Nutrient Requirements - The Merck Veterinary Manual

Nutrient Requirements

Water is essential for normal hydration. The ability of arid species to conserve water is not indicative of a reduced intake requirement. In several species, reduced water availability has resulted in lowered growth rates without apparent changes in the physiologic status of the animals.

The protein content of the diet has traditionally been recommended to be ~18-20% for carnivores and 11-12% for herbivores. Amino acid requirements are identical to those of mammals, with the addition of histidine in reptiles. Inadequate protein levels result in weight loss, muscle wasting, increased susceptibility to secondary infections, failure to reproduce, and slower healing after injury. A nonresponsive infection can be the result of a primary nutritional deficiency. Many newer commercial diets offer protein levels up to 28-32%, which may prompt rapid growth but can have severe longterm consequences (eg, hyperuricemia, see below). Consequently, lower protein levels are currently recommended, particularly for uricotelic reptiles.

Excess protein is common in the diet of carnivorous lizards when excessive meat products are fed rather than whole animals. Feeding excessive amounts of high-protein cat foods has been implicated in cases of excess protein and vitamin D₃. Many nutritionists recommend not feeding cat foods to reptiles. Dog food, especially low-fat varieties, can be used sparingly as part of a complete and balanced diet in both carnivores and omnivores. The overuse of high-protein diets prepared for carnivores has been incriminated in causing disease in tortoises and iguanas.

Feeding excess protein can result in hyperuricemia, in which uric acid is deposited in internal organs; this may lead to primary visceral gout, a debilitating and often fatal condition. Uric acid levels can also be increased by dehydration or renal damage. Hyperuricemia leading to visceral gout from these causes is referred to as secondary visceral gout. (See also Urinary System.)

Most protein deficiencies are seen in herbivorous species on “salad-type” diets or in anorectic individuals. Herbivore diets may be supplemented with alfalfa sprouts, bean sprouts, soy beans or meal, invertebrates, or soft-moist or low-fat dog food (used sparingly). Anorectic reptiles may require force feeding, environmental alteration, or sufficient variety in the diet to identify a preferred food item.

Carbohydrates do not appear to be essential to carnivorous species but, in many cases, caloric requirements can be met by adding carbohydrates to the diet or through gluconeogenesis of dietary protein. Crocodilians appear unable to assimilate certain polysaccharides. Blood glucose values are variable for each order and may remain increased for as long as 1 wk after a meal. Blood glucose is increased during breeding seasons, especially in males.

Clinical hypoglycemia has been reported in captive crocodilians. Signs include mydriasis, tremors, opisthotonos, loss of the righting reflex, and death. Overcrowding and stress with the prolonged release of adrenergic compounds is thought to be causative. Hypoglycemia without clinical signs is normally seen in alligators during the winter.

Fiber is required for the normal functioning of the digestive tract. In large land tortoises and other herbivorous species, adding roughage (eg, hay) to the diet has eliminated chronic malodorous diarrhea.

Specific fatty acid requirements have not been determined for reptiles, but 0.2% linoleic acid in the diet is recommended. Deficiencies have not been reported, but reduced stores in the visceral fat have been associated with small clutch size during the breeding season. Atherosclerosis has been reported; restriction of cholesterol may be an important longterm dietary consideration in captive reptiles.

Mineral deficiencies are seen frequently in captive reptiles, especially chelonians and lizards. Vitamin and mineral deficiencies are rare in snakes that are fed nutrient-rich whole prey. A vitamin/mineral supplement should be added to the diet of every captive reptile; many products specific for use in reptiles are commercially available.

Calcium is the most important mineral deficiency in reptile nutrition. A calcium: phosphorus ratio of at least 1.2:1 is generally recommended. However, in some situations (eg, females laying large numbers of calcareous eggs, or rapidly growing juveniles), a ratio approaching 2:1 or greater, is more appropriate. With carnivorous diets, skeletal muscle has a calcium:phosphorus ratio of ~1:25; beef heart and liver, ~1:44. Feeding a pure meat diet not only provides excessive protein but also is extremely poor in calcium and rich in phosphorus. Such carnivorous diets should be altered to include whole prey or a low-fat, low-protein dog food. Calcium should be supplemented with products developed for reptiles that ideally contain no phosphorus.

