Canine Immune-Mediated Myositis: Diagnostic and Therapeutic Approach

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-08-11

Key Takeaways

• Canine immune-mediated myositis presents as focal (masticatory muscle myositis, extraocular myositis) or generalized (polymyositis) acquired inflammatory myopathies, characterized by immune system attack on muscle tissue leading to weakness and atrophy.
• Masticatory muscle myositis (MMM) specifically targets type 2M muscle fibers, presenting with trismus and masticatory muscle atrophy; diagnosis is strongly supported by a positive 2M antibody titer, with muscle biopsy serving as a confirmatory test, especially in seronegative cases.
• Generalized polymyositis involves symmetric weakness of proximal limb and axial muscles, often with dysphagia and megaesophagus; elevated creatine kinase (CK) and aspartate aminotransferase (AST) are key laboratory findings, with marked elevations favoring generalized forms.
• Muscle biopsy with histopathology, including immunohistochemistry for MHC class I and II expression, is the gold standard for diagnosis, aiding in differentiation from infectious, endocrine, or neoplastic myopathies.
• Immunosuppression, primarily with corticosteroids, is the cornerstone of therapy, with adjunctive agents considered for refractory cases or steroid intolerance; a critical concern is the paraneoplastic association, where neoplasia (most commonly lymphoma) may develop within 12 months of polymyositis diagnosis, necessitating a thorough search for occult malignancy.
• Serial CK measurements are crucial for monitoring treatment response, with declines expected within one to two weeks of initiating immunosuppression, though clinical improvement may take longer; relapse is common with rapid corticosteroid tapering.

Immune-mediated myositis in dogs encompasses a group of acquired inflammatory myopathies in which the immune system targets muscle tissue, producing weakness, atrophy, and dysfunction that ranges from focal to generalized. This article provides a diagnostic and therapeutic framework for the practicing veterinarian, covering the recognized clinical forms, the immunopathologic basis of disease, a structured approach to laboratory and biopsy testing, and current treatment principles. The content assumes familiarity with neurologic and musculoskeletal examination and focuses on clinical decision-making instead of exhaustive pathophysiology.

The diagnostic challenge in these cases is substantial. Clinical signs overlap with infectious myositis, endocrine myopathy, degenerative neuromuscular disease, and neoplasia, and the distinction carries direct therapeutic consequences. Immunosuppressive treatment is not benign, and a confident diagnosis supported by serologic and histopathologic evidence is preferable to empiric therapy. This article answers the practical questions of which tests to pursue, how to interpret them, and how to monitor response to treatment.

At a Glance

Classification of Canine Inflammatory Myopathies

The classification of canine inflammatory myopathies rests on a retrospective review of 200 diagnostic muscle biopsies from the Comparative Neuromuscular Laboratory at the University of California, San Diego. That clinicopathologic review of 200 cases divided inflammatory myopathies into generalized and focal forms. Generalized inflammatory myopathy includes immune-mediated polymyositis, infectious and preneoplastic myositis, and rarely dermatomyositis-like or overlap syndromes. Focal inflammatory myopathy includes masticatory muscle myositis and extraocular myositis.

This distinction is clinically meaningful because the focal forms carry a better prognosis and a more predictable response to immunosuppression. The generalized forms demand a broader diagnostic search, particularly for underlying infection or neoplasia.

Masticatory Muscle Myositis

Masticatory muscle myositis is the most recognized focal form. The disease targets the type 2M muscle fibers that are unique to the muscles of mastication, including the temporalis, masseter, and pterygoid muscles. The immune attack is directed specifically at these fibers, sparing the limb and axial musculature. Clinical signs include inability to open the jaw, masticatory muscle atrophy, and pain on jaw manipulation. Acute cases may show muscle swelling and pain, while chronic cases present with marked atrophy, particularly of the temporalis muscles.

The immunopathology of MMM has been characterized by immunohistochemical studies of MHC class I and class II antigen expression. These antigens are expressed on the sarcolemma of affected muscle fibers even in the absence of inflammatory cell infiltration, suggesting that MHC expression participates in the initiation and maintenance of the disease instead of occurring as a secondary consequence of local inflammation. This finding has diagnostic relevance: biopsy samples from chronic MMM cases may show minimal cellular infiltrate despite clear clinical disease, and MHC immunohistochemistry can support the diagnosis in such cases.

