Monensin in Horses – The Latest Update on the Horse Poisonings
Just this past October, a case of monensin toxicity at a horse barn in Florida claimed the immediate lives of three horses and affected 19 others. A mistake at the feed company caused monensin — a type of drug called an ionophore, which is added to cattle, swine, and poultry feed to increase weight gain — to be inadvertently mixed into horse feed that was used at Masterpiece Equestrian Center in Davie, Florida.
Days later, several horses were found with various signs typical of monensin toxicity: elevated temperature, rapid heart rate, inability to rise, trembling, sweating, and hind limb paralysis. Those that don’t die from the acute toxicity suffer permanent heart damage.
Monensin has always been a mystery to me. We are hammered with the following mantra in vet school: monensin kills horses, monensin kills horses. By why horses? Horses are ten times more sensitive to the drug than cattle and in cattle this stuff is very commonly used, especially in the feedlot. In addition to increasing feed efficiency and rate of gain (two things that are important for feedlot cattle packing on pounds prior to slaughter), monensin also prevents against coccidiosis, a disease that causes diarrhea. Mixed into the feed, it’s fed to feedlot steers and heifers on a daily basis, no problemo.
Make no mistake, monensin can be toxic to cattle, too, but the doses at which this occurs are far higher than for horses. For some reason, cattle are way more tolerant of the stuff. Most cattle monensin toxicity cases show a group of cattle becoming anorexic for a period of days or weeks. When the drug is removed, re-calculated, and its proper dose (toxicity in cattle is almost always caused by a calculation or mixing error) is given, the cattle recover. Only at very high doses do cattle exhibit the cardiotoxic effects that horses show with the tiniest amount.
Monensin doesn’t just attack a horse’s heart. It affects all skeletal muscle in the body. Muscle cells begin to break down, releasing myoglobin into the blood stream, which, in an unfair irony, is toxic as well, outside the cell. Free myoglobin in the blood causes kidney damage and failure, so those that can make it through the cardiac effects of the toxicity then usually succumb to multiple organ failure as the kidneys and liver try to rid of the body of myoglobin from damaged muscle.
In other words, monensin toxicity in horses stinks. It’s painful, there’s no antidote, and survivors really don’t survive in the best sense of the word. They eventually succumb to the toxicity one way or another.
I feel terrible for the horses that were affected by this most recent feed mix-up but unfortunately it won’t be the last case. It seems like every couple of years there is a monensin toxicity case that hits the news because where horse barns order large amounts of feed from mills that also process cattle, swine, or poultry feed, this is an accident waiting to happen. Usually it’s an honest mistake. Labels get confused, deliveries are inadvertently switched. Wires get crossed. It happens. But it still stinks. It’s also a handy plot for a Dick Francis novel when the mistake isn’t honest. But that’s for an entirely different blog.
Dr. Anna O'Brien