Polymyositis is an inflammatory polymyopathy with an immune-mediated aetiology most commonly seen in adult large breed dogs. Polymyositis can be caused by other systemic conditions but in many cases the aetiology is unknown. Breed-specific myositis is not reported within the veterinary literature. We wish to report an idiopathic syndrome characterised by severe pharyngeal dysphagia in young Hungarian Viszlas which is appears to be caused by myositis of the masticatory and pharyngeal musculature.

The clinical records of fourteen Hungarian Viszlas with similar clinical signs were obtained by the authors via the Hungarian Viszla breed society after one such dog presented at Dick White Referrals. The presenting signs were marked salivation and drooling (14/14, 100%), dysphagia of varying severity but always moderate to severe and often with "turtling" of the neck when the dog attempted to swallow (14/14, 100%), thin body condition (14/14, 100%), significant temporal muscle atrophy (13/14, 92%), pharyngeal erythema and/or tonsillar enlargement on visual inspection (9/10, 90%), marked elevation of creatine kinase (5/7, 85%. mean value 13,306 iu/l), mild-moderate elevation of alanine transaminase (6/11 dogs, 54%; mean value 491 iu/l) and identification of oesophageal dilatation on lateral thoracic radiography (5/13 dogs, 38%). The mean age of onset of clinical signs was 14 months (range 9-30 months) with 10 male and 4 female dogs identified. Three of the fourteen dogs were assessed and managed in primary veterinary practices whilst eleven were referred to recognised specialist referral hospitals. Seven of the dogs underwent EMG testing and biopsy of the temporal muscles; all bar one of these dogs revealed a diagnosis of lymphocytic myositis whilst the seventh dog in this group was diagnosed with severe inflammatory/necrotising myositis caused by antibodies against a sarcommel antigen. Five dogs had anti-type II muscle antibody testing undertaken, all were negative. Anti-acytelcholine receptor antibody testing was negative in the three dogs assessed. Megaoesophagus was diagnosed in six dogs whilst three had no definite diagnosis reached. Eight of the fourteen dogs (57%) survived, four dogs (31%) were euthanased due to recurrent clinical signs (euthanased at an mean age of 16.5 months), one dog died at home without resolution of the clinical signs (12 months old) and one was lost to follow-up. The only treatment that appeared to generate significant prolonged improvement were immunosuppressive steroids (6/6 dogs), although four dogs have survived without treatment.

This is the first report of pharyngeal dysphagia and myositis in young Hangarin Viszlas in the UK and further work is required to further elucidate the cause and possible inheritance of the condition.