Morbity and mortality in Texel sheep following feed-based monensin overdose in Brazil.

Monensin is an antibiotic ionophore used as feed additive in production animals, however, overdose with monensin is associated with poisoning in livestock. This study describes a mortality outbreak in sheep associated with ingestion of a feed supplement containing elevated concentrations of monensin. The objectives were characterize pathological lesions from monensin toxicosis, correlate these findings with serum creatine kinase myocardial band (CKMB) to estimate the extent of myocardial injury, as well as with electrocardiogram to evaluate the progression and severity of cardiac damage. A farm with 49 Texel sheep provided 275 Kg of supplement containing 1.102 mg/kg of monensin undiluted, freely available in the trough for seven days (40 Kg/day). From the 5th day onward animals presented sternal recumbency, submandibular edema, dyspnea and tachycardia followed by death in 15 animals. At necropsy, the main lesions were globular heart with eccentric dilatation of cardiac chambers, pale myocardium, lungs with edema and congestion, hydrothorax, hydropericardium, ascites, liver with enhanced lobular pattern and pale skeletal musculature. Histologically, in six sheep that died within the first days necrotic myocarditis multifocal to coalescing, mild to moderate with discrete degree of fibrosis, and in nine sheep that died later fibrosis became pronounced. Mapping of cardiac lesions revealed predominance of lesions in left and right ventricles, atria, and interventricular septum, with degree varying between 2 and 3. In apex, right and left papillary muscles lesions ranged from grades 0-2. There was evidence of discrete multifocal necrotic myositis, pulmonary edema and congestion, necrotic hepatitis and centrilobular congestion. In the animals which the CKMB enzyme was measured, the mean value was 1008.88 u/L (104-2480 u/L). Electrocardiogram in four animals showed sinus tachycardia, atrial fibrillation and decreased wave P amplitude. Monensin poisoning caused predominant damage to heart with right and left congestive heart failure, which continued to be present in the surviving animals.