Acquired myasthenia gravis (MG) is an immune-mediated disorder in which autoantibody (autoAb) is directed at nicotinic acetylcholine receptors (AChR) at the neuromuscular junction. Antibody-mediated destruction of AChR leads to muscular weakness that may be life-threatening. Weakness is typically exacerbated by exercise and improved with rest. Weakness can be generalized or focal in nature, and restricted to ocular, pharyngeal, oresophageal skeletal muscle. Canine breeds considered disproportionately affected include Akitas, German Shepherd Dogs, and Dachshunds. Because of its varied clinical presentation, acquired MG should be considered for a dog presenting with generalized or focal muscle weakness. While the Ab-mediated immune response to muscle nicotinic AChR is one of the best characterized autoimmune disease, what initiates and sustains the autoimmune response remains unknown. The molecular pathogenesis of the disease is discussed here. The "gold standard" for diagnosis of acquired MG in dogs is demonstration of serum AChR Ab titer > 0.6 nmol/L via immunoprecipitation assay. A positive response to the administration of short-acting anticholinesterases (i.e., edrophonium) can be used to provide a tentative diagnosis, but must be interpereted with caution as other neuromuscular disorders also may show a positive response to edrophonium. Treatment includes the administration of long acting anticholinesterases, immunosuppression, and supportive care of other constitutional signs. Management strategies and prognosis will be discussed.