Ryan S. De Voe, DVM, MSpVM, DACZM, DABVP (Avian)
In this lecture we will discuss the basics of insectivorous reptile nutrition, paying particular attention to the role vitamin A and Vitamin D play in a healthy diet. Captive animals that receive diets that contain deficient or excessive amounts of both these vitamins are frequently seen by veterinarians. Therefore, it is important that the reptile veterinarian be able to recognize signs of malnutrition and provide treatment as well as correct the diet.
Captive insectivorous reptiles can be difficult for the casual keeper to maintain. In addition to providing an appropriate captive environment that meets the animal's requirements for heat, light, humidity, etc., a complete diet must be offered. With so many variables to address, even the most dedicated and educated keepers rarely get everything perfect. It should be noted that wild "insectivorous" reptiles rarely limit their intake to just insects. Most species will eat any living thing that they can overpower and consume. This means that wild animals will consume smaller mammals, reptiles, amphibians, birds, fish, crustaceans, and arthropods besides insects. The limiting factor seems to be the ability of the reptile to overpower the prey and fit it in their mouths!
Unfortunately the majority of insectivorous reptiles in captivity subside on a diet consisting solely of crickets and mealworms plus the occasional wax worm. There is nothing magical about the nutritional content of these insects, and in fact they are deficient in a number of nutrients (Vitamin A & D, protein, and calcium). The fact of the matter is these insects are easy to maintain and propagate; therefore they are the most readily available. Luckily, in recent years there has been interest in finding new food insect species for captive propagation. Some of the fly larvae offered for sale (ex/"Phoenix worms") purportedly have better nutritional profiles than those of crickets and mealworms. This author believes that provision of a diet as varied as possible is the best approach to maintaining insectivorous reptiles. The author has personally raised many species of insectivorous lizards on diets consisting of commercially available insects plus field collected insects with no additional supplementation. Many deficient insect diets can be completed with the addition of the occasional vertebrate prey animal or prepared meat diet (canned cat food, etc.).
Frequency of feeding captive reptiles is a topic of some debate. Some keepers advocate feeding insectivorous reptiles relatively large meals 1-2 times weekly. Many animals will get by with this type of schedule, but a more natural approach would be to offer small quantities of food daily. This approach keeps the animal active, and helps avoid problems such as food impactions or constipation. When feeding frequency is increased the keeper also has more chances to offer variety in the food items offered, as well as the method of presentation. This can help enrich the lives of captive reptiles and encourage more natural behaviors.
Vitamin and mineral supplementation is tricky, as the quality of commercially available products varies greatly, sometimes according to batch. Many zoos with nutrition departments produce their own vitamin and mineral supplements and perform frequent analysis for quality control. The greatest difficulty lies in the fact that we simply do not know the exact dietary requirements of all species so sometimes we are using a best guess when developing diets. It is relatively easy to recognize when a diet is completely inappropriate as the animals may develop overt signs of malnutrition. The greater difficulty is when malnutrition does not cause overt disease, but results in reproductive failure or a slightly debilitated state which makes the animal more susceptible to infectious disease. These cases are more difficult to figure out and correct.
Many vitamin and mineral supplements come in powdered form and are intended to be "dusted" onto the prey item prior to feeding. Success in delivering the supplement in this manner varies according to a large number of variables. Even products that stick well to a chitinous exoskeleton can be groomed off if the insect is not consumed in time. Do not assume that adequate amounts of supplement are being delivered via insect "dusting".4
Most veterinarians are capable of making educated guesses regarding the level of supplementation appropriate for certain reptiles. All husbandry parameters need to be considered, especