Toxicosis in cattle from concurrent feeding of monensin and dried distiller's grains contaminated with macrolide antibiotics

Consumption of monensin-containing feed contaminated with macrolide antibio tic residues resulted in the death of cattle from multiple feedlots in sout h-central Kansas. Cattle were fed mile 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 p receded by either no premonitory signs or 1 or more of the following: anore xia, depression, dyspnea, locomotor deficits, and recumbency. Significant g ross lesions were pulmonary and mesenteric edema, hepatomegaly, and general ized myocardial and skeletal muscle pallor that was confirmed histologicall y as acute myodegeneration and necrosis. Other significant histologic lesio ns included centrolobular hepatocellular necrosis, congestion, and pulmonar y interstitial and alveolar edema with fibrin exudation. Animals that survi ved beyond 6 weeks had poor weight gain and coalescing foci of myocardial f ibrosis with residual myocardial degeneration. Analysis of trace mineral su pplements for monensin were within the manufacturer's label range. The DDG samples from affected feedlots had 50-1,500 ppm of erythromycin, clarithrom ycin, and related macrolide antibiotic analogues, which originated in the a lcohol residue. In a preliminary feeding trial, cattle fed this contaminate d DDG in combination with monensin had clinical signs and died with gross a nd 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 resid ues in the contaminated feed appeared to affect the biotransformation of ot herwise nontoxic levels of monensin, leading to clinical ionophore toxicosi s.