Your dog has refused to eat for two days...

Not because he's sulking about his bowl, but because he literally can no longer open his mouth.

Or perhaps he stumbles slightly, gets out of breath quickly during walks, or you notice that his temple muscles have wasted away in a few weeks.

These signs do not evoke the classic pathologies associated with dogs (dysplasia, arthritis, cruciate ligament rupture).

Yet, they may point to a myopathy: a disease affecting the muscles themselves.

Canine myopathies form a heterogeneous group of pathologies, ranging from localized autoimmune diseases to generalized genetic dystrophies. Although uncommon, canine myopathies encompass a wide range of diseases that are often mistaken for orthopaedic or neurological disorders.

Evans et al., J Vet Intern Med     Evans et al., 2004                     University of Pennsylvania, dvm360

Muscle, the forgotten organ

Skeletal muscle accounts for 40 to 50% of a dog's body mass.

It is involved in every movement, every deep breath, every swallow. When it gets sick, everything else suffers.

The term "myopathy" literally means a disease of the muscle ("myo" = muscle, "pathy" = disease).

This term encompasses very different entities depending on their origin: immune, infectious, genetic, or drug-induced.

The common point: the muscle fibers themselves are altered or destroyed.

Masticatory Myositis (MMM): The Locked Jaw

This is the most common focal myopathy in dogs.

Masticatory Muscle Myositis (MMM) is an autoimmune disease in which the immune system specifically attacks type 2M fibers of the jaw muscles.

These fibers are unique: they are only found in the masticatory muscles (temporalis, masseter, pterygoids).

No other muscle in the body has them, and this explains why the disease is strictly localized to the jaw.

Acute Phase: When it Starts

The temporal muscles swell, the eyes appear prominent (exophthalmos) due to the swelling of the pterygoid muscles behind the eyeballs.

The dog drools, refuses to touch its meal, and whimpers if one tries to open its mouth.

In some cases, the mouth remains closed even under general anesthesia (this is trismus, a characteristic sign of advanced MMM).

Chronic Phase: If you wait too long

The muscles are no longer swollen: they have atrophied and been replaced by fibrous tissue. The cheekbones protrude, the eyes appear sunken (enophthalmia).

At this stage, even with aggressive treatment, recovery remains partial.

Functional sequelae can be permanent.

Diagnosis and treatment

Diagnosis is based on the 2M antibody blood test (ELISA 2M), developed in 2004 by Professor Diane Shelton's team at the University of California San Diego.

Ideally performed before corticosteroid therapy whenever possible, since prolonged immunosuppressive treatment may reduce antibody concentrations and increase the risk of false-negative results.

Muscle biopsy remains the gold standard examination to assess the degree of fibrosis and guide the prognosis.

Treatment is based on immunosuppression with prednisone (cortisone), administered for a minimum of 6 months.

In a 17-year study by the University of Pennsylvania involving 22 cases, 91% of dogs treated early recovered normal masticatory function within 4 weeks. Approximately 27% experienced a relapse.

Polymyositis: when inflammation becomes generalized

Unlike MMM, polymyositis usually affects several muscle groups simultaneously.

The seminal study by Evans et al. (J Vet Intern Med, 2004), based on 200 canine muscle biopsies, describes the most frequent signs as generalized weakness, stiff gait, dysphagia (difficulty swallowing), muscle atrophy, and episodes of fever. Myalgia upon palpation is curiously rare: do not confuse the absence of apparent pain with the absence of disease.

Polymyositis can be idiopathic (unknown cause, the most frequent), infectious (Neospora caninum, Toxoplasma), or paraneoplastic.

This latter case is particularly well-documented in Boxers: in Evans' study, lymphoma was observed in 6 of 32 Boxers with polymyositis within 12 months of the muscle diagnosis. This multi-causal nature requires a complete workup before any immunosuppression.

Hereditary Myopathies: When the Problem is in the Genes

Less frequent but often more severe, hereditary myopathies are linked to genetic mutations affecting the structure or metabolism of muscle fibers. The best-known example: canine Duchenne muscular dystrophy, reported in Golden Retrievers (GRMD model).

