Ionophore Toxicosis in Horses
26 July 2010 Ionophore Toxicosis in Horses
- A Cautionary Tale Word from Woodwedge
A recent report of the death of three horses in Alberta5, alleged to have resulted from eating feed medicated or contaminated with the ionophore, Rumensin (crystalline monensin sodium), prompts the writing of this article.
Monensin is one of several biologically active compounds categorized as ionophore antibiotics in use routinely as feed additives to control coccidiosis in poultry and to improve feed efficiency in pasture and feedlot cattle, also of use in the dairy industry6. The concentrated product is rarely to be found on the farm, available only in formulated ruminant and poultry rations at the feed mill. Used properly the compounds are effective but the level of safety is small, and careless use has caused major losses4. Ionophores are specifically prohibited for use in horses at any time because of the unique species sensitivity and toxicity at a very low level intake. There is general agreement that access to ruminant feed, mixing errors, accidental contamination of horse feed in a mill producing poultry, cattle and horse feed are the most common causes for intoxication1,2,3,4.
The heart is the primary target organ of monensin toxicosis. In horses ingesting a sublethal dose of monensin, heart muscle is damaged and replaced by fibrous tissue during the healing process. The result is a structurally weakened heart that can succumb to stress and cause acute collapse of the horse. Myocardial injury and death in horses may occur from a single acute toxic dose of monensin as low as 1 to 2 mg/kg body weight, shown to be several to one hundred times more susceptible than other species.
Monensin toxicosis is suspected when horses show clinical signs of feed refusal, abdominal discomfort, muscle weakness, and heart failure and when a possible exposure to contaminated feed has occurred. Clinically, signs in horses with ionophoretoxicity vary with the type, quantity and concentration of the ionophore, and with the pre-existing health and body condition of the horse. Predisposing factors may include vitaminE/selenium deficiency, T-2 toxin exposure, and any number of drug interactions associated with impaired ionophore metabolism3. Peracute toxicity is manifest as progressive, severehemoconcentration, hypovolemic shock and death within a few hours of ingestion. The acute form is characterized by feed aversion, colic, diarrhoea, profuse sweating, muscle weakness, progressive ataxia, rapid heart rate, difficult breathing and excessive urination, along with signs of central nervous system malfunction. These cases may show signs for 1 to 4 days before collapse and death. Horses surviving sublethal doses of monensin exhibit signs of reduced athletic performance, unthiftiness, and cardiac failure.
Diagnosis of monensin toxicity may be difficult. Laboratory tests must be run soon after the syndrome develops. Many agents are potential causes if sudden death is the only observation, including selenium toxicity, grain overload, ethylene glycol, botulism, vitamin E/selenium deficiency, various plant varieties and neurogenic myopathies3.
A definitive diagnosis of ionophore toxicity is based on detection of the ionophore in the feed or stomach contents of exposed horses4.
Postmortem findings range from no visible lesions to heart muscle pallor and signs of congestive heart failure. If death occurs suddenly, few lesions will be present. If death is delayed, myopathy and congestive heart failure are more apt to be evident3.
Treatment of horses acutely affected may be attempted, usually on a symptomatic basis. Intensive intravenous fluid therapy, activated charcoal or mineral oil orally may be administered4. Although heroic therapy may support the horse during the initial crisis, the prognosis is always guarded because longer term actions of monensin, particularly on the heart, may still cause death. All affected horses are susceptible to cardiac damage, which may be permanent. A critical evaluation of cardiac function and the integrity of any previously intoxicated horse destined to return to some form of athletic endeavour is well advised. A cautionary word – Biosecurity on the farm or ranch extends to a careful evaluation of all feeds and supplements provided for your horses
. Your dealer should be known for quality feeds, properly formulated, stored and delivered. Purchased feed for horses should be kept in a clean, secure, separate area away from other livestock feed and medications or potentially harmful products. If repackaging feed, be sure to use clean bags or containers to avoid accidental contamination5. The integrity of fences/corrals should be assured so there is no possibility of horses gaining access to ruminant or poultry feed.
A healthy CVP (client-veterinarian-patient) relationship always pays dividends, especially in an emergency. You may have little time to develop one in the unfortunate event of ionophore toxicosis involving your horses.
B.W.R. Rothwell, D.V.M 2010.07.22
- Radostits, O.M. et al, Veterinary Medicine 9th Edition pp1624-26
- Canadian Animal Health Institute, Compendium of Veterinary Products 9th Edition, pp 683
- Blakley, Barry: WCVM Student Notes “Ionophores” via email current to 2010.07.19
- Lohmann, Katharina: Excerpts from Reed and Bayly Equine Internal Medicine pp 449 (cardiovascular diseases), 527-28 (Disorders of the Musculoskelatal system), 1393-1394 (Toxicologic Problems) via email 2010.07.21
- desBarres, Wm., Fwd. copy of email 20.10.07.15 “Important News to Horse Owners” originating from Ms. Anita Doonan, ATRA 2010.07.14
- Merck Veterinary Manual 9th Edition pp 2175, 226