Fibrous osteodystrophy in a dromedary camel. (January 2021)

• Record Type: Journal Article
• Authors: Hines, Elizabeth S.; Stevenson, Valentina B.; Patton, Molly E.; Leventhal, Hannah R.; Diaz-Portalatin, Noah; Meyerhoeffer, Mitchell A.; Dahlgren, Linda A.; Sponenberg, D. Phillip
• Is Part Of: Journal of veterinary diagnostic investigation. Volume 33:Number 1(2021)
• Page Start: 144
• Page End: 148
• Publication Date: 2021-01
• Subjects: bone diseases -- camelus -- hyperparathyroidism -- metabolic disease; Veterinary medicine -- Diagnosis -- Periodicals; 636.0896075
• DOI: 10.1177/1040638720965252
• Languages: English
• ISSNs: 1040-6387

Abstract

A 6-y-old female dromedary camel ( Camelus dromedarius L.) was presented for assessment of firm, bilateral swellings rostral and ventral to the eyes. Serum biochemistry revealed hyperglycemia (28.5 mmol/L), hypocalcemia (1.27 mmol/L), hyperphosphatemia (3.39 mmol/L), hypoproteinemia (total protein 50 g/L), and hypoalbuminemia (20 g/L). Based on the poor prognosis associated with the presumptive diagnosis of fibrous osteodystrophy, the camel was euthanized. Gross postmortem findings revealed expanded fibrous tissue replacing the maxilla and mandible, and bilaterally prominent parathyroid glands. Histology of the maxilla revealed proliferative loose fibrous tissue with widely scattered, regularly spaced, small spicules of mineralized bone. The parathyroid glands were prominent bilaterally; the internal and external parathyroid glands were composed of plump cells with abundant pale basophilic cytoplasm and open nuclei. The pathologic findings were consistent with the antemortem diagnosis of fibrous osteodystrophy. The camel's diet, which was not specifically balanced for a camel, included grass hay, sweet feed, and alfalfa pellets. The camel's caregivers reported feeding her treats of cookies. A feed analysis was not available. The biochemistry abnormalities and clinical and postmortem findings, along with a diet that was not balanced for a camel, are consistent with a diagnosis of nutritional secondary hyperparathyroidism.