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Monensin Poisoning in Horses

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Originally Posted On: https://madbarn.com/monensin-poisoning-in-horses/

 

Monensin Poisoning in Horses: Risk Factors, Symptoms & Prevention

Monensin is a type of ionophore antibiotic commonly found in livestock feed that is highly toxic to horses. These antibiotics are frequently used in animal feed for parasite control and to promote growth in livestock and poultry species.

The most common cause of monensin toxicosis in horses is accidental ingestion of livestock feeds that contain ionophores. Horses who live and graze on farms where ionphore antibiotics are used have the highest risk of exposure.

All ionophores are toxic to horses, but monensin is the most toxic. Ingestion of as little as 0.9 grams (0.03 ounces) can cause death in an average adult horse.

In horses, monensin poisoning most commonly impacts the cardiovascular system, causing symptoms of cardiac muscle tissue damage, including collapse, rapid heart rate, and sudden death.

Unfortunately, there is currently no antidote, and treatment options are primarily supportive. The prognosis for monensin toxicosis is poor, with most horses dying rapidly after exposure.

Monensin Poisoning in Horses

Ionophore antibiotics like monensin are among the most common causes of myocardial necrosis (heart muscle tissue death) in horses. Since the 1970s, these medications have been a common additive to cattle and poultry feed to promote weight gain and protect livestock from bacterial infections. [1][2]

Commercially available ionophores include: [3]

  • Lasalocid
  • Laidlomycin propionate
  • Maduramycin
  • Monensin
  • Narasin
  • Salinomycin
  • Semduramycin

Among ionophores, monensin poses the highest threat to horses as it is the most toxic. Ingestion of as little as 0.9 g (0.03 oz) is sufficient to cause poisoning in a typical adult 1,000 lb (450 kg) horse. [4]

Causes of Monensin Toxicosis

Ionophore poisoning in horses is caused by the ingestion of monensin (or other ionophores), usually from a treated livestock feed. This can occur as the result of accidental exposure to cattle or poultry feed on farms where treated feeds are in use, or due to feed contamination.

Accidental Exposure

The most common cause of monensin toxicosis in horses is accidental consumption of feed intended for other livestock species. These feeds often incorporate ionophores such as monensin to control infections and promote growth in cattle and poultry.

Feed manufacturers are required to list all active ingredients, including monensin and other additives on the feed label. Attentive reading of feed labels helps minimize accidental equine exposure. [5][6]

Once ingested, monensin is rapidly absorbed by the gastrointestinal tract and enters the bloodstream, where it forms complexes with electrolyte minerals (sodium, magnesium, calcium, and potassium) in the body. These mineral complexes are transported through cell membranes where they disrupt the cell’s pH balance and function, ultimately causing cell and tissue death. [3]

Feed Contamination

While accidental ingestion of ionophore-treated cattle or poultry feed is the most common cause of equine monensin toxicosis, poisoning occasionally occurs as the result of manufacturing contamination of feeds labelled for horses. [7]

The risk of cross-contamination is higher in facilities that produce feed for multiple animal species. If the equipment used for processing monensin-containing feed for cattle or poultry is not cleaned sufficiently before transitioning to horse feed production, residual traces of monensin within the machinery can contaminate equine feed. [4]

It is also possible for a manufacturer to mis-label treated cattle feed as safe and intended for horses, and for a feed mill to add monensin to a horse feed lot in error.

To mitigate this, regulations for feed manufacturing outline mandatory equipment cleaning procedures and other quality control guidelines that must be followed.

Specific mitigating practices to prevent monensin contamination at feed manufacturing plants include: [6][8]

  • Cleaning and sanitation: all equipment used in the production of medicated feeds must be completely cleared of the previous batch and any leftover ingredients. Cleaning procedures include washing, vacuuming, and sweeping to remove any feed particles of the previous lot from the production machinery.
  • Priming: the equipment lines are flushed with grain after cleaning. Running grains through the entire production system removes any residual monensin (and other medications) that might still be present in trace amounts within the machinery.
  • Production sequencing: involves producing feeds in a specific order to reduce the risk of contamination. If possible, non-medicated feeds for other livestock species are produced in between processing a medicated feed and horse feed.
  • Documentation: production staff must confirm in writing that all waste and ingredients have been removed from the manufacturing area between production lots. This practice creates traceability and reduces human error when ingredients are added to a batch.

While the feed industry is highly regulated and required to follow strict rules, errors can occur. Always monitor your horses when introducing new feeds and contact a veterinarian promptly if there are any signs of discomfort or other abnormal reactions to dietary changes.

Risk Factors

Accidental exposure to monensin-treated feed is the leading cause of ionophore toxicosis in horses.

Risk factors include: [4]

  • Horses living on multispecies farms are at a higher risk of accidental exposure to contaminated feed
  • Foals and miniature horses are at a higher risk of ingesting a fatal dose of monensin due to their smaller size and weight
  • Selenium and vitamin E deficiency can increase the severity of tissue damage in affected horses
  • Inadequate access to appropriate feed can increase the probability of horses consuming feed intended for other animals

Environmental Exposure

Monensin is commonly used for growth promotion and parasite control in feeds for the following livestock species: [2][4]

  • Cattle
  • Pigs
  • Poultry
  • Sheep
  • Goats

Ionophores promote growth in ruminant livestock by controlling the proliferation of specific bacteria populations in the digestive system. This results in more efficient digestion of grain and increased energy absorption, leading to weight gain. [9]

While monensin and other ionophores are effective management tools for production livestock, there is some concern around their potential environmental impact. In particular, cattle who consistently consume monensin-treated feeds have high concentrations of monensin in their manure. [10]

Runoff from cattle manure can lead to detectable levels of monensin in groundwater and other aquatic environments. [11][12] The impact of ionophore contamination on the water supply and aquatic ecosystems requires further study, but contaminated water sources are another potential route of exposure to horses.

Processing cattle manure with anaerobic bacteria before disposal or further processing has been shown to reduce monensin concentration by as much as 70%. [10] Adopting this practice may reduce the impact of ionophore contamination in the environment and decrease the risk of exposure for horses.

Symptoms of Acute Monensin Toxicosis

Symptoms of acute monensin toxicosis in horses vary depending on which organ system is most affected. Monensin has the most impact on the cardiovascular system, but muscular and nervous system symptoms may occur in some cases. [2][4]

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Cardiovascular Symptoms

The most commonly affected organ in horses is the heart, with most horse developing heart muscle tissue death (myocardial necrosis).

Cardiovascular symptoms of monensin toxicosis include: [4]

  • Exercise intolerance
  • Elevated heart rate
  • Collapse
  • Congestive heart failure (swelling of the legs and abdomen, rapid breathing, jugular pulse)
  • Sudden death

Neurological Symptoms

Neurological symptoms can occur 12 to 36 hours from ingestion in horses, and may include: [4]

  • Incoordination (ataxia)
  • Generalized weakness
  • Muscle tremors

Gastrointestinal Symptoms

Gastrointestinal symptoms of monensin poisoning generally begin within one hour of ingestion and are caused by the adverse effect of the antibiotic on the horse’s intestinal flora. Clinical signs include: [4]

  • Reduced appetite
  • Colic
  • Diarrhea

Musculoskeletal

Musculoskeletal symptoms in horses include: [4]

  • Generalized weakness
  • Sweating

Horses that survive acute toxicosis can develop muscle atrophy weeks after exposure.

Symptoms of Chronic Monensin Toxicosis

While rare, horses that consume sublethal amounts of monensin can develop chronic toxicosis.

Symptoms of chronic monensin toxicosis include: [14][15]

  • Abdominal swelling (ventral edema)
  • Exercise intolerance
  • Decreased performance
  • Poor mane condition
  • Chronic heart failure

Diagnosis

Since monensin is highly toxic to horses, it is unusual to obtain a diagnosis before death. Diagnosis of monensin toxicosis is also challenging as there is no specific test available.

In cases where a veterinary intervention is sought for a living horses suspected of monensin poisoning, an initial diagnosis is based on physical examination, a known or suspected history of exposure to monensin-containing feed, and the presence of characteristic symptoms.

Further investigation is required to confirm diagnosis. Diagnostic testing may include: [2][15]

  • Blood tests: serum and complete blood count tests can detect elevated levels of troponin I (cTnI), a cardiac regulator protein indicating damage to heart muscle
  • Diagnostic imaging: echocardiography is used to detect the presence of dilated heart chambers
  • Feed analysis: although feed analysis is a useful tool in confirming monensin poisoning, it poses challenges as the distribution of the antibiotic can be inconsistent throughout feed samples. Testing multiple samples of feed is advised.

Differential Diagnosis

In cases without a known history of exposure, other toxins and conditions that can cause similar symptoms should be ruled out, these include: [4]

  • Cantharidin toxicosis
  • Myocarditis
  • Cardiotoxic plant poisoning
  • Botulism
  • Stroke or brain hemorrhage

Post-Mortem Findings

Unfortunately, monensin is highly toxic to horses, and ingestion of as little as 2-3 g/kg can result in fatal poisoning. Horses that die prior to diagnosis may be submitted for post-mortem examination (necropsy) to confirm the cause of death.

Common post-mortem findings include: [4]

  • Pale spots on the myocardium (muscle layer of the heart)
  • Chamber dilatation
  • Lesion of heart and nervous tissue
  • Monensin in stomach contents

Treatment

Monensin poisoning is a severe condition, and affected horses require urgent hospitalization. Currently, no antidote is available, and treatment is aimed at early detoxification and supportive care.

Treatment options include: [4][15]

  • Gastric lavage: if horses are promptly hospitalized (within 10 hours from ingestion), gastric lavage can be administered to reduce further absorption of monensin
  • Gastric administration of magnesium sulfate or activated charcoal
  • Intravenous fluid therapy
  • Vitamin E and selenium supplementation
  • Magnesium sulfate and lidocaine to treat ventricular arrhythmias

It’s important to note monensin poisoning is often rapidly fatal in horses. Affected horses are unlikely to survive long enough to receive medical intervention.

