Rickets in a Thoroughbred-cross foal: case report and review of the literature.
Abstract: 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.
Publication Date: 2021-06-23 PubMed ID: 34160312PubMed Central: PMC8366248DOI: 10.1177/10406387211025232Google 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.
- Case Reports
- Journal Article
- Review
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.
The article discusses a case of a six-month-old Thoroughbred-cross foal diagnosed with Rickets, a metabolic bone disease usually caused by deficiency in Vitamin D and phosphorus. The study highlights the characteristic abnormalities and gross features seen in affected animals, along with the altered levels of certain nutrients in the blood.
Understanding Rickets
- Rickets is a metabolic bone disease that hampers the normal process of bone development and mineralization in young animals. Failure of endochondral ossification, a process where cartilage is transformed into bone or bone-like tissue, is one of the significant issues with this disease. Also, the absence or reduced levels of certain critical nutrients, namely vitamin D and phosphorus, often cause Rickets.
Case Details of the Thoroughbred-cross foal
- A detailed postmortem examination of a six-month-old Thoroughbred-cross foal revealed numerous bone malformations, confirming the case of Rickets. The common features included enlargement of costochondral junctions of the ribs creating a “rachitic rosary” appearance, presence of multiple fracture calluses in the ribs, and noticeable widening of epiphyses and metaphyses of the long bones.
- Microscopic findings revealed a poorly organized structure of hypertrophic chondrocytes (specialized cells that produce and maintain cartilage) within the physes of affected bones, along with the presence of these cells embedded within the primary and secondary spongiosa – a soft, sponge-like part of the bone containing marrow and blood vessels.
- Traces of poorly mineralized osteoid bones were also detected. Some sections also showed increased osteoclastic activities – a process that breaks down bone tissues, indicating more complex metabolic imbalance in bones.
Probable Causes and Pathogenesis
- Antemortem examination of the foal revealed low levels of calcium and 25-hydroxyvitamin D in the blood, pointing towards deficiency of these essential constituents leading to the disease.
- The exact cause of these imbalances could not be determined accurately, but some possibilities highlighted include lack of sunlight exposure, lack of Vitamin D precursors in the diet due to malnutrition, or a combination of both. However, a genetic basis driving the onset of the disease was not ruled out.
Cite This Article
APA
Asin J, Murphy BG, Samol MA, Polanco J, Moore JD, Uzal FA.
(2021).
Rickets in a Thoroughbred-cross foal: case report and review of the literature.
J Vet Diagn Invest, 33(5), 987-992.
https://doi.org/10.1177/10406387211025232 Publication
Researcher Affiliations
- California Animal Health and Food Safety Laboratory System, San Bernardino branch, University of California-Davis, CA, USA.
- Department of Pathology, Microbiology & Immunology, University of California-Davis, CA, USA.
- Department of Pathology, Microbiology & Immunology, University of California-Davis, CA, USA.
- California Animal Health and Food Safety Laboratory System, San Bernardino branch, University of California-Davis, CA, USA.
- California Animal Health and Food Safety Laboratory System, San Bernardino branch, University of California-Davis, CA, USA.
- California Animal Health and Food Safety Laboratory System, San Bernardino branch, University of California-Davis, CA, USA.
- California Animal Health and Food Safety Laboratory System, San Bernardino branch, University of California-Davis, CA, USA.
- Department of Pathology, Microbiology & Immunology, University of California-Davis, CA, USA.
MeSH Terms
- Animals
- Bone and Bones
- Calcium
- Horse Diseases
- Horses
- Rickets / veterinary
Conflict of Interest Statement
Declaration of conflicting interests: The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
References
This article includes 25 references
- Azarpeykan S. Influence of blanketing and season on vitamin D and parathyroid hormone, calcium, phosphorus and magnesium concentrations in horses in New Zealand. Domest Anim Endocrinol 2016;56:75–84.
- Breidenbach A. Peculiarities of vitamin D and of the calcium and phosphate homeostatic system in horses. Vet Res 1998;29:173–186.
- Craig LE. Bones and joints. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. 6th ed. Vol. 1. Elsevier, 2016:16–163.