Generalized Immune-Mediated Polymyositis

Generalized polymyositis produces weakness that is typically symmetric and affects the proximal limb muscles, axial muscles, and often the pharyngeal and esophageal musculature. Affected dogs present with a stilted gait, exercise intolerance, dysphagia, regurgitation from megaesophagus, and a weak or changed bark. Muscle atrophy may be generalized or subtle in early disease. The retrospective series noted that myalgia was rarely described, so the absence of apparent pain does not argue against the diagnosis.

The same series reported that creatine kinase and aspartate aminotransferase concentrations were significantly higher in generalized than focal inflammatory myopathies, a useful but not absolute discriminator. Marked CK elevation supports generalized disease, while normal or mildly elevated CK does not exclude either form.

Immunopathologic Basis

The immune mechanisms driving canine myositis parallel those described in human polymyositis. In human disease, T cell mediated destruction of muscle fibers is central, and autoantibodies directed against cytoplasmic antigens such as Jo-1 define clinical subsets. The Jo-1 antigen, histidyl-transfer RNA synthetase, can serve as a chemokine for immature dendritic cells and T lymphocytes, bridging innate and adaptive immune responses and contributing to breakdown of tolerance. Whether analogous antigen-specific mechanisms operate in canine disease remains incompletely defined, but the MHC class I and II expression documented in canine MMM supports an antigen-driven process.

The presence of autoantibodies in canine myositis has been demonstrated indirectly. In a study of dogs with myasthenia gravis, titin antibodies were identified in a small number of dogs with polymyositis, suggesting shared autoimmune mechanisms across neuromuscular disorders. The clinically important serologic test in dogs remains the antibody against type 2M fibers, which is specific for MMM and distinguishes it from generalized polymyositis.

Paraneoplastic Considerations

The association between polymyositis and neoplasia warrants particular attention. In the 200-case series, neoplasia developed in 12 of 200 dogs within 12 months of polymyositis diagnosis, with lymphoma being the most common tumor identified. This temporal relationship means that a diagnosis of polymyositis should prompt a thorough search for occult neoplasia, including thoracic radiography, abdominal ultrasound, and lymph node evaluation. The paraneoplastic form may be clinically indistinguishable from primary immune-mediated polymyositis, and the muscle disease may precede the tumor diagnosis by months.

Diagnostic Reasoning Framework

The diagnostic approach proceeds from recognition of the clinical syndrome to confirmation of immune-mediated disease and exclusion of mimics. A dog with masticatory muscle atrophy, inability to open the jaw, and elevated CK should be tested for circulating antibodies against type 2M fibers. A positive result confirms MMM and makes biopsy unnecessary in most cases. A negative result does not exclude the disease, particularly in chronic cases, and biopsy of the temporalis or masseter muscle should follow.

For generalized weakness with elevated CK and no obvious cause, the differential list includes infectious myositis from protozoal, bacterial, or rickettsial agents, endocrine myopathy, muscular dystrophy, and polymyositis. Serologic testing for infectious agents, endocrine screening, and electromyography help narrow the field. Muscle biopsy remains the definitive test, and the biopsy site should be selected based on electromyographic abnormalities or clinically affected muscles. The pathologist should be asked to perform MHC immunohistochemistry in addition to routine histochemistry, particularly when cellular infiltration is sparse.

The paraneoplastic search should run in parallel with the myositis workup instead of after treatment is initiated. Thoracic radiographs, abdominal imaging, and lymph node cytology are reasonable first steps, with more advanced imaging guided by clinical findings.

Clinical Assessment and Examination Findings

The physical examination should begin with observation of the patient at rest and during movement. Gait assessment often reveals a short-strided, stilted pattern that worsens with exercise. Affected dogs may resist rising, show reluctance to jump, or display obvious muscle pain on palpation. In a retrospective review of 200 inflammatory myopathy cases, generalized weakness, stilted gait, and dysphagia were among the most frequently recorded clinical signs, while myalgia was rarely described by owners or clinicians Evans J, Levesque D, Shelton GD, clinicopathologic review of 200 cases.

Masticatory muscle myositis (MMM) produces a distinctive examination profile. Palpation of the temporalis and masseter muscles may reveal swelling in the acute phase or marked atrophy in chronic disease. Inability to open the jaw, or trismus, is a hallmark finding that distinguishes MMM from most other myopathies. Dogs with MMM may also show exophthalmos due to swelling of the temporalis muscle within the orbit. Extraocular muscle involvement can produce strabismus or impaired globe retraction.

