MBD in exotic cats

Metabolic Bone Disease in Exotic Pets

Metabolic bone disease, nutritional secondary hyperparathyroidism, fibrous osteodystrophy, osteoporosis, osteomalacia, rickets, simian bone disease, osteogenesis imperfecta, cage paralysis, bone atrophy, juvenile osteoporosis, paper-bone disease, goundou, Paget's disease, Recklinghausen's disease, osteitis fibrosa cystica; whichever name is used to describe this disease, it remains a frequently diagnosed condition in reptiles, and it is also seen in exotic animals, such as non-human primates and exotic cats that have been improperly fed and maintained. While MBD may occur in birds, it is uncommon in psittacines, but occurs occasionally in raptors and mustophagids that are fed an inappropriate diet.

Metabolic bone disease should be considered to be a disease caused by dietary and husbandry mismanagement. It is characterized by metabolic defects affecting the morphology and functioning of bone. Metabolic bone disease is most often seen in young, growing animals, however, it may also occur in older animals, usually housed indoors. MBD is manifested by a number of clinical signs. MBD animals often show a reluctance to move. Limbs may become distorted, and from weight bearing, may develop valgus deformities. The tail may have angular bends to it, and the vertebral column may also become misshapen. If the ribs are deformed, this may cause protrusion of the abdominal organs. The lower jaw may become deformed and may make normal prehension of food difficult.


Radiographs will show decreased bone density, and fractures, in various stages, will usually be present. Many types of skeletal deformities may be present, as well, including bowed legs, kyphosis, scoliosis, lordosis and collapsed pelvis. Collapsed pelvis may result in constipation or obstipation, and in adult females, dystocia is likely.

Serum calcium levels are usually decreased, and phosphorus levels may be increased, however, in some cases, levels are normal. Serum alkaline phosphatase levels are elevated in any condition involving osteoblastic or osteoclastic activity. Although radiographs and testing are helpful, the history, evaluation of the diet, clinical signs and physical exam are often diagnostic.

Facial deformities are common, and anorexia is common and may be due to poor mastication. Stertorous breathing is common as facial swelling impinges on the nares. Swelling of the jaw may prevent proper closing of the mouth and may interfere with mastication. Teeth may erupt in a haphazard fashion or may simply fail to erupt.

Prolonged hypocalcemia may result in cataract formation and strabismus in juveniles. Paraplegia may result from compression fractures of the vertebrae. Retarded growth of infants is common, and quadrupeds may develop a narrow chest and prominent sternum, caused by gravitational drooping.

Canines and felines are highly susceptible to MBD. New World NHPs are likely to develop fibrous osteodystrophy with deformities of the face and jaw. Juvenile carnivorous birds fed an all-meat diet may develop rickets in 10-14 days. In sub-acute or chronic cases, birds may show poor feather structure and poor molting. Birds may also develop hypocalcemic tetany. Birds consuming a high fat diet (sunflower seed, coconut meat and rape seed) have a high incidence of MBD. Snakes are rarely affected by MBD because they eat whole animals.

Lizards, crocodilians and chelonians are susceptible, however adult chelonians rarely show clinical signs. Juvenile chelonians with early-onset MBD often develop abnormal shells. A normally hard-shelled turtle may have a soft shell, and the carapace may curve upward along the edges. The skull often develops abnormally, and the chelonian's maxilla may grow excessively, resulting in a parrot-beaklike appearance. Normally, chelonians lift their bodies 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 dragging.

Hoofed animals are usually exposed to sunlight, and are thus assured a source of vitamin D. Herbivorous diets are more likely to contain sufficient calcium. However, with improper husbandry and diet, it may occur in any species.

Caution must be exercised when handling and examining animals with suspected MBD, as demineralized bones may fracture easily.

Adult animals presented with MBD may show subtle muscle fasciculation, occasional twitching of a toe, limb or tail, and these signs may be exacerbated by stress or exercise. Tremors will progress and will become more severe and frequent. Eventually, the tremors will progress to seizures or tetany. Flaccid paralysis may result.

