Myasthenia gravis (MG) is a relatively common neuromuscular disease of dogs. It’s caused by an abnormality in the transmission of information from one nerve to another. Specifically, it’s the result of a reduction in the numbers of receptors for a chemical crucial to this transmission: the neurotransmitter, acetylcholine.
Two kinds of myasthenia gravis are recognized in veterinary medicine: The congenital form, which carries a very poor prognosis, happens when dogs are born with a reduced number of receptors for acetylcholine. The acquired version is considered a less ominous disease in which the immune system attacks it’s own acetylcholine receptors, thereby hindering normal nerve communication.
In the congenital form, MG is inherited a an autosomal recessive trait and is seen in very young dogs. For the acquired disease, the mode of inheritance is unknown. It’s most common in middle-aged to older dogs.
Symptoms and Identification
The most common symptom associated with myasthenia gravis is regurgitation. This symptom, commonly confused with vomiting, happens when the smooth muscle of the esophagus (the tube leading from the mouth to the stomach) is unable to function well enough to move swallowed food into the stomach. Dogs so affected will bring up undigested food, will lose weight or fail to thrive, and may have respiratory symptoms consistent with aspiration pneumonia (coughing, fever, malaise and/or difficulty breathing). These symptoms are more common with the acquired form of the disease.
Other symptoms include generalized weakness, difficulty walking, and poor tolerance of exercise. Affected pups and older dogs, alike, will display a significant reduction of symptoms after resting.
Diagnosis of the acquired condition is achieved through blood testing to determine the presence of acetylcholine receptor antibodies. This test provides definitive confirmation of the disease.
In the case of the congenital condition, however, diagnosis is not so straightforward. Nerve conduction studies and monitoring the muscle’s response to an injected drug that improves neurotransmission are required before a definitive diagnosis can be established.
Congenital myasthenia gravis is most commonly seen in the Jack Russell Terrier, Springer Spaniel and smooth-haired Fox Terrier. The acquired kind is mostly seen in large breeds like German Shepherds, Golden Retrievers and Labrador Retrievers.
For the acquired form, treatment relies on a drug that reduces acetylcholine breakdown, thereby allowing more time for neurotransmission to occur. Mestinon (pyridostigmine hydrochloride) is the drug of choice in canine medicine. Trial and error is required to effect an acceptable dose.
For the congenital form, things are not so straightforwardly achieved. Though the same drug is employed, pups don’t respond as well. Most progressively worsen until they can no longer walk normally. The great majority are eventually euthanized.
Unfortunately, because treatment of the condition is commonly not fruitful in congenital cases, its expense is not high. Diagnosis, however, can prove a sizable burden for owners who choose to pursue a definitive explanation for their pup’s problems. They can expect to pay anywhere between $500 and $2,000 in the process.
For acquired cases where diagnosis is relatively simple, the long-term costs of the medication are often the worst of the expenses. But the cost of treatment is not insignificant should serious secondary effects of the disease make themselves known. Aspiration pneumonia, in particular, can be very expensive to treat. This is especially true should intensive care be required.
For both congenital and acquired forms, neither parents nor siblings of affected dogs should be bred. This is the mainstay of effective prevention.
Shelton, G.D. 1992. Canine myasthenia gravis. In R.W. Kirk and J.D. Bonagura (eds.) Kirk's Current Veterinary Therapy XI Small Animal Practice. pp.1039-1042. W.B. Saunders Co., Toronto.
Braund, K.G. 1995. Peripheral nerve disorders. In S.J. Ettinger and E.C. Feldman (eds.) Textbook of Veterinary Internal Medicine, pp. 701-726. W.B. Saunders Co., Toronto.