FREE SHIPPING over $40
OVER 10000 FIVE-STAR REVIEWS
5% OFF ALL SUBSCRIPTIONS
100% HAPPINESS GUARANTEE
Analyze Diet
0
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.
© 2025 EVJ Ltd.
Get Full Text
Publication Date: 2025-01-06 PubMed ID: 39763093DOI: 10.1111/evj.14464Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
LinkedInCopy
  • Journal Article

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

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

References

This article includes 26 references
  1. Finno CJ, Gianino G, Perumbakkam S, Williams ZJ, Bordbari MH, Gardner KL. A missense mutation in MYH1 is associated with susceptibility to immune‐mediated myositis in Quarter Horses.. Skelet Muscle 2018;8:7.
  2. Finno CJ, Spier SJ, Valberg SJ. Equine diseases caused by known genetic mutations.. Vet J 2009;179:336–347.
  3. Gianino GM, Valberg SJ, Perumbakkam S, Henry ML, Gardner K, Penedo C. Prevalence of the E321G MYH1 variant for immune‐mediated myositis and nonexertional rhabdomyolysis in performance subgroups of American Quarter Horses.. J Vet Intern Med 2019;33:897–901.
  4. Valberg SJ, Henry ML, Perumbakkam S, Gardner KL, Finno CJ. An E321G MYH1 mutation is strongly associated with nonexertional rhabdomyolysis in quarter horses.. J Vet Intern Med 2018;32:1718–1725.
  5. Durward‐Akhurst SA, Valberg SJ. Immune‐mediated muscle diseases of the horse.. Vet Pathol 2018;55:68–75.
  6. Valberg SJ. Genetics of equine muscle disease.. Vet Clin North Am Equine Pract 2020;36:353–378.
  7. Sponseller BT, Wong DM, Ruby R, Ware WA, Wilson S, Haynes JS. Systemic calcinosis in a quarter horse gelding homozygous for a myosin heavy chain 1 mutation.. J Vet Intern Med 2022;36:1543–1549.
  8. Lewis SS, Valberg SJ, Nielsen IL. Suspected immune‐mediated myositis in horses.. J Vet Intern Med 2007;21:495–503.
  9. Valberg SJ, Schultz AE, Finno CJ, Bellone RR, Hughes SS. Prevalence of clinical signs and factors impacting expression of myosin heavy chain myopathy in quarter horse‐related breeds with the MYH1E321G mutation.. J Vet Intern Med 2022;36:1152–1159.
  10. Tan J‐Y, Valberg SJ, Sebastian MM, Davis GD, Kelly JR, Goehring S. Suspected systemic calcinosis and calciphylaxis in 5 horses.. Can Vet J 2010;51:993–999.
  11. Veterinary microbiology and microbial disease. Chichester, West Sussex: Wiley‐Blackwell; 2011.
  12. Bianchi MV, Mello LS, Ribeiro PR, Wentz MF, Stolf AS, Lopes BC. Causes and pathology of equine pneumonia and Pleuritis in southern Brazil.. J Comp Pathol 2020;179:65–73.
  13. de Albuquerque AL, Zanzarini Delfiol DJ, Andrade DGA, Albertino LG, Sonne L, Borges AS. Prevalence of the E321G MYH1 variant in Brazilian quarter horses.. Equine Vet J 2022;54:952–957.
  14. Delfiol DJZ, de Oliveira‐Filho JP, Battazza A, de Souza CP, Badial PR, Araujo JP Jr. Prevalência da mutação causadora da paralisia periódica hipercalêmica em equinos da raça Quarto de Milha no Brasil.. Ciênc Rural 2015;45:854–857.
  15. Zanzarini Delfiol DJ, de Oliveira‐Filho JP, Badial PR, Battazza A, Araujo JP Jr, Borges AS. Estimation of the allele frequency of type 1 polysaccharide storage myopathy and malignant hyperthermia in quarter horses in Brazil.. J Equine Vet Sci 2018;70:38–41.
  16. Aleman M, Scalco R, Malvick J, Grahn RA, True A, Bellone RR. Prevalence of genetic mutations in horses with muscle disease from a neuromuscular disease laboratory.. J Equine Vet Sci 2022;118:104129.
  17. Zhang P, Cox CJ, Alvarez KM, Cunningham MW. Cutting edge: cardiac myosin activates innate immune responses through TLRs.. J Immunol 2009;183:27–31.
  18. Durward‐Akhurst SA, Finno CJ, Barnes N, Shivers J, Guo LT, Shelton GD. Major histocompatibility complex I and II expression and lymphocytic subtypes in muscle of horses with immune‐mediated myositis.. J Vet Intern Med 2016;30:1313–1321.
  19. Schott HC. Chronic renal failure in horses.. Vet Clin North Am Equine Pract 2007;23:593–612.
  20. Odriozola ER, Rodríguez AM, Micheloud JF, Cantón GJ, Caffarena RD, Gimeno EJ. Enzootic calcinosis in horses grazing Solanum glaucophyllum in Argentina.. J Vet Diagn Invest 2018;30:286–289.
  21. Lam J, Taekshita S, Barker JE, Kanagawa O, Ross FP, Teitelbaum SL. TNF‐α induces osteoclastogenesis by direct stimulation of macrophages exposed to permissive levels of RANK ligand.. J Clin Invest 2000;106:1481–1488.
  22. Howie AJ. Handbook of renal biopsy pathology.. Cham: Springer International Publishing; 2020.
    doi: 10.1007/978-3-030-40939-5google scholar: lookup
  23. Munday JS. Pathologic basis of veterinary disease, 6th Edition. Edited by James F. Zachary.. US Vet Dermatol 2017;28:258.
  24. Gaspar BL, Vasishta RK, Radotra BD. Myopathology: a practical clinico‐pathological approach to skeletal muscle biopsies.. Singapore: Springer Singapore; 2019.
    doi: 10.1007/978-981-13-1462-9google scholar: lookup
  25. Honda T, Ota H, Yamazaki Y, Yoshizawa A, Fujimoto K, Sone S. Proliferation of type II pneumocytes in the lung biopsy specimens reflecting alveolar damage.. Respir Med 2003;97:80–85.
  26. Kraler S, Blaser MC, Aikawa E, Camici GG, Lüscher TF. Calcific aortic valve disease: from molecular and cellular mechanisms to medical therapy.. Eur Heart J 2022;43:683–697.

Citations

This article has been cited 0 times.
Subscribe to our newsletter
Join 99,850 horse owners like you who receive our email updates on horse health and nutrition.