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Veterinary pathology1975; 12(5-6); 405-414; doi: 10.1177/0300985875012005-00607

[Systemic cutaneous and subcutaneous amyloidosis in the horse].

Abstract: A 9-year-old horse had numerous firm, painless nodules of the skin and subcutis. Moderately vascular granulation tissue with numerous uni- or multinuclear reticuloendothelial cells was in the nodules and the regional lymph nodes but not in the viscera. By using special stains and electron microscopy, widespread amyloid deposits, mainly in the cytoplasm of reticuloendothelial cells, were identified. Amyloid was probably produced within the reticuloendothelial cells, then expelled from the dying cell and deposited in the intercellular space.
Publication Date: 1975-01-01 PubMed ID: 1229055DOI: 10.1177/0300985875012005-00607Google Scholar: Lookup
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  • English Abstract
  • Journal Article

Summary

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The research article discusses a case of an aged horse showing numerous firm, painless skin and subcutis nodules caused by systemic cutaneous and subcutaneous amyloidosis, and suggests amyloid was produced within the horse’s reticuloendothelial cells.

Introduction and Background

  • The study investigates a case of systemic cutaneous and subcutaneous amyloidosis, especially in a 9-year-old horse.
  • Amyloidosis is a general term for several different types of disease associated with an abnormal deposition of a specific protein, known as amyloid, in various tissues and organs throughout the body.
  • In the horse, the disease presented as numerous firm, painless skin and subcutis nodules. These are abnormal growths or lumps that were found to contain moderately vascular granulation tissue and many uni- or multinuclear reticuloendothelial cells.

Research Methodology and Findings

  • The researchers used special staining techniques and electron microscopy to investigate the nodules and surrounding tissue. With these techniques, they were able to identify widespread amyloid deposits mostly in the cytoplasm of reticuloendothelial cells – cells that play an important role in immune response.
  • These deposits were not found in the viscera, implying a localized rather than systemic distribution of the amyloid protein.
  • The researchers posit that the amyloid was likely produced within the reticuloendothelial cells. These cells were then believed to die off, releasing the newly-formed amyloid into the intercellular space where it was deposited.

Implications of the Research

  • This study provides valuable findings on the occurrence and development of systemic cutaneous and subcutaneous amyloidosis in horses. The identification of the disease’s prevalence in a specific cell type (reticuloendothelial cells) can contribute to a better understanding of the pathogenesis and potential disease management strategies.
  • However, the exact mechanism by which these reticuloendothelial cells produce and release the amyloid protein remains to be explored.

Cite This Article

APA
Stünzi H, Ehrensperger F, Wild P, Leemann W. (1975). [Systemic cutaneous and subcutaneous amyloidosis in the horse]. Vet Pathol, 12(5-6), 405-414. https://doi.org/10.1177/0300985875012005-00607

Publication

ISSN: 0300-9858
NlmUniqueID: 0312020
Country: United States
Language: ger
Volume: 12
Issue: 5-6
Pages: 405-414

Researcher Affiliations

Stünzi, H
    Ehrensperger, F
      Wild, P
        Leemann, W

          MeSH Terms

          • Amyloidosis / pathology
          • Amyloidosis / veterinary
          • Animals
          • Female
          • Horse Diseases / pathology
          • Horses
          • Lymph Nodes / pathology
          • Mononuclear Phagocyte System / ultrastructure
          • Respiratory Tract Diseases / pathology
          • Skin Diseases / pathology
          • Skin Diseases / veterinary

          Citations

          This article has been cited 2 times.
          1. Østevik L, Gunnes G, de Souza GA, Wien TN, Sørby R. Nasal and ocular amyloidosis in a 15-year-old horse. Acta Vet Scand 2014 Aug 27;56(1):50.
            doi: 10.1186/s13028-014-0050-6pubmed: 25159190google scholar: lookup
          2. Linke RP, Trautwein G. Immunoglobulin lambda-light-chain-derived amyloidosis (A lambda) in two horses. Blut 1989 Mar;58(3):129-32.
            doi: 10.1007/BF00320431pubmed: 2495038google scholar: lookup