Canine Dermatomyositis : Genetics, Diagnosis and Treatment

Canine dermatomyositis (DM) is an inflammatory ischemic vasculopathy, of immune origin with strong genetic predisposition, that primarily affects the skin and, to a lesser extent, striated musculature. We present a comprehensive pathogenic, diagnostic and therapeutic overview of this dermatosis.

June 2025

Introduction

Initially recognized in the Collie and Shetland Sheepdog, this condition serves as a particularly relevant spontaneous model for the study of human juvenile dermatomyositis (JDM), a systemic autoimmune disease presenting striking clinical and histopathological similarities. Canine DM is therefore not only a clinical concern for veterinary practitioners, but also a valuable field of translational research.

Over the last decade, understanding of canine DM has undergone a radical transformation. The concept of a simple hereditary disease with autosomal dominant transmission with variable penetrance and inconsistent expressivity has been superseded by a much more nuanced model of complex genetic disorder. Advances in genomics have enabled the identification of specific risk loci and their epistatic interactions, providing a predictive framework for the disease. Simultaneously, fundamental research has highlighted the central role of dysregulation of the type I interferon (IFN) signaling pathway as a major pathogenic driver, similar to what is observed in human JDM. This convergence of genetic and immunopathological knowledge has paved the way for more targeted diagnostic and therapeutic approaches, which are redefining the management of this disease in 2025. We present a current state of knowledge on canine dermatomyositis, integrating the most recent discoveries on its pathogenesis, diagnosis and emerging therapeutic strategies.

Etiopathogenesis

The etiopathogenesis of canine dermatomyositis is the result of a complex interaction between polygenic genetic predisposition, dysregulation of the innate immune system, and environmental triggers. Understanding this cascade of events, from gene to lesion, is fundamental to comprehending the disease and justifying modern therapeutic approaches.

1.1 The Genetic Component of Canine Dermatomyositis

The historical notion of autosomal dominant transmission with incomplete penetrance has been refined by genome-wide association studies (GWAS) that have revealed a complex and epistatic inheritance pattern. The risk of developing DM in predisposed breeds, such as the Collie and Shetland Sheepdog, is now understood as being determined by the interaction of variants within three independent genetic loci.

Identification of Risk Loci

Research has identified three major chromosomal regions whose specific alleles modulate DM risk.

• Locus A (Chromosome 10): A very strong association has been found with a missense mutation in the PAN2 gene. The PAN2 gene codes for a subunit of the poly(A) nuclease deadenylation complex, which plays a crucial role in regulating messenger RNA (mRNA) degradation. This function is particularly important for regulating the inflammatory response, notably by stabilizing transcripts of pro-inflammatory genes containing adenine-uracil rich elements (ARE), such as that of interleukin 6 (IL-6), a cytokine known to be overexpressed in human JDM. This mutation therefore establishes a direct link between a fundamental genetic defect and predisposition to immune dysregulation.
• Locus B (Chromosome 31): A second significant association has been identified with an insertion/deletion (indel) in a 5′ non-coding region of the MAP3K7CL gene. Although the precise function of this gene, which codes for a kinase, is still poorly studied, it is primarily expressed in peripheral blood leukocytes, suggesting a role in immune function.
• Locus C (Canine MHC): A significant association has been observed with a specific haplotype of the canine major histocompatibility complex (MHC) class II. The association is particularly strong in individuals homozygous for this haplotype. However, the high frequency of this risk haplotype in healthy dogs indicates that it is not sufficient alone to cause the disease and that its influence is modulated by the other risk loci.

Epistatic Interaction and Risk Stratification

Combined analysis of genotypes from these three loci has revealed a risk model that is not simply additive, but epistatic, where the effect of one gene is modified by the presence of one or more other genes. Research has shown that 9 of the 27 possible genotypic combinations confer moderate (33-50% penetrance) or high (90-100% penetrance) risk of developing DM, explaining 93% of cases studied. For example, AABB genotypes (homozygous for risk alleles at loci A and B) present 100% penetrance when associated with at least one risk allele at locus C (AABBCc or AABBCC).