The Biochemistry of Metabolic Bone Disease

Metabolic bone disease occurs as a result of biochemical reactions regulated by the parathyroid glands, small glands located near the thyroid glands in the neck. The regulation of calcium homeostasis is delicately balanced by the interaction of three hormones: parathyroid (PTH), calcitonin (thyrocalcitonin, TCT) and 1,25-dihydroxycholecalciferol (1,25-DHCC), which is the biologically active form of vitamin D. Major organs involved in the process include the intestine, liver, kidney, parathyroid gland, thyroid gland and bone. In birds that possess a uropygial gland, this gland is also involved in calcium metabolism.

Calcium is necessary for normal neuromuscular function, cardiac contraction, blood clotting, membrane permeability and activation of enzymes as well as for serving as the structural foundation of the skeleton. Calcium is absorbed by the intestines under the influence of 1,25-DHCC. Diseases of the small intestine and liver may interfere with calcium absorption. It is also important to know that ingestion of a high fat diet (such as may occur with birds eating a primarily sunflower or safflower seed diet) may be detrimental because fats may reduce calcium absorption.

Calcium and phosphorus in the body are in a ratio of 2:1. The optimal ratio in the diet should be between 1:1.5 and 2:1. Most dietary errors involve too much phosphorus, an excess of which ties up the calcium ions present in the ingesta to form insoluble absorbed, resulting in hyperphosphatemia. The resulting hypocalcemia causes stimulation of parathyroid hormone production.

The parathyroid glands are responsible for the minute-to-minute regulation of calcium. When serum calcium is low, this stimulates secretion of PTH, which has two major functions. First, it promotes calcium mobilization from bone (vitamin D must be present for this.) PTH also promotes the excretion of phosphate in the urine, and calcium reabsorption is enhanced.

In avian species, the ultimobranchial glands are involved with calcium regulation. Calcitonin is a hormone secreted by the thyroid gland in mammals. It is secreted when the serum calcium level is elevated. Calcitonin inhibits calcium resorption from the bone and acts in opposition to parathyroid hormone to reduce serum calcium levels.

Interestingly, in birds that possess an uropygial gland, the secretion from this gland plays an important role in calcium metabolism. The secretions from this gland include vitamin D3 precursors that are spread on the feathers when the bird preens. Then when the bird's feathers are exposed to ultraviolet light, the precursors are converted to vitamin D3, which is then ingested when the bird next preens. So, if the bird has a poorly functioning uropygial gland (often due to hyperkeratosis from hypovitaminosis A or if the bird has plucked out all of the wick feathers of the gland), it may develop hypocalcemia problems. Hypocalcemia problems may also result if the bird is not exposed to ultraviolet light to activate the vitamin D on the feathers.

Vitamin D need not be supplemented in animals that receive some ultraviolet radiation. However, animals kept indoors require a dietary source. Vitamin D2 is ergocalciferol, and is synthesized by the irradiation of ergosterol, a plant constituent. Ergocalciferol is utilized for vitamin D activity by most mammals. Cholecalciferol, vitamin D3, is derived by synthesis of 7-dehydrocholesterol in the skin from cholesterol. Ultraviolet light induces the transformation. Liver malfunctions and kidney disease may prevent the transformation from occurring.

It should be noted that recently, a major manufacturer of New World primate biscuits has greatly increased the levels of vitamin D3 in their product, which, while wonderful for primates, is very dangerous for other species that may consume them! Birds and reptiles that are fed primate biscuits are at significant risk for hypervitaminosis D, which may result in mineralized organs, toxicosis and even death.

