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Basics ⬇

Outline

BASICS

Overview!!navigator!!

  • Monensin is used as an anticoccidial agent and growth promotant in livestock species
  • Horses are the most sensitive non-target species (LD50 2–3 mg/kg)
  • Most affected organ systems are:
    • Cardiovascular—severe myocardial necrosis with secondary systemic congestion
    • Musculoskeletal—severe muscle necrosis

Signalment!!navigator!!

No age, genetic, or sex predilection.

Signs!!navigator!!

  • Onset of clinical signs commonly occurs within 24 h but can be delayed for days to months
  • Anorexia
  • Ataxia
  • Tremors
  • Sweating
  • Dyspnea
  • Depression with hypoactivity or reluctance to move
  • Weakness
  • Recumbency with attempts to rise and thrashing of legs
  • Sudden death

Causes and Risk Factors!!navigator!!

  • Exposure to premix or feed containing monensin
  • Feeding rations containing monensin, e.g. cattle, poultry, or swine feed
  • Feed mixing errors in which monensin is inadvertently added to the ration
  • Feed contamination at mills that mix cattle, poultry, or swine feed
  • Gaining access to and consumption of bagged premix

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Other causes of myopathies including rhabdomyolysis, hyperkalemic periodic paralysis, vitamin E/selenium deficiency, seasonal pasture myopathy
  • White snake root
  • Cantharidin toxicosis
  • Selenium toxicosis

CBC/Biochemistry/Urinalysis!!navigator!!

  • Often, there is minimal to no effect on hematopoietic parameters
  • Owing to the potential delayed onset of clinical signs, serum chemistry abnormalities may not be observed as changes in serum chemistry typically occur within 24 h preceding death
  • Creatine kinase and aspartate aminotransferase may be increased because of cardiac and skeletal myocyte damage
  • Electrolyte abnormalities may be observed but typically occur late. Electrolyte changes include increased serum phosphorus and decreased serum calcium and potassium
  • Urine glucose, protein, myoglobin, and hemoglobin can be increased, accompanied by a decrease in urine specific gravity and pH

Other Laboratory Tests!!navigator!!

Cardiac troponins may be elevated.

Imaging!!navigator!!

N/A

Other Diagnostic Procedures!!navigator!!

  • A quantitative analysis for monensin and other ionophores, which can cause similar clinical signs, in a representative feed sample through liquid chromatography mass spectrometry
  • Feed samples may not be representative of what was consumed if the feed in question is gone, there is a delayed onset of clinical signs, or if the ration is hand-mixed for each feeding

Pathologic Findings!!navigator!!

  • In cases of peracute death, gross and microscopic lesions may not be observed
  • Gross findings include areas of pallor and streaking of cardiac and skeletal muscle along with epicardial and endocardial hemorrhage. Secondary lesions associated with heart failure include hydropericardium, pulmonary edema, hydrothorax, nutmeg liver, and ascites
  • Microscopic findings include myocardial degeneration and necrosis characterized by vacuolization, loss of striation, and mineralization with chronic cases exhibiting myocardial fibrosis and lymphoplasmacytic infiltrate

Treatment ⬆ ⬇

TREATMENT

  • There is no specific antidote for monensin toxicosis
  • Remove suspect feed immediately to prevent further access and consumption
  • Administration of vitamin E to minimize oxidative damage to tissues
  • Gastric lavage or administration of activated charcoal immediately to minimize absorption.
  • Administration of mineral oil to expedite gastrointestinal transit
  • Restrict activity of affected horses for up to 3 months

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

Echocardiograms can be used to monitor for cardiomyopathies in surviving individuals.

Prevention/Avoidance!!navigator!!

  • Store feeds or premixes containing monensin away from horse feed and in an area inaccessible to horses
  • Implementation of good feed-mixing practices

Possible Complications!!navigator!!

May observe acute death months later without prior clinical signs.

Expected Course and Prognosis!!navigator!!

  • The prognosis depends on the quantity of monensin ingested and the amount of damage to cardiac and skeletal muscle
  • Poor to grave once clinical signs are observed
  • Death is attributed to severe myocardial damage and decreased function

Miscellaneous ⬆ ⬇

MISCELLANEOUS

Abbreviations

LD50 = median lethal dose

Suggested Reading ⬆ ⬇

Divers TJ, Kraus MS, Jesty SA, et al. Clinical findings and serum cardiac troponin I concentrations in horses after intragastric administration of sodium monensin. J Vet Diagn Invest 2009;21(3):338–343.

Hall JO. Ionophores. In: Plumlee KH, ed. Clinical Veterinary Toxicology. St. Louis, MO: Mosby, 2004:120–127.

Novilla NM. Ionophores . In: Gupta RC, ed. Veterinary Toxicology, 2e. San Diego, CA: Elsevier, 2012:1281–1299.

Poppenga RH. Feed additives. In: Smith BP, ed. Large Animal Internal Medicine, 5e. St. Louis, MO: Elsevier Mosby, 2015:1609–1610.

Author(s) ⬆ ⬇

Author: Scott L. Radke

Consulting Editors: Wilson K. Rumbeiha and Steve Ensley

Additional Further Reading ⬆

Click here for Additional Further Reading