G. D. Shelton

Dilatation of the right atrium in a dog with polymyositis and myocarditis.

A nine-year-old, female, neutered golden retriever was referred for investigation of weakness. Immune-mediated polymyositis with mixed mononuclear cell inflammation and fibrosis was diagnosed in muscle biopsy specimens from several sites. A soft tissue opacity was noted radiographically cranial to the cardiac silhouette. The dog failed to respond to treatment with prednisolone and was euthanased. At post-mortem examination, the structure observed radiographically was showed to be an enlarged right atrium. Histopathological examination of samples collected at post-mortem confirmed polymyositis. Additionally, mononuclear cell infiltrations and fibrosis were observed in areas of endocardium and/or myocardium in the walls of all four cardiac chambers. Myocarditis has not been reported previously in canine polymyositis but is well recognised in people. Enlargement of the right atrium has also been reported in association with polymyositis and myocarditis in people.

Dystrophin-deficient muscular dystrophy in a Norfolk terrier

A six-month-old male entire Norfolk terrier was presented with a 3-month history of poor development, reluctance to exercise and progressive and diffuse muscle atrophy. Serum creatine kinase concentration was markedly elevated. Magnetic resonance imaging of the epaxial muscles revealed asymmetrical streaky signal changes aligned within the muscle fibres (hyperintense on T2-weighted images and short-tau inversion recovery with moderate contrast enhancement on T1-weighted images). Electromyography revealed pseudomyotonic discharges and fibrillation potentials localised at the level of the supraspinatus, epaxial muscles and tibial cranialis muscles. Muscle biopsy results were consistent with dystrophin-deficient muscular dystrophy. The dog remained stable 7 months after diagnosis with coenzyme Q10 and l-carnitine; however after that time, there was a marked deterioration and the owners elected euthanasia. This case report describes the clinical presentation, magnetic resonance imaging, electrodiagnostic and histopathological findings with immunohistochemical analysis in a Norfolk terrier with confirmed dystrophin-deficient muscular dystrophy, which has not been previously described in this breed.

Dystrophin‐deficient muscular dystrophy in two lurcher siblings

Two cases of dystrophin-deficient muscular dystrophy in 16-week-old male lurcher siblings are reported. The myopathies were characterised by regurgitation, progressive weakness and muscle wastage. The dogs had generalised weakness in all four limbs, with more pronounced weakness in the pelvic limbs. Reduced withdrawal in all limbs, muscle contracture and lingual hypertrophy were noted. Serum creatine kinase activities were markedly elevated. Electromyographic abnormalities included fibrillation potentials. Histopathological and immunohistochemical staining were consistent with dystrophin-deficient muscular dystrophy. Clinical improvement was noted in one of the cases with L-carnitine supplementation and supportive therapy. Genetic transmission of the disease was postulated as the dogs were siblings.

Late‐onset Becker‐type muscular dystrophy in a Border terrier dog

A 9-year-old Border terrier was presented to a referral hospital after a 1-year history of progressive stiffness and exercise intolerance. Neurological examination was consistent with a neuromuscular disorder. Serum creatine kinase activity was mildly elevated. A myopathy was suspected based on MRI findings and electrophysiological examination. Muscle histopathology was consistent with a severe non-inflammatory myopathy of a dystrophic type. Immunofluorescence and western blotting confirmed a dystrophinopathy with an 80-kDa truncated dystrophin fragment similar to Becker muscular dystrophy in people. To our knowledge, this is the first description of a late-onset Becker-type muscular dystrophy in a dog, and the first description of a dystrophinopathy in a Border terrier. Muscular dystrophy in dogs should not be ruled out based on late onset clinical signs and only mildly elevated creatine kinase.

Identification of the mutation causing centronuclear myopathy in a border collie

WE would like to inform colleagues and border collie breeders that the mutation causing centronuclear myopathy in the only reported case …