Abstract

BackgroundA retrospective study of the clinicopathological features of presumed and confirmed cases of idiopathic inflammatory polymyopathy in the Hungarian Vizsla dog and guidelines for breeding.Results369 medical records were reviewed (1992–2013) and 77 Hungarian Vizslas were identified with a case history consistent with idiopathic inflammatory polymyopathy. Inclusion criteria were: group 1 (confirmed diagnosis); histopathology and clinical findings compatible with an inflammatory polymyopathy and group 2 (probable diagnosis); clinical findings compatible with a polymyopathy including dysphagia, sialorrhea, temporal muscle atrophy, elevated serum creatine kinase (CK) activity, and sufficient clinical history to suggest that other neuromuscular disorders could be ruled out. Some group 2 dogs had muscle biopsy, which suggested muscle disease but did not reveal an inflammatory process. The mean age of onset was 2.4 years; male dogs were slightly overrepresented. Common presenting signs were dysphagia, sialorrhea, masticatory muscle atrophy, and regurgitation. Common muscle histopathological findings included degenerative and regenerative changes, with multifocal mononuclear cell infiltration with lymphoplasmacytic myositis of variable severity. A positive response to immunosuppressive treatment supported an immune-mediated aetiology. The mean age at death and survival time were 6.4 and 3.9 years, respectively. Recurrence of clinical signs and aspiration pneumonia were common reasons for euthanasia.ConclusionsDiagnosis of Vizsla idiopathic inflammatory polymyopathy can be challenging due to lack of specific tests, however the presence of dysphagia, regurgitation and masticatory muscle atrophy in this breed with negative serological tests for masticatory muscle myositis and myasthenia gravis, along with muscle biopsies suggesting an inflammatory process, support the diagnosis. However, there is an urgent need for a more specific diagnostic test. The average of inbreeding coefficient (CoI) of 16.3% suggests an increased expression of a Dog Leukocyte Antigen Class II haplotype, leading to an increased disease risk. The prognosis remains guarded, as treatment can only manage the disease. Recurrence of clinical signs and perceived poor quality of life are the most common reasons for humane euthanasia.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-015-0408-7) contains supplementary material, which is available to authorized users.

Highlights

  • A retrospective study of the clinicopathological features of presumed and confirmed cases of idiopathic inflammatory polymyopathy in the Hungarian Vizsla dog and guidelines for breeding

  • The aim of this study was to describe the clinicopathological features of idiopathic inflammatory polymyopathy in the Hungarian Vizsla, in particular to emphasise the diagnostic approach, treatment, outcome, and to recommend guidelines for breeding practices

  • Two cases were shown to have acetylcholine receptor antibodies and they were excluded from the study

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Summary

Introduction

A retrospective study of the clinicopathological features of presumed and confirmed cases of idiopathic inflammatory polymyopathy in the Hungarian Vizsla dog and guidelines for breeding. The immune-mediated inflammatory myopathies are acquired diseases, characterised by immunological processes primarily involving the skeletal muscle. In human medicine these disorders are divided into five major subsets: dermatomyositis, generalised polymyositis, focal myositis, necrotizing autoimmune myositis and inclusion-body myositis [1]. Histopathology of inclusion body myositis is characterised by cytoplasmic filamentous inclusions, membranous structures and myeloid bodies, in addition to cellular infiltration and increased expression of MHC antigen [7]. Focal myositis is characterised by immune-mediated damage of specific muscle groups such as the masticatory muscles (e.g. temporalis, masseter, pterygoid, rostral portion of the digastricus) in masticatory muscle myositis (MMM) and the extraocular muscles in extraocular myositis. MMM is characterised by the presence of muscle-specific serum autoantibodies, most notably against masticatory myosin binding protein-C [8]

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