|First Posted: Apr 6, 2009|
Apr 8, 2011
Monensin Sodium and Horses
"Summary: Monensin, a growth promotant used in some cattle feeds, can be lethally toxic to horses if it's consumed in large enough doses. Sub-lethal levels, though, can lead to heart damage. This study looked at the long-term effects of sub-lethal doses of monensin on horses or ponies who had consumed the product unintentionally. Of the 37 animals evaluated nearly a year after consuming monensin, 21 had returned to athletic or reproductive use. The study confirmed that not all horses who consume monensin need to be retired or euthanized, and also validated several tests as methods of monitoring recovery.
The take-home message: Don't feed horses medicated cattle feed!
The Latest Research - Long-term assessment of horses and ponies post exposure to monensin sodium in commercial feed.
Hughes KJ, Hoffmann KL, Hodgson DR. Veterinary Science, University of Sydney 410 Werombi Road, Camden, New South Wales 2570, Australia. Equine Vet J. 2009 Jan;41(1):47-52. REASONS FOR PERFORMING STUDY: Acute monensin intoxication in equids is well described; however, the long-term effects of sublethal intoxication and ability to return to previous use are less well understood. Long-term observations may allow improved estimation of prognosis in cases of sublethal intoxication.
OBJECTIVES: To assess horses and ponies exposed to sublethal amounts of monensin for evidence of chronic sequelae and ability to return to prior/intended use.
METHODS: Twenty-nine horses and 8 ponies were assessed utilizing serum biochemistry, treadmill exercise stress testing, electrocardiography, and pre- and post exercise echocardiography > or = 6 weeks after ingestion of monensin-contaminated feed. Animals with evidence of monensin-induced cardiomyopathy were re-examined after a period of rest of > or = 11 months. Follow-up information was obtained by owner telephone interview > or = 52 months after exposure.
RESULTS: During resting echocardiography, 11 animals had reduced/low-normal left ventricular fractional shortening (FS); an increase in FS in 8 of these animals was measured > or = 11 months later. Six animals had reduced or low-normal FS during post exercise echocardiography. Two horses had ventricular premature depolarizations during exercise. Follow-up information was available for 35 animals: 21 returned to athletic/reproductive use, 13 were retired immediately and one died. Mean FS increased significantly (P < 0.001) between initial and second examination in 15 animals that underwent resting echocardiography on 2 occasions.
CONCLUSIONS: Some equids exposed to sublethal doses of monensin may not develop permanent myocardial disease and a return to athletic/reproductive use is possible.
POTENTIAL RELEVANCE: Exercise stress testing, echocardiography and electrocardiography may be useful for detection and monitoring of cardiac dysfunction in equids exposed to monensin and determining whether a return to athletic/reproductive use is possible. PMID: 19301581 [PubMed - in process]"