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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 BVSc, PhD, DACVS, DECVS, FRCVS

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.

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