Myasthenia Gravis (MG) is a disorder of neuromuscular transmission in which autoantibodies against nicotinic acetylcholine receptors (AChRs) at the neuromuscular junction results in reduction of AChRs and muscle weakness (Lindstrom et al., 1987). The disease is characterized by muscle weakness and fatigue (Shelton, 1995). MG occurs in both acquired and congenital forms (Pedroia, 1989). It has been reported that although acquired MG in dogs is seen to begin from eight weeks to eleven years of age, however, it is usually observed between the ages of one and eight years (Hopkins, 1992). The clinical symptoms of congenital MG have been reported to arise in 6-8 week-old puppies (Pedroia, 1989). The cause of MG is the reduction in the number of functional acetylcholine receptors in the postsynaptic membrane of the neuromuscular junctions (Fluckiger, 1978). Acquired MG is characterized by the presence of autoantibodies against acetylcholine receptors (Cuddon, 1989). Although the cause of autoantibodies is not exactly known, it has been suggested that the thymus may play a role (Shelton, 1995). Thymoma has been observed in some cases (Klebanow, 1992); however, autoimmunity signs have been reported to be absent in congenital MG (Shelton, 1995).

 

MG is a disorder which appears with exercise and is characterized by fatigue in skeletal muscles (Fluckiger, 1978). Most patients show clinical such signs as dysphagia, salivation and megaesophagus along with regurgitation. It has been reported that, as a result of clinical symptoms, aspiration pneumonia can occur (Pedroia, 1989). According to some authors (Hopkins, 1992), the definitive diagnosis for MG can be made by its reply to cholinesterase drugs, electrodiagnostics and the presence of antiAChR antibodies in the sera of the patients. Treatments for MG in dogs have been reported to be mainly cholinesterases and immunosupressive drugs (Shelton, 1995). German shepherd and Labrador/Golden retriever breeds are the most commonly diagnosed with this disease (Lee et al., 2005).

 

A four years old male Golden Retriever weighing 25 kg was presented with complaints of exhaustion and fatigue for the past month and inability to stand on its hind legs, loss of voice, regurgitation and anorexia. The dog was regularly vaccinated and dewormed. The owner reported vomiting and regurgitation of undigested food a few minutes after eating, change in the voice and progressive pelvic limb weakness one week prior to presentation. Mild dyspnea was observed after light exercise on the day before presentation. Physical examination revealed a thin body condition, hoarse voice, hypersalivation and pelvic limb weakness. On thoracic auscultation, mild respiratory crackle was detected. The dog was ambulatory but obviously weak and reluctant to bear weight on the hind limbs. Lateral thoracic radiograph revealed enlarged thymus gland and megaesophagus (Figure 1).

Clinical findings were evaluated and, on the assumption of MG, Edrophonium Chloride (Enlon®, Indya Pharmaceuticals) was administered intravenously (IV) at a dose of 0.1 mg/kg and a positive clinical reply occurred within 30 minutes. The disease was diagnosed as MG. Following drug use, heart frequency decreased and defecation was observed; however, cholinergic crisis findings such as salivation, vomiting and diarrhoea did not occur. Although Edrophonium therapy was initiated, megaesophagus did not return to normal status. The dog was severely emaciated in spite of treatment and the clinical signsincluding weight loss and dehydration were progressing. The treatment was continued, however the dog died after ten days.

 

Although the most common findings of MG are reported to be walking disorders following exercise (Shelton, 1995), such symptoms are also seen in peripheral neuropathy and polymyositis. In these diseases, the walking abnormalities are continuous, and there is atrophy in the muscles, and other findings associated with MG are not present (Watson, 1994). In this case, also swaying of the backside after walking, symptoms such as loss of voice, regurgitation, total inability to stand up and difficulty in lifting the head were observed.

 

According to some investigators (Shelton et al., 1990), AChR antibodies can be determined in 80 to 90% of canine and human patients with acquired MG; however, no complete correlation has been determined between a single antibody concentration and the severity of disease. Receptor antibodies in humans with thymoma and MG are always positive and are inclined to have higher concentrations than MG patients without thymoma (Hopkins, 1992). MG requries the long-term combination therapy (Schütt and Kersten, 1986). Cholinesterase inhibitor drugs are the principal agents used in the management of canine MG (Hopkins, 1992). Anticholinesterase drugs inhibit enzymatic hydrolysis of ACh at the neuromuscular junction, prolonging the interaction of ACh released at the nerve terminus with the remaining AChRs, thereby increasing the effective concentration and duration of the effect of ACh in the synaptic cleft (Shelton, 1995). Some investigators (Schütt and Kersten, 1986) have reported using anticholinesterases for a period between 6 weeks and 6 years. Corticosteroids have been reported to be widely used in the treatment of acquired MG (Cuddon, 1989). The primary beneficial effect of corticosteroids in this disease is related to suppression of initiating aberrant immune response against acetylcholine receptors (Hopkins, 1992). It has been reported that corticosteroids have also been reported to be successful on their own in the treatment of acquired MG (Maddison et al.,1984). On the other hand, although the myasthenic crisis and signs of the MG during treatment can quickly be cured by the use of corticosteroids and cholinesterases (Cuddon, 1989). However, it has been reported that corticosteroids cannot be recommended in all cases of MG (Shelton, 1995).

 

All the authors have seen the manuscript and there is no conflict of interest or interests among authors.

 

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http://dx.doi.org/10.1111/j.1939-1676.1990.tb03124.x