A SUDDEN-DEATH-SYNDROME INDUCED IN POULTS AND CHICKS FED DIETS CONTAINING FUSARIUM-FUJIKUROI WITH KNOWN CONCENTRATIONS OF MONILIFORMIN

A sudden death syndrome was induced in chicks and poults fed diets con taining Fusarium fujikuroi, formulated to contain 0-330 mg/kg monilifo rmin (M) with or without the maximum recommended therapeutic concentra tion of monensin. Lesions of monensin toxicosis were not observed. Cli nical signs were referable to cardiac dysfunction (sudden death, dyspn ea, cyanosis, depression). Poults and chicks dying early in the study had no gross lesions or had lesions of right ventricular dilation. Tre ated poults and chicks dying late in the study or euthanatized at term ination of the study had lesions of bilateral myocardial hypertrophy, usually concentric. Absolute heart weights and relative heart weights, expressed asa percentage of body weight, were significantly greater i n treated birds than controls (P < 0.05), whereas body weights were si gnificantly less (P < 0.05). Microscopically, lesions progressed from acute myocardial degeneration to necrosis, fibrosis, and hypertrophy. Ultrastructural findings were consistent with the gross and microscopi c lesions. Serum pyruvate concentrations were a useful indicator of M- induced cardiotoxicosis. Concentrations of serum pyruvate increased wi th increased concentration-of dietary M, but were not affected by addi tion of monensin to the diet. In chicks ingesting 40-300 mg/kg M, seru m pyruvate concentrations were significantly greater (P < 0.05) than t hose in controls (controls, 0.28 +/- 0.08 mmol/liter; exposed 0.38 +/- 0.11-0.55 +/- 0.13 mmol/liter). Poults ingesting 80-330 mg/kg M had s ignificantly greater serum pyruvate concentrations than controls (cont rols 0.33 +/- 0.09 mmol/liter; exposed 0.43 +/- 0.13-1.00 +/- 0.06 mmo l/liter). The Vetronics System(R) was used to evaluate electrocardiogr aphic alterations in a limited number of chicks and poults surviving t o the end of the feeding trial. Electrocardiographic alterations in po ults and chicks fed dirts containing greater than or equal to 40 mg/kg and greater than or equal to 160 mg/kg M, respectively, were consiste nt with ventricular hypertrophy, myocardial injury, and hypoxia. Elect rocardiographic alterations were more striking in poults than in chick s. Altered myocardial metabolism due to M toxicosis, in conjunction wi th the unusual susceptibility of domestic poultry to altered cardiac m etabolism, is believed to be the cause of the organ-specific lesions i n these birds. These findings suggest that cardiac injury with subsequ ent alterations in cardiac electrical conductance may be a cause of th e sudden deaths observed in poultry chronically intoxicated with dieta ry M.