Fibrotic myopathy and contracture of the caudal thigh musculature: a prospective study of 41 dogs (2019–2022)

Sarah A. Wilson Comparative Genetics and Orthopaedic Research Laboratory, Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI

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Emily E. Binversie Comparative Genetics and Orthopaedic Research Laboratory, Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI

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Nyah Kohler Comparative Genetics and Orthopaedic Research Laboratory, Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI

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Margaret M. Patterson Comparative Genetics and Orthopaedic Research Laboratory, Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI

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Susannah J. Sample Comparative Genetics and Orthopaedic Research Laboratory, Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI

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Peter Muir Comparative Genetics and Orthopaedic Research Laboratory, Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI

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Abstract

OBJECTIVE

To determine the presentation, diagnosis, progression, and family risk of fibrotic myopathy, a disease with marked breed predisposition in the German Shepherd Dog (GSD).

ANIMALS

41 dogs prospectively recruited to the University of Wisconsin-Madison Comparative Genetics and Orthopedic Laboratory between November 2019 to August 2022.

METHODS

Medical records of dogs diagnosed with fibrotic myopathy were reviewed upon referral. The following data were recorded: sex, age, weight, regio interscapularis (withers) height, date of neutering, coat color and length, and age at fibrotic myopathy diagnosis. A pedigree was also obtained.

RESULTS

In the study population, breeds included 37 GSDs, a Belgian Malinois, a Belgian Malinois cross, and 2 dogs with a GSD phenotype and no pedigree. Mean age at fibrotic myopathy diagnosis was 5.9 ± 2.0 years, and duration of lameness before diagnosis was 5.6 months and ranged from 0.75 to 18 months. Males were overrepresented at 61% of the study population. Inherited familial risk for fibrotic myopathy in the GSD was supported by pedigree analysis.

CLINICAL RELEVANCE

This was the largest case series of fibrotic myopathy to date, providing a more comprehensive look at presentation and progression of the disease. The longer duration of lameness in bilaterally affected dogs likely represents disease progression rather than a more severe phenotype. Family history data support a genetic contribution to fibrotic myopathy, suggesting that further genetic investigation is warranted.

Abstract

OBJECTIVE

To determine the presentation, diagnosis, progression, and family risk of fibrotic myopathy, a disease with marked breed predisposition in the German Shepherd Dog (GSD).

ANIMALS

41 dogs prospectively recruited to the University of Wisconsin-Madison Comparative Genetics and Orthopedic Laboratory between November 2019 to August 2022.

METHODS

Medical records of dogs diagnosed with fibrotic myopathy were reviewed upon referral. The following data were recorded: sex, age, weight, regio interscapularis (withers) height, date of neutering, coat color and length, and age at fibrotic myopathy diagnosis. A pedigree was also obtained.

RESULTS

In the study population, breeds included 37 GSDs, a Belgian Malinois, a Belgian Malinois cross, and 2 dogs with a GSD phenotype and no pedigree. Mean age at fibrotic myopathy diagnosis was 5.9 ± 2.0 years, and duration of lameness before diagnosis was 5.6 months and ranged from 0.75 to 18 months. Males were overrepresented at 61% of the study population. Inherited familial risk for fibrotic myopathy in the GSD was supported by pedigree analysis.

CLINICAL RELEVANCE

This was the largest case series of fibrotic myopathy to date, providing a more comprehensive look at presentation and progression of the disease. The longer duration of lameness in bilaterally affected dogs likely represents disease progression rather than a more severe phenotype. Family history data support a genetic contribution to fibrotic myopathy, suggesting that further genetic investigation is warranted.

