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Veterinarians are increasingly being presented with reptile patients, many which suffer from a nutritional related illness. Metabolic bone disease, vitamin D3 deficiency and hypovitaminosis A are three of the most commonly diagnosed illnesses in reptiles1. It is important for reptile owners to understand how to correctly identify and prevent these conditions in reptilian pets.
Calcium and
Vitamin D3 Deficiency In carnivorous reptiles, calcium deficiency usually is associated with diets comprised of skeletal muscles and viscera, or neonatal prey with little skeletal development. These meats have a negative Ca:P ratio of 1:302. Insects also have a negative Ca:P ratio, and therefore should be fed a calcium rich diet 2-3 days prior to being used as food2. In herbivores, deficiencies are due to an unsupplemented diet of greens, or diets containing high amounts of phytates (soy products) or oxalates (spinach) that impair calcium absorption3. Herbivorous diets usually contain little calcium (Ca) and excessive phosphorus (P). An ideal Ca:P ratio is 1:<1, which is only achieved with captive herbivores via supplementation4. It is imperative veterinarians thoroughly evaluate each patient’s diet to establish if nutrition is adequate. Nutritional secondary hyperparathyroidism involves an excess production of parathyroid hormone in response to hypocalcemia (low calcium). Calcium is reabsorbed from the bone to compensate for the low blood calcium. Over time, if dietary calcium fails to replenish bone reservoirs, bone weakens. This disease can affect all reptiles, but is most common in lizards and aquatic turtles5. Two distinct forms of MBD are possible and although it is commonly seen in juveniles, it is also associated with adults. Growing lizards are prone to classic MBD, with most symptoms arising from the skeletal system, including skeletal deformities, fibrous osteodystrophy and pathologic fractures. The second form is more common in adult lizards with symptoms secondary to hypocalcemia, including muscle tremors, paresis and seizures. MBD affects all reptiles differently and veterinarians must be alert for any of the signs, as some patients may exhibit all of the classic symptoms, while some patients may exhibit only one sign of the disease. The earliest and most consistent sign of MBD is partial or complete lack of truncal lifting2. Healthy lizards lift their bodies and proximal tails off the ground when they walk. Often times, lizards with MBD drag their pelvis’ or slide around on their trunks, unable to lift their bodies off the ground. Signs of fibrous osteodystrophy include the appearance of a very robust, or well-muscled lizard. The mandible may also be pliable. Generally, there is a gradual decline in appetite and weight loss associated with MBD. Radiographs are not essential but useful to diagnose MBD and can serve as a basis for evaluating progress during therapy. Radiographic findings include an overall decrease in bone density and poor contrast of bone and soft tissue opacities2,3. Epiphyses are often widened and very radiolucent. Plasma Ca and P levels can aid in diagnosing MBD and also guide therapy regimens. As the disease progresses, plasma Ca levels generally decrease (often less then 8.5 mg/dl) and plasma P levels generally increase3, however, symptomatic lizards may have normal plasma Ca and P levels. An inverse Ca:P ratio is strongly suggestive of MBD2. Treatment begins with stabilizing the life threatening conditions, such as hypocalcemic tetany, dehydration and some pathologic fractures. All the medical care known to be effective will be useless if the owner does not agree to alter the reptile’s current diet and environment. Goals of therapy include not only the correction of nutritional deficiencies, but also the reversal of bone loss and promotion of new bone, depending on the severity of the disease6. It is important that the animal remains in a safe environment during therapy, as handling and climbing could lead to multiple fractures. Strict cage rest is advised. If the reptile is still eating, instructions on the appropriate diet and supplement (calcium carbonate or glubionate dusted on greens) must be given. If the patient is anorexic or not eating enough to maintain it’s body weight, it should be force fed the appropriate enteral diet via a red rubber feeding tube or syringe. For large herbivores and turtles, one part alfalfa pellets and two parts water blended to a slurry works well2. Feed 20ml/kg every other day. For debilitated carnivorous reptiles, a high fat, high protein feline enteral diet is recommended3. On alternate days, give the same amount of water. Begin oral calcium supplementation with 1ml/kg calcium glubionate every 12 hours2. If the patient is too weak for oral administration, give 100mg/kg 10% calcium gluconate IM every 6 hours2, or as needed to prevent muscle tremors. Switch to oral supplementation as soon as possible. Oral Ca supplementation should be continued for 1-3 months. 