This discovery transforms understanding of the disease. The former concepts of “incomplete penetrance” and “variable expressivity” can now be reinterpreted in light of this quantitative genetic model. These phenotypic variations are not random but are the direct reflection of each individual’s polygenic risk profile. A dog with a high-risk genotype is almost certain to develop the disease if exposed to appropriate triggers, while a dog with a moderate-risk genotype may never express the disease or may only present mild and transient signs. Genetics thus provides a predictive framework that replaces uncertainty. This has profound implications for genetic counseling, which moves from simply recommending not to breed clinically affected dogs to a proactive strategy for selecting breeding pairs aimed at minimizing the production of puppies carrying high-risk genotypic combinations.

Genotype-Phenotype Correlation

A significant inverse correlation has been established between the number of risk alleles at the PAN2 and MAP3K7CL loci and the age of disease onset. Dogs carrying four risk alleles (homozygous for risk at both loci) develop DM at a median age of 5 months, while those with only two risk alleles develop it at a median age of 18.5 months. This correlation suggests a gene dose effect on predisposition severity, where a higher genetic load requires a lower environmental triggering threshold to initiate the disease.

 

Table 1: Genetic Risk Loci for Canine Dermatomyositis

Locus Name	Associated Gene	Chromosome	Normal Allele (notation)	Known/Hypothetical Biological Function
Locus A	PAN2	10	Wildtype (a)	Regulation of mRNA degradation, stabilization of inflammatory response transcripts
Locus B	MAP3K7CL	31	Wildtype (b)	Kinase expressed in immune tissues, potential role in immune signaling
Locus C	DLA-DRB1	12 (MHC)	Other DLA haplotypes (c)	Antigen presentation, regulation of adaptive immune response

 

Table 2: DM Risk Stratification Based on Genotype (Combinations of Loci A and B, modified by Locus C)

Locus A / Locus B Genotype	Risk with Locus C = cc	Risk with Locus C = Cc	Risk with Locus C = CC
aa bb	Low	Low	Low
Aa bb	Low	Low	Low
aa Bb	Low	Low	Low
AA bb	Unknown	Moderate	Moderate
Aa Bb	Low	Low	Low
aa BB	Low	Moderate	Moderate
AA Bb	Unknown	Moderate	High
Aa BB	Unknown	Moderate	High
AA BB	Unknown	High	High
Table adapted from UC Davis Veterinary Genetics Laboratory data, based on research by Evans et al.

1.2 The Immune Dysregulation Cascade: Vasculopathy and Interferon

Genetic predisposition is only the first step. The pathogenesis of DM is fundamentally a disease of the immune system that targets blood vessels, resulting in tissue ischemia.

Ischemic Vasculopathy as Primary Lesion

DM is primarily an inflammatory vasculopathy. The central pathological process is an immune-mediated attack directed against the endothelium of small blood vessels, particularly endomysial capillaries in muscles and dermal vessels in skin. This endothelial inflammation, or endotheliitis, leads to narrowing of the vascular lumen, microthrombosis and, ultimately, hypoperfusion of downstream tissues. The resulting ischemia is responsible for the characteristic clinical manifestations: atrophy and necrosis of hair follicles and epidermis (causing alopecia and ulceration) and degeneration of muscle fibers (causing atrophy and weakness).

Type I Interferon (IFN) as Central Pathogenic Driver

Overwhelming evidence from human and canine models indicates that hyperactivation of the type I interferon signaling pathway is the primary driver of this vasculopathy. This “IFN signature” is manifested by systemic and tissue (skin, muscle, blood) overexpression of a set of genes whose transcription is induced by IFN, such as MXA, ISG15 and CXCL10. The strength of this signature in the skin is directly correlated with cutaneous disease activity and decreases or disappears in patients in remission, making it a potential biomarker of disease activity. Type I interferons have pleiotropic effects that may explain the vasculopathy: they can activate endothelial cells, promote a pro-inflammatory and pro-thrombotic state, and recruit immune cells to the site of inflammation, thus perpetuating vascular damage.

Role of Autoantibodies and Circulating Immune Complexes (CIC)

Although research on myositis-specific autoantibodies is less advanced in dogs than in humans, older studies have established a positive correlation between the clinical severity of canine DM and serum levels of circulating immune complexes (CIC) and immunoglobulin G (IgG). It is postulated that these CIC can deposit in the walls of micro-vessels, activate the complement cascade there and thus contribute to endotheliitis and vasculopathy.