Introduction

Fibrotic myopathy is a disease process in which normal muscle is replaced with fibrous tissue. This process is well described in humans and horses.1 It is known to affect the infraspinatus, supraspinatus, iliopsoas, sartorius, gracilis, and semitendinosus muscles in dogs.2,3 The fibrotic transformation has historically been considered a consequence of muscle strain injury.4 Fibrotic myopathy is a rare condition in dogs that affects the gracilis and semitendinosus muscles. The condition has a strong breed predilection and principally affects the German Shepherd Dog (GSD), particularly younger male dogs in the age range of 2 to 7 years.4 Fibrotic myopathy has also been reported in Doberman Pinschers, Saint Bernards,5 and an Old English Sheepdog.6

Diagnosis of fibrotic myopathy can be made via palpation of the affected muscle bellies as well as observation of a characteristic gait.4,5 In the affected pelvic limb, there is a short stride with a rapid, elastic medial rotation of the paw, external rotation of the hock, and internal rotation of the stifle during the mid- to late swing phase.5 Palpation of the affected muscle bellies reveals a firm, taut band of fibrous tissue extending from the midline of the pelvis at the medial aspect of the proximal thigh to the caudomedial stifle.2,5 In some dogs, palpation of the affected muscles may elicit a pain response.5,7 Pain in affected muscles may be related to stage of disease, with greater pain in the early phase of the disease. Fibrosis of affected muscle bellies typically progresses over time, leading to limited passive range of motion of pelvic limb abduction.4,5

Treatment options include conservative medical management with rest and nonsteroidal anti-inflammatory medication, surgical transection or resection of the fibrotic band, and mesenchymal stem cell injection into the affected muscles.7 Intensive rehabilitation and physical therapy have been recommended to try to slow the progression of contracture and combat pelvic limb muscle atrophy. Recurrence of lameness within 3 to 5 months of surgical treatment is typical.5 Subsequent surgical treatment has a shorter time to recurrence.5 Treatment with autologous adipose-derived stem cells injected into the lesion as well as IV subjectively reported long-term resolution in 4 of 11 dogs.7

Proposed etiologies for fibrotic myopathy include acute muscle trauma, chronic muscle microinjury, immune-mediated disease, drug reaction, infectious disease, neurogenic disturbance to muscle homeostasis, or vascular anomalies.5,7 Canine fibrotic myopathy shares some clinical features with congenital muscular torticollis (CMT) in humans including histopathologic findings of interstitial fibrosis.8 The etiology of CMT is not clearly understood, but there is evidence that CMT is a recessive Mendelian disease,9 with a recent study8 on gene expression concluding that CMT may be defined as a developmental disorder. The outcome of both fibrotic myopathy in dogs and CMT in humans is replacement of muscle tissue with dense fibrous tissue, leading to functional shortening of the affected muscle belly. One important difference between the 2 disease processes is prognosis; it is reported that 90% of patients with CMT are cured with stretching exercises without long-term musculoskeletal complications.8 Given the evolution and genetic architecture of dog breeds, substantial breed predisposition to a rare disease implies a genetic etiology.10 However, review of pedigree data information from 6 GSDs in a previous study2 yielded no evidence of a common ancestor within 4 generations.

To date, the largest published study5 on fibrotic myopathy consisted of 18 dogs. Other occasional reports of fibrotic myopathy range from 1 to 13 dogs over the course of 43 years for a total of 56 dogs.1,4,5 The purpose of this prospective study was to evaluate the clinical presentation and family history of fibrotic myopathy more comprehensively in a large series of dogs recruited to a genetic discovery study.

Methods

Case selection

Patients were prospectively recruited at the University of Wisconsin-Madison School of Veterinary Medicine Comparative Genetics and Orthopedic Research Laboratory between November 2019 and August 2022. Dogs were recruited through the UW Veterinary Hospital and in-person consultation or through referral and subsequent virtual consultation. Dogs were included in the study if a diagnosis of fibrotic myopathy was made on the basis of physical and gait examinations and clinical findings were available from the medical record and patient videos. The presence of the pathognomonic gait and a palpable fibrous band in the caudomedial thigh musculature were criteria for diagnosis of fibrotic myopathy.

Medical records review

Medical records were obtained from all dogs enrolled. The following data were recorded for each dog as appropriate: date of birth, date of death, neuter status and date of ovariohysterectomy/castration, American Kennel Club number, coat color and length, age at fibrotic myopathy diagnosis, weight, regio interscapularis (withers) height, and any comorbidities.

