monensin and Poisoning

Topics: Animals; Antiprotozoal Agents; Aspartate Aminotransferases; Bird Diseases; Creatine Kinase; Diagnosis, Differential; Female; Greece; L-Lactate Dehydrogenase; Male; Monensin; Poisoning; Struthioniformes

Consumption of monensin-containing feed contaminated with macrolide antibiotic residues resulted in the death of cattle from multiple feedlots in south-central Kansas. Cattle were fed milo dried distiller's grains (DDG) with solubles from a common source in conjunction with the ionophore antibiotic, monensin. Deaths occurred as early as 72-96 hours after feeding and were preceded by either no premonitory signs or 1 or more of the following: anorexia, depression, dyspnea, locomotor deficits, and recumbency. Significant gross lesions were pulmonary and mesenteric edema, hepatomegaly, and generalized myocardial and skeletal muscle pallor that was confirmed histologically as acute myodegeneration and necrosis. Other significant histologic lesions included centrolobular hepatocellular necrosis, congestion, and pulmonary interstitial and alveolar edema with fibrin exudation. Animals that survived beyond 6 weeks had poor weight gain and coalescing foci of myocardial fibrosis with residual myocardial degeneration. Analysis of trace mineral supplements for monensin were within the manufacturer's label range. The DDG samples from affected feedlots had 50-1,500 ppm of erythromycin, clarithromycin, and related macrolide antibiotic analogues, which originated in the alcohol residue. In a preliminary feeding trial, cattle fed this contaminated DDG in combination with monensin had clinical signs and died with gross and histologic findings comparable to those of the field cases. Even though rations supplemented with the contaminated DDG contained approved levels of monensin, the clinical and postmortem findings were consistent with those expected for monensin toxicosis. The presence of macrolide antibiotic residues in the contaminated feed appeared to affect the biotransformation of otherwise nontoxic levels of monensin, leading to clinical ionophore toxicosis.

Topics: Animal Feed; Animals; Anti-Bacterial Agents; Cattle; Cattle Diseases; Edible Grain; Food Contamination; Foodborne Diseases; Macrolides; Male; Monensin; Poisoning

A total of 42 birds from a flock of 104 farmed ostriches showed signs of toxicity after the accidental inclusion of monensin in their concentrate ration. The initial clinical signs were muscle weakness and ataxia which progressed to recumbency, dyspnoea and death, despite intensive supportive therapy. The serum activity of the enzymes creatine kinase, aspartate aminotransferase and lactate dehydrogenase was high in the affected birds, indicating significant muscle pathology. Few gross lesions were identifiable postmortem, but widespread lesions of degenerative myopathy were present at the histopathological level. However, these degenerative changes were restricted to the skeletal muscle and there was no evidence of cardiomyopathy in any of the birds examined. The birds were fed a ration which contained 215 to 224 ppm monensin for 13 days. New clinical cases ceased to occur shortly after the withdrawal of the source of monensin, but all the individuals which showed clinical signs of toxicity died or were euthanased on humane grounds.

Topics: Animal Feed; Animals; Aspartate Aminotransferases; Bird Diseases; Birds; Creatine Kinase; Diet; Digestive System; Hemoglobins; Ionophores; L-Lactate Dehydrogenase; Liver; Lung; Male; Monensin; Muscle, Skeletal; Poisoning; Scotland; Spleen

Topics: Animals; Monensin; Muscle Fibers, Skeletal; Muscle, Skeletal; Myocardium; Necrosis; Poisoning; Swine; Swine Diseases

Four female fistulated camels (Camelus dromedarius), 4-5 years of age, were each given two grams of 10% monensin intraruminally daily for six days to study the effect of monensin on the rumen fermentation pattern. Signs of toxicity appeared on the sixth day, and included depression, anorexia, muscular weakness, inability to stand, salivation and regurgitation of ruminal contents. On the eighth day, two animals died. The ruminal contents were replaced in the survivors, but they died on the tenth and eleventh day from the start of the experiment.

Topics: Animals; Camelus; Female; Fermentation; Monensin; Poisoning; Rumen

A clinical case of monensin poisoning in ostriches is presented. Analytical results and histopathologic changes in intercostal muscles and liver supported the ionophore toxicity diagnosis.

Topics: Animals; Bird Diseases; Birds; Monensin; Poisoning

As the percentage of rabbit feed is very small compared to the bulk of animal feeds, there is a fair chance that rabbit feed will be contaminated with constituents (additives) of batches previously prepared for other animals. Contamination of rabbit feed with monensin derived from previous runs could occur. This contamination may result in anorexia, abortion, high mortality in breeding does and outbreaks of bacterial infections (pasteurellosis and staphylococcal infection) in affected populations.

Topics: Animal Feed; Animals; Diagnosis, Differential; Female; Food Contamination; Male; Monensin; Poisoning; Rabbits

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