Metabolic Bone Disease

An owner purchases a baby green iguana and proudly brings it home and sets it up in its new cage. The new owner doesn't receive much information when the new lizard is purchased, and he feeds it the diet that he was instructed to: a variety of greens, vegetables and fruits. He neglected to purchase a thermometer for the cage, nor did he acquire a full-spectrum light or proper equipment to heat the cage. The iguana has a bowl for water, and rarely, if ever, is allowed to swim in a tub or pool. While the young iguana has a good appetite, the owner notices that the limbs are beginning to look muscle-bound and the lizard doesn't seem to be able to lift up his trunk normally. During one cage-cleaning, when the iguana is jumping around the cage, the owner notices that one front leg appears to be broken.

This is, unfortunately, a common scenario that occurs most often in rapidly growing young green iguanas (Iguana iguana), but also may be seen in any reptile or amphibian species. This description is the classic presentation for juvenile metabolic bone disease (MBD), also called nutritional secondary hyperparathyroidism and fibrous osteodystrophy. MBD encompasses many different clinical syndromes, but all result in bone and calcium problems.

Let's look at what went wrong in the case of the young green iguana that was described. MBD in juvenile herps is usually the result of a calcium-deficient diet, combined with vitamin D deficiency, an incorrect calcium: phosphorus ratio and/or a lack of necessary exposure to ultraviolet light. What actually happened to that iguana that resulted in a bone fracturing with normal cage activity?

To understand why this iguana's legs became swollen and became prone to breaking, we need to have a good understanding of how a reptile and amphibian absorb and utilize calcium for strong bones. The mineral, calcium, is essential for proper bone development. However, it is not as simple as that. The mechanism for calcium absorption involves a vitamin, D3, that a herp will manufacture when exposed to proper ultraviolet light. In the absence of a calcium-rich diet, and without correct lighting, a rapidly growing iguana (they can optimally grow 30-60 cm per year) will not be able to produce normal bone. To try and support calcium-deficient soft bones, supportive fibrous connective tissue is laid down around the bone, resulting in the muscle-bound appearance to the limbs. This is called fibrous osteodystrophy. Often with fibrous osteodystrophy, the lower jaw will become rubbery and the head, spine, limbs or tail may become misshapen.

In mammals, exposure to ultraviolet (UV) irradiation in the 290-320 nm wavelength range will allow the production of vitamin D3 in the body, also called cholecalciferol. It is thought that reptiles utilize this form of vitamin D, as well. There is another form of vitamin D, called ergocalciferol, or D2, that is derived from plants and is not thought to perform the same functions as D3 in reptiles.

For proper growth and health and to prevent metabolic bone disease, it is always best to allow reptiles exposure to natural sunlight, not filtered through glass or plastic. Many owners believe that they are providing adequate ultraviolet light by placing a cage or tank in a sunny window. However, both glass and plastic will filter out the necessary ultraviolet rays. Window screens will only minimally affect transmission of ultraviolet light, so a screened open window can allow natural sunlight, as long as the herp is not contained in a glass or plastic cage. While natural sunlight is always best, it is usually necessary for the herp owner to provide UV light by the use of a full-spectrum fluorescent light. There are several excellent companies that produce fluorescent lights that emit the proper ultraviolet spectrum necessary for vitamin D synthesis in the body. However, these lights should optimally be placed within 18 inches of the animal for maximum utilization (or follow recommendations that come with the bulb), and the light should not be placed so that glass or plastic is between the light source and the animal. For maximum effect the light should remain on for 12 hours per day, unless specific conditions deem otherwise. Also, the most significant ultraviolet radiation will diminish from the fluorescent light over time, so for maximum efficiency, the bulb should be replaced every six months (or at the maximum every 18 months). Over time, while the light emitted will look the same, the ultraviolet portion will not be emitted in significant strength to be of use to the herp. Some herpers use a combination of a full-spectrum fluorescent light and a black light, as black lights emit slightly more ultraviolet light (particularly UV A). It is the UV B portion of the ultraviolet light that serves as the catalyst for vitamin D3 activation, however.

In addition to requiring ultraviolet light for proper utilization of calcium, young growing reptiles require the proper amount of calcium. Another mineral, phosphorus, is closely related to calcium metabolism. For proper bone development, a diet should contain a ratio of calcium to phosphorus of approximately 1.5-2 to 1. Herbivores are prone to bone problems because many diets are very low in calcium and have excessive phosphorus. Fruit and lettuce are both low in calcium and high in phosphorus. To create the correct calcium to phosphorus ratio in a diet for herbivores, it is essential that the foods chosen to be fed are high in calcium and low in phosphorus. In addition to providing an appropriate diet, in most cases, a calcium supplement is required. Multiple vitamin supplements usually contain calcium, but this is not usually enough to prevent MBD.