How MBD Occurs

When a growing animal, or an older animal, is fed a diet with a negative calcium: phosphorus ratio, and vitamin D is lacking in the animal, the parathyroids begin producing excessive hormone. This pulls calcium out of the bones to maintain the blood calcium levels within life-sustaining limits. Parathyroid hormone also causes the kidneys to reabsorb calcium and causes phosphorus to be excreted. Calcium is also absorbed from the intestines at an increased rate. As the bones are broken down by osteoclasts, the body starts to put fibrous connective tissue around the bones to try to give the bones some stability. This may result in a swollen appearance to the limbs, especially in reptiles. Often, the jaw becomes rubbery and swollen, and this is often very obvious in monkeys and big cats. MBD most often affects the mandible, long bones and vertebral column. When calcium can no longer be pulled from the bones in amounts to maintain blood levels, the serum calcium will drop to dangerously low levels. At this point, twitching may develop, progressing to seizures from hypocalcemia.

In birds, in addition to the thyroids and parathyroids, there are two ultimobranchial glands found in the thoracic inlet that are also involved in calcium metabolism. There are four types of cells in the ultimobranchial gland: c-cells, parathyroid nodules, vesicles and lymphoid tissue. The c-cells secrete calcitonin, which blocks the transfer of calcium from bone to blood, but its physiological role in birds is not clear. It may be relatively unimportant in regulating the level of plasma calcium but significant in preventing excessive bone resorption by parathyroid hormone.

Diet and MBD

In juvenile carnivores, such as big cats, calcium deficiency is usually associated with diets of skeletal muscle and viscera, but not bone, or diets of neonatal prey (baby chicks, for example). Lack of full-spectrum lighting, especially unfiltered sunlight, will exacerbate the problem. In older animals, most often marmosets and tamarins in my experience, MBD is often associated with a lack of unfiltered sunlight, inadequate vitamin D3 in the diet, and an incorrect calcium: phosphorus ratio.

Metabolic bone disease is a common nutritional disease in some birds, most commonly musophagids (turacos, Go-Away Birds and Plantain-Eaters.) MBD is most likely to occur when the natural diet of birds being kept is not known or only partially defined. Young growing birds are more likely to be affected. MBD and calcium deficiency may also be involved in the higher incidence of dystocia and egg-binding that occur in these birds. Most fruit is low in calcium and has an incorrect calcium: phosphorus ratio. Birds (and other species of animals, as well), when offered a large amount of fruit in the diet, may choose these items preferentially, even if the diet as a whole is balanced and contains adequate calcium. Therefore, it may be preferable to limit the amount of fruit in the diet or to blend the entire diet into a homogeneous mixture to ensure that all the dietary items offered are consumed. Calcium supplements may be added to the diet, as well.

In reptiles, rubber jaw is common, and limbs may become misshapen. Green iguanas grow very rapidly during the first year of life, and if fed and housed improperly, MBD is likely to occur. Adult herps with MBD may present with uncontrollable twitching or seizures due to hypocalcemia.

In mammals, exposure to ultraviolet (UV) radiation in the 290-320 nanometer (nm) wavelength range will allow the production of vitamin D3, cholecalciferol. For maximum effect of full-spectrum fluorescent lights, the light should remain on 12 hours per day and the light should be placed within 18 inches of the animal for maximum effect (follow the recommendations that come with the bulb).


A drug used to treat osteoporosis in post-menopausal women, works well to treat the effects of, and even works to reverse, MBD in all of the animals this author has used it on. It is a synthetic calcitonin, called calcitonin-salmon (Calcimar TM, Miacalcin TM) that is also used to treat Paget's disease in humans, a disease characterized by abnormal bone formation and resorption in long bones. In humans, calcitonin is also used for early treatment of hypercalcemic emergencies along with other appropriate therapy. Calcitonin works by inhibiting bone resorption, and it pulls circulating calcium and phosphorus out of the blood, and will help put calcium into bone and other body tissues. It decreases osteoclast activity and stimulates osteoblast activity. It also causes increased calcium excretion in the urine.

