Posted by BabyHerp on August 18, 2000 at 02:17:39:
Thought this might be of interest to anyone wanting a more in depth look at what the vet sees when an ig dies of MBD. Done in 1996
Chondromatosis and osteoporosis in a green iguana (Iguana iguana)due to nutritional osteodystrophy. (HE, 400X, 113K)
History: The iguana was reported to be lethargic and dehydrated prior to death. The diet consisted solely of fruits and vegetables. The house had recently been fumigated for insects and the owner was concerned about the possibility that the iguana was poisoned by eating a poisoned insect.
Gross Pathology: An immature male green iguana in fair body condition weighing approximately 70 gm was presented for necropsy. Both femurs were markedly enlarged in diameter and there was a pathologic fracture of the distal right femur. Both femurs cut easily with a scalpel blade. The mandible was rubbery and bent easily without breaking. Approximately 3.0 mls of serous fluid was present in the abdominal cavity. The thyroid glands were mildly enlarged but the parathyroid glands were not observed grossly. No other significant gross changes were observed in the carcass.
Laboratory Results: Morganella morgani and a Flavobacterium spp. were isolated from femoral bone. Flavobacterium spp., Alicaigenes xylosoxidans and Citrobacter freundii were isolated from an abdominal swab. Flavobacterium spp. was also isolated from liver. None of these organism were considered to be significant in this case. Viral culture was not performed. Blood was not available for hematology and blood chemistry analysis.
Contributor's Diagnosis and Comments: Femur, chondromatosis, diffuse, severe, bilateral with severe osteoporosis, compatible with nutritional osteodystrophy.
Sections of undecalcified diaphyseal femur are submitted for conference participants. The diaphysis of each femurs is markedly thickened. There is a diffuse lack of cortical bone with a proliferating cuff of hyperplastic cartilage that has largely replaced and compressed the diaphyseal cortical bone. Numerous scattered osteoclasts and a row of osteoblasts line most of the remaining spicules of cortical bone. Periosteal reaction is minimal. Bone marrow elements are present in low, but adequate numbers. Sections of mandible (not submitted) have a diffuse lack of cortical bone with marked diffuse osteoclastic activity and replacement of bone with a loose areolar fibrous connective tissue compatible with fibrous osteodystropy (osteodystrophia fibrosa) . In addition, sections of thyroid gland exhibited mild to moderate diffuse hypertrophy and hyperplasia of follicles containing abundant colloid. Parathyroid tissue was not observed on gross or histologic examination.
The proliferating cuff of diaphyseal hyperplastic cartilage is unique to the iguana with nutritional osteodystrophy (secondary nutritional hyperparathyroidism). Fibrous osteodystrophy commonly occurs in the horse and its relatives (zebra, etc.), goats, pigs, cattle, sheep (rarely), and a variety of other species, including non-human primates. Fibrous osteodystrophy is characterized by extensive osteoclastic resorption of bone and formation of fibro-osseus tissue which fills the marrow space in response to excessive secretion of parathyroid hormone. These changes are particularly prominent in the bones of the face and mandible in some species resulting in the syndromes of "bighead" (horse) and/or "rubber jaw" (dog). There is a high susceptibility to pathologic fractures and avulsion of ligaments resulting from slight trauma.
The most common causes of fibrous osteodystrophy are deficiency of calcium, calcium/phosphorous imbalance (high dietary phosphorous), vitamin D deficiency and occasionally renal failure. These conditions result in excessive secretion of parathyroid hormone. Parathyroid hormone (PTH) increases resorption of calcium via an osteoblast mediated stimulation of osteoclasts and decreases resorption of phosphate from the glomerular filtrate. Osteoclasts do not have receptors for PTH and only respond to PTH in the presence of osteoblasts which appear to release unknown paracrine factors that locally stimulate osteoclastic bone resorption.
AFIP Diagnosis: Femur, cortex: Osteodystrophy, chondroproliferative, diffuse, severe, with osteopenia, green iguana (Iguana iguana), reptile.
Conference Note: Captive iguanas are often fed a diet of fruits and vegetables which contain low levels of calcium. The calcium deficient diet results in low serum levels of calcium and relatively high levels of serum phosphorous, inducing the secretion of PTH from chief cells in the parathyroid. Parathyroid hormone elevates serum calcium by increasing the active osteoclast pool, resulting in osteoclasis and skeletal remodeling, and by increasing absorption of calcium in the distal tubules of the kidney. There is also a concomitant decrease in serum phosphate due to PTH-mediated decreases in absorption of phosphates in the proximal tubules of the kidney. Continued osteoclastic activity in the face of calcium deficiency results in the lesions associated with osteodystrophy.
It is believed that the cartilaginous proliferation is an adaptation to mechanical stresses placed upon the weakened bone. It is not understood why iguanas develop proliferations of cartilaginous rather than fibrous tissue, as is seen in other species with nutritional osteodystrophy.
Green iguanas have also been shown to develop fibrous osteodystrophy if they are not allowed access to ultraviolet light in the range of 285-315 nm (UV-B). Ultraviolet light is required by iguanas to convert provitamin D3 to the active form of vitamin D3. It has been speculated that the hypovitaminosis D causes an exaggerated parathyroid hormone response resulting in decalcification of bone and fibrous osteodystrophy. An unusual and characteristic feature of this condition is widespread metastatic calcification of soft tissues in the face of hypovitaminosis D.
Contributor: Veterinary Diagnostic and Investigational Laboratory, College of Veterinary Medicine, University of Georgia, P.O. Box 1389, Tifton, Georgia 31793.
References:
1. Anderson, M.P. and Capen, C.C. 1976. Nutritional osteodystrophy in captive green iguanas (Iguana iguana). Virchows Arch. B Cell Pathol. 21:229-247.
2. Anderson, M.P. and Capen, C. C. 1976. Fine structural changes of bone cells in experimental nutritional osteodystrophy of green iguanas. Virchows Arch. B Cell Pathol. 20:169-174.
3. Jacobson, E. R. 1981. Diseases of reptiles. Part I. Noninfectious diseases. Compend. Contin. Educ. Pract. Vet. 3:122-126.
4. Jacobson, E. R. 1984. Biology and diseases of reptiles In: Laboratory Animal Medicine. Eds. J.G. Fox. , F. J. Cohen and F. M. Loew. Academic Press, Inc., New York. chap. 15, pp. 470-471.
5. Palmer, N. 1993. Bones and Joints In: Pathology of Domestic Animals. Eds. K. V. F. Jubb, P. C. Kennedy and N. Palmer. Academic Press, Inc., new York. Chap. 1, pp. 72-77.
6. Richman L, Montali R, Allan M, and Oftedal O: Widespread metastatic soft tissue mineralization in vitamin D deficient Green Iguanas. Abstract, American College of Veterinary Pathologists 46th Annual meeting, 1995.
International Veterinary Pathology Slide Bank: Laser disc frame #2589, 2590, 6097, 6305, 6309-11, 8223, 9152, 9399, 9981-9988, 15293, 15294, and 15299.