Generalized polymyositis presents with more variable findings. Appendicular muscle atrophy, particularly of the epaxial, gluteal, and proximal limb muscles, is common. Some dogs develop megaesophagus with associated regurgitation and aspiration pneumonia. Dysphonia and changes in bark quality reflect laryngeal or pharyngeal muscle involvement. Cardiac muscle involvement is uncommon but should be considered when arrhythmias or syncope are present.

Diagnostic Testing Strategy

Laboratory Evaluation

Serum creatine kinase (CK) and aspartate aminotransferase (AST) are the primary screening tests. In the 200-case series, mean CK and AST concentrations were significantly higher in generalized inflammatory myopathies than in focal forms such as MMM Evans J, Levesque D, Shelton GD, clinicopathologic review of 200 cases. Marked CK elevation supports active muscle necrosis, but a normal CK does not exclude myositis, particularly in chronic or end-stage disease where muscle mass is depleted.

A complete blood count, serum biochemistry panel, and urinalysis should accompany CK measurement to screen for concurrent disease. Thoracic radiographs are indicated to evaluate for megaesophagus, aspiration pneumonia, or a cranial mediastinal mass suggestive of thymoma. Abdominal ultrasound may be considered in older dogs given the reported association between polymyositis and neoplasia, with lymphoma diagnosed in a subset of dogs within 12 months of polymyositis diagnosis Evans J, Levesque D, Shelton GD, clinicopathologic review of 200 cases.

Serologic Testing

The 2M antibody test is the definitive serologic marker for MMM. Antibodies directed against type 2M muscle fibers are highly specific for MMM and distinguish it from generalized polymyositis and other inflammatory myopathies. Testing should be performed before immunosuppressive therapy is initiated, as treatment may reduce antibody titers and compromise diagnostic sensitivity.

For dogs with suspected generalized polymyositis, serologic testing for acetylcholine receptor antibodies is warranted to exclude concurrent myasthenia gravis. In one study of dogs with autoimmune neuromuscular disorders, titin antibodies were detected in dogs with polymyositis, and ryanodine receptor antibodies were found in a dog with polymyositis Shelton GD, Skeie GO, Kass PH, Aarli JA, titin and ryanodine receptor autoantibodies. These antibodies are more commonly associated with thymoma and late-onset myasthenia gravis, but their presence in polymyositis cases supports a shared autoimmune background.

Electrodiagnostics

Electromyography (EMG) can identify abnormal spontaneous activity including fibrillation potentials and positive sharp waves in affected muscles. EMG is useful for guiding muscle biopsy site selection and for detecting subclinical involvement. Motor and sensory nerve conduction studies are typically normal in myositis and help exclude peripheral neuropathy. Electrodiagnostic findings are supportive instead of diagnostic, and biopsy remains the confirmatory test.

Muscle Biopsy

Biopsy is the gold standard for confirming immune-mediated myositis and excluding other causes of myopathy. Selection of the biopsy site is critical. For MMM, samples should be taken from the temporalis or masseter muscles. For generalized polymyositis, the vastus lateralis, triceps, or biceps femoris are commonly sampled. Avoid sampling muscles that have undergone recent needle EMG, as needle insertion can produce artifactual changes.

Histopathologic features include lymphocytic infiltration, myofiber necrosis, phagocytosis, and variable fibrosis. In MMM, immunohistochemical studies have demonstrated expression of major histocompatibility complex class I and class II antigens on muscle fiber sarcolemma, independent of inflammatory cell infiltration Paciello O, Shelton GD, Papparella S, MHC class I and II expression in canine masticatory muscle myositis. This finding supports an immune-mediated pathogenesis and may aid diagnosis in cases with minimal cellular infiltrate.

Differential Diagnosis Prioritization

The differential list for a dog presenting with weakness, muscle atrophy, and CK elevation includes both immune-mediated and non-immune causes. Infectious myositis due to protozoal agents such as Neospora caninum or Toxoplasma gondii should be considered, particularly in young dogs or those with systemic signs. Endocrine myopathies including hypothyroidism and hyperadrenocorticism can produce weakness and atrophy without marked CK elevation. Toxic myopathies, such as those associated with certain drugs, and nutritional myopathies are less common but remain possibilities.

Diagnostic Workup Checklist

The following sequence provides a structured approach to the suspected myositis case.