The convergence of these data allows the establishment of a unified causal chain that was not evident a decade ago. First, genetic predisposition, notably via mutations in inflammatory regulatory genes such as PAN2, creates fertile ground for an aberrant immune response. Second, in the presence of triggers, this predisposition leads to excessive and sustained production of type I IFN, the central mechanism of the disease. Third, this IFN-rich environment induces vasculopathy by directly damaging endothelial cells. Fourth, vasculopathy compromises blood supply, causing ischemia in vulnerable tissues. Finally, this ischemia manifests clinically as the characteristic cutaneous and muscular lesions of DM. This unified understanding of pathogenesis fully justifies the current therapeutic paradigm shift, which moves away from general immunosuppressors toward therapies that target and specifically block the IFN signaling pathway.

1.3 Environmental and Endogenous Triggers

In a genetically predisposed individual, triggering factors are often necessary to initiate or exacerbate the disease.

• Documented Risk Factors: Several factors are known to play a role in triggering clinical flares.

• • Mechanical Trauma: The typical localization of lesions on bony prominences (face, carpi, tarsi) and pressure points strongly suggests that repeated microtrauma acts as a local trigger, a Koebner phenomenon.
  • Ultraviolet (UV) Radiation Exposure: The photodistribution of certain facial lesions and reported worsening after sun exposure implicate UV as an important triggering factor, probably by inducing keratinocyte apoptosis and releasing autoantigens.
  • Hormonal Factors: Disease flares have been associated with estrus, suggesting hormonal influence on immune regulation.

• The Role of Vaccination: The link between vaccination and DM is an important topic for discussion. There is a well-recognized syndrome of post-vaccination ischemic dermatopathy, notably after rabies vaccination, which is clinically and histologically indistinguishable from DM. A retrospective study of 177 cases of ischemic dermatopathy estimated that an association with recent vaccination was probable in 48.3% of cases. Rather than considering post-vaccination dermatopathy as an entirely distinct entity, it is more logical to view it as genetic DM unmasked by the powerful immune stimulus that vaccination represents. For a puppy carrying a high-risk genotype (for example, AABB), the intense immune stimulation induced by a vaccine could be the “stress test” sufficient to initiate the IFN pathogenic cascade and trigger clinical disease. This has important clinical implications: for puppies of at-risk breeds with unknown or high-risk genetic status, it is not a matter of avoiding vaccination, but of informing owners and implementing close monitoring to detect the appearance of cutaneous lesions in the weeks and months following injections, to allow early intervention.

Clinical Spectrum and Diagnostic Approach

The clinical presentation of canine DM is variable, ranging from mild and self-limiting cutaneous forms to severe systemic involvement. Diagnosis relies on a multimodal approach combining signalment, clinical signs and targeted complementary examinations.

2.1 Breed Predisposition and Disease Classification

• Familial DM: The Collie and Shetland Sheepdog are the emblematic breeds of the disease, in which a hereditary basis has been proven and genetic risk loci have been identified.
• DM-like Syndromes (Dermatomyositis-like): Similar clinical and histological presentations have been described in a growing number of other breeds, notably the Beauceron, Welsh Corgi, Lakeland Terrier, Chow Chow, German Shepherd and Kuvasz.

The historical distinction between “familial DM” (in predisposed breeds) and “DM-like” (in other breeds) is increasingly considered semantic rather than biological. The underlying histopathology is identical, suggesting common pathogenic pathways. The term “ischemic dermatopathy” is a more precise and unifying histopathological diagnosis that encompasses these different clinical presentations. The modern diagnostic approach should therefore not stop at breed, but rather search for genetic and pathological markers of the disease in any dog presenting a compatible clinical picture, regardless of breed.

2.2 Clinical Manifestations

The clinical signs of DM vary considerably from one individual to another, but generally follow a recognizable pattern.

Cutaneous Signs

Cutaneous involvement is the most constant manifestation of the disease.

• Initial Lesions: They typically appear in young dogs, before 6 months of age, and often as early as 7 to 11 weeks. The initial presentation may be subtle, with transient papules, pustules or vesicles that rapidly evolve into more characteristic lesions of erythema, alopecia, scales and crusts.
• Characteristic Distribution: Lesions have a predilection for areas of trauma and poor collateral circulation: the face (periocular and peribuccal regions, nasal bridge), ear pinnae (particularly the tip and folds), tail tip, and skin overlying bony prominences of the limbs (carpi, tarsi, digits).
• Chronic Lesions: Over time, lesions evolve toward permanent cicatricial alopecia, cutaneous atrophy and pigmentary alterations (hyperpigmentation or hypopigmentation), creating a mottled appearance called poikiloderma. Nail involvement (onychodystrophy, onychorrhexis, onychoschizia) may also be observed.

