Steve Sachtleben, PhD, PAS
It’s been over 35 years since Elanco Animal Health (Indianapolis, Indiana) registered Rumensin® (1975) for use in beef cattle for the improvement of feed efficiency through its modification of rumen fermentation. Subsequently, additional claims have been approved by the FDA for use in lactating dairy cattle and meat goats.
There are probably thousands of articles in print on the use of Rumensin® (monensin sodium) in beef cattle as stockers, beef replacement heifers, and feedlot cattle fed for slaughter. The greatest response to Rumensin® is found in cattle fed diets with significant amounts of roughage. It is the ability of Rumensin® to alter rumen fermentation so that more energy is created through the shift from acetate to propionate production. This shift in volatile fatty acids also reduces the production of CO2 and methane gases thus reducing the potential risk of grain bloat.
When Rumensin® was first approved; feedlot finishing diets contained substantially more roughage than typical finishing diets today, so the improvement in energy efficiency was greater than it is currently. However, with the use of co-products, the trend toward higher dietary fiber in finishing diets will perhaps improve the ionophore’s effectiveness.
Why does Rumensin® decrease intake in feedlot diets? There are two mechanisms that influence dry matter intake; rumen distension and chemostatic/thermostatic feedback. The first mechanism is straight forward in that the rumen can only hold so much feed and then the calf stops eating. This is typical of high-roughage diets. The second mechanism halts feed intake when an energy threshold is reached. This is why finishing cattle stop eating even though the rumen can physically hold more. In the case of Rumensin®, because more energy is produced per pound of feed, cattle consume less dry matter.
The energy threshold mechanism gives Rumensin® the ability to help keep intake more consistent during changing weather patterns and large swings in ambient temperature like those experienced in the spring and fall. Essentially, cattle are unable to eat more and gorge themselves because their energy threshold has been reached. This is most likely the reason Elanco submitted a claim for and received clearance from the FDA for a higher concentration of Rumensin® per ton of air-dried feed (40 grams/ton).
Rumensin® has claims other than feed efficiency in cattle fed for slaughter (at 50-480 mg/head/day, 5-40 g/ton of 90% dry matter diet). It can be used for the prevention and control of coccidiosis in all beef cattle types except veal calf production. For growing cattle on pasture, an increased weight gain claim can be made as well as feed efficiency in mature, reproducing beef cows. Rumensin® is also cleared by the FDA to be fed in combination with other feed additives such as MGA®, Tylan®, Optaflexx®, Deccox® and Zilmax®. Check with your feed specialist to determine actual clearance combinations permitted and the concentrations of the additives allowed by beef animal type.
The safety of Rumensin® in livestock species has been a topic of discussion in the industry for years. There is no doubt it is toxic to horses in relatively small doses as is Bovatec® (Alpharma). No feed labeled “for cattle only” should be offered to horses or their equine cousins, EVER. Strict sequencing of feeds must be followed at the manufacturing plant to prevent cross contamination of beef and horse feeds. Goats can safely consume Rumensin®, but NOT sheep.
So how does monensin sodium toxicity occur? There is little data in the literature discussing such cases. Three papers were found when an initial literature review was conducted. These papers were written in 1981 (Janzen et al.), 1983 (Potter et al.) and 2009 (Anderson and Grooms). The 1981 and 2009 papers were actual case studies, which involved beef bulls and dairy heifer replacements, respectively. In the 1981 case, the offending diet had been fed up and it was presumed to be ionophore toxicity due to the diagnostic work involved. It was theorized that the bulls had perhaps consumed monensin at 20-30 times the recommendation. The report by Anderson and Grooms (2009) involved heifers and the feeding of Rumensin 80 rather than a diluted premix. It was estimated the cattle consumed about 400 times the formulated rate. Both cases were errors of human origin and not the fault of the ionophore. Potter and coworkers (1983) also presented a paper on monensin toxicity in cattle. This report summarizes research where cattle were given known amounts of monensin in order to determine the LD50s (lethal dose where 50% mortality was recorded). The work (Potter et al, 1983) outlined the symptoms observed in cattle overdosed with monensin. Initially feed intake declines and, dependent on dose, may drop to zero. Diarrhea may also be present at this time. Depending on dose, depression, rapid breathing, ataxia and death might occur. An overdose is most likely responsible for these symptoms as cattle do not detect the monensin the first day, but subsequently back off feed and probably do not consume enough feed for further overdosing to occur. However, the damage has been done.
Monensin toxicity causes cell death by disrupting cell ion stability, thus destabilizing cell membranes. This effect is most readily found in cardiac muscle. Lesions are also found in skeletal muscle and general degeneration, necrosis and mineralization is detected in both sites. This is why cattle that do not die from monensin toxicity are generally lethargic and short of breath. There is no recovery when they have advanced this far down the path of monensin toxicity. There is no treatment or antidote for monensin toxicity.
Anderson, John and Dan Grooms. 2009. Rumensin Toxicity in Heifers: A case Study. Michigan Dairy Review. Vol.14. No.3.
Jansen, E.D., O.M. Radostits and J.P. Orr. 1981. Possible Monensin Poisoning in a Group of Bulls.Can. Vet. J. 22:92-94.
Potter, E.L., R.L. VanDuyn and C.O. Cooley. 1983. Monensin Toxicity in Cattle. J. Anim. Sci. 59:1499-1511.