1. Obtain a complete history including onset, progression, exposure to toxins or drugs, and vaccination status.
2. Perform a full physical and neurologic examination with specific attention to masticatory muscle size and jaw mobility.
3. Measure serum CK and AST. Repeat CK after 24 to 48 hours if the initial value is normal but clinical suspicion remains high.
4. Run a complete blood count, biochemistry panel, and urinalysis to screen for concurrent disease.
5. Obtain thoracic radiographs to evaluate for megaesophagus, aspiration pneumonia, or thymoma.
6. Submit serum for 2M antibody testing if MMM is suspected. Collect the sample before starting immunosuppressive therapy.
7. Submit serum for AChR antibody testing in generalized polymyositis cases.
8. Perform EMG to identify affected muscles and guide biopsy site selection.
9. Obtain muscle biopsy from an affected muscle. Submit samples for routine histopathology and consider immunohistochemistry for MHC class I and II expression.
10. Consider infectious disease testing based on signalment and geographic exposure.
11. In older dogs, screen for neoplasia with abdominal ultrasound and additional imaging as indicated.

Monitoring and Prognostic Indicators

Serial CK measurement is the most practical monitoring tool during treatment. CK should decline within one to two weeks of initiating immunosuppressive therapy. Clinical improvement in gait, jaw mobility, and muscle mass typically follows over several weeks. Muscle atrophy may persist despite successful immunologic control, particularly in chronic MMM.

Repeat 2M antibody titers are not routinely recommended for monitoring treatment response, as titers may remain positive for months after clinical remission. Instead, clinical examination and CK trends guide therapeutic decisions. Relapse is common when immunosuppressive drugs are tapered too rapidly, and recurrence of atrophy has been documented in immune-mediated myositis cases Lewis SS, Valberg SJ, Nielsen IL, suspected immune-mediated myositis in horses. While this observation comes from equine cases, the principle of relapse with rapid corticosteroid withdrawal applies across species.

Prognosis depends on the underlying type and severity. Dogs with MMM generally have a good prognosis if treated early and maintained on appropriate immunosuppression. Dogs with generalized polymyositis have a more guarded prognosis, particularly when megaesophagus or concurrent neoplasia is present. The paraneoplastic association with lymphoma and other malignancies within 12 months of polymyositis diagnosis warrants ongoing surveillance in older patients Evans J, Levesque D, Shelton GD, clinicopathologic review of 200 cases.

Recognized Complications and Failure Modes

Treatment failure in immune-mediated myositis usually follows one of several recognizable patterns. The first is incomplete initial immunosuppression, where the chosen protocol controls but does not eliminate the aberrant immune response. Affected dogs improve partially, then plateau with persistent muscle atrophy or weakness. Detection relies on serial creatine kinase (CK) measurement at each recheck, a CK that remains above the reference interval after 4 to 6 weeks of treatment should prompt escalation instead of acceptance.

The second pattern is relapse during corticosteroid taper. This occurs when the taper proceeds faster than the underlying immune response subsides. Early detection depends on owner vigilance for return of presenting signs, particularly dysphagia or jaw opening difficulty in masticatory muscle myositis, and on recheck CK before each dose reduction. A rising CK without clinical signs warrants returning to the previous dose and slowing the taper schedule.

The third pattern is corticosteroid intolerance. Polydipsia, polyuria, panting, and muscle weakness are expected during induction, but gastrointestinal signs, pancreatitis, or behavioral changes require dose adjustment or transition to a steroid-sparing agent. Routine monitoring of body weight, appetite, and stool quality at each visit identifies these problems before they become emergencies.

Aspiration pneumonia is the most serious complication, especially in dogs with masticatory muscle myositis and dysphagia. Owners should be instructed to report coughing, gagging, or nasal discharge immediately. Thoracic radiographs are indicated for any suspected aspiration event, and feeding posture modification may be needed during the acute phase.

Common Diagnostic Errors

The most frequent error is diagnosing masticatory muscle myositis without serologic confirmation or biopsy. Swelling of the temporalis and masseter muscles is not pathognomonic, and conditions such as infectious myositis, neoplasia, or trauma can mimic the presentation. The 2M antibody test is highly specific and should be performed whenever the diagnosis is suspected, with biopsy reserved for seronegative cases.

A second error is attributing generalized weakness to polymyositis without excluding other neuromuscular diseases. Myasthenia gravis, polyneuropathy, and degenerative myelopathy can all present with weakness and muscle atrophy. The diagnostic workup must include acetylcholine receptor antibody testing and electrodiagnostics before committing to long-term immunosuppression, particularly in older dogs where paraneoplastic polymyositis is a consideration. Neoplasia developed in 12 of 200 dogs within 12 months of a polymyositis diagnosis in one retrospective series, supporting a thorough search for underlying malignancy in middle-aged and older patients Evans et al., clinicopathologic review of 200 cases.