General physical exam findings were evaluated and any relevant data recorded. If available, radiographs and radiograph reports were reviewed to rule out other orthopedic disease. Orthopedic exam findings were evaluated for pathognomonic gait changes and presence of a fibrotic band in the caudal thigh musculature. Cases were classified as bilateral or unilateral, and, if unilateral, the affected leg was recorded. If the dog received treatment for fibrotic myopathy, the treatment and clinical response to treatment were determined. This included surgical as well as medical management.

Gait analysis

Gait analysis was performed in person at UW Veterinary Care for local dogs and via video evaluation for distant patients. Gait was assessed for functional lameness of the pelvic limbs, characterized by medial rotation of the paw, external rotation of the hock, and internal rotation of the stifle.5 This characteristic gait change (Supplementary Video S1) in combination with palpation of a fibrotic band in the caudal thigh musculature is diagnostic for fibrotic myopathy.

Pedigree analysis

Complete 4- to 7-generation pedigree information was obtained for each dog. A master pedigree map was compiled using Illustrator (version 25.2.1; Adobe Inc.) to study repeated use of popular dams/sires and the family relationship between individual dogs. A total of 1,195 dogs were included in the master pedigree. The pedigree was evaluated for relationships between affected dogs to gain insight into mode of inheritance, particularly patterns that could reflect a recessive versus dominant mode of inheritance. Videos and medical records were reviewed for control siblings as for cases when available. When unavailable, phenotype-negative littermates were designated on the basis of owner/breeder reports. The pedigree key indicated which dogs were identified by medical records/veterinary examination versus owner/breeder reports.

Statistical analysis

Descriptive data were generated for the dogs diagnosed with fibrotic myopathy. Results are reported as the mean ± SD for data that approximate a normal distribution and median (range) for data that do not approximate a normal distribution. Clinical variables in the unilateral group were compared to the bilaterally affected group using the Student t test, the Mann-Whitney test or the Fisher Exact test as appropriate. Results were considered significant at P < .05.

Results

Study population

Of the 41 dogs, 37 were purebred GSDs confirmed by pedigree data. Pedigree data were not available for the remaining 2 dogs with a GSD phenotype. There was 1 Belgian Malinois confirmed by pedigree data and 1 Belgian Malinois cross. In the GSD population, there were 27 dogs with a German working dog genetic background, 4 dogs with an American or German show dog genetic background, 1 GSD with a mixed working/show genetic background, and 7 GSDs whose genetic background was not known. Three dogs were working police dogs, and 4 dogs were actively participating in Shutzhund, search and rescue, or Mondoring before being diagnosed with fibrotic myopathy. Of the 39 GSDs, 18 had a black and tan coat color, 10 had black and red, 7 were sable, 3 were black, and 1 was white. There were 3 long-haired GSDs and 36 with medium-length/stock fur.

Of the 41 dogs, 10 were sexually intact males, 15 were castrated males, 2 were sexually intact females, and 14 were ovariohysterectomized females. The mean age at diagnosis was 5.9 ± 2.0 years and ranged from 2.0 to 11.7 years. Subject weight was 35.7 ± 6.55 kg, and withers height was 63.3 ± 4.1 cm. Mean duration of reported lameness before diagnosis of fibrotic myopathy was 5.4 ± 5.2 months. There were no significant differences in clinical variables between the dogs affected unilaterally and dogs affected bilaterally (Table 1). Duration of lameness was longer in the bilaterally affected dogs than in the unilaterally affected dogs.

Table 1

Comparison of population data for 41 dogs with fibrotic myopathy diagnosed unilaterally (n = 20) versus bilaterally (21) between November 2019 and August 2022.

Variable Unilateral Bilateral P value
Age at diagnosis (y) 5.73 ± 2.2 6.1 ± 1.9 .54
Weight (kg) 36.11 ± 7.9 35.38 ± 4.7 .71
No. of sexually intact males 4 6 .72
No. of castrated males 8 7 .75
No. of sexually intact females 1 1 1.00
No. of spayed females 7 7 1.00
Duration of lameness (mo) 3.9 (0.75, 12) 7.38 (1, 18) .082

Continuous variables are presented as mean ± SD or median (range) as appropriate. There were 25 males and 16 females.