The chitinous exoskeleton of insects is devoid of calcium and, therefore, insectivores must obtain dietary calcium from insects “gut loaded” and powdered with calcium supplements (see Management).

Herbivores should be encouraged to eat items rich in calcium, including cabbage, kale, okra, sprouts, collard greens, and bok choy. These foods typically are also rich in vitamin A. A calcium supplement with no phosphorus should be routinely given to herbivores, up to twice weekly in normal specimens.

Vitamin D is also required for proper calcium metabolism and balance. Animals housed outside with access to natural, unfiltered sunlight usually have adequate levels of vitamin D₃ because inactive vitamin D precursors in the skin are converted to vitamin D₃ when the skin is exposed to ultraviolet (UV) light. Access to UV light has been recommended in reptiles not exposed to unfiltered sunlight (see lighting requirements Management). Reptiles fed whole mammalian prey generally consume adequate levels of preformed vitamin D₃ . The food items of insectivores should be fortified by gut loading and powdering. Herbivores that have limited exposure to UV light should receive supplemental vitamin D₃. Most reptile supplements that contain calcium also contain limited (but adequate) amounts of vitamin D₃ . Excessive levels of oral vitamin D₃ can lead to the excessive absorption and utilization of calcium.

An inappropriate calcium:phosphorus ratio or inadequate levels of vitamin D can result in nutritional secondary hyperparathyroidism, fibrous osteodystrophy, osteomalacia, cystic calculi, cloacal calculi, and rickets. Pathologic fractures, bone deformities, and soft or deformed shells in turtles may occur. Terminal signs may include tetanic seizures. The skeletal maladies that result from abnormal calcium:phosphorus metabolism are referred to as metabolic bone disease.

Nutritional secondary hyperparathyroidism, iguana

Nutritional secondary hyperparathyroidism, iguana

Treatment consists of correcting the calcium:phosphorus ratio and administering vitamin D₃, if appropriate, either by injection, per os, or by exposure to an appropriate UV source. A dietary history should be obtained and evaluated, and deficiencies corrected. If a calcium supplement is to be provided in the initial stages of treatment, it should not contain phosphorus. An excellent calcium source is calcium glubionate, given PO at 1 mL/kg, as long as is needed. Other sources of dietary calcium include crushed cuttlebone, crushed oyster shell, crushed or pulverized calcium lactate, or commercially available products. In severe cases, a calcium injection can be given before the oral supplementation. Calcium gluconate (10%) can be given at 250 mg/kg, IP, for 1 dose only, and calcium lactate at 5 mg/kg, IM or SC, daily for 1-7 days.

To avoid toxicity, vitamin D should not be injected more than once every 2-4 wk at a dosage of 200 IU/kg, IM. Excessive supplementation of vitamin D combined with plentiful calcium may result in soft-tissue calcification. Green iguanas fed excessive levels of cat food developed calcification of soft tissues thought to be due to hypervitaminosis D. Oversupplementation of vitamin D and calcium is thought to be one of the main causes of renal disease in mature lizards, especially green iguanas and bearded dragons.

Calcitonin has been used at dosages of 50 IU/kg, IM, once a week for 2 treatments in green iguanas with metabolic bone disease caused by nutritional secondary hyperparathyroidism. Calcitonin inhibits bone resorption and acts as an antagonist to parathyroid hormone, but there is debate whether calcitonin accomplishes for reptiles what it does for mammals. Calcium supplements should begin before the calcitonin is used, because the latter can cause severe hypocalcemia.

Iodine deficiency can manifest as lethargy and an abnormal swelling at the thoracic inlet (goiter). Feeding of goitrogenic compounds, including certain green forages, may precipitate the problem. The imbalance is corrected by supplementation with a balanced vitamin-mineral mixture containing iodine, or iodized salt (0.5% of the diet).