1000IU/kg vitamin D, IM, should be given once a week for two treatments2. An unfiltered ultraviolet light must also be available to the patient for 12 hours a day7. Recently, calcitonin has shown promising success in the treatment of MBD11, however, the patient must be normocalcemic before calcitonin is given (between 8-11mg/dl). Hypocalcemic patients must be pretreated for 7 days with calcium glubionate (1cc/kg, PO, BID) before calcitonin therapy is initiated2.Doses of salmon calcitonin at 50IU/kg, IM, in the front legs once a week for two treatments appears to be beneficial in case studies8. Without treatment, patients showing clinical signs of MBD will die. Patients can be treated on an outpatient basis, except those exhibiting paresis, which should be stabilized before release. Most veterinarians treating reptiles agree that the prognosis depends on the owner’s desire to follow through with the prescribed recommendations, which takes a substantial commitment. A complete cure from MBD depends, of course, on the severity of the disease. Success often depends on an early diagnosis and aggressive treatment. Vitamin D3 deficiency occurs with diets that contain only vitamin D2, are devoid of vitamin D3 or low exposure to ultraviolet wavelengths via direct sunlight or full-spectrum lamps. Limited research data and clinical impressions suggest that dermal synthesis of 1,25-dihydroxycholecalciferol may be more efficient than gastrointestinal absorption of dietary D39. Specific calcium and Vitamin D3 requirements are unknown for most reptiles. General recommendations for birds are often substituted for reptiles and are as follows: 1.8-3.0g calcium /kcal or .5-1.5% of dry matter intake, and 200-500IU/kg of dry matter for vitamin D3. Oversupplementation of calcium inhibits intestinal absorption of zinc and copper and thyroid uptake of iodine5. Supplementation should be recommended, but quantities should be measured. Generally, invertebrate prey and salads should be dusted with vitamin and minerals 1-2 times per week for adults, 3-4 times per week for juveniles. Ultraviolet lights are thought to be essential for photochemical production of the active form of vitamin D, which is cholecalciferol, or D3. Vitamin D3 absorption is enhanced by encouraging clients to use UV lights in the 290-320 nm wave length, replacing bulbs every 6 months and allowing the reptile to sit within 18 inches of the bulb7. Natural sunlight is only beneficial if the reptile is allowed to bask in direct light, as glass filters out a substantial amount of the beneficial ultraviolet rays. Vitamin A deficiency Young, aquatic turtles are most commonly diagnosed with hypovitaminosis A. These turtles are often maintained on diets of unsupplemented greens, meat, and poor commercial diets. Turtles may present with a history of anorexia and poor growth or shell development. Physical examination often reveals edema and inflammation of the eyelids. Chronic cases will often have whitish-yellow cellular debris underneath the eyelids. Other symptoms may include anorexia, lethargy and a nasal or ocular discharge. Diagnosis is usually based on dietary history, clinical signs and response to therapy. Injectable and oral preparations of vitamin A are the treatment of choice. 1500-2000 IU of vitamin A/kg, SQ, once a week for 2-6 weeks, depending on the severity, is the recommended dose10. Higher doses do not speed recovery and increases the likelihood of vitamin A toxicosis, characterized by anorexia and skin sloughing. Secondary illnesses, such as upper respiratory infections and anorexia should also be addressed. Prevention of hypovitaminosis A includes expanding the diet to include dark green leafy vegetables (dandelions, turnips, mustard greens and bok choy), foods rich in betacarotene (squashes, carrots, sweet potatoes and cantaloupe) and fish (for aquatic turtles). Several commercial reptile foods also contain adequate vitamin A11. Nutritional Support of Debilitated Reptiles Diets for nutritional support are selected after considering energy sources, nutrient contents, digestibility, and form. For example, a diet for a starved snake (carnivore) should provide calories mostly from fat and protein, with little carbohydrate and no fiber. In contrast, a diet for an herbivorous lizard would contain less fat and more carbohydrate, especially fiber. Often times, the veterinarian’s first choice is a liquid enteral diet3. Enteral diets designed for cats and critical care human patients usually contain more fat and less carbohydrates, and are therefore suitable for carnivorous reptiles. Those designed for dogs and most human beings are suitable for omnivores and diets with fiber are suitable for herbivores, although fiber supplementation is recommended9. Liquid diets can be blended with other foods to insure the reptile is getting adequate nutrition. Conclusion Nutritional management is an extremely important part of the care of healthy and sick reptile patients. Primary nutritional disorders are common in reptiles, often due to inappropriate management and poorly formulated diets. Clinically, deficiencies of calcium, vitamin D3 and A are most common. |