- Chavez LS. Molecular basis for pseudo vitamin D-deficiency rickets in the Hannover pig. J Nutr Biochem 2003;14:378–385.
- Dittmer KE. Skeletal deformities associated with nutritional congenital rickets in newborn lambs. N Z Vet J 2017;65:51–55.
- Dittmer KE, Thompson KG. Vitamin D metabolism and rickets in domestic animals: a review. Vet Pathol 2011;48:389–407.
- Dursun F. Genetic and clinical characteristics of patients with vitamin D dependent rickets type 1A. J Clin Res Pediatr Endocrinol 2019;11:34–40.
- El Shorafa WM. Effect of vitamin D and sunlight on growth and bone development of young ponies. J Anim Sci 1979;48:882–886.
- Geisen V. Vitamin D-dependent hereditary rickets type I in a cat. J Vet Intern Med 2009;23:196–199.
- Kumar V. Chapter 9: Environmental and nutritional diseases. In: Kumar V, et al.., eds. Robbins and Cotran Pathologic Basis of Disease. 9th ed.Elsevier, 2016:437–442.
- LaDouceur EEB. Osteomalacia with hyperostosis in captive lesser hedgehog tenrecs (Echinops telfairi). Vet Pathol 2020;57:885–888.
- LeVine DN. Hereditary 1,25-dihydroxyvitamin D-resistant rickets in a Pomeranian dog caused by a novel mutation in the vitamin D receptor gene. J Vet Intern Med 2009;23:1278–1283.
- Madson DM. Rickets: case series and diagnostic review of hypovitaminosis D in swine. J Vet Diagn Invest 2012;24:1137–1144.
- Mair TS, Divers TJ. Self-Assessment Color Review of Equine Internal Medicine. 1st ed. Manson Publishing, 1997:157–158.
- Molin A. Vitamin D-dependent rickets type 1B (25-hydroxylase deficiency): a rare condition or a misdiagnosed condition?. J Bone Miner Res 2017;32:1893–1899.
- Nicolescu R. Vitamin D-resistant rickets and cinacalcet-one more favorable experience. Front Pediatr 2018;6:376.
- Pozza ME. Serum vitamin D, calcium, and phosphorus concentrations in ponies, horses and foals from the United States and Thailand. Vet J 2014;199:451–456.
- Stechman MJ. Genetic causes of hypercalciuric nephrolithiasis. Pediatr Nephrol 2009;24:2321–2332.
- Sykes AR. Experimental production of osteoporosis in growing lambs by continuous dosing with Trichostrongylus colubriformis larvae. J Comp Pathol 1975;85:549–559.
- Teshima T. A genetic variant of CYP2R1 identified in a cat with type 1B vitamin D-dependent rickets: a case report. BMC Vet Res 2019;15:62.
- Thompson KG, Cook RG. Rickets in yearling steers wintered on a swede (Brassica napus) crop. N Z Vet J 1987;35:11–13.
- Toribio RE. Disorders of calcium and phosphate metabolism in horses. Vet Clin North Am Equine Pract 2011;27:129–147.
- Toribio RE. Effects of hypercalcemia on serum concentrations of magnesium, potassium, and phosphate and urinary excretion of electrolytes in horses. Am J Vet Res 2007;68:543–554.
- Uhl EW. The pathology of vitamin D deficiency in domesticated animals: an evolutionary and comparative overview. Int J Paleopathol 2018;23:100–109.
- Wilkens MR. Trans- and paracellular calcium transport along the small and large intestine in horses. Comp Biochem Physiol A Mol Integr Physiol 2017;204:157–163.
Use Nutrition Calculator
Check if your horse's diet meets their nutrition requirements with our easy-to-use tool Check your horse's diet with our easy-to-use tool
Talk to a Nutritionist
Discuss your horse's feeding plan with our experts over a free phone consultation Discuss your horse's diet over a phone consultation
Submit Diet Evaluation
Get a customized feeding plan for your horse formulated by our equine nutritionists Get a custom feeding plan formulated by our nutritionists
