Horses accidentally exposed to monensin contaminated-feed.

Because of the extreme toxicity of monensin, a common feed additive for cattle, usually very rapid death ensues ingestion. Here is a report of a large number of horses receiving sublethal acute doses and important information on monitoring and prognosis. The main message is if you buy a home made feed from a mill make doubly sure they are aware of the problem or ever better: they do not use ionophore growth promoters in their livestock feed. See the article for more on this.
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Equine Vet J. 2020 Mar 7. doi: 10.1111/evj.13258. [Epub ahead of print]
Acute, subacute and chronic sequelae of horses accidentally exposed to monensin contaminated-feed.
Gy C1, Leclere M1, Belanger MC1, Allano M1, Beauchamp G2, Lavoie JP1.

Author information:
1. Department of Clinical Sciences, Faculty of Veterinary Medicine, Université de Montréal, St-Hyacinthe, Quebec, Canada.
2. Faculty of Veterinary Medicine, Université de Montréal, St-Hyacinthe, Quebec, Canada.
Abstract
BACKGROUND:

Monensin is highly toxic to horses and inadvertent ingestion can result in cardiac injury and death.
OBJECTIVES:

To describe sequelae of monensin ingestion, and to determine clinical predictors of outcome.
STUDY DESIGN:

Observational clinical study METHODS: Physical examination, electrocardiogram and echocardiography were performed on 76 horses accidentally exposed to monensin-contaminated feed. Four horses were examined within 14 days of exposure (acute period), 29 horses were examined between 15 and 45 days post-exposure (subacute period) and 70 horses were examined four to 10 months after exposure (chronic period). Follow-up information was obtained for 56 horses by telephone interviews approximately 16 months after exposure.
RESULTS:

Cardiac abnormalities were detected in 4/4, 19/29 and 31/70 horses during the acute, subacute, and chronic periods, respectively. Sixteen months post-exposure, 34 of the 64 horses (53%) for which the outcome was known had returned to their previous use, 13 (20%) were reported to be exercise intolerant, three (5%) were retired, and 14 (22%) were dead (two deaths, 12 euthanasia). Thinning of the myocardium observed at any point in time was associated with a negative outcome. Heterogeneity of the myocardium observed in the acute/subacute period was associated with a negative outcome while subjective contractile intraventricular dyssynchrony, cardiac chamber dilation, decreased fractional shortening, and multiple premature ventricular complexes observed in the chronic period were associated with a negative outcome. Some horses with significant changes associated with a negative outcome in the chronic phase still returned to their previous work.
MAIN LIMITATIONS:

No control group and only 27 horses were examined more than once.
CONCLUSIONS:

Clinical outcome of horses exposed to sublethal doses of monensin is highly variable. The presence of heterogeneity and thinning of the myocardium shortly after intoxication was associated with a negative outcome.