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Thirty-two lactating Holstein cows, blocked according to level of milk production, were fed cottonseed meal contaminated with aflatoxin B1, (AFB1) (0, 94, 241 and 500 μg/kg) as 20% of their ration (equivalent to 0, 20, 48 and 104 μg/kg in complete feed). Within 12 h, aflatoxin M1 (AFM1) appeared in the milk of all cows receiving contaminated feed. The mean AFM1 concentrations in the milk approached steady-state conditions (0.35, 0.63 and 1.61 μg/L for treatments of 20, 48 and 104 μg AFB1/kg, respectively) at 24 h and returned to the Food and Drug Administration action level of 0.5 μg/L or lower within 24 h after removal of the contaminated feed. The ratio of AFB1 in the feed to AFM1 in the milk averaged 66:1. The mean percent of daily AFB1 intake that was transferred to AFM1 was 1.74. This value was unaffected by the concentration of AFB1 in the feed (1.89, 1.55 and 1.81% transferred for treatments of 20, 48 and 104 μg AFB1/kg, respectively). Although increased milk production had no effect on the concentration of AFM1 in the milk, it had a positive effect (P ≤ 0.01) on the percent of AFB1 intake transferred to AFM1 (2.14 vs 1.35%). In a second trial, 16 additional cows were fed either naturally contaminated cottonseed meal or corn (44 and 49 μg/kg, respectively, on a complete feed basis). The percent of AFB1 intake secreted as AFM1 was affected (P ≤ 0.02) by the source of contamination (1.73 vs. 1.32% for the cottonseed meal and corn treatments, respectively). The AFM1 concentrations in the milk were not significantly different (P>0.05).

Abstract. One hundred ninety-two male broiler chicks were dosed with monensin at concentrations of 0, 121, or 242 mg/kg feed throughout the normal growing period (50 days). Body weight gain and feed efficiency were determined weekly, and cardiac muscle was examined grossly and histologically at the end of the experiment. Livers also were weighed and examined grossly. Feed intake was determined daily, allowing continuous monitoring of drug intake. No depressing effects of the drug on growth rate and efficiency were observed until after four weeks, and then were evident only in the chicks receiving the 242 mg/kg diet. Subepicardial hemorrhage and congestion occurred in 40% of the hearts from the chickens fed the high monensin dose and were nonexistent in the other treatments. There appeared to be an inverse relationship between monensin dose and liver weight. The paralytic effects previously reported from acute dosing experiments were not observed. The results show that the heart and probably the liver are sensitive indicators of monensin toxicity and that the subchronic toxic dose is less than 18 mg/kg body weight per day.Monensin, a monovalent carboxylic ionophore, is used widely in the United States as an anticoccidial agent for poultry. It is approved for use in the feed of broiler chickens at concentrations of 90 to 110 g/ton. Reports of monensin poisoning in birds have appeared recently in the literature [l, 4, 6, 7, 11, 121. These incidents involved chickens, turkeys, and guinea fowl; two of the occurrences have been ascribed to contaminated or improperly prepared feed [6] and to drug incompatibility [ 121. Signs of toxicity have been reported in birds exposed to monensin concentrations [161 parts per million (ppm)] which were only slightly greater than the approved concentration (121 pprn). In drug incompatibility, toxic signs were observed at a monensin concentration of 80 pprn 1121. The toxicity manifests itself primarily as a neuromuscular dysfunction which can result in paralysis and death of the poisoned birds.This study was conducted to investigate the subchronic toxicity in broiler chickens fed monensin throughout the growing period at the approved use concentration and at two times the approved concentration. Histologic examinations were done on the hearts from these birds because of recent reports of cardiotoxic effects of monensin in mammalian species [3, 8, 9, 131 and chickens [4].

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