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Journal of veterinary internal medicine1999; 13(6); 534-539; doi: 10.1892/0891-6640(1999)013<0534:daeopf>2.3.co;2

Detection and effects on platelet function of anti-platelet antibody in mule foals with experimentally induced neonatal alloimmune thrombocytopenia.

Abstract: Horse mares carrying mule foals were immunized during the last trimester of pregnancy with whole acid-citrate-dextrose-anticoagulated donkey blood to experimentally induce neonatal alloimmune thrombocytopenia. Thrombocytopenia occurred in the neonatal mule foals born to immunized horse mares within 24 hours after ingestion of their dams' colostrum. Mule foals born to mares not immunized with donkey blood did not develop thrombocytopenia. These findings suggest that antibodies may have been directed against a donkey platelet antigen present in the mule foals but not present in their dams. The objectives of this study were to determine whether anti-platelet antibody could be detected in mule foals with experimentally induced neonatal alloimmune thrombocytopenia, to identify any platelet proteins recognized by serum antibody in these foals, and to determine if platelet function was altered by sera from these mule foals. An indirect enzyme-linked immunosorbent assay demonstrated significantly higher absorption at 1:200 of platelet-bindable immunoglobulin G in serum from thrombocytopenic mule foals, compared with nonthrombocytopenic mule foals. Sera from thrombocytopenic and nonthrombocytopenic mule foals produced similar binding patterns in western immunoblots with donkey platelet proteins separated on sodium dodecyl sulfate polyacrylamide gels. Maximal platelet aggregation and relative slope of aggregation in response to collagen were significantly inhibited after incubation with sera from thrombocytopenic mule foals. These results suggest that mule foals with induced alloimmune thrombocytopenia have serum antibodies that bind to platelets and may compete with collagen binding sites to impair platelet aggregation.
Publication Date: 1999-12-10 PubMed ID: 10587252DOI: 10.1892/0891-6640(1999)013<0534:daeopf>2.3.co;2Google Scholar: Lookup
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  • Journal Article

Summary

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The research article discusses an experimental study on mule foals to investigate the occurrence and effects of anti-platelet antibody in neonatal alloimmune thrombocytopenia (a condition called NAIT, which can cause low platelet levels and bleeding). It was conducted on pregnant horse mares carrying mule foals and induced by immunization with acid-citrate-dextrose-anticoagulated donkey blood. The findings suggest that antibodies, potentially against a donkey platelet antigen, may be causing the thrombocytopenia in mule foals.

Experiment Design

  • The researchers immunized horse mares carrying mule foals in their last trimester with whole acid-citrate-dextrose-anticoagulated donkey blood to experimentally induce neonatal alloimmune thrombocytopenia.

Results of the Study

  • Thrombocytopenia (low platelet count leading to bleeding) occurred in mule foals born to these immunized mares within 24 hours of drinking their mothers’ colostrum. Conversely, mule foals born to mares not immunized with donkey blood did not develop thrombocytopenia.
  • This indicated the possibility of antibodies being directed against a donkey platelet antigen present in the mule foals but not their mothers.

Objectives of the Study

  • The primary goals of this study were to determine if anti-platelet antibody can be detected in affected mule foals, to identify any platelet proteins recognized by serum antibody in these foals, and to ascertain if the platelet function was altered by sera from these mule foals.

Methodology

  • An indirect enzyme-linked immunosorbent assay demonstrated significantly higher absorption of platelet-bindable immunoglobulin G in serum from thrombocytopenic mule foals compared with foals that were not thrombocytopenic.
  • Sera from thrombocytopenic and nonthrombocytopenic mule foals produced similar binding patterns in western immunoblots with donkey platelet proteins separated on sodium dodecyl sulfate polyacrylamide gels.

Conclusions

  • Maximum platelet aggregation and the relative slope of aggregation in response to collagen were significantly inhibited after incubation with sera from thrombocytopenic mule foals.
  • The results suggest that mule foals with induced alloimmune thrombocytopenia have serum antibodies that bind to platelets. This binding may compete with collagen binding sites, ultimately impairing platelet aggregation.

Cite This Article

APA
Ramirez S, Gaunt SD, McClure JJ, Oliver J. (1999). Detection and effects on platelet function of anti-platelet antibody in mule foals with experimentally induced neonatal alloimmune thrombocytopenia. J Vet Intern Med, 13(6), 534-539. https://doi.org/10.1892/0891-6640(1999)013<0534:daeopf>2.3.co;2

Publication

ISSN: 0891-6640
NlmUniqueID: 8708660
Country: United States
Language: English
Volume: 13
Issue: 6
Pages: 534-539

Researcher Affiliations

Ramirez, S
  • Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, USA. santos_ramirez@ncsu.edu
Gaunt, S D
    McClure, J J
      Oliver, J

        MeSH Terms

        • Animals
        • Antibodies / immunology
        • Antigens, Human Platelet / immunology
        • Autoimmune Diseases / congenital
        • Autoimmune Diseases / immunology
        • Autoimmune Diseases / veterinary
        • Binding, Competitive
        • Blood Platelets / immunology
        • Blood Platelets / physiology
        • Collagen
        • Equidae
        • Female
        • Horse Diseases / congenital
        • Horse Diseases / immunology
        • Horses
        • Immunization / veterinary
        • Maternal-Fetal Exchange
        • Platelet Aggregation
        • Pregnancy
        • Thrombocytopenia / congenital
        • Thrombocytopenia / immunology
        • Thrombocytopenia / veterinary

        Citations

        This article has been cited 1 times.
        1. Mendoza FJ, Toribio RE. An Overview of Donkey Neonatology. Animals (Basel) 2025 Jul 6;15(13).
          doi: 10.3390/ani15131986pubmed: 40646885google scholar: lookup