A third error is interpreting a normal CK as excluding myositis. While average CK concentrations are significantly higher in generalized inflammatory myopathy than in focal forms, normal values do not rule out masticatory muscle myositis, where CK may be normal or only mildly elevated Evans et al., clinicopathologic review of 200 cases. The diagnosis rests on clinical signs, serology, and biopsy, not on a single laboratory value.

Limitations of Current Evidence

The evidence base for canine immune-mediated myositis rests largely on retrospective case series and expert opinion. Prospective randomised trials comparing immunosuppressive protocols are lacking, and no published data define the optimal duration of treatment or the most effective steroid-sparing agent. Expert consensus statements from the American College of Veterinary Internal Medicine provide general frameworks for immune-mediated disease management, but they do not address myositis specifically ACVIM consensus statements.

The immunopathologic understanding continues to evolve. Major histocompatibility complex class I and class II antigen expression on muscle fibers in masticatory muscle myositis occurs independently of inflammatory cell infiltration, suggesting these molecules participate in disease initiation instead of arising as a consequence of local inflammation Paciello, Shelton, and Papparella, MHC class I and II expression in canine masticatory muscle myositis. The clinical implications of this finding for treatment timing or monitoring are not yet defined.

Opinion differs on when to biopsy versus treat empirically. Some clinicians biopsy all suspected cases to confirm the diagnosis and rule out infectious causes. Others treat empirically when serology is positive and clinical signs are classic, reserving biopsy for nonresponders. Both approaches are defensible, but the decision should be made explicitly and documented.

Referral and Escalation Criteria

Referral to a veterinary neurologist or internal medicine specialist is warranted when the diagnosis remains uncertain after initial testing, when a dog fails to respond to appropriate immunosuppression within 4 to 6 weeks, or when repeated relapse occurs during taper. Specialist centers offer advanced electrodiagnostics, muscle biopsy interpretation through experienced neuromuscular laboratories, and access to broader immunosuppressive options.

Laboratory consultation is appropriate for biopsy interpretation, particularly when inflammatory infiltrates are sparse or when distinguishing immune-mediated from infectious myositis. The Comparative Neuromuscular Laboratory at the University of California, San Diego, has published extensively on this disease and provides a diagnostic service that includes immunohistochemistry and serology Evans et al., clinicopathologic review of 200 cases.

Regulatory reporting is not typically required for canine immune-mediated myositis. It is a sporadic autoimmune condition, not a notifiable disease under international animal health standards WOAH terrestrial animal health standards. However, if multiple cases present in a single household or region, or if an infectious aetiology is suspected, consultation with local veterinary authorities is prudent.

Troubleshooting Guide

Frequently Asked Questions

How Should I Manage Suspected Immune-Mediated Myositis When Advanced Diagnostics Are Not Available?

When muscle biopsy, serology, or electrodiagnostics are unavailable, base the working diagnosis on signalment, physical examination, and serial creatine kinase measurements. A strong suspicion of masticatory muscle myositis can be supported by selective masticatory muscle atrophy, inability to open the jaw, and elevated CK. A therapeutic trial with immunosuppressive glucocorticoids is reasonable, provided the client understands the diagnosis is presumptive. Document response objectively using jaw gape measurements, muscle mass scores, and CK trends at defined recheck intervals. If the patient fails to improve within two to four weeks, reassess the diagnosis instead of escalating immunosuppression. Referral for biopsy remains preferable whenever feasible, as the clinicopathologic review of 200 inflammatory myopathy cases demonstrates substantial overlap in clinical presentation across myopathy categories.

What Is the Role of MHC Class I and II Immunohistochemistry on Biopsy Samples?

Immunohistochemistry for MHC class I and class II adds diagnostic value when inflammatory infiltrates are sparse or absent. In masticatory muscle myositis, MHC class I and II antigens are expressed on the sarcolemma of muscle fibers independent of cellular infiltration, and this expression co-localizes with dystrophin. This finding suggests antigen expression participates in disease initiation instead of merely reflecting secondary inflammation. Requesting MHC immunohistochemistry on biopsy specimens can therefore support an immune-mediated diagnosis even when routine histopathology shows minimal inflammation. Discuss this testing option with the pathology laboratory before submission, as fixation and processing protocols affect antigen preservation. The immunohistochemical study of canine masticatory muscle myositis provides the evidence base for this recommendation.

