Lizard Metabolic Bone Disease

Introduction

Metabolic bone disease (MBD) is a complex disease that is associated with derangement of the metabolism of calcium, phosphorus and vitamin D3, poor husbandry and other diseases.

MBD is the most common disease in captive lizards, especially green iguanas; it is usually a result of poor husbandry. For example, deficiency in Vitamin D3 and/or UVB in combination with calcium deficiency leads to metabolic bone disease. Associated terms include fibrous osteodystrophy, nutritional secondary hyperparathyroidism, osteoporosis, osteomalacia and rickets.

Extreme care should be taken when examining animals with MBD as their bones are weakened and easily fractured.

Clinical signs

These include:

Lethargy and reluctance to move
Difficulty in lifting body off ground
Ataxia, paresis and paralysis of hindlimbs
Poor appetite to anorexia
Weight loss to poor weight gain
Softening, swelling and deformities of bones e.g. soft mandibles
Pathological fractures
Muscle fasciculations and seizures

When juveniles have been affected during growth, they may have poorly mineralized and pliable mandibles which is a sign of prolonged MBD. This results in distorted jaw bones and a characteristic facial 'smile'. In chameleon species, MBD causes difficulty protruding or retracting the tongue.

Tremors, muscular fasciculations, paresis and seizures usually develop in more severe cases of MBD with developed hypocalcaemia. However in most cases, calcium and phosphate levels usually appear normal.

In some cases, hindlimbs may appear very muscular as a result of thickening of the bone cortex caused by marked fibrous osteodystrophy in the long bones. Palpation or radiography suffice to differenciate from healthy tissue. In addition, the costochondral junctions may appear enlarged and distorted.

Diagnosis

Diagnosis is dependent on:

History - dietary and environmental evaluation; directed towards identifying possible causes of calcium and vitamin D3 deficiency.
Physical examination
Radiography - hypomineralisation of skeleton, pathological fractures, fibrous osteodystrophy. Radiographs are very effective in confirming the diagnosis; indeed, radiolucent transverse processes in the caudal vertebrae are pathognomonic of MBD in lizards.
Biochemistry - calcium is generally within normal limits but may be low, especially in neurological cases; the calcifediol assay can be done on plasma to determine the status.

Treatment

Initial focus should be on improving calcium intake as well as access to appropraite UVB light. Parenteral injections of calcium or oral solutions can be used on animals with clinical hypocalcaemia (when renal failure has been ruled out).

Administer oral calcium for non-neurological cases - calcium glubionate (NeoCalglucon, Sandoz) at 1 ml/kg bw q12-24h for 1-3 months.
Administer parenteral calcium for neurological cases, preferably IV or ICo by slow infusion (100-500 mg/kg q6h) and concurrent diuresis with serial plasma calcium and phosphorus measurements.
Calcitonin has previously been suggested as a treatment - 50 iu/kg IM weekly for 1-4 weeks, but its clinical effects have not been established (do not give to hypocalcaemic patients).
Vitamine D deficiency can be addressed by UVB exposure as long as the kidney and liver functions are normal.
Treatment should be given every 6-12 hours until noticeable clinical signs have ceased (e.g. seizures, fasciculations).

Carry out supportive care.

Attempt only conservative repair of fractures by stabilizing bones with external coaptation .

Prevention

MBD is prevented by providing correct housing and diet. However, caging and dietary requirements vary depending on the species of lizard.

Literature Search

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Lizard Metabolic Bone Disease publications

References

Girling, S.J. and Raiti, P. (2004). BSAVA Manual of Reptiles. British Small Animal Veterinary Association, 2nd Edition. pp. 350. ISBN 978-0905214757