Severe tail involvement with alopecia and crusty lesions

 

Essentially unilateral palpebral involvement in this dog

 

Lesion that can perfectly mimic dermatophytosis

Myopathic Signs

Muscular involvement is more variable and, when clinically apparent, is generally a sign of a more severe form of the disease.

• Correlation with Cutaneous Signs: Clinical myositis usually occurs after the appearance of cutaneous lesions, and its severity is often proportional to that of the dermatological involvement.
• Muscle Atrophy: Atrophy of masticatory muscles (temporal and masseter) is the most frequent muscular sign and may be the only myopathic manifestation. In more severe cases, bilaterally symmetrical atrophy of muscles of the head, neck, trunk and limbs may develop.
• Functional Signs: Atrophy and inflammation of mastication and swallowing muscles can lead to difficulties grasping food (prehension), chewing and swallowing (dysphagia). An abnormal, stiff and stilted gait (“stiff-stilted gait” or “goose step”) is also described.
• Severe Complications: Development of megaesophagus (dilatation and hypomotility of the esophagus) is a serious complication, leading to regurgitation, weight loss and high risk of aspiration pneumonia, a frequent cause of mortality in severe forms of DM.

2.3 Definitive Diagnosis: A Multimodal Strategy

The diagnosis of DM is never based on a single test, but on the convergence of several elements, after excluding common differential diagnoses such as demodicosis, bacterial pyoderma, dermatophytosis and discoid lupus erythematosus.

• Histopathology (Cornerstone): Biopsy is the key examination to confirm the ischemic nature of the lesions.

• • Cutaneous Biopsy: Taken from a recent and active lesion, it reveals characteristic changes of ischemic dermatopathy: pauci-cellular interface dermatitis (with few inflammatory cells), hair follicle atrophy, vacuolization of basal layer keratinocytes, presence of apoptotic cells (Civatte bodies), and fibrosis or mucin accumulation in the dermis. Vascular changes may be subtle, manifesting as a “blurred” and eosinophilic appearance of perivascular collagen (“smudged collagen”) rather than obvious necrotizing vasculitis.
  • Muscle Biopsy: Although less systematically performed in routine practice, it is indicated in cases of suspected myopathic involvement. It typically shows interstitial and perivascular myositis, predominantly lymphocytic, plasmacytic and histiocytic, associated with signs of muscle fiber suffering (degeneration, necrosis, regeneration and atrophy).

• Electrodiagnostic (EMG): Electromyography is a very sensitive tool for detecting myopathy, even in the absence of obvious clinical signs. The examination, performed under anesthesia, reveals abnormal spontaneous electrical activities in affected muscles, such as fibrillation potentials, positive sharp waves, and bizarre or myotonic high-frequency discharges.
• Genetic Tests: For Collies, Shetland Sheepdogs and their crosses, testing the three risk loci (PAN2, MAP3K7CL, DLA) has become an essential diagnostic and prognostic tool. It allows confirmation of genetic predisposition and risk stratification of the animal (low, moderate or high), which helps guide owner counseling.
• Clinical Biochemistry: Serum creatine kinase (CK) measurement is useful. Marked elevation is an indicator of active myositis and muscle damage. However, a normal CK value does not exclude diagnosis, as muscular involvement may be minimal, focal or chronic with little active inflammation.

Table 3: Diagnostic Modalities for Canine Dermatomyositis

Diagnostic Modality	Expected Results / Key Abnormalities
Cutaneous Histopathology	Pauci-cellular interface dermatitis, follicular atrophy, basal vacuolization, Civatte bodies, dermal fibrosis/mucinosis, “smudged collagen”
Muscle Histopathology	Interstitial and perivascular myositis (lympho-plasmacytic), muscle fiber degeneration/regeneration/atrophy
Electromyography (EMG)	Abnormal spontaneous activity: fibrillation potentials, positive sharp waves, high-frequency myotonic/bizarre discharges
Genetic Test (3 loci)	Identification of risk alleles at PAN2, MAP3K7CL and DLA loci; calculation of risk score (Low, Moderate, High)
Biochemistry (Creatine Kinase)	Elevation (often marked) in active myositis, but may be normal in chronic forms or with minimal muscular involvement

Therapeutic Strategies and Management in 2025

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Prognosis and Long-Term Evolution

The prognosis of canine DM is highly variable and depends on multiple factors. Understanding these indicators and the evolutionary profiles of the disease is essential for providing owners with realistic expectations and for adapting long-term management.