How Do I Distinguish Relapse From Treatment Failure During Maintenance Therapy?

Relapse and treatment failure require different responses. A relapse occurs when a patient previously stable on maintenance therapy develops recurrent weakness, atrophy, or CK elevation. Treatment failure means the initial induction protocol never achieved remission. Before reclassifying either, exclude non-inflammatory causes of deterioration, including corticosteroid myopathy, intercurrent infection, and neoplasia. The retrospective review of 200 inflammatory myopathy cases found neoplasia developed in 12 of 200 dogs within 12 months of polymyositis diagnosis, so new or worsening signs warrant re-evaluation for paraneoplastic disease. For confirmed relapse, increase immunosuppression to the previous effective dose and taper more slowly. For true treatment failure, reconsider the diagnosis, review biopsy quality, and consider referral for second-opinion histopathology.

What Monitoring Parameters Are Most Useful in General Practice?

Serial creatine kinase measurement is the most practical objective monitor, but it does not always correlate with clinical severity. Track muscle mass using body weight and targeted palpation of the temporalis, masseter, and epaxial muscles. For masticatory muscle myositis, measure jaw gape with calipers at each visit. Document dysphagia severity by observing the dog eating a standardized meal. Aspartate aminotransferase follows a similar trajectory to CK but is less muscle-specific. Recheck CK every two to four weeks during induction, then every eight to twelve weeks during maintenance. Instruct clients to report acute weakness, voice change, or regurgitation promptly, as these may indicate megaesophagus or laryngeal involvement. The clinicopathologic review of inflammatory myopathies notes that dysphagia, megaesophagus, and dysphonia are among the most common presenting signs.

How Should I Discuss the Diagnosis and Prognosis With the Owner?

Explain that immune-mediated myositis is an inflammatory muscle disease caused by the immune system attacking muscle tissue, not an infection or injury. Describe the diagnostic process in stages, starting with blood tests and progressing to biopsy if needed. Be explicit that treatment is immunosuppressive, not curative, and that lifelong monitoring is usually required. Discuss the realistic timeline: visible improvement often takes two to four weeks, and medication tapering occurs over months. Address financial commitment honestly, including costs of serial blood work, medications, and potential complications. For masticatory muscle myositis, the prognosis is generally favourable with treatment, but for generalized polymyositis, the retrospective case series documents a meaningful risk of associated neoplasia, which warrants mentioning when discussing long-term outlook.

When Should I Refer a Case to a Specialist?

Refer when the diagnosis is uncertain after initial testing, when a patient fails to respond to an appropriate immunosuppressive trial, or when complications such as megaesophagus, aspiration pneumonia, or suspected paraneoplastic neoplasia arise. Referral is also appropriate when muscle biopsy is needed but the practice lacks surgical or sample-handling experience, since poor biopsy technique compromises histopathologic interpretation. Cases requiring second-line immunosuppressive agents, such as mycophenolate or leflunomide, benefit from specialist input on dosing and monitoring. If clinical signs progress despite treatment, referral allows repeat biopsy and broader investigation. The ACVIM consensus statements provide a framework for evidence-based decision-making that can support referral discussions with owners.

Related Clinical & Scientific Guides

• Feline Hepatic Lipidosis: Nutritional and Medical Management
• Canine Respiratory Infection: Diagnostic Approach and Treatment
• Canine Respiratory Virus: Diagnostic and Management Considerations

References and Further Reading

• Canine inflammatory myopathies: a clinicopathologic review of 200 cases.. 2004.
• Expression of major histocompatibility complex class I and class II antigens in canine masticatory muscle myositis.. 2007.
• Titin and ryanodine receptor autoantibodies in dogs with thymoma and late-onset myasthenia gravis.. 2001.
• Prevalence of the E321G MYH1 variant for immune-mediated myositis and nonexertional rhabdomyolysis in performance subgroups of American Quarter Horses.. 2019.
• Suspected immune-mediated myositis in horses.. 2007.
• The role of Jo-1 in the immunopathogenesis of polymyositis: current hypotheses.. 2003.
• ACVIM Consensus Statements. Journal of Veterinary Internal Medicine.
• MSD Veterinary Manual, Professional Edition. MSD Veterinary Manual.
• American Veterinary Medical Association Practice Resources. American Veterinary Medical Association.

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This article is educational professional reference material for veterinary audiences. It is not a substitute for veterinary diagnosis, individual clinical judgment, current product labeling, or applicable regulatory requirements.