moniliformin. Dose-dependent differences in protein or ATP production from those observed in controls were not noted in myoblasts exposed to moniliformin. Myoblasts grown in medium containing moniliformin and A23187, beauvericin or monensin had similar degrees of cytotoxicity as parallel cultures receiving only these ionophores. These findings suggest that cytotoxicity due to moniliformin in L6 myoblasts may be due in part to oxidative damage and altered pyruvate metabolism, and that moniliformin does not predispose myoblasts to ionophore toxicosis.

Degree

Ph.D.

Advisors

Harrington, Purdue University.

Subject Area

Animal diseases|Veterinary services

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