Iron and copper deficiencies associated with anemia have been reported in turtles.

Vitamin A deficiency is seen frequently in captive turtles. Aquatic turtles rarely are involved because they typically eat whole prey that contain preformed vitamin A. However, some adult aquatic turtles eat a more herbivorous diet, and the first documented case of hypovitaminosis A was in a red-eared slider. Terrestrial turtles are more commonly affected. Herbivorous tortoises fed correctly eat diets high in β-carotene that is converted to vitamin A and rarely exhibit signs. Box turtles, particularly in the USA, appear most at risk usually due to diets (fed in captivity) that contain little vitamin A. Signs of hypovitaminosis A include palpebral edema, chronic respiratory disease, and renal disease. Squamous metaplasia of epithelial structures is characteristic, especially of the lacrimal glands, producing a thickened, sticky discharge in addition to swollen eyelids. The eyes may eventually remain closed, impairing the ability of the turtle to find food. Secondary infections of the eyes, respiratory system, and skin are common. Treatment consists of short daily soaks to allow the turtle to drink and wash its eyes, application of an antibiotic ophthalmic ointment for both moisture and secondary infections, and administration of vitamin A at 200 IU/kg, once every 2 wk for no more than 2 injections. For less severe cases, oral vitamin A can be supplied via cod liver oil at a rate of 1 drop in the food twice a week. Oral supplementation is generally preferred due to the potential toxicity of the injections. Commercially available vitamin products are also available for reptiles. Dietary levels of vitamin A should be increased for up to 6 wk before hibernation in turtles and tortoises. Severe hyperkeratosis and dysecdysis, which in the past have been associated with hypovitaminosis A, are more commonly due to hypervitaminosis A. Vitamin A administered at dosages recommended in the past would induce severe skin irritation and shedding, often within days.

Hypovitaminosis A, slider turtle

Hypovitaminosis A, box turtle

Vitamin A deficiency, turtle

Vitamin B₁ deficiency can result from diets containing fish with high thiaminase levels, and exogenous supplementation is required. Weight loss with adequate food intake is characteristic, but neurologic signs can also occur. Goldfish have low thiaminase activity, while smelt have extremely high levels. Freezing of fish decreases parasite loads but increases thiaminase levels. Posterior paresis progressing to flaccid paralysis and the loss of the righting reflex has been seen in iguanas and garter snakes, respectively, and is associated with a B-complex deficiency. Deficiencies of the water-soluble vitamins often involve more than 1 vitamin and require treatment with a multivitamin preparation.

Biotin deficiency, associated with the feeding of unfertilized, uncooked chicken eggs, has been reported in helodermatids, some varanids, tegus, and larger skinks. Anorexia and weakness are the primary signs. Avidin, an antibiotin substance, is found in ovalbumin. Feeding fertilized eggs reduces the amount of avidin in the egg, and biotin supplementation reduces the frequency of the condition.

Vitamin C is produced endogenously in reptile kidneys. Vitamin C deficiency has been incriminated (but never proved) in cases of infectious stomatitis, and oral or injectable supplementation of vitamin C (from 25 mg to several grams, depending on the size of the reptile, daily or as needed) has been suggested, especially when renal disease is present. While not proved beneficial, vitamin C supplementation at this dosage is safe and will do no harm.

Vitamin-K-responsive coagulopathies characterized by prolonged gingival bleeding after loss of deciduous teeth have been reported in crocodilians. Treatment with vitamin K at 0.5 mg/kg body wt has been suggested.

Steatitis has been reported in crocodilians fed mackerel and tuna and in snakes fed obese rats. Ceroid deposition was seen at necropsy. Vitamin E supplementation at 100 IU/kg has been recommended as a preventive, but it is more important to avoid feeding fish that have been frozen and thawed improperly, stored too long, or left uneaten for ≥1 day.