Kyphosis and Metabolic Bone Disease in an Infant Lowland Gorilla (Gorilla gorilla gorilla)
American Association of Zoo Veterinarians Conference 2007

Michael T. Barrie, DVM; Gwen E. Myers, DVM

Columbus Zoo and Aquarium, Powell, Ohio, USA


An 8-month-old, hand-raised, female, lowland gorilla (Gorilla gorilla gorilla), was diagnosed with kyphosis by radiographs and magnetic resonance imaging (MRI). The degree of deformity was considered severe by orthopedic specialists consulted on the case. Infant humans with kyphosis, depending on severity, have the potential of developing instability, narrowing of the spinal canal and cord compression as the misshapen hemivertebrae grow. Posterior paresis or paralysis, and urinary or bowel incontinence can result. Treatment in infant humans often involves stabilization surgery where the affected vertebral bodies are fused with a bone graft, limiting the potential for narrowing of the spinal canal during growth. Because the gorilla weighed only 4.2 kg, the procedure for her would require both a ventral and dorsal surgical approach. External fixation in a body cast would also be necessary, likely for 6 months, as the gorilla was too small to accommodate internal fixation devices. Naturally, there were concerns about the serious surgical risks involved and the postoperative management.

Concurrently, the gorilla suffered from metabolic bone disease (generalized demineralization), indicated on survey radiographs. A dual energy X-ray absorptiometry (DEXA) was performed to quantify bone density. On the initial DEXA, the lumbar bone mineral density was 0.25 g/cm2. This is below the 1st percentile for 10 kg human infants (mean = 0.40 g/cm2, 1st percentile = 0.31 g/cm2).

Surgery was postponed until the bone density problem could be addressed. Serum parathyroid hormone (PTH), 25-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol levels were 161 pg/ml, 9 ng/ml, and 250 pg/ml, respectively. These values were consistent with vitamin D deficiency (diagnosed by low 25-hydroxycholecalciferol level; human reference ranges for serum parathyroid hormone, 25-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol are 7.0–53 pg/ml, 8.0–36 ng/ml, and 22–67 pg/ml respectively) which can cause poor calcium absorption, and diminished calcium and phosphorous incorporation into bone. The suspected etiologies of her vitamin D deficiency were likely to have been insufficient vitamin D intake and diminished sunlight exposure. Metabolic bone disease, when caused by insufficient vitamin D, calcium, and phosphorous intake, can usually be corrected with high levels of calcium and vitamin D supplementation. The milk formula was adjusted to increase the daily calories and was supplemented with calcium glubionate (Calcionate syrup, Rugby Laboratories, Duluth, GA, USA; 3.6 g, PO) and ergocalciferol (Calciferol drops, Schwarz Pharma, Inc., Milwaukee, WI, USA; 16,000 IU, PO). The keeper staff also made an effort to move the gorilla outdoors to facilitate sun exposure for short periods as weather permitted. After 3 months the serum PTH level had returned to normal (46 pg/ml).

A repeat DEXA 5 months later showed improvement in bone density (0.31 g/cm2). Periodically, radiographs and MRI of the spine were repeated. Overall bone density continued to subjectively improve during this time. Narrowing of the spinal canal did not occur as the gorilla grew. No symptoms of spinal cord damage (incontinence, hind limb weakness) were observed. Surgical stabilization was therefore postponed indefinitely with the caveat that it may become necessary in the future if symptoms developed.

At 6 years of age and weighing 30 kg, no outward signs of spinal cord compromise have been observed. The gorilla has always behaved and ambulated normally. At this time, it is thought that surgery will be unnecessary. Destabilization of the spine may be less likely to occur in gorillas due to their quadrupedal stance and more horizontal posture compared to humans. Metabolic bone disease may affect gorillas in captivity and must be considered in any assessment of treatment of bone disease in this species.


The authors wish to thank the gorilla keepers and zoo hospital staff, and all of the specialists for their generous help with the management of this case. Special thanks to Dr. Joe Donovan who assisted with anesthesia and to Kathy Boston for providing MRI support.


Speaker Information
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Michael T. Barrie, DVM
Columbus Zoo and Aquarium
Powell, OH, USA

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