4.1 Prognostic Indicators: Predicting the Future

Several factors allow estimation of the probable evolution of the disease in a given dog.

• Clinical Factors:

• • Disease Severity: This is the most direct prognostic factor. Mild cases, with only a few non-ulcerated cutaneous lesions, have an excellent prognosis and may even enter spontaneous remission without sequelae. Moderate cases have a good prognosis for control, but often with residual cicatricial alopecia. Severe cases, with extensive ulcerations and/or significant muscular involvement, have a guarded to poor prognosis.
  • Muscular and Esophageal Involvement: The presence of clinically significant myopathy, and particularly the development of megaesophagus, considerably darkens the prognosis. The risk of malnutrition, aspiration and aspiration pneumonia becomes a major life threat.

• Demographic Factors: A retrospective study of 177 cases of ischemic dermatopathy (excluding classic familial DM) identified two factors associated with poorer evolution: body weight less than 10 kg and older age at time of biopsy.
• Genetic Factor: Integration of genetic risk profile (based on the 3 loci) into prognostic assessment represents a major advance. This test allows a shift from reactive prognosis, based on clinical signs already present, to proactive and predictive prognosis. A Collie or Shetland puppy tested at birth and revealing a high-risk genotype (e.g., AABBCC) has an intrinsically more guarded prognosis, even before the appearance of any clinical sign. It is predicted to develop the disease earlier and potentially in a more severe form. This information allows early patient stratification and implementation of enhanced surveillance and aggressive therapeutic intervention strategy from the first signs, which could improve long-term outcomes.

4.2 Disease Evolution and Long-Term Management

By analogy with human JDM, canine DM can follow different evolutionary patterns over time.

• Evolutionary Profiles:

• • Monocyclic: The disease manifests as a single episode, often in slightly affected animals, which enters complete remission (sometimes spontaneously) and does not recur. The prognosis is excellent.
  • Polycyclic: The disease evolves in flares, with remission periods interspersed with relapses. These flares are often initiated by triggering factors (UV exposure, trauma, estrus). Management aims to control flares and prolong remission periods.
  • Chronic-continuous: The disease remains persistently active, without complete remission periods. These cases require lifelong treatment and are associated with the most guarded prognosis.

• Chronic Management: Management of chronic forms (polycyclic or continuous) is challenging. The goal is to keep the disease under control with the minimum effective dose of medications to limit cumulative side effects. Use of steroid-sparing agents (such as cyclosporine) and, increasingly, targeted therapies such as JAK inhibitors, is at the heart of this strategy. Regular clinical and biological monitoring is essential to adjust treatment and monitor for complications, including potentially increased risk of kidney disease in dogs suffering from long-term chronic inflammation.

Conclusion

In 2025, canine dermatomyositis has evolved from the status of an enigmatic hereditary disease to that of a complex genetic disorder whose molecular mechanisms are increasingly well understood. Recognition of its etiopathogenesis, centered on an ischemic vasculopathy driven by dysregulation of the type I interferon pathway and underpinned by specific genetic interactions, has transformed its clinical approach.

This paradigm shift has profound and concrete implications. Diagnosis has evolved to integrate genetic tests as an essential pillar alongside histopathology and electromyography, enabling early risk stratification and more precise prognosis. Therapeutically, the arsenal has been enriched, moving from broad-spectrum immunosuppressors, effective but burdened with side effects, to targeted therapies that specifically block identified pathogenic pathways. The use of Janus Kinase inhibitors, in particular, represents the new frontier of treatment, offering hope for more effective and safer disease control.

Future research perspectives are clear. They must focus on identifying risk loci in other canine breeds, large-scale validation of the efficacy and long-term safety of targeted therapies through randomized clinical trials, and development of blood biomarkers (such as IFN signature) for non-invasive monitoring of disease activity and increased treatment personalization. The canine dermatomyositis model, through its relevance and complexity, will continue to be an invaluable resource for advancing understanding and treatment of this debilitating disease, both for the welfare of dogs and for the knowledge it brings to human medicine.

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