Equine Moldy Hay and Feed Toxins – NAVLE Study Guide

Overview and Clinical Importance

Feed-related toxicoses represent a significant category of equine multisystemic disease on the NAVLE. Horses are uniquely susceptible to several feed contaminants due to their sensitive gastrointestinal physiology and metabolic pathways. Mycotoxins, ionophores, and endophyte alkaloids are the three major categories of feed-borne toxins that veterinarians must recognize and manage. These conditions often present with nonspecific clinical signs initially, making a thorough dietary history essential for diagnosis.

Understanding the source, mechanism, clinical presentation, and management of these toxicoses is critical for both clinical practice and board examinations. Horses are extremely sensitive to ionophores (20 times more than cattle) and fumonisins, making feed contamination potentially fatal even at low concentrations.

Mycotoxins in Equine Feed

Mycotoxins are toxic secondary metabolites produced by filamentous fungi. The major mold genera producing mycotoxins relevant to equine health include Fusarium, Aspergillus, and Penicillium. Fusarium toxins typically develop in the field during cool, wet conditions, while Aspergillus and Penicillium toxins form during improper storage in warm, humid environments.

Major Mycotoxins Affecting Horses

Equine Leukoencephalomalacia (ELEM)

Equine leukoencephalomalacia (ELEM), also known as moldy corn poisoning or blind staggers, is a devastating neurological disease caused by fumonisin mycotoxins produced by Fusarium verticillioides (formerly F. moniliforme) and F. proliferatum. The disease is characterized by liquefactive necrosis of the cerebral white matter.

Pathophysiology

Fumonisins disrupt sphingolipid biosynthesis by inhibiting ceramide synthase, leading to accumulation of sphinganine and sphingosine. This disruption causes: damage to cell membranes, particularly in the CNS and liver; vascular dysfunction leading to cerebral edema; and liquefactive necrosis of the subcortical white matter. The neurotoxic form (ELEM) results from chronic ingestion of lower doses, while the hepatotoxic form occurs with acute, high-dose exposure.

Clinical Signs

Clinical signs typically appear 7-21 days after exposure to contaminated feed. The onset can be peracute to chronic:

• Early signs: Anorexia, depression, lethargy
• Neurological signs: Ataxia, circling, head pressing, blindness
• Advanced signs: Hyperexcitability, aimless wandering, recumbency
• Terminal signs: Tonic-clonic seizures, coma, death
• Hepatotoxic form: Icterus, photosensitization (less common)

Diagnosis

• History: Corn-based diet, multiple horses affected
• Clinical chemistry: Elevated AST, GGT, SDH (hepatic involvement)
• CSF analysis: Xanthochromia, elevated protein, pleocytosis
• Feed testing: HPLC for fumonisin quantification (greater than 5 ppm is toxic)
• Necropsy: Liquefactive necrosis of cerebral white matter, often unilateral or asymmetrically bilateral

Treatment and Prognosis

Fescue Toxicosis

Fescue toxicosis results from ingestion of tall fescue grass (Festuca arundinacea) infected with the endophytic fungus Neotyphodium coenophialum (formerly Acremonium coenophialum). The endophyte produces ergot alkaloids, primarily ergovaline, which cause profound reproductive effects in pregnant mares. Approximately 85% of tall fescue pastures in the United States are infected with this endophyte.

Pathophysiology

Ergovaline acts as a dopamine D2 receptor agonist, which inhibits prolactin secretion from the pituitary gland. The consequences include: suppressed prolactin leading to agalactia; prolonged gestation due to hormonal dysregulation; impaired placental development and function; and vasoconstriction affecting placental blood flow.

Clinical Signs in Pregnant Mares

Treatment

Domperidone is the treatment of choice. It is a dopamine D2 receptor antagonist that blocks ergovaline effects and restores prolactin secretion.

