Monensin Toxicosis in Horses

Monensin poisoning can be characterized as acute or chronic.

Acute monensin toxicosis occurs when large amounts of antibiotic-containing feed are ingested over a short period of time. In these cases, symptoms develop suddenly.

Chronic monensin toxicosis occurs when small amounts of monensin-containing feed are ingested over an extended period of time. Initially, these cases may show no symptoms, and exercise intolerance and weakness develop over time. Chronic toxicosis is rare in horses due to the highly toxic nature of the antibiotic in this species, which makes even small amounts of the toxin more likely to cause severe, sudden symptoms.

Monensin toxicosis is rare in horses, and usually occurs when there are mixing errors at the feed plant or horses gain access to medicated cattle or poultry feed. Monensin toxicosis is commonly life threatening and must be treated as an emergency.

As little as 2 milligrams of monensin per one kg of body weight is toxic to horses. Horses that live on a farm with cattle or poultry are at higher risk of monensin toxicosis.

Monensin toxicosis is caused by ingestion of a toxic dose of monensin, an ionophore antibiotic commonly found in cattle and poultry feed. In these species, ionophores are used as growth promoters. In horses, monensin damages muscle cells, particularly those found in the heart.

Cross-contamination between feeds intended for different types of animals or allowing horses access to cattle or poultry feed are the most common causes of monensin toxicosis.

In some cases, multiple horses ingesting the same feed products are affected.

Diagnosis of monensin toxicosis is often based on symptoms, physical examination, and history of exposure. Diagnostic tests that can identify the heart damage characteristic of this toxin include:

• Blood work
• Diagnostic imaging, including ultrasound and X-rays
• Electrocardiograms

Definitive diagnosis is obtained by identifying the presence of monensin in feed or the animal's stomach contents.

There is no antidote or definitive treatment for monensin toxicosis. Treatment options include:

Decontamination:

• Gastrointestinal decontamination to remove contaminated feed
• Activated charcoal to bind the toxin

Note: decontamination is only effective if contaminated feed is still in the stomach. Activated charcoal should only be administered by a veterinarian. There is no safe way to decontaminate the GI tract at home.

Supportive and symptomatic care:

• IV fluid therapy and supplemental oxygen
• Stall rest to reduce workload of the heart
• Thiamine or vitamin E supplementation
• Antiarrhythmic drugs to stabilize the heart rhythm

Prognosis of monensin toxicosis is guarded and depends on the amount of antibiotic ingested and the resulting degree of heart damage.

Severe heart damage is often permanent, and the horse may suffer from decreased performance and long-term exercise intolerance. Horses recovering from monensin toxicosis must be withdrawn from riding activities or athletic pursuits for a minimum of 4 months, then evaluated for heart disease. Some horses continue to have heart arrhythmias for the rest of their lives, making them unsafe for riding. Long term, affected horses may develop congestive heart failure.

Monensin toxicosis is not contagious. Strategies to prevent exposure include:

• Selecting feed from companies that use separate machinery for producing horse feed, or have thorough cleaning procedures between batches
• Restricting access to cattle and poultry feed

Monensin toxicosis is rare in horses. It is more common in horses on farms with cattle and poultry.

• Decontamination
• IV fluid therapy
• Supplemental oxygen
• Stall rest
• Vitamin E and thiamine supplementation
• Antiarrhythmic medications