INTERNAL MEDICINE CASE STUDIES
Immune mediated polymyositis in a male neutered 4 year
old Boxer
A four year old male neutered Boxer was referred to the R(D)SVS Medicine Service with a 2
week history of stiffness and dyspnoea. On clinical examination, the dog was dull, weak and
had a very stiff, shortened gait and was walking on his toes. The dog had reduced muscle
mass but no evidence of muscle pain on palpation. Proprioception was normal but
withdrawal reflexes were very weak. Patellar and triceps reflexes were absent bilaterally and
the gag reflex was markedly reduced. Haematology revealed a mature neutrophilia
(23.7x109/l, ref. range 3.6-12). Serum biochemistry revealed a moderate increase in creatine
kinase (1242 iu/l, ref. range 50-200). Thoracic radiographs were generally unremarkable and
serology for Toxoplasma and Neospora was negative. In light of the reduced reflexes and
increase in creatine kinase concentration, a myopathy was suspected to be the cause of the
dog’s clinical signs and so biopsies of the cranial tibial, biceps femoris, vastus lateralis and
triceps muscles were taken. Histopathology of the muscle biopsies revealed a mixed
inflammatory cell population of granulocytes and macrophages with mild to severe myofibre
atrophy and loss. No infectious agents were seen. Consequently, a diagnosis of immune
mediated polymyositis was made. The dog was treated with immunosuppressive doses of
prednisolone and azathioprine, with sucralfate for gastro-protection. At a recheck 2 weeks
after discharge, the owner reported that the dog was doing well, the dyspnoea had resolved
and the dog was walking better but was still stiff.
Primary immune mediated polymyositis is an inflammatory myopathy not associated with
any other systemic or infectious causes1. There appears to be a predilection towards larger,
mature dogs and commonly observed clinical signs include weakness, exercise intolerance
and a stiff gait. The criteria for a definitive diagnosis of immune mediated polymyositis is
poorly defined in veterinary medicine although most authors agree that the disease can be
diagnosed if the following features are present 1) clinical signs of muscle weakness, 2)
elevated serum creatinine kinase concentrations, 3) abnormal electromyography
examination with normal motor nerve conduction velocities, 4) absence of an underlying
cause based on clinical examination, diagnostic imaging and infectious agents screens and
5) a muscle biopsy which shows an inflammatory infiltrate. Canine polymyositis has been
associated with systemic lupus erythematous and recent drug administration although the
link between the associated condition and polymyositis is often poorly defined.
Treatment of immune mediated polymyositis is based on immunosuppression, initial pain
relief and supportive care. Prednisolone is the most commonly used immunosuppressive
drug although other drugs such as aziathioprine may also be helpful, particularly if long term
therapy is required to control the clinical signs. The prognosis for dogs with idiopathic
page 1 of 2 polymyositis is poorly characterised although is generally considered to be reasonably good.
Muscle fibrosis and secondary contracture is a possible consequence of polymyositis which
may lead to permanent gait abnormalities.
Reference
1
Evans et al (2004) Canine inflammatory myopathies: a clinicopathologic review of 200
cases. JVIM. 18, 679-91
The University of Edinburgh is a charitable body, registered in Scotland, with registration number SC005336.
www.ed.ac.uk/vet/hfsa-int-med
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Immune Mediated Polymyositis
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