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Case Description—A 17-month-old 7-kg (15.4-lb) Shih Tzu was evaluated because of progressive thoracic limb weakness of 3 months' duration.
Clinical Findings—Neuroanatomic diagnosis was consistent with a lesion affecting the cervicothoracic (C6 through T2) spinal cord segments. Electrophysiologic testing revealed abnormal spontaneous activity in the thoracic limbs. Via magnetic resonance (MR) imaging, a lesion in the spinal cord that extended from the C5 through C7 vertebrae was detected, as were symmetric lesions in the cranial portion of the cervical spinal cord, caudal colliculi, and vestibular and cerebellar nuclei. Tests to detect metabolites indicative of inborn errors in metabolism revealed no abnormalities.
Treatment and Outcome—Prior to undergoing MR imaging, the dog received clindamycin (14 mg/kg [6.4 mg/lb], PO, q 12 h), trimethoprim-sulfadiazine (17 mg/kg [7.7 mg/lb], PO, q 12 h), and prednisone (1 mg/kg [0.45 mg/lb], PO, q 24 h). Because of its deteriorating condition, the dog was euthanized. During necropsy, gross lesions were identified in the cervical spinal cord, caudal colliculi, and vestibular and cerebellar nuclei (corresponding to lesions detected via MR imaging). Microscopic evaluation of the brain and spinal cord revealed polioencephalomyelopathy; there was severe spongiosis of the neuropil with reactive astrocytes (many with high numbers of swollen mitochondria) and preservation of large neurons.
Clinical Relevance—The form of polioencephalomyelopathy in the Shih Tzu of this report was similar to that described for Australian Cattle dogs; the similarity of findings in dogs with those in humans with Leigh disease is suggestive of a mitochondrial defect.