• Medientyp: E-Artikel
  • Titel: Rickets in a Thoroughbred-cross foal: case report and review of the literature
  • Beteiligte: Asin, Javier; Murphy, Brian G.; Samol, Monika A.; Polanco, Jose; Moore, Janet D.; Uzal, Francisco A.
  • Erschienen: SAGE Publications, 2021
  • Erschienen in: Journal of Veterinary Diagnostic Investigation, 33 (2021) 5, Seite 987-992
  • Sprache: Englisch
  • DOI: 10.1177/10406387211025232
  • ISSN: 1040-6387; 1943-4936
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  • Beschreibung: Rickets is a metabolic bone disease associated with failure of endochondral ossification and impaired osteoid mineralization in growing animals. As a consequence, affected individuals can develop gross and microscopic bone malformations. The most common causes of rickets in domestic species include vitamin D and phosphorus deficiency. Rickets has been described in multiple species; however, comprehensive postmortem characterizations with confirmatory histopathology in equids have not been published. A 6-mo-old, Thoroughbred-cross foal was diagnosed with rickets based on gross autopsy findings and microscopic examination of the ribs and long bones. Grossly, all costochondral junctions of the ribs were enlarged with a “rachitic rosary” appearance, and there were multiple fracture calluses in the rib bodies. Epiphyses and metaphyses of the long bones appeared widened on sagittal section, and their physes were irregularly thickened. Histologically, there were poorly organized columns of hypertrophic chondrocytes within the physes of affected bones, islands of chondrocytes embedded within the primary and secondary spongiosa, and faintly eosinophilic seams of poorly mineralized osteoid within the bone trabeculae. Areas of focally increased osteoclastic activity were observed in some of the sections, perhaps pointing to a more complex metabolic bone disease in a growing animal. Low serum concentrations of calcium and 25-hydroxyvitamin D were detected in an antemortem sample. The pathogenesis of these imbalances was not definitively established, but lack of sunlight exposure, low concentration of vitamin D precursors in the diet (perhaps secondary to malnutrition), or both, were suspected; a genetic basis cannot be ruled out.
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