Nutritional Problems in Reptiles
World Small Animal Veterinary Association World Congress Proceedings, 2008
Bairbre O'Malley, MVB, CertVR, MRCVS
Bairbre O'Malley Veterinary Hospital
Bray, Co. Wicklow, Ireland


Nutritional problems are commonly seen in pet reptiles. This is mainly caused by poor feeding habits, poor quality foods and general ignorance by reptile owners of their pet's dietary needs. Problems range from simple starvation to deficiencies of Vitamin A, D & E and calcium to the converse of obesity and hepatic lipidosis. Excess supplementation of Vitamin A and D can also lead to vitamin toxicities.


Reptiles are ectothermic so do not rely on food intake to maintain body temperature. Consequently they do not have to eat as frequently as birds and mammals. In the wild they are also capable of long periods of physiological starvation during times of drought, temperature extremes, food shortage and hibernation. Unfortunately many pet owners assume their pet is undergoing this physiological hibernation / brumation when the pet is actually starving due to illness or poor husbandry. Consequently reptiles are often presented to veterinary clinics in an advanced state of debilitation.

Reptiles are commonly kept under suboptimal conditions leading to stress and maladaptation. Common causes are inappropriate food, low temperatures and competition from tank mates. Food of appropriate size and familiar colour are often not provided.

Treatment of Starvation

These animals are often chronically debilitated and any medical problems must first be ruled out. Any underlying dehydration problems should be addressed with fluids, electrolytes and warm water soaks. Assist feeding calories and nutrients until normal feeding resumes--this can be done by stomach tube feeding or by placing a pharyngostomy tube under anaesthetic. As the problem is usually a chronic one increase the feeds slowly. Overfeeding can lead to fatal hypokalemia and hyperphosphatemia.

Husbandry issues like subnormal temperatures, lack of basking lamps and more natural diet must be addressed. Suitable cage furniture like hidey holes, foliage or branches must be provided. For example, the royal python is known to be a difficult feeder in captivity. In the wild this species is secretive, nocturnal and feeds on gerbils. They 'sit and wait' for their prey and then feed under cover in burrows. To stimulate feeding in captivity it is important to provide plenty of hidey holes and feed brown coloured mice scented with gerbil smell.


A captive reptile will expend a lot less energy than a wild one so will have lower energy needs. Feeding fatty foods like obese mice, waxworms and goldfish may lead to excessive rapidity of growth in juveniles and obesity in adults.

Obesity is also commonly seen in sedentary species like savannah monitors, tegus, pythons and boas. Owners also need to be aware of their pet's natural lifestyle--for example in some wild habitats, savannah monitors often fast from December to late May and live off fat stores. The Horsfield tortoise that comes from the Russian steppes only spends about 15 minutes a day feeding and is active for only 3 months of the year so overfeeding of this species is common.


Firstly rule out any medical problems like ascites and pregnancy. Restrict amounts of crickets and feed lean prey in small amounts. Increase the size of the enclosure and provide an enriched environment to increase exercise. Herbivores can be given increased fibre and encouraged to forage for food. Commercial pellet foods which are higher in fat should be avoided.

Hepatic Lipidosis

This is caused by the excessive accumulation of triglycerides in hepatocytes and is often triggered by a period of starvation. It is commonly seen in obese animals fed a high fat diet (e.g., obese laboratory mice and waxworms) and also non-breeding females. Biochemical evaluation of liver enzymes can be helpful but the most accurate method is via liver biopsy.


Animals with mild hepatic lipidosis are usually in good body condition and can be given assisted feeding in moderate amounts for a short period. More severe cases will need to be stabilized first with fluids and may take months to start feeding. In many case a pharyngostomy tube will need to be placed so the owner can feed the reptile long-term at home.

Nutritional Secondary Hyperparathyroidism

Nutritional secondary hyperparathyroidism (NSHP) or metabolic bone disease is commonly seen in reptiles. It occurs when a low intake of calcium stimulates parathyroid hormone to mobilise calcium from the bone to maintain normal blood levels. This condition mainly affects juvenile lizards and chelonians but can occur in adults too. It is uncommon in snakes as they are fed a vertebrate diet rich in calcium. Juvenile and small snakes fed pinkies (neonatal mice) that have no mineralised skeleton can be affected.


Many owners seem to believe that insects live on thin air and never actually feed them. Basically if the prey is under nourished so will be the predator. Insects like mealworms and crickets have an inverse Ca:P ratio. This can be helped by two methods.

 Gut loading--feed the crickets a high calcium food with a bit of fruit / vegetables for moisture (e.g., milk powder, porridge oats with a slice of apple). This should be supplemented with a calcium powder. Vetark Nutrobal is good as it has a Ca:P ratio of 46:1.

 Dusting--prior to feeding, the crickets should be put in a plastic bag and lightly dusted with a good quality calcium powder.


Feed a wide variety of mixed leafy greens high in calcium like dandelions, romaine lettuce, and kale.

Common Causes

 Diets low in calcium and high in phosphorus (e.g., crickets, skeletal muscle meat, day old chicks, pinkie mice).

 Lack of Vitamin D3 (cholecalciferol) in the diet or lack of ultraviolet light. Vitamin D is produced by the action of ultraviolet light on skin and the crucial wavelengths are UVB 290-315 nm. The amount of UV needed will depend on the individual species--some nocturnal lizards like the leopard gecko can absorb Vitamin D very rapidly by exposing themselves to sun briefly at dawn and dusk.

 General poor husbandry--production of Vitamin D is very slow at suboptimal temperatures, lack of exercise due to too small a vivarium, too rapid growth due to over feeding of juveniles.

Clinical Signs

Lizards often present with fractured limbs or hind limb paresis due to poor mineralisation of the bones. The limbs may appear swollen due to flabby muscle mistakenly giving the appearance of plumpness. The mandible can be swollen (rubber jaw) and there is general anorexia and lethargy. Severe cases get hypocalcaemic tetany and seizures. Poorly mineralized eggs, dystocia, cloacal prolapse are also commonly seen.

Juvenile chelonians are at high risk because of the high calcium requirements for their shell during growth. They present with anorexia and with a soft shell. Often the shell may appear deformed, asymmetric and too small for animal.


This is made via the husbandry history (poor diet and lack of UV light), clinical signs and radiography.


Generalised osteopenia of skeleton is particularly evident at extremities (digits and lateral vertebral processes of tail) where the bone assumes the same soft tissue opacity as surrounding tissues. Thin cortices of long bones with folding fractures may be seen. There is often evidence of past healed fracture and / or spinal deformities like scoliosis, lordosis etc.


Many patients are anorexic and dehydrated and may need to be hospitalized for fluid therapy and assisted feeding. Oral calcium should be given or parenteral calcium (Ca gluconate 100 mg/kg sc) if there are muscle tremors or seizures. The owner must correct any underlying husbandry problems like subnormal temperatures and lack of ultraviolet light and dietary calcium. Access to unfiltered sunlight (i.e., not through a window) is important where possible. Gentle handling is required.

Vitamin D Toxicity

Vitamin D is toxic when given in high doses. This can happen with overzealous supplementation or where the owner is feeding dog / cat food to herbivorous species. Signs of toxicity are soft tissue calcification of many body organs which can be visible on radiographs. Treatment is with aggressive fluid therapy.

Hypovitaminosis A

This is seen commonly in young aquatic turtles fed poorly supplemented commercial foods (dried shrimp mix) and muscle meats. It can also be seen in tortoises and some lizards. Carnivores have to get vitamin A from animal sources (e.g., liver) while herbivores can get it via conversion from beta-carotene in plant foods. Lack of vitamin A leads to squamous cell metaplasia and hyperkeratosis and may also affect growth and cartilage development.

Clinical Signs

Affected turtles often show poor growth and anorexia. They develop blepharoedema of the eyes due to squamous metaplasia of the Harderian glands. They can develop secondary respiratory infections like rhinitis and pneumonia. Aural abscesses can be seen plus inguinal and axillary oedema due to secondary kidney problems.


Injectable Vitamin A (1000-5000 iu/kg q 7-10 days for 4 treatments) and oral preparations. Be careful to avoid overdosing with vitamin A injections. Severely anorexic animals may need hospitalisation for force-feeding. Secondary pneumonia will need to be treated with antibiotics.

Turtles with vitamin A deficiency are also likely to be deficient in other nutrients as well, so a balanced diet must be provided. Turtle pellets should be given along with dark leafy greens and the turtles weaned off shrimp mixes and muscle meats. Fresh prey like earthworms, mealworms and small fish are recommended. Liver and dried cat food can also be given.

Vitamin A Toxicity

Great care must be taken when injecting vitamin A as overdosage can cause intoxication. This can occur if 100 times the recommended dose is given. Clinical signs are anorexia, erythema and sloughing of skin. Treatment is symptomatic.

Hypovitaminosis B1 (Thiamin)

This is seen in aquatic carnivorous species like the garter and Eurasian water snakes and turtles. It is common when a diet of sea or frozen fish is fed. Sea fish are high in thiaminases and frozen fish left to thaw for too long gets depleted in thiamin.

Clinical Signs

Affected snakes show neurological signs like ataxia, opisthotonos, torticollis, muscle tremors, blindness and death.


Thiamin can be given parenterally (50 mg/kg) or orally (25 mg/kg) by stomach tube if anorexic. The diet should be corrected--feed only freshwater fish, fresh caught fish or well-thawed fish.

Hypovitaminosis E (Tocopherol)

This occurs when reptiles are fed oily fish like mackerel, goldfish and whitebait. It can also be seen in snakes fed obese laboratory rodents. Treatment is with Vitamin E (1 iu/kg). The patient should be tube fed if anorexic and dietary imbalance addressed.

Clinical Signs

Anorexia, painful nodules under the skin.

Speaker Information
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Bairbre O'Malley, MVB, CertVR, MRCVS
Bairbre O'Malley Veterinary Hospital
Kilmantain Place
Bray, Co. Wicklow, Ireland

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