Acute monensin toxicosis in sheep: light and electron microscopic changes

Area of Science:

• Veterinary Toxicology
• Animal Pathology
• Pharmacology

Background:

• Monensin is an ionophore antibiotic commonly used in livestock.
• Monensin toxicosis can occur with excessive dosing, leading to significant health issues in animals.

Purpose of the Study:

• To investigate the clinical and pathological effects of monensin toxicosis in sheep.
• To elucidate the cellular mechanisms underlying monensin-induced muscle damage.

Main Methods:

• Oral administration of monensin to sheep at escalating doses (12, 16, and 24 mg/kg).
• Clinical observation for toxicosis signs, serum biochemistry analysis, necropsy, and ultrastructural examination of tissues.
• Focus on liver, diaphragm, and myocardium for ultrastructural changes.

Main Results:

• Clinical signs of toxicosis, including CNS depression and anorexia, appeared within 24-36 hours.
• Elevated serum creatine phosphokinase and aspartate aminotransferase indicated muscle damage.
• Necropsy revealed skeletal muscle hemorrhages, pale myocardium, and pulmonary edema.
• Ultrastructural analysis showed mitochondrial swelling, cristolysis, sarcoplasmic reticulum swelling, and myofibrillar disruption, particularly in diaphragm and myocardium.

Conclusions:

• Monensin causes muscle cell necrosis through its ionophorous properties, disrupting cellular Na+:Ca2+ balance.
• Increased intracellular calcium due to disrupted ionic processes leads to mitochondrial dysfunction and cell death.
• Diaphragm and myocardium are particularly susceptible to monensin-induced ultrastructural damage.