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Home / Equine Research Bank / Equine Vet J / Systemic calcinosis in horses: Pathological and genetic aspe...
Equine veterinary journal2025; doi: 10.1111/evj.14464

Systemic calcinosis in horses: Pathological and genetic aspects.

Abstract: In horses, systemic calcinosis is a rare syndrome characterised by muscle lesion associated with the mineralisation of large muscle groups or other organs, in the absence of an alternative cause for the calcification, such as toxic, enzootic or metabolic. Molecular and histopathological aspects of the disease are still poorly elucidated. Objective: To describe the epidemiological, pathological and molecular aspects of systemic calcinosis in a convenience sample of six horses submitted to necropsy in the Southern and Midwestern regions of Brazil. Methods: Retrospective exploratory study. Methods: Post-mortem necropsy records of six horses with a cause of death compatible with systemic calcinosis, were reviewed followed by histopathology, immunohistochemistry, microbiology and molecular investigation. Results: The affected horses were all Quarter Horses with a mean age of 16.8 months, and an average disease course of 15.5 days. Muscle necrosis and mononuclear infiltration were observed in all animals in association with mineral deposition variably affecting the muscle tissue and/or other organs such as heart, lung and kidney. All tested animals (5/6) showed positive PCR results for the E321G MYH1 gene variant, which encodes the heavy chain of fast-contracting skeletal muscle myosin and is associated with myopathy. Three horses demonstrated positive immunostaining for Streptococcus equi, which is a known trigger for immune responses. Conclusions: The study was limited by the small sample size, molecular evaluation was not completed in one animal due to technical limitations, lack of pre-mortem evaluation of calcium metabolism and lack of accurate descriptions in the necropsy reports of involvement of each muscle individually. Conclusions: In horses, systemic calcinosis syndrome causes immune-mediated muscle lesions in association with calcification of organs and tissues, varying greatly among animals. The E321G MYH1 variant was present in all horses tested for the variant and could be involved in the pathophysiology of systemic calcinosis.
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Publication Date: 2025-01-06 PubMed ID: 39763093DOI: 10.1111/evj.14464Google Scholar: Lookup
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Summary

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This research investigates systemic calcinosis, a rare syndrome in horses characterized by muscle lesions and mineralization in organs, by examining the pathology of the disease and genetic aspects in six horses that underwent necropsy in Brazil. The study found that the E321G MYH1 gene variant was present in all tested animals and could potentially be implicated in the disease’s development.

Understanding Systemic Calcinosis in Horses

  • The research focuses on systemic calcinosis, a condition where muscle damage is accompanied by the calcification of large muscle groups or other vital organs like the heart, lungs, and kidneys.
  • This condition is rare in horses and occurs without any discernable explanation such as toxicity, epidemics, or metabolic disorders.
  • The researchers aimed to understand the pathological and molecular aspects of this disease.

Methodological Approach

  • This study involved retrospective exploration, where the records of six horses that had undergone necropsy were reviewed.
  • These horses, all Quarter Horses, were found to have died due to causes compatible with systemic calcinosis.
  • Their age averaged at about 16.8 months, and they exhibited the disease for roughly 15.5 days.
  • Post-mortem investigations involved histopathology, immunohistochemistry, microbiology, and molecular investigation methods.

Findings of The Study

  • The horses showed symptoms of muscle necrosis and mononuclear infiltration, together with variable mineral deposits in the muscle tissue or other organs.
  • Genetic testing indicated that all tested animals showed the presence of the E321G MYH1 gene variant. This gene is responsible for fast-contracting skeletal muscle myosin and its variation is associated with myopathy.
  • Besides, three horses showed immunostaining positive for Streptococcus equi, which is an organism known to trigger immune responses.

Limitations and Conclusions

  • However, the research was limited by a small sample size and because one test subject’s molecular evaluation could not be completed due to technical constraints.
  • Lack of pre-mortem evaluation of calcium metabolism and absence of detailed descriptions in necropsy reports also somewhat grouped the understanding of the syndrome.
  • Despite these limitations, the study concluded that systemic calcinosis in horses results in immune-mediated muscle lesions and calcification of tissues and organs. The MYH1 variant’s presence could have a significant role in the onset and progression of the disease.

Cite This Article

APA
Carvalho Serena G, Marchezan Piva M, Viezzer Bianchi M, Fernandes da Fonseca HC, Chitolina Pupin R, Martins Basso R, Secorun Borges A, Monteiro Nunes M, Driemeier D, Panziera W, Oliveira-Filho JP, Gomes DC, Pavarini SP. (2025). Systemic calcinosis in horses: Pathological and genetic aspects. Equine Vet J. https://doi.org/10.1111/evj.14464

Publication

Equine veterinary journal
ISSN: 2042-3306
NlmUniqueID: 0173320
Country: United States
Language: English

Researcher Affiliations

Carvalho Serena, Guilherme
  • Setor de Patologia Veterinária, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, RS, Brazil.
Marchezan Piva, Manoela
  • Setor de Patologia Veterinária, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, RS, Brazil.
Viezzer Bianchi, Matheus
  • Setor de Patologia Veterinária, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, RS, Brazil.
Fernandes da Fonseca, Helena Carolina
  • Laboratório de Anatomia Patológica-Faculdade de Medicina Veterinária e Zootecnia, Universidade Federal de Mato Grosso do Sul, Campo Grande, Mato Grosso do Sul, Brazil.
Chitolina Pupin, Rayane
  • Laboratório de Anatomia Patológica-Faculdade de Medicina Veterinária e Zootecnia, Universidade Federal de Mato Grosso do Sul, Campo Grande, Mato Grosso do Sul, Brazil.
Martins Basso, Roberta
  • Departamento de Ciências Clínicas Veterinárias, Laboratório de Biologia Molecular Universidade Estadual Paulista (Unesp), Faculdade de Medicina Veterinária e Ciência Animal, Botucatu, São Paulo, Brazil.
Secorun Borges, Alexandre
  • Departamento de Ciências Clínicas Veterinárias, Laboratório de Biologia Molecular Universidade Estadual Paulista (Unesp), Faculdade de Medicina Veterinária e Ciência Animal, Botucatu, São Paulo, Brazil.
Monteiro Nunes, Marcelo
  • EquineMed-Clínica Veterinária, Campo Grande, MS, Brazil.
Driemeier, David
  • Setor de Patologia Veterinária, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, RS, Brazil.
Panziera, Welden
  • Setor de Patologia Veterinária, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, RS, Brazil.
Oliveira-Filho, José Paes
  • Departamento de Ciências Clínicas Veterinárias, Laboratório de Biologia Molecular Universidade Estadual Paulista (Unesp), Faculdade de Medicina Veterinária e Ciência Animal, Botucatu, São Paulo, Brazil.
Gomes, Danilo Carloto
  • Laboratório de Anatomia Patológica-Faculdade de Medicina Veterinária e Zootecnia, Universidade Federal de Mato Grosso do Sul, Campo Grande, Mato Grosso do Sul, Brazil.
Pavarini, Saulo Petinatti
  • Setor de Patologia Veterinária, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, RS, Brazil.

Grant Funding

  • Universidade Estadual Paulista
  • Coordenau00e7u00e3o de Aperfeiu00e7oamento de Pessoal de Nu00edvel Superior
  • Universidade Federal do Rio Grande do Sul
  • Universidade Federal de Mato Grosso do Sul
  • Conselho Nacional de Desenvolvimento Cientu00edfico e Tecnolu00f3gico

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