In the absence of the correct calcium to phosphorus ratio, and without exposure to ultraviolet light, the body will begin to produce excessive amounts of parathyroid hormone. Normally, healthy bone is an excellent reservoir for calcium, containing 99% of a vertebrate's calcium. Vertebrates require a continual supply of calcium as a cellular ion, especially for normal functioning of nerves and muscles. The heart cannot beat regularly and normally without calcium ions in the bloodstream. In young animals, if not enough calcium is reaching the bloodstream, parathyroid hormone (PTH) levels will increase. This stimulates bone to break down, releasing calcium into the bloodstream and also releasing phosphorus from the bone. PTH will also enhance phosphorus excretion through the kidneys, and will decrease the excretion of calcium through the kidneys. PTH also stimulates cholecalciferol synthesis in the body, which also stimulates calcium absorption from the small intestines. Over time, if the animal cannot consume or absorb enough calcium to put back into the bones, the bones will weaken. At this point, fibrous connective tissue is laid down around the long bones, to try to support them, and the limbs will look swollen. Eventually, unless the problem is identified and corrected, the reptile will continue to worsen, and will eventually die.

Some calcium supplements contain vitamin D3. However, there is some question as to whether this is absorbed well from the gastrointestinal tract when supplied orally.

Herbivores, such as green iguanas, aren't the only reptiles to suffer from MBD. Carnivorous reptiles may develop MBD if the diet they are fed does not contain bone. Organ meats (such as liver, heart, kidney or gizzard) or muscle meats (ground beef, chicken, turkey) have an incorrect calcium to phosphorus ratio. For example, hamburger has a ca: phos ratio of 1:16. So, you can see that even with calcium supplementation, it may be difficult to supply the correct ca: phos ratio. It is always best to offer whole prey items, if possible, as the bone in the whole animal (fish, mouse, rat or bird) will provide a positive ca: phos ratio. The exception is pinky mice and rats, as their skeletons have not yet sufficiently calcified and thus will not provide the correct ratio. Since snakes usually consume whole prey items, they rarely suffer from MBD.

Reptiles that ingest primarily insects are also prone to MBD, as insects also contain a negative ca: phos ratio. For this reason, all insects offered to herps should be fed a calcium- rich diet for several days prior to being used as food, or they should be dusted with a calcium supplement just before being fed.

There is an array of clinical signs of MBD. In young animals, an early sign, especially in green iguanas, is the inability to lift the trunk normally. This may be partial or complete. Normal iguanas will lift their body and tail closest to the body up off the ground while walking on any surface. Often, in early MBD, the iguana will lift the front half of the body up while walking, while dragging the pelvis and tail on the ground. In advanced cases, the iguana will drag itself along, unable to lift off the ground at all. This will progress to the complete inability to move in a forward motion, in spite of frantic fore and hind limb movements.

The mandible may become rubbery, and the maxilla may become soft, as well. Eventually, the lower jaw will retract, so that an underbite develops. This may be made even more evident by fibrous osteodystrophy of the jaw. It becomes difficult for a reptile to eat normally when the jaw is misshapen, so weight loss may be a sign of MBD.

A reptile or amphibian with MBD is often lame or reluctant to move. They are often weak. Since weakened bones are prone to fracturing, spontaneous fractures may occur, or fractures may occur from normal activity or handling. Deformities of the spine commonly occur. The rear limbs may become very weak or even paralyzed. If this occurs, the chance for recovery is poor, as this often interferes with urination and defecation.

Chelonians (turtles and tortoises) with early onset MBD often develop abnormal shells. Normally hard-shelled turtles and tortoises may have soft shells and the carapace may curve upwards along the edges. The skull often develops abnormally, and the chelonian often has an overgrown maxilla, resulting in the appearance of a parrot beak. Normally, turtles and tortoises lift their body up off the ground while walking, and with MBD, they may not be able to do so. Examination of the plastron may show signs of being dragged.

Adult reptiles and amphibians that develop MBD will not show the same problems as juveniles. Since they are not rapidly growing, bone and developmental problems do not occur. Usually, a lizard with adult-onset MBD presents with nervous system problems. Subtle signs, such as occasional twitching of toes, a limb or tail are the first signs. As problems with low calcium in the bloodstream (hypocalcemia) progress, twitching and muscle tremors become more evident, especially after exercise, such as swimming or walking. Tremors of the muscles become more severe and frequent. Without proper diagnosis and treatment, the muscle tremors can progress to seizures or tetany (prolonged seizure activity and twitching). Eventually, the herp will become very weak and the muscles will become flaccid. While this can occur in adult iguanas commonly, chelonians rarely, if ever, show signs of adult MBD.

