CASE DESCRIPTION: A 7-month-old neutered male ferret was evaluated for episodic pelvic limb weakness of 2 weeks' duration. CLINICAL FINDINGS: Neurologic examination revealed flaccid tetraparesis with decreased spinal reflexes suggestive of a neuromuscular disease. Results of hematologic and CSF analyses, thoracic radiography, and abdominal ultrasonography were unremarkable. Electrodiagnostic testing revealed subtle spontaneous activity localized to pelvic limb interosseous muscles, unremarkable motor nerve conduction velocities, and lower than typical compound muscle action potential (CMAP) amplitude for tibial nerve stimulation only. A severe decremental response of the CMAP was detected with repetitive nerve stimulation (45.5% at the third ulnar nerve). An esophagogram revealed mild megaesophagus. Intravenous neostigmine methylsulfate administration resulted in immediate resolution of muscle weakness. Cross-reacting anti-acetylcholine receptor (AChR) antibodies were detected in serum (0.35 nmol/L) by use of a canine- and feline-specific muscle extract. Clinical signs and ancillary test results were diagnostic of acquired myasthenia gravis. TREATMENT AND OUTCOME: Pyridostigmine bromide was administered (1 mg/kg [0.45 mg/lb], PO, q 8 h), resulting in complete remission of clinical signs. However, 1 month after the diagnosis, the ferret was euthanized because of recurrence of weakness despite anticholinesterase treatment. CLINICAL RELEVANCE: To the authors' knowledge, this is the first report of acquired myasthenia gravis in a ferret and the first identification of anti-AChR antibodies in this species. Autoimmune myasthenia gravis should be considered in ferrets when weakness and flaccid paresis suggest a neuromuscular disease. Electrodiagnostic testing, anticholinesterase challenge, and AChR antibody titer determination were helpful for diagnosis of this condition.
CASE DESCRIPTION: A 7-month-old neutered male ferret was evaluated for episodic pelvic limb weakness of 2 weeks' duration. CLINICAL FINDINGS: Neurologic examination revealed flaccid tetraparesis with decreased spinal reflexes suggestive of a neuromuscular disease. Results of hematologic and CSF analyses, thoracic radiography, and abdominal ultrasonography were unremarkable. Electrodiagnostic testing revealed subtle spontaneous activity localized to pelvic limb interosseous muscles, unremarkable motor nerve conduction velocities, and lower than typical compound muscle action potential (CMAP) amplitude for tibial nerve stimulation only. A severe decremental response of the CMAP was detected with repetitive nerve stimulation (45.5% at the third ulnar nerve). An esophagogram revealed mild megaesophagus. Intravenous neostigmine methylsulfate administration resulted in immediate resolution of muscle weakness. Cross-reacting anti-acetylcholine receptor (AChR) antibodies were detected in serum (0.35 nmol/L) by use of a canine- and feline-specific muscle extract. Clinical signs and ancillary test results were diagnostic of acquired myasthenia gravis. TREATMENT AND OUTCOME: Pyridostigmine bromide was administered (1 mg/kg [0.45 mg/lb], PO, q 8 h), resulting in complete remission of clinical signs. However, 1 month after the diagnosis, the ferret was euthanized because of recurrence of weakness despite anticholinesterase treatment. CLINICAL RELEVANCE: To the authors' knowledge, this is the first report of acquired myasthenia gravis in a ferret and the first identification of anti-AChR antibodies in this species. Autoimmune myasthenia gravis should be considered in ferrets when weakness and flaccid paresis suggest a neuromuscular disease. Electrodiagnostic testing, anticholinesterase challenge, and AChR antibody titer determination were helpful for diagnosis of this condition.