Comorbidities identified by medical record review were common in the population. These included allergic skin disease (n = 4), lumbosacral disease (3), hip dysplasia (3), intervertebral disc disease (2), hypothyroidism (2), urinary tract infection with pyelonephritis (1), ear disease (1), spinal osteoarthritis (1), gastroenteritis (1), benign prostatic hyperplasia (1), immune-mediated polyarthritis (1), medial shoulder instability (1), elbow dysplasia (1), and tetanus (1).

Gait analysis

All 41 dogs were confirmed to have the characteristic abnormal pelvic limb gait with medial rotation of the paw, external rotation of the hock, and internal rotation of the stifle (Supplementary Video S1), either unilaterally (n = 20) or bilaterally (21).

Management

Overall, 14 of the 41 dogs received some form of therapeutic treatment. No specific treatment was reported in the remaining 27 dogs.

Medical treatment—In the study group, 11 of the 41 dogs underwent physical rehabilitation as the sole treatment by a canine rehabilitation specialist. Treatments included chiropractic manipulation, acupuncture, cold laser therapy, therapeutic ultrasound, active/passive range of motion, underwater treadmill, vibration plate, and cast stretching. Medical treatment included carprofen (n = 2), meloxicam (1), losartan (1), methocarbamol (1), gabapentin (1), and vitamin E and vitamin C (1). No treatment effectively resolved the fibrosis or functional lameness.

Surgical or biological therapy—A left-sided gracilis tenotomy, partial tenomyectomy and a semitendinosus tenotomy was performed in 1 dog. Initial improvement was reported 3 weeks after surgery. The lameness subsequently recurred, and the dog was euthanatized 6 months after surgery. Intensive physical therapy was performed in another dog, followed by adipose-derived stromal vascular fraction injections intralesionally as well as IV. After an unsatisfactory response to the injections, a left gracilis myectomy was performed with continued intensive rehabilitation therapy after the myectomy surgery. The dog was also treated with losartan, methocarbamol, and carprofen. The lameness of the dog improved after this treatment but did not return to normal. Lameness remained static after the treatment, based on owner reports and serial range of motion performed by a rehabilitation specialist. An injection of platelet-rich plasma into the affected right semitendinosus was performed in another dog, but outcome could not be determined from the medical record.

One dog had 3 rounds of IM injections into the diseased muscle. Initially, a homeopathic mixture containing 11 ingredients called Spascupreel, combined with polysulfated glycosaminoglycan (Adequan), and triamcinolone were injected into the left gracilis. A homeopathic mixture of 14 ingredients called Traumeel and Spascupreel were subsequently injected into both gracilis muscles 2 months later, and this treatment was then repeated 5 days later. This dog was transiently improved after the first injection; however, the lameness recurred without improvement from subsequent injections.

Pedigree

Review of the overall pedigree of 1,195 dogs identified 2 families in which a dog affected with fibrotic myopathy was used for breeding. These families within the overall pedigree were studied in detail. In the first family, breeding of an affected female produced a male case and a female case 2 generations later (Figure 1). The dam of the affected female was a phenotype-negative control. In the second family, breeding of an affected male produced a male case and a female case as progeny. Further breeding of the female progeny produced a male case as progeny as well as 8 littermates that were phenotype-negative controls.

Figure 1
Figure 1
Figure 1

Pedigrees describing use of an affected German Shepherd Dog for breeding and the associated progeny fibrotic myopathy phenotypes. Squares = male; circle = female; red filled = fibrotic myopathy case; green filled = fibrotic myopathy phenotype–negative control; and unfilled = unknown fibrotic myopathy status. Solid line around shape = status determined by medical records or veterinary examination, dashed line around shape = status based on owner/breeder reports. A—Five-generation pedigree of affected family with 2 fibrotic myopathy cases included in the present study. Breeding of an affected female produced a male case and a female case 2 generations later. The dam of this dog was a control dog. B—Four-generation pedigree of an affected family with 1 fibrotic myopathy case included in the present study. Breeding of an affected male produced a male case and a female case as progeny. Further breeding of the female progeny produced a male case as progeny as well as 8 phenotypically negative littermates.

