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Furazolidone induces a cardiotoxicosis when fed in toxic concentrations to newly hatched ducklings. This preliminary experiment was designed to determine if creatine kinase (CK) isoenzymic activities or other serum analytes would be useful as indicators of these cardiac alterations. Sera from 12 ducklings (six fed a control ration and six fed the control ration with 700 mg furazolidone added per kg of feed [700 ppm] for 28 days) were analyzed for CK isoenzymic activities, electrolytes, nitrogenous metabolites, hepatic enzymic activities, bilirubin, and glucose. Statistically significant differences between control and treated groups were detected for creatine kinase MB (CK-MB, cardiac muscle origin) isoenzymic activity and bilirubin, potassium, calcium, and total carbon dioxide concentrations. Differences other than CK-MB isoenzymic activity were generally explained by factors related to the toxicosis or sample handling. These findings suggest that CK-MB isoenzymic activity may be useful to detect and monitor the progress of cardiac injury in furazolidone toxicosis, thereby increasing the usefulness of this model of dilated cardiomyopathy. Our findings, analyzed on the Kodak Ektachem 700 Dry Chemistry Analyzer, are compared with serum chemistry values reported in the literature.

Clinical and pathologic alterations during the development of furazolidone-induced toxicosis were investigated in a group of 35 newly hatched male Pekin ducklings fed a ration containing 700 mg of furazolidone/kg of feed for 27 days. A control group (n = 25) was fed the same ration without added furazolidone. Every 3 days, ducklings were weighted and palpated for ascites and 3 were chosen at random for euthanasia to determine the severity of lesions and to obtain hearts for gross measurements and ultrastructural study. Clinical alterations in treated ducklings consisted of decreased feed consumption with lower weight gain and nervous signs. Gross pathologic alterations included cardiomegaly with dilatation of all chambers and thinning of the myocardium, pericardial effusion, pulmonary edema and congestion, ascites, and testicular enlargement. Gross lesions were not observed before day 8. The earliest lesion (day 9) was cardiac chamber dilatation, with the left ventricle and left atrium most commonly and most severely dilated. Hearts from ducklings euthanatized on days 6, 12, 18, 24, and 27 were examined ultrastructurally. Myofibrillar lysis was first observed on day 12 in 1 duckling (of 3) and in at least 1 duckling from subsequent euthanasia periods. Myofibrillar lysis did not appear to be uniform among the cardiac chambers.

Long-term treatment (eighteen months) with a medicated feed containing 400 ppm of furazolidone gave rise to side-effects on a pig farm on which the animals were affected with persistent oedema disease. These side-effects disappeared on discontinuation of the medication. In view of this suspected case of chronic furazolidone intoxication the court formulated several questions for a panel of experts. The questions and the replies given are stated.

Studied was the morphologic picture in a total of 13 calves spontaneously intoxicated with furazolidon following its overrating and use once and severalfold as a therapeutic means against infectious enteritis. There were hemorrhages in the subcutaneous tissue and the muscles, kidneys, abomasum, spleen, and heart as well as liver dystrophia and hyperemia and edema of the leptomeninges and the brain cortex. Histologically, there were hyperemia, strong and diffuse pericellular and perivascular edema of the cerebrum and the cerebellum with degenerative changes in the Purkinje layer, fatty degeneration and biliary thrombi in the liver, hemorrhages and activation of the endothelial cells and glomeruli of the kidneys, hyperemia and fatty infiltration of the myocardium, and hemorrhages in the spleen.

Prolonged administration of furazolidone to calves may give rise to chronic furazolidone poisoning: retardation of growth, thrombocytopenia and leucopenia, occasionally changing into haemorrhagic diathesis. In acute nitrofuran poisoning neurological signs are observed as a consequence of monoamine oxidase inhibition. Five incidents of acute nitrofuran poisoning on veal calf farms are reported in the present paper, each with a mortality rate varying frm 46.7 per cent ot 70 per cent. Ten times the recommended dose of furazolidone or furadoltone was administered in each case.

We examined 41 samples of calf urine in order to determine the urinary furazolidone excretion. 26 calves were administered furazolidone in the form of Terapeutan T in a therapeutic dose of 5 kg per os individually, which represents approx. 3 mg of furazolidone per kg body weight per day over 5 days. 11 calves were administered with twice the therapeutic dose, i.e. 6 mg furazolidone per kg live body weight over the same 5 days. A triple strength dose was administered to two calves on the 2nd and 3rd days and after administration we observed the furazolidone excretion in urine. The dynamics of furazolidone excretion in urine of one calf we determined even after the fivefold dose in comparison with the therapeutic dose, administered in the course of 2 days after application of the double dose, which was administered over 4 days. During administration of 3 mg and 6 mg furazolidone respectively per kg of live weight per kg furazolidone was excreted in urine minimally and only rarely (7.6%). During administration of higher doses furazolidone was found in the urine of all individuals. The highest urinary concentration of furazolidone in calves was determined after administration of the fivefold dose in comparison with the therapeutic dose, i.e. 15 mg furazolidone per kg live weight in the 4th hour after urine collection (23.0 mg furazolidone per liter urine). When this dose was administered over 2 days, it did not effect any clinical symptoms of disease. It has proved to be well founded to determine the furazolidone level in calf urine in laboratory diagnostics. The examination contributes to the estimation of the furazolidone dose, administered to calves. Urinary furazolidone concentrations greater than 1.0 mg.l-1 provide warning signals of overdosage with this chemotherapeutic. For urine furazolidone determination we utilized the photometric method, described by Herret and Buzard (1960).