• Dose: 1.1 mg/kg PO once daily
• Timing: Begin 25-30 days before expected foaling date
• Effect: Restores normal gestation length, prevents dystocia, allows lactation

Prevention

• Remove mares from fescue pastures 60-90 days before foaling
• Test pastures and hay for endophyte levels
• Consider novel endophyte or endophyte-free fescue varieties
• Domperidone prophylaxis if removal not possible

Ionophore Toxicosis

Ionophores are polyether antibiotics used as growth promoters and coccidiostats in cattle, poultry, and swine feed. The most common ionophores include monensin, lasalocid, and salinomycin. Horses are exquisitely sensitive to ionophores, with a lethal dose of monensin being only 2-3 mg/kg (compared to 20-80 mg/kg in cattle).

Mechanism of Toxicity

Ionophores are lipid-soluble molecules that transport cations (Na+, K+, Ca2+) across cell membranes, disrupting normal ionic gradients. This causes: mitochondrial dysfunction and ATP depletion; intracellular calcium overload; oxidative stress and cell death; and preferential damage to cardiac and skeletal muscle (myocardiocytes are highly susceptible).

Clinical Signs

Severity depends on dose ingested. Clinical presentation ranges from subclinical to peracute death:

• Peracute: Sudden death within hours (high dose)
• Acute: Anorexia, colic, profuse sweating, tachycardia, weakness, ataxia
• Subacute: Exercise intolerance, arrhythmias, progressive weakness
• Chronic: Heart failure, poor performance, myoglobinuria

Diagnosis

• History: Access to cattle/poultry feed, new batch of horse feed
• Cardiac enzymes: Markedly elevated CK, LDH, AST, troponin I
• ECG: Arrhythmias (VPCs, tachycardia, conduction disturbances)
• Echocardiography: Myocardial thinning, reduced contractility
• Feed analysis: HPLC for ionophore quantification

Treatment and Prognosis

Slaframine Toxicosis (Slobbers Syndrome)

Slaframine toxicosis, commonly called slobbers, is caused by the mycotoxin slaframine produced by the fungus Rhizoctonia leguminicola (now Slafractonia leguminicola). This fungus causes black patch disease primarily in red clover, but can also affect white clover, alsike clover, and alfalfa. The condition is most common during cool, wet spring and fall conditions.

Pathophysiology

Slaframine is an indolizidine alkaloid that acts as a parasympathomimetic agent. It is metabolized in the liver to an active form that stimulates muscarinic receptors on salivary glands, lacrimal glands, and other exocrine tissues. This causes the characteristic excessive salivation.

Clinical Signs

• Profuse salivation: Most prominent sign; frothy, dripping saliva
• Lacrimation: Excessive tearing
• Diarrhea: Mild to moderate
• Polyuria: Frequent urination
• Mild bloat: Occasional

Treatment and Prognosis

• Remove contaminated forage: Primary treatment
• Atropine: May help control salivation (anticholinergic)
• Fresh water: Ensure adequate hydration
• Prognosis: EXCELLENT; signs resolve within 24-48 hours after removal

Recurrent Airway Obstruction (Heaves)

While not a true toxicosis, moldy hay causes Recurrent Airway Obstruction (RAO), also known as heaves or equine asthma. This is an allergic inflammatory condition triggered by inhalation of mold spores (Aspergillus, Alternaria, Faenia rectivirgula) and organic dust in hay. RAO affects approximately 12% of mature horses.

Clinical Signs

• Chronic cough, especially with exercise or feeding
• Nasal discharge (mucopurulent)
• Increased respiratory rate and effort
• Heave line: Abdominal muscle hypertrophy from labored breathing
• Exercise intolerance

Treatment

• Environmental management: Most important; pasture turnout, avoid dusty hay
• Corticosteroids: Dexamethasone, inhaled fluticasone/beclomethasone
• Bronchodilators: Clenbuterol, inhaled albuterol
• Hay alternatives: Soaked hay, hay cubes, complete pelleted feeds

Prevention of Feed Toxicoses