Clinical History
A 6 year old female spayed mixed breed dog was presented for evaluation of excessive salivation and regurgitation.  Approximately one year prior to presentation, the groomer noticed that the dog’s temporal muscles were atrophied.  The dog then developed difficulty opening its mouth and prehending food.  At that time, it developed profuse regurgitation and salivation which worsened with excitement.  A serum antibody titer against masticatory muscle type 2M fibers (2M antibody) was negative.  Enlarged salivary glands were noted, which on aspirate revealed normal salivary tissue.  The dog was treated with phenobarbital for presumed sialadenosis but had no improvement.  It was then referred once the salivation and regurgitation did not improve on the phenobarbital.

Physical and Neurological Examination
Routine physical examination revealed weight loss (2 kg in three weeks) and normal TPR.  Bilaterally enlarged (2-3 cm), symmetrical, firm, painless salivary glands were palpable.  There was decreased temporal muscle mass and the jaw was difficult to open, but no pain was elicited.  The tongue appeared normal and withdrew normally.  Abdominal palpation was within normal limits.  Other than sluggish direct and consensual papillary light responses, the neurological examination was within normal limits. Fundic examination was unremarkable.

Diagnostic Testing
CBC – Plasma protein 8.1 g/dl (normal 5.7-7.2)

Serum Chemistry Profile -
Phosphorous 2.6 mg/dl ("reference" 3.2-8.1)
Potassium 2.6 mEq/l ("reference" 4.2-5.4)
Chloride 98 mEq/l ("reference" 109-120)
Bicarbonate 27 mmol/L ("reference" 16-25)
ALT 95 IU/L ("reference" 10-55)
AST 75 IU/L ("reference" 12-40)
Cholesterol 342 mg/dl ("reference" 80-315)

Urinalysis -
Trace protein
USG >1.040

Thyroid - T4- 0.85 ug/dl (normal 0.5-2.1)
Phenobarbital level - 16.1 ug/dl (range 15-40)

Thoracic radiographs - A moderate amount of gas and fluid was noted within the thoracic esophagus, however, there was no overt esophageal dilatation.

Esophagram
Nasopharyngeal regurgitation, and regurgitation from the cervical esophagus, were noted.  No megaesophagus was present.  Barium was retained in the pharynx and cervical esophagus, with only a small amount of barium getting to the stomach.  Radiographic interpretation was oropharyngeal dysphagia and suspected cranial esophageal dysmotility.

Oral examination
No abscess noted.  The tonsils were inflamed and enlarged, with the right tonsil about 2 times larger than the left.

Esophagoscopy - The esophagus appeared grossly normal with a mild amount of fluid present.  The lower esophageal sphincter was initially wide open, then appeared to regain normal size.  The stomach was grossly normal, but the pylorus was large and open.  The duodenum appeared grossly normal and possibly hypermotile.

Histopathology of duodenum, stomach, and tonsils - Mild lymphoid hyperplasia of tonsils and mild lymphoplasmacytic gastritis.  Normal duodenum.

Histopathology of temporalis muscle - Inflammatory myopathy/myositis (See image below).  Multifocal areas of mononuclear, predominantly lymphocytic, cellular infiltrations were present having an endomysial and perivascular distribution. Fiber loss and fibrosis were not noted. Prominent staining of the muscle sarcolemma using SPA-HRPO was present (not shown), consistent with polymyositis. Antibodies were not detected against type 2M fibers in direct (within the muscle biopsy) or indirect (within the serum) assays.   

Acetylcholine receptor (AChR) antibody titer– 0.86 nmol/L (normal <0.6 nmol/L)

Diagnosis
Myasthenia gravis (MG) and inflammatory myopathy (most likely polymyositis). The elevated AChR antibody is diagnostic of immune-mediated MG. The cellular infiltrates present within the temporalis muscle biopsy are indicative of a concurrent myositis. Since clinical signs indicated involvement of more than just the masticatory muscle group, the 2M antibody titer was negative and sarcolemmal staining was apparent with the immunoreagent SPA-HRPO, a diagnosis of polymyositis is more likely than masticatory muscle myositis. Both oropharyngeal  dysphagia and esophageal motility disorders can be associated with underlying MG and polymyositis. Myasthenia gravis and polymyositis have been reported to occur concurrently with thymoma, which was not identified in this case. Also, MG and polymyositis may be part of a generalized autoimmune disorder, which was suspected in this case.

Outcome
The dog was treated with cephalexin, metaclopramide, famotidine, and potassium supplementation.  Once the results of the AChR antibody test and muscle histopathology were reported, pyridostigmine bromide and increasing doses of corticosteroids were initiated.  The dog did well for about three weeks, then presented to the referring veterinarian with an extremely low temperature, profuse regurgitation, and expired during resuscitation efforts.