It is caused by a mutation in the dystrophin gene (exactly the same as in humans with Duchenne myopathy), which explains the considerable scientific interest in dogs as a therapeutic model.

More recently, an inherited inflammatory myopathy was characterized in the Dutch Shepherd: a mutation in the SLC25A12 gene, coding for a mitochondrial transporter, leads to rapid muscle degeneration.

Affected puppies develop tremors, stiffness, and weakness from 3 to 9 months of age.

The prognosis is very severe: all described cases were euthanized before 2 years of age due to painful degeneration. These forms justify genetic testing before breeding in affected breeds.

Although hereditary forms are uncommon, they have played a major role in advancing research into human neuromuscular diseases, particularly Duchenne muscular dystrophy.

Predisposed Breeds: What the Literature Says

Large breeds are generally overrepresented in published studies, but certain specific breeds present particular, well-documented forms.

Diagnosis: Why it's often a long process

Diagnosing canine myopathies is an exercise in exclusion: joint conditions, neuropathies, dental problems, endocrine diseases, and infections must be ruled out before a conclusion can be reached. The complete diagnostic pathway includes:

• Blood test with CK measurement: early sign of active muscle damage.

• 2M antibody test (MMM): must be performed before any corticosteroids.

• Electromyogram (EMG): measures the electrical activity of muscles and locates the affected area.

• Muscle biopsy: gold standard examination to confirm the inflammatory or dystrophic nature.

• MRI: increasingly used to target muscles for biopsy.

• Infectious serology (Neospora, Toxoplasma): essential before any immunosuppression.

Treatment and prognosis

For autoimmune forms (MMM, idiopathic polymyositis): immunosuppression is the cornerstone of treatment, based on prednisone in immunosuppressive doses, gradually tapered. In case of insufficient response or relapse, azathioprine, cyclosporine or mycophenolate are added. The minimum duration is 6 months. Too early weaning is the primary cause of relapse.

For infectious forms: treatment of the primary triggering cause. Treating Neospora polymyositis with prednisone alone would be a serious error.

For hereditary myopathies: there is currently no curative treatment. Management is symptomatic, focused on comfort and quality of life.

The prognosis for treatable inflammatory forms is favorable when diagnosis is early. Forms with extensive fibrosis (often cases observed late) may retain permanent functional sequelae even with appropriate treatment.

Are canine myopathies contagious?

Most canine myopathies are not contagious and cannot be transmitted to other dogs or people. Only some infectious myopathies result from parasites or infectious agents, but even these are not spread through simple contact between dogs.

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Sources 

1. Evans J., Lévesque D. et Shelton GD (2004). Canine inflammatory myopathies: clinicopathologic review of 200 cases. J Vet Intern Med, 18(5) : 679-691. PubMed 15515585
2. Shelton GD (2007). From dog to man: the broad spectrum of inflammatory myopathies. Neuromuscular disorders, 17(9-10) : 663-670. PubMed 17629703
3. Tauro A. et coll. (2015). Clinical characteristics of idiopathic inflammatory polymyopathy in the Hungarian Vizsla. BMC Veterinary Res, 11 : 97. PMC4414416
4. Shelton GD et coll. (2019). A mitochondrial aspartate/glutamate transporter mutation induces inflammatory myopathy in the Dutch Shepherd. J Neuromuscul Dis, 6(4) : 485-501. PubMed 31594244
5. Massey J. et coll. (2013). Association of a class II MHC haplotype with accumulated risk of polymyositis in the Hungarian Vizsla dog. PLoS One, 8(2) : e56490. PubMed 23457575
6. VCA Veterinary Hospitals: Masticatory myositis in dogs
7. Merck Veterinary Manual (2025). Polymyositis in dogs and cats. msdvetmanual.com
8. Comparative Neuromuscular Laboratory, UCSD: Masticatory Muscle Myositis FAQ (Pr Diane Shelton)