Canine Myasthenia Gravis (MG)

Myasthenia gravis in dogs is a neuromuscular disease marked by defective signal transmission at the motor end-plate, resulting from either congenital receptor deficiency or acquired autoantibodies targeting nicotinic acetylcholine receptors. This leads to skeletal muscle weakness, commonly manifesting as exercise-induced collapse, megaesophagus, and—in severe cases—respiratory compromise.

Diagnosis requires advanced testing, including serum AChR antibody titers and electromyography. Management combines anticholinesterase drugs, immunosuppressive strategies, and supportive care to prevent complications such as aspiration pneumonia.

Definition & Etiology

Myasthenia gravis (MG) is a neuromuscular disorder characterized by impaired communication between nerves and muscles, leading to muscle weakness and fatigue. It occurs in two forms:

Congenital MG – Rare, caused by a deficiency of acetylcholine receptors. Reported in Jack Russell Terriers, Springer Spaniels, Fox Terriers, and Dachshunds.

Acquired MG – More common, immune-mediated, caused by autoantibodies against acetylcholine receptors at the neuromuscular junction. Seen in breeds like Akitas, German Shepherds, Golden Retrievers, and Labrador Retrievers.

Pathophysiology

Autoantibodies block and degrade acetylcholine receptors, preventing effective nerve signal transmission. This results in exercise-induced muscle weakness and rapid fatigue.

Clinical Signs

Generalized Weakness – Worsens with exercise, improves with rest.
Megaesophagus – Regurgitation due to esophageal dilation, increasing risk of aspiration pneumonia.
Focal Muscle Weakness – Affects facial, pharyngeal, and ocular muscles, causing dysphagia, change in voice, and ptosis.
Acute Fulminant MG – Severe, rapidly progressive paralysis, leading to respiratory failure.

Diagnosis

Acetylcholine Receptor Antibody Test (AChR-Ab Test) – Gold standard, highly sensitive and specific for acquired MG.
Tensilon Test – IV edrophonium chloride briefly improves muscle strength.
Electromyography (EMG) – Detects abnormal decremental response in muscle activity.
Chest Radiographs – Assess for megaesophagus and aspiration pneumonia.

Treatment

Anticholinesterase Therapy – Pyridostigmine bromide (first-line drug) inhibits acetylcholinesterase, improving neuromuscular transmission.
Immunosuppressive Therapy – Corticosteroids (used cautiously), azathioprine, or mycophenolate for immune-mediated cases.
Supportive Care – Elevated feedings to manage megaesophagus, monitoring for aspiration pneumonia.
Thymoma Removal – If a thymoma is present, surgical excision may improve clinical signs.

Prognosis

Varies based on severity. Many dogs enter spontaneous remission within 6–8 months, but those with aspiration pneumonia have a poorer prognosis. Regular monitoring is essential

📚 References

Merck Veterinary Manual. Inflammatory Disorders of the Peripheral Nerves and Neuromuscular Junction in Animals.🔗
Forgash AJ, et al. (2021). Clinical features and outcome of acquired myasthenia gravis in 94 dog. 🔗
Journal of Veterinary Internal Medicine. Case Series of Canine Myasthenia Gravis: A Classification Approach With Consideration of Seronegative Dogs. 🔗
AVMA Publications. Acute fulminating myasthenia gravis in five dogs. 🔗