Citation: Journal of the American Veterinary Medical Association 261, 11; 10.2460/javma.23.04.0183

Additionally, 2 families were identified in which the unaffected dam and sire produced progeny that were affected with fibrotic myopathy. In 1 family, a litter of 4 puppies included 1 case (Figure 2). In a second family, a litter of 3 puppies included 1 case and 2 phenotype-negative dogs. In this second family, the 2 sibling littermates of the dam were also phenotype negative controls.

Figure 2
Figure 2
Figure 2

Pedigrees describing the scenario in which breeding 2 phenotypically normal German Shepherd Dogs yielded progeny affected with fibrotic myopathy. Squares = male; circle = female; red filled = fibrotic myopathy case; green filled = fibrotic myopathy phenotype–negative control; yellow filled = currently phenotype negative, too young to be considered a control; and unfilled = unknown fibrotic myopathy status. Solid line around shape = status determined by medical records or veterinary examination, dashed line around shape = status based on owner/breeder reports. A—Three-generation pedigree in which 2 unaffected parents produced 1 affected offspring and 3 unaffected offspring. B—Three-generation pedigree in which 2 unaffected parents produced 3 offspring: 1 affected puppy and 2 unaffected puppies. Both pedigrees support the hypothesis of a recessive Mendelian mode of inheritance.

Citation: Journal of the American Veterinary Medical Association 261, 11; 10.2460/javma.23.04.0183

Discussion

Fibrotic myopathy is a rare disease with marked predisposition in the GSD.4 In the present study, 41 dogs with a diagnosis of fibrotic myopathy were prospectively evaluated to characterize the clinical features of fibrotic myopathy more fully. This large sample size enabled assembly of a comprehensive pedigree map of the 1,195 dogs to further investigate familial risk. All the affected dogs were GSDs and dogs with a GSD phenotype or the closely related Belgian Malinois breed or were a Belgian Malinois cross.

Fibrotic myopathy most often affects the gracilis or semitendinosus muscles. However, case reports have also described fibrotic myopathy of the tensor fascia lata in a Whippet11; the infraspinatus contracture in a German Pointer, a GSD, and a Belgian Shepherd12,13; and the iliopsoas in a Pointing Griffon,3 a GSD,14 and an English Pointer associated with a migrating foreign body.15 The gracilis is a muscle with a unique innervation pattern that has neuromuscular compartments.16 A study17 of rat gracilis muscle demonstrated 2 motor end plates within the muscle belly and that these end plates mark the central portions of 2 relays of muscle fibers. Further investigation is warranted to determine the significance of this unique innervation as it pertains to fibrotic myopathy of the gracilis. When compared to 6 other dog breeds, GSDs were found to have the highest ratio of gastrocnemius to quadriceps muscle width and the lowest ratio of quadriceps to hamstrings.18 GSDs were also found to have the most angular pelvic limbs18 and a decreased range of motion in their stifle joint when compared to Labrador Retrievers.2 The dominance of the caudal thigh musculature and their angulated posture in dogs with a GSD-type confirmation may be a specific risk factor contributing to disease pathogenesis for fibrotic myopathy. When considering fibrotic myopathy as a recessive Mendelian disease or a dominant one with incomplete penetrance, a dog with 1 or 2 copies of the mutation may have alterations to muscle homeostasis leading to disease development. As muscle microtrauma builds up in these often very active dogs, there is an inappropriate healing response. The gracilis muscle may be particularly susceptible due to its unique innervation and compartmentalization, and the caudal thigh muscles in the GSD could be at highest risk because their pelvic limb musculature is dominated by the caudal muscle bellies.

Mean age of diagnosis was 5.9 years, like the previously reported age at diagnosis of 5 years old.5 Earlier studies report a higher incidence in males than females,1,4,5 a finding corroborated in the present study in which 61% of the cases were males. Bilaterally affected dogs were compared to unilaterally affected dogs to explore the possibility of fibrotic myopathy being a progressive disease. There was no significant difference between any of the variables studied. Although not a significant result, the duration of lameness in the bilaterally affected dogs was 89% longer than in the unilaterally affected dogs. Most bilaterally affected dogs were initially diagnosed as unilateral cases and later found to be bilaterally affected at subsequent evaluation. These observations suggest that the condition is progressive over time rather than the possibility that bilaterally affected dogs represent a more severe clinical expression of the disease. Comorbidities were common in the dogs of this report. The most frequently occurring comorbidity was spinal pathology, such as lumbosacral disease, intervertebral disc disease, and spinal osteoarthritis, which could contribute to an abnormal pelvic limb gait. Gait evaluation and clinical examination of the dogs of this report confirmed the pathognomonic gait in all 41 dogs, which was associated with varying degrees of palpable fibrotic tissue in the caudal thigh musculature.

