monensin and Cardiomyopathies

Acute monensin intoxication in equids is well described; however, the long-term effects of sublethal intoxication and ability to return to previous use are less well understood. Long-term observations may allow improved estimation of prognosis in cases of sublethal intoxication.. To assess horses and ponies exposed to sublethal amounts of monensin for evidence of chronic sequelae and ability to return to prior/intended use.. Twenty-nine horses and 8 ponies were assessed utilising serum biochemistry, treadmill exercise stress testing, electrocardiography, and pre- and post exercise echocardiography > or = 6 weeks after ingestion of monensin-contaminated feed. Animals with evidence of monensin-induced cardiomyopathy were re-examined after a period of rest of > or = 11 months. Follow-up information was obtained by owner telephone interview > or = 52 months after exposure.. During resting echocardiography, 11 animals had reduced/low-normal left ventricular fractional shortening (FS); an increase in FS in 8 of these animals was measured > or = 11 months later. Six animals had reduced or low-normal FS during post exercise echocardiography. Two horses had ventricular premature depolarisations during exercise. Follow-up information was available for 35 animals: 21 returned to athletic/reproductive use, 13 were retired immediately and one died. Mean FS increased significantly (P < 0.001) between initial and second examination in 15 animals that underwent resting echocardiography on 2 occasions.. Some equids exposed to sublethal doses of monensin may not develop permanent myocardial disease and a return to athletic/reproductive use is possible.. Exercise stress testing, echocardiography and electrocardiography may be useful for detection and monitoring of cardiac dysfunction in equids exposed to monensin and determining whether a return to athletic/reproductive use is possible.

Topics: Animal Feed; Animals; Blood Chemical Analysis; Cardiomyopathies; Dose-Response Relationship, Drug; Echocardiography; Electrocardiography; Exercise Test; Female; Follow-Up Studies; Food Contamination; Horse Diseases; Horses; Ionophores; Male; Monensin; Time Factors

Topics: Animal Feed; Animals; Cardiomyopathies; Cattle; Cattle Diseases; Monensin

Topics: Animals; Cardiomyopathies; Cattle; Cattle Diseases; Female; Monensin; Poisoning; Selenium

Feedlot calves given monensin in their feed developed an excessive mortality which peaked 3-4 mo after monensin was withdrawn. Typically the calves died suddenly and necropsy revealed areas of paleness in the skeletal muscles (early cases) and in the myocardium (more chronic cases). Histology (in 19 calves) showed swollen myocytes with loss of striation and sarcoplasmic vacuolization, followed by the appearance of necrotic fibres and infiltration with macrophages and neutrophils, and finally local and generalized fibrosis. Calcification was not evident. A differential diagnosis ruled out an etiology of nutritional and toxicological origin, thus leaving the probability of atypical (chronic) monensin toxicosis.

Topics: Animal Feed; Animals; Cardiomyopathies; Cattle; Cattle Diseases; Foodborne Diseases; Furans; Male; Monensin; Muscles; Muscular Diseases; Myocardium

The acute toxicity of lasalocid and monensin was studied in 36 Holstein steers. The cattle were given (orally) a single dosage of lasalocid (1, 10, 50, or 100 mg/kg of body weight) or monensin (25 mg/kg of body weight) or rice hulls. Animals were observed once a day until they died or were euthanatized at 32 days after the dose was given. All cattle were necropsied. Heart, kidney, adrenal gland, liver, spleen, pancreas, lungs, brain, sciatic nerve, skeletal muscle, small intestine, large intestine, and rumen tissue sections, stained with hematoxylin and eosin, were studied microscopically. Lasalocid was lethal at dosages of 50 and 100 mg/kg, and monensin was lethal at the dosage given (25 mg/kg). Cattle dying of lasalocid and monensin toxicoses had gross and microscopic lesions consistent with cardiomyopathy. Dilated heart or petechial and ecchymotic hemorrhages were observed with both drugs. Microscopically, multifocal areas of myocyte necrosis were observed. Those cattle that died within 3 days of dosing with either drug had a marked degranulation of pancreatic acinar cells. Changes were not observed in any other tissues.

Topics: Animals; Cardiomyopathies; Cattle; Cattle Diseases; Lasalocid; Male; Monensin; Pancreas; Respiratory System

Monensin, A Na+-selective carboxylic ionophore, produces left atrial damage in pigs given toxic doses. Eight weanling pigs were given mycelial monensin orally (40 mg/kg body weight) and were killed on days 1, 2, 4, and 16 (two animals at each time interval) for ultrastructural study of the left atrial lesions. On days 1-4, extensive necrosis with contraction bands was present. Rapid macrophagic invasion and phagocytosis of sarcoplasmic debris was seen on days 2 and 4. Missing necrotic myocytes were outlined by persistent "tubes" of external laminas. In some surviving myocytes, sublethal injury was evident on day 1 by mitochondria with condensed conformation and on days 2, 4, and 16 by moderate to marked myofibrillar lysis and sarcoplasmic vacuolation. Monensin cardiotoxicity in pigs constitutes a unique example of selective injury to atrial myocardium.

Topics: Acute Disease; Animals; Cardiomyopathies; Cattle; Dose-Response Relationship, Drug; Female; Furans; Heart Atria; Macrophages; Male; Monensin; Myocardial Contraction; Myocardium; Necrosis; Swine

Three outbreaks of fatal cardiomyopathy in feedlot sheep are reported which were associated with the introduction of pelleted feed that contained greater than recommended concentrations of monensin. Gross and histopathological examination of some of these sheep revealed evidence of cardiomyopathy. Myocardial lesions which had a predominantly epicardial distribution are described. Lesions were also observed in skeletal muscle and in brain.

Topics: Animals; Cardiomyopathies; Disease Outbreaks; Food Additives; Furans; Monensin; Myocardium; Sheep; Sheep Diseases

Thirty-two horses were examined with a history of poor performance and unthriftiness several months after the ingestion of feed containing monensin sodium. Cardiac abnormality was diagnosed in 8 cases and suspected in 4 others. Necropsy examinations were performed on 6 cases with marked clinical symptoms and evidence of circulatory failure was found. Marked cardiac myopathy and fibrosis was a consistent feature. It is concluded that ingestion of monensin sodium by horses may cause either acute death or delayed cardiac circulatory failure as a result of specific cardiac myodegeneration.

Topics: Animals; Cardiomyopathies; Furans; Horse Diseases; Horses; Monensin