Two experiments were performed in order to determine the toxic effects of varying doses of aflatoxins in calves. Clinical, productive and pathologic aspects of affected calves were considered. In the first experiment, nine 2 to 4-month-old calves Holstein Friesian calves were fed, for two months, daily amounts corresponding to 1.5% of their body weight of a ration containing 500±100 ppb of aflatoxins. Three calves of similar age and weight were used as controls and, except for being a ration free of aflatoxins, were kept in the same condition as the treated calves. In the second experiment, three 4-5-month old Holstein Friesian calves, were orally fed daily small parcels of a concentrate of aflatoxins diluted in 500 ml of water corresponding to 1,250, 2,500 e 5,000 ppb of B1 aflatoxin (AFB1). A male 4-month-old Holstein Friesian calf was used as control. During all the experimental period of the first experiment, the weight gain of the calves receiving AFB1 was equivalent to that of the control group. In the first experiment no differences were observed between treated and control calves when the values of serum activity of aspartate transaminase (AST), serum albumin (SA), total serum protein (TP), and PVC, determined weekly, were compared. However there was a significant difference between treated and control groups in the serum activities of alkaline phosphatase (AP) and gamma glutamyl transferase when the serum sampled on the 63th day of the experiment was considered. During the whole experimental period and up to three weeks after the final of the experiment, no clinical signs or histopathological changes associated with the consumption of aflatoxins were observed in any of the calves of the first experiment. In the second experiment, clinical signs observed in three treated calves included loss of appetite, decrease in weight gain, and loss of weight. Jaundice, intermittent diarrhea, tenesmus and apathy were only observed in the calf receiving 5,000 ppb of AFB1. Due to these clinical signs the calf was euthanized. Increased activity of AF and GGT were observed in all the calves of the treated group during most part of the experimental period. A marked drop in the serum levels of SA was observed in the serum sampled on the 49º day of the experiment in the calf receiving the largest dose of aflatoxin. No changes were observed regarding PCV, TP, total bilirubin, direct bilirubin and in the serum activity of AST in any of the calves of the second experiment. Histopathological changes in intoxicated calves included bile duct proliferation, cytoplasmic vacuolar hepatocelular degeneration consistent with hepatocelular deposit of lipids, periportal to bridging fibrosis, megalocytosis, subendothelial edema and fibrosis in terminal hepatic veins. Necropsy findings in the euthanatized calf which receive de largest doses of AFB1 included slight enlargement of the liver which was firm and diffusely light-yellow, mild ascites, and edema of the mesentery and of abomasal folds. Data stemmed from these two experiments allow to conclude that AFB1 doses of 500±100 in the ration do not cause pathologic changes or decrease in productivity in calves kept in experimental conditions, but can be associated to minimal serum biochemistry; while AFB1 doses of 1.250, 2.500 e 5.000 ppb in the ration cause chronic hepatic disease in calves in kept in experimental conditions.
Diseases of cattle; mycotoxicosis; aflatoxina; aflatoxicosis; hepatic diseases; pathology
