Rumensin® Toxicity in Heifers: A Case Study
John Anderson, West Michigan Veterinary Services
Many dairy producers use Rumensin® (Elanco Animal Health) for dairy heifers as an aid to controlling coccidiosis and for improved feed efficiency. Rumensin® also is approved for use in lactating cows as a tool for improving milk production efficiency.
Monensin, the active compound in Rumensin®, has a very wide safety margin for humans and cattle. But, it can be toxic if not fed according to the Food Drug Administration-approved label. In other species, such as horses, monensin can be extremely toxic.
The heifers were housed in a single sloped three-sided barn on a bedded pack. They were fed a totally mixed ration (TMR) consisting of haylage (80%), corn silage (10%), straw (10%) and a mineral/vitamin supplement that was formulated to meet the specific needs of the heifers. Included in the mineral mix was Rumensin® added at a concentration formulated to provide 50 mg/head per day when mixed into the TMR.
The initial sign that something was wrong in this group of heifers was an acute drop in appetite. It was noted by the morning feeder that the heifers had not cleaned up their TMR from the previous day.
Not suspecting any major problem, the employee feeding these heifers mixed and fed a new batch of TMR. Again the heifers had no appetite at all, even for the new feed. The feed was being mixed and delivered to the heifers by a relatively new and inexperienced employee who had been on the job for about 3 weeks.
Upon being informed of the lack of appetite, the herdsman investigated the feed and how it was mixed and discovered that concentrated Rumensin® 80 was being mixed into the TMR instead of a mineral premix containing the Rumensin®. The mineral premix was designed to deliver 50 mg/head per day of monensin when mixed into the TMR.
Rumensin® is available to provide different concentrations of monensin. Rumensin® 80 contains 80 grams of monensin and is designed to be added to TMRs. Rumensin® is often mixed into custom mineral mixes at various concentrations depending on how they are to be delivered (e.g., free choice or mixed into rations).
Saturday morning (day 3 after exposure) a dead heifer was discovered in the group, but the others were starting to chew their cuds and looking brighter and more alert. On Sunday (day 4 after exposure) two more dead heifers were discovered. It was noted that some of the remaining heifers appeared more lethargic, but most were chewing their cuds.
On Monday morning (day 5 after exposure) there were 11 dead heifers. At this point, the herdsman called the herd veterinarian. Based on the history, it was suspected that acute monensin toxicity was the most likely cause of the heifer deaths.
Necropsies were conducted and based on recommendations from the Michigan State University Diagnostic Center for Population and Animal Health (DCPAH) and Elanco Animal Health, samples were collected and submitted for diagnostic analysis. Upon diagnosis, the primary lesion observed was a “gritty” feel when the heart muscle was cut.
This was later confirmed to be mineralization deposits in the heart tissue. No other gross abnormalities were noted. Samples were submitted to DCPAH and lesions consistent with monensin toxicity were found in the heart.
Most of these heifers failed to thrive and were eventually culled. Some heifers were not clinically affected and appear normal today. It is assumed that the spectrum of effects
The LD50 (lethal dose in which 50% of exposed cattle die) of monensin is estimated to be between 10 to 40 mg/lb (20 to 80 mg/kg) of body weight. Using the lowest LD50 estimate, for a heifer weighing 500 lbs, the dose where 50% of exposed animals would be expected to die would be 5000 mg/head per day.
The normal rate that Rumensin® is fed to heifers is 50 to 200 mg/ head per day. In this case, if heifers had even ingested only 25% of their normal daily diet, they would have ingested a potentially lethal dose of monensin.
In cattle, the clinical signs of acute monensin toxicity are loss of appetite (24 to 36 hours post ingestion), diarrhea, dullness, weakness, loss of balance or stumbling, difficulty breathing, and death within 3 to 14 days after ingestion of the incriminated feed.
Monensin causes cell death by disturbing intra-cellular ion homeostasis and destabilizing cell membranes. Cell damage is most evident in heart and skeletal muscle.
Lesions most commonly seen with monensin toxicity in cattle are heart and skeletal muscle degeneration, necrosis and mineralization. Secondary lesions and clinical signs occur from acute heart failure or chronic cardiovascular insufficiency. There is no specific treatment or antidote for monensin toxicity.
Gonzalez, M. Barkema, H.W., and Keefe, G.P. Monensin toxicosis in a dairy herd. Can Vet J. 2005 October; 46: 910–912.
Novilla, M.N. The veterinary importance of the toxic syndrome induced by ionophores. Vet Hum Toxicol 1992;34:66–70.
Potter, E.L. VanDuyn, R.L. Cooley, C.O. Monensin toxicity in cattle. J Anim Sci 1984 Jun;58:1499-511.
Rumensin® 80 Product Label, http://elms.xh1.lilly.com/rumensin_80_label.pdf (last accessed 4-10-09).
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