So, the main effect of calcitonin is to help rebuild bone more quickly. What used to take weeks or months to correct, can now take just a few weeks to reverse. The synthetic calcitonin-salmon actually reverses the effects of parathyroid hormone.

It is important to remember that calcitonin pulls calcium out of the bloodstream, so prior to using it, the animal should be pretreated with calcium, either by injection, orally, or by a combination of the two, prior to using it. Providing an exogenous source of vitamin D3 to facilitate calcium utilization, is also a good idea.

Treatment with calcitonin-salmon should only be undertaken by a vet experienced with this drug. It is an expensive drug, but doses given to most exotic animals are quite small. Because calcitonin pulls calcium out of the bloodstream, it can precipitate a hypocalcemic crisis if the animal has not been adequately pretreated with calcium. And prior to treatment, the diet must be corrected, and proper husbandry instituted (including adequate exposure to ultraviolet light).

For most species, calcium glubionate (Neo-Calglucon) should be given at 1 ml/kg PO q12hr, for several months. Once the animal is pre-treated with calcium, Neo-Calglucon can be administered in the drinking water, 1 ml. per ounce of water. Injectable vitamin D should be given (even though the efficacy may not be completely known or understood). For calcitonin, a dosage of 50 IU/kg, IM, repeated in 7 days, is recommended for herps. In marmosets and tamarins, this author has used a dosage of 10 IU/kg, on days 0, 3, 6, 10, 15, and 22. Please be aware that this dosage is empirical, and scaled down from human dosages. However, this regime worked very well and resulted in excellent clinical response in several cases. In the case big cats with MBD, following dietary correction and support therapy, treatment with calcitonin-salmon will usually result in stabilization of the cat, and although recovery will be slow, eventually, many will be able to stand and walk unaided. The dosage of calcitonin-salmon used by this author (also an empirical dose) was 5 IU/kg body weight IM q48 hr. (The human dosage range for Paget's disease is 4-8 IU/kg q12 hr. to q6 hr.) However, the dosage for humans with osteoporosis is 100 IU per day SQ or IM, or every other day. Calcitonin comes as a sterile solution in 2 ml. vials, containing 200 IU per ml.

Handling MBD patients should be kept to a minimum to prevent additional damage to the skeletal system. Herps should be placed in a warm cage with all climbing branches removed to prevent falls. Strict cage rest in a small confined space is recommended and the patient should be isolated to prevent competition for food, and this will also allow better monitoring of food intake.

Calcium binders that use aluminum are popular to lower phosphorus levels, however, it has been discovered that aluminum can be nephrotoxic, which can compound any pre-existing renal problems, so it is safer to use calcium to bind phosphorus and therefore lower the hyperphosphatemia. If aluminum-containing phosphorus binders are used, they should only be used short-term to minimize any renal damage.

Fractures may be splinted, however, often the bones will fracture on either side of the splint, so often cage rest is the safest way to manage fractures.

In addition to treating the hypocalcemia and related problems, support care is necessary. Fluids, thermal support, nutritional support and any other therapy needed should be administered, based on results of the lab tests.

Typical MBD in a Big Cat

I examined a cougar recently, called out for a second opinion. The cat had been seen within the week by a practitioner who had his veterinary license suspended and had diagnosed a "vaccine reaction" in the cat. When I examined the cat, on emergency at 1:00 a.m., it was found to be paralyzed in the hind legs, and had severe paresis of the front legs. There was crepitus of the hips and hind legs. Bilateral cataracts were present. Renal failure was developing. By the time the cat was treated, it was in lateral recumbency. The diet had been hamburger and cooked chicken meat.

The owners had purchased the cub from a breeder in Oklahoma, and were given no instructions regarding diet, husbandry or veterinary care. They were a wealthy couple with little common sense. They had not researched anything about owning a big cat before foolishly purchasing the cougar. They had been working with the vet with the suspended license, who did not believe in prophylactic vaccines, nor did he use common pharmaceuticals, relying solely on homeopathic treatments and herbs. It was this veterinarian who had suggested the diet that was being fed when the cat became ill. This is a typical scenario when a young animal is presented with MBD: incorrect and inappropriate diet, ignorant (but usually well-meaning) owners and poor husbandry.