The diagnosis of MBD, either in an adult or juvenile, may often be presumed based on the history (diet, husbandry, etc.) and physical examination. Radiographs may be helpful in determining the bone density (an indication of the amount of calcium present in the bone), any skeletal abnormalities (including irregularities of the skeletal system, fractures, etc.) and they may be useful in follow-up evaluation of treatment. However, rads are not essential for diagnosis of MBD in the juvenile form.

Blood tests may show low blood calcium and an elevation of the phosphorus level. With hypocalcemic adult MBD, the calcium level may be in the normal range, unless the blood is drawn during or immediately after a seizure or twitching episode. An inverse ca: phos ratio of the blood is strong evidence of MBD. Juveniles with MBD often have a low calcium level and an elevated phosphorus level, however some young herps with MBD may show levels within the normal range.

Treatment for MBD will depend on the severity of clinical signs and how long the herp has been ill. Before beginning any therapy, the owner must understand the commitment involved. Also, the owner must be willing and able to correct the diet and husbandry conditions that led to the herp developing MBD in the first place.

Any fractures should be identified. Small lizards may do best if broken bones are managed conservatively, meaning that cage rest is often adequate for healing, unless the limbs are in grossly abnormal positions. Fractures may be splinted, but in severe cases, the bones may bend or break on either side of the splinted areas. So, it may be best to allow them to heal naturally, once the calcium problems have been corrected. The soft bones are too weak to withstand surgical correction with pins. Until the herp has healed, it should only be handled for medication.

Juveniles with MBD should be treated with calcium. I often begin treatment with an injection of vitamin A and D3, calcium gluconate and intracoelomic (IC) fluids. An injection of vitamin D3 should only be administered if the history reflects deficiency, and it is not known how well exogenous vitamin D will actually help the MBD herp. Injections must be given very carefully to prevent further damage to the skeletal system. Ill herps should be kept near the high end of their optimal temperature range. If the physical exam or blood tests show signs of bacterial infection, antibiotics may be administered. To minimize stress, the herp may be dewormed, based on the results of the fecal parasite examination.

Calcitonin salmon, a synthetic hormone derived from fish, is an excellent addition to therapy for juvenile MBD herps. This is an injectable medication. I will usually treat the herp with calcium, by injection or orally, for three days prior to commencing treatment with calcitonin salmon. In questionable cases, it may be safest to run a blood calcium level prior to instituting calcitonin therapy. This drug is extremely beneficial in speeding the recovery of juvenile MBD herps. The action of calcitonin is to pull calcium out of the bloodstream, and putting it into bones and other tissues needing it. Its use will greatly facilitate healing of fractured bones and the strengthening of weak, calcium-deficient bones. Calcitonin injections may be given every 7 days, for at least two treatments, or longer, if required.

Many publications have issued strong warnings about the possible dangers of using calcitonin in the treatment of juvenile MBD because if it is given without first pre-treating with calcium for several days (or until the blood calcium level has normalized), it can result in seizures, collapse or death. However I have used calcitonin in many, many herps (and other species, such as marmosets, tamarins, cougars and bobcats) with no adverse effects. The key is to make sure that the animal has received adequate calcium supplementation for an adequate length of time, so that once the calcitonin is given and it begins drawing calcium out of the bloodstream and into bone, this will not precipitate a hypocalcemic crisis.

If the herp is unable to eat on its own, it may be hospitalized for tube feedings. So, in addition to IC fluids, injectable calcium, injectable vitamins and heat, tube feedings may be necessary. All the while, we must remember that we must first do no harm, meaning that during treatment, we need to ensure that we don't cause additional damage when handling this fragile animal. Often, treatment on an outpatient basis is satisfactory. The herp should begin exposure to UV light as soon as possible. All patients, whether hospitalized or treated at home, should be weighed weekly, at least, to monitor weight gains. If the herp is not gaining, then supplemental feedings may be necessary.

At home, the herp should be placed in a warm cage, and all climbing branches should be removed to prevent dangerous falls. Strict cage rest in a small confined space is recommended, and the patient should be isolated to prevent cage-mates from possibly injuring it and to prevent competition for food (which also allows the owner to closely monitor food intake).