In 34% of cases, specific medical or surgical treatment was provided. Management was variable in terms of invasiveness and length of treatment and included surgical myectomy in 2 dogs. Overall, outcomes were like those of previous reports.4,5 In both dogs treated with surgery, lameness returned or persisted after treatment. No treatment provided long-term resolution of the abnormal gait or resolved the muscle fibrosis. Clinical outcomes in the dogs of this report suggest that intensive physical rehabilitation may help to maintain range of motion in the affected limb and slow disease progression. For many of the study dogs, only palliative medical treatment was provided and the owners of affected dogs were given a poor prognosis regarding the resolution of the gait abnormality.

There is a lack of consensus on the etiology of fibrotic myopathy. Rupture of the gracilis muscle is a common major muscle injury among racing Greyhounds.19 However, there are no reports to date of this severe injury to the muscle resulting in fibrotic myopathy in racing Greyhounds. Within the population of GSDs, fibrotic myopathy has historically been associated with working dogs.7 In the present study, a German working dog genetic background was commonly identified in affected dogs. The high impact activity and subsequent muscle microtrauma from athletic activity may contribute to the pathogenesis of fibrotic myopathy and merits further investigation of the muscle pathology in case and control dogs.

Given the genetic architecture of dog breeds as isolated ancestral populations,20 marked breed predisposition and breed subpopulation predisposition suggest a genetic basis for fibrotic myopathy. However, a previous study2 did not support this hypothesis, given the lack of a common ancestor across 4 generations in 6 dogs. Detailed analysis of the pedigrees of the dogs of this report identified 4 families in which an affected dog was used for breeding or an affected dog was the progeny of unaffected parents. The observation that breeding an affected dog produces progeny that are affected with many littermates that are unaffected could represent a recessive mode of inheritance or a dominant one with incomplete penetrance as an explanation for the disease. This hypothesis is further supported by the observation that affected dogs can be the progeny of an unaffected sire and dam, making a dominant mode of inheritance much less likely unless there is incomplete penetrance. While our data suggest familial risk, the mode of inheritance is yet to be determined. Fibrotic myopathy could have a Mendelian or polygenic mode of inheritance. Further discovery work that confirms the genetic basis of this disease could be very impactful, as it would enable development of a genetic screening test that could identify heterozygote carriers of the fibrotic myopathy mutation if a Mendelian mode of inheritance was confirmed or enable polygenic risk score testing for disease risk.

There were several limitations to this study. Not all of the dogs were examined at the University of Wisconsin-Madison. Based on medical records, it was not possible to determine whether the gracilis, semitendinosus, or both were affected. More detailed physical or ultrasound examination of these cases could have provided additional information of the pattern of muscle fibrosis in these cases and which muscle bellies were affected. The rarity of the disease makes statistical analysis of the model of inheritance difficult to accomplish, as it often relies on owner/breeder contact and cooperation.

In conclusion, this report describes the largest prospective case series of dogs diagnosed with fibrotic myopathy to date. Our findings confirm a predisposition to males and strong breed predisposition in the GSD, particularly those dogs with a German working genetic background. As the disease progresses, unilaterally affected dogs commonly become bilaterally affected. Review of the pedigree data provides evidence supporting the hypothesis of an inherited disease with a recessive component. Further research is needed to determine the mode of inheritance. Further discovery research is needed to characterize the genetic contribution to this disease and rule out other modes of inheritance, including polygenic and dominant with incomplete penetrance or variable expressivity. High-impact athletic activity with associated muscle microtrauma may also have a role in disease pathogenesis.

Supplementary Materials

Supplementary materials are posted online at the journal website: avmajournals.avma.org

Acknowledgments

The authors have nothing to declare.

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