Activated charcoal should only be administered to horses with veterinary guidance.

 

Prognosis

The prognosis of monensin toxicosis is poor, and many horses that develop clinical signs of myocardial necrosis die within a few days from the ingestion of a toxic dose of monensin, and rapidly from the onset of symptoms.

Early diagnosis and aggressive therapy can improve the chances of survival. However, even with treatment, some horses may die of severe cardiac damage. [4]

Long-Term Complications

Horses that survive the acute phase of the toxicosis are likely to suffer from long-term health complications linked to cardiovascular damage.

A 2020 study found that 20% of horses suffering from exercise intolerance were unable to return to previous levels of performance a year and a half after exposure. Fourteen percent of affected horses succumbed to cardiac complications. [13]

Horses recovering from monensin poisoning should not be ridden for up to three months after medical intervention, and all recovering equines require medical clearance before returning to previous levels of activity. Ongoing veterinary monitoring is required for recovering regardless of intent to return to work. [4][13][15]

Prevention

Due to the high mortality rate, limited treatment options, and current lack of antidote, prevention is the best method to ensure the well-being of horses at risk of monensin poisoning.

Prevention strategies include: [4]

  • Diligent feed storage, especially on multiple-species farms
  • Thorough sanitation of shared feed tubs and transportation trucks
  • Use of dedicated feeding equipment for medicated feeds
  • Preventing horse access to other livestock grazing pasture, stalls, barns, and paddocks
  • Appropriate training of farm personnel
  • Buying feed from reliable producers
  • Purchasing feed from equine-only feed producers
  • Diligent reading of feed labels
  • Prompt and proper disposal of any known or potentially contaminated feed
  • Prompt veterinary attention for horses that might have been exposed to monensin-treated feeds, even if asymptomatic

Summary

Monensin is an ionophore antibiotic, commonly found in livestock and poultry feed, that poses a severe and often fatal threat to horses. The ingestion of as little as 0.9 g (0.03 oz) can cause death in horses.

  • The most frequent cause of toxicosis is accidental ingestion of contaminated feed
  • Symptoms of acute monensin toxicosis include rapid heart rate, collapse, incoordination, reduced appetite, diarrhea, sweating, and sudden death
  • No antidote is currently available. Treatment focuses on early detoxification and supportive care
  • The prognosis is poor, with most symptomatic horses dying within days of exposure
  • Horses that survive the acute phase face long-term cardiovascular issues, with affected horses often dying months after exposure
  • Prevention is critical through careful feed management practices

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References

  1. McCoy, C. P. Characterization of Monensin Poisoning in the Horse. Oklahoma State University. 1982.
  2. Mercer, M. A. Ionophores Use in Animals – Pharmacology. MSD Veterinary Manual. 2022.
  3. Novilla, M. N. Ionophores. Veterinary Toxicology (Third Edition). Academic Press. 2018. doi: 10.1016/B978-0-12-811410-0.00078-7.
  4. Hovda, L. R., Blackwell’s Five-Minute Veterinary Consult Clinical Companion Equine Toxicology. Wiley Blackwell. 2022.
  5. Cuneo, S. P. et al., Ionophore Toxicity in Horses. The Informed Arizona Equestrian. 2018.
  6. Code of Federal Regulations Title 21- Part 507—Current Good Manufacturing Practice, Hazard Analysis, And Risk-Based Preventive Controls for Food for Animals. 21CFR225. 1976.
  7. Judd, B. Monensin Poisoning in Horses. VIN.com. 2020.
  8. Team, H. Feed Mixing Sequencing. Halverson.
  9. Smith. B. P., Large Animal Internal Medicine. 6th edition. Elsevier Inc, St Louis, MO. 2019.
  10. Arikan. O. A. et al., The Fate and Effect of Monensin during Anaerobic Digestion of Dairy Manure under Mesophilic Conditions. PLoS ONE. 2018.
  11. Watanabe. N. et al., Environmental Occurrence and Shallow Ground Water Detection of the Antibiotic Monensin from Dairy Farms. Journal of Environmental Quality. 2008.
  12. Pérez. D. J. et al., Monensin Occurrence in Surface Water and Its Impact on Aquatic Biota in a Stream of the Southeast Pampas, Argentina. Environmental Science and Pollution Research. 2021.
  13. Gy, C. et al. Acute, Subacute and Chronic Sequelae of Horses Accidentally Exposed to Monensin-Contaminated Feed. Equine Veterinary Journal. 2020. View Summary
  14. Blomme, E. A. G. et al. Ionophore Toxicity in Horses. Equine Veterinary Education. 1999.
  15. Marr, C. M. and Bowen, I. M., Eds., Cardiology of the Horse. 2nd ed. Saunders Elsevier, Edinburgh. 2010.

 

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