The calcium supplementation will be given orally when recovery indicates that the herp is strong enough. Neo-CalgluconTM (calcium glubionate) is available as a liquid children's calcium supplement and works well when dosed by syringe. Once the patient is stable and eating well on its own, a calcium carbonate supplement may be sprinkled over the food items consumed. TumsTM work well, as they are available in fruit flavored chewable tablets and are easily calibrated for proper dosage. Calcium supplements with phosphorus should not be used, as many MBD herps already have elevated phosphorus levels and additional supplementation with it may be deleterious. In the past, phosphorus binders containing aluminum were often used to lower phosphorus levels, however, studies in humans have shown that aluminum may cause kidney damage, which may compound pre-existing renal problems. So, if phosphorus binders containing aluminum are used, they should only be used for a short period of time to initially lower phosphorus levels, then the patient should be switched to calcium carbonate, which will also lower phosphorus levels.

The prognosis for juvenile MBD recovery is good with early diagnosis and aggressive therapy. Without treatment, many MBD patients will die. However, if skeletal abnormalities have occurred, such as abnormal bending of the spine, those changes are most likely irreversible. Fractures will heal with time, and even more quickly with calcitonin treatment, but an underbite of the jaw will remain, although the bones will harden. If damage to the spine results in injury to the spinal cord (as evidenced by a flaccid tail, incontinence or the inability to defecate) the prognosis is poor. With chelonians, once the shell has become misshapen, it is impossible to correct. Overgrown beaks may be trimmed. As the chelonian grows, the abnormal shell may cause deformities to the limbs or abnormal placement of internal organs. This can be quite devastating.

With adult MBD, resulting in hypocalcemia, the treatment should attempt to normalize the blood calcium level slowly, as rapid infusion of calcium intravenously can be very dangerous. The cause of the hypocalcemia should be determined, if possible, so that corrections may be made in the diet and husbandry of the patient. The resolution of clinical signs (twitching, flaccid weakness) can be quite dramatic once injectable calcium is administered. However, often these patients are dehydrated and will benefit from IC fluids, and possibly injectable vitamin D3 and support care. Once home, dietary and husbandry changes must be made to prevent the reoccurrence of hypocalcemic MBD.

There is much controversy about the use of "full-spectrum" incandescent light bulbs. Some practitioners feel that herps exposed to the light from these bulbs develop normally and do not develop MBD. Some tests indicate that these bulbs do indeed emit UV A and UV B. Others feel that incandescent bulbs cannot emit the correct wavelengths at the proper strength for vitamin D3 synthesis. No matter what type of bulbs you use, full-spectrum, black light or incandescent, remember that natural, unfiltered sunlight is always best and safest (however, never leave a herp unattended in direct sunlight, as overheating and death can rapidly occur). Always strive to allow your herps access to natural sunlight when possible. Even an hour per week should be beneficial.

In addition to traditional full spectrum fluorescent lights (a straight tube that fits into a special fixture), there are now fluorescent full spectrum lights that will screw into a traditional light socket. These are more compact and will provide correct ultraviolet light. When deciding on a full spectrum fluorescent light, make sure that you choose one that emits ultraviolet light. Fluorescent lights for growing plants and for aquariums do not produce ultraviolet light. Also, don't be fooled by bulbs that tout producing natural true sunlight colors, as these do not emit ultraviolet light, either.

When choosing a vitamin supplement for your herps, make sure that the label specifies cholecalciferol, and not ergocalciferol. If the label does not specify which type of vitamin D it contains, then it is best to not take chances with it, as the ergocalciferol is less expensive to produce, and may be what it contains. Preparations with cholecalciferol should be what you choose, even though oral absorption is questionable.

While we have discussed the two most common forms of MBD, there are other forms. Any condition that disrupts vitamin D absorption or metabolism (kidney, liver, intestinal, thyroid or parathyroid disease) may result in MBD. Other clinical syndromes involved with MBD include osteoporosis, osteomalacia and rickets.

Metabolic bone disease is a nasty problem and one that is completely avoidable by properly caring for your pet herp. Unfortunately, this disease is still all too common today, due to misinformation or lack of accurate data concerning diet and husbandry. I truly feel that by acquiring any animal for pet or breeding purposes, we owe it to them, as their stewards, to learn all that we can about how to provide them with the necessary diet and caging requirements to ensure that they live a long and healthy life. If we all did this, I would never have to treat another case of MBD again, and that would make me a very happy veterinarian.

Copyright 2006 Margaret A. Wissman, D.V.M., D.A.B.V.P.
All Rights Reserved

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