Osteodystrophia Fibrosa and Scurvy in Guinea Pigs

There have been cases reported in the literature of nutritional secondary hyperparathyroidism due to Ca-P imbalance as the underlying cause of OF in guinea pigs. Scurvy (scorbutus) can be involved with nutritional secondary hyperparathyroidism, as clinical signs can develop in as little as two weeks of ascorbic acid deprivation. Scurvy occurs most commonly in young, rapidly growing young animals. Lack of dietary vitamin C results in defective collagen formation, which is necessary for structural integrity of blood vessels. Resulting clinical signs may include leaky blood vessels and hemorrhage, most often into joints and gingiva and loose, maloccluded teeth due to the teeth not being anchored tightly in the sockets. Other clinical signs of scurvy include a rough haircoat, anorexia, diarrhea, teeth grinding and vocalizations due to pain, delayed wound healing, lameness and increased susceptibility to bacterial infections.

Radiographs may show generalized mild osteopenia (no double cortical line), a scorbutic lattice and a subtle zone of debris on the proximal tibia. The double cortical line sign is one of the few pathognomonic Roentgen signs of osteopenia, which has been reported in humans and guinea pigs. The specific Roentgen signs of scurvy are very similar in humans and guinea pigs.

I recently consulted for a vet treating a male (intact), 17 month old guinea pig with pathologic fractures of the left and right humerus bones. The guinea pig was on an appropriate diet (according to the owner), but it developed fractures with normal ambulation. Lab results were as follows: WBC 7,700 (n 5.5-11.0 x 103/ul), PCV 35 % (n 33-50%), MCV 77 (n 60-70 fL), differential: neutrophils 76% (5852) high, lymphocytes 8% (616) low, monocytes 11% (847) high, eosinophils 5% (385) high, platelets increased at 804 x103/ul. The chemistries that were abnormal included: alkaline phosphatase 246 (elevated) (n15-45 IU/L), total protein 4.4 (low) (4.5-6.5 g/dL), calcium 7.9 (low) (n 8-12mg/dL), phosphorus 8.4 (n 4.2-8.5 mg/dL). Radiographs, evaluated by a board certified radiologist, confirmed metabolic bone disease in this patient. Any time there is osteoclast activity, the alkaline phosphatase will be elevated. Unfortunately, this patient died before calcitonin could be administered.

Metabolic Bone Disease in Psittacines

I recently consulted on a case of a young (approximately 14 months of age) sun conure that was reluctant to move. Diet was a seed mix, pellets, table food, fruits and vegetables. Radiographs evaluated by a board certified radiologist demonstrated the unusual diagnosis of metabolic bone disease, which was supported by lab tests indicating hypocalcemia, hyperphosphatemia and increase in alkaline phosphatase. The bird also showed signs of secondary bacterial infection. No specific cause could be identified for this diagnosis.


Calcitonin-salmon is an effective treatment for metabolic bone disease in many different species of exotic animals. However, it must be stressed that correcting the diet and husbandry practices are essential for reversing this disease. Offering calcium carbonate chewable tablets, such as flavored antacid tablets, as a dietary supplement, is a simple way to provide an excellent source of available calcium for many animals. Providing full-spectrum (UVA and UVB) fluorescent lighting which is replaced every six months, or better yet, allowing an animal to be exposed to natural sunlight, unfiltered through glass or plastic (approximately one hour per week as a minimum) is essential, even if vitamin D is supplemented in the diet. Because this disease is almost always completely preventable, I hope that the day comes when I need never treat another case of MBD again. Let's all work to educate our clients and owners of exotic animals regarding appropriate diets and husbandry practices.

Copyright © 2006 Margaret A. Wissman, D.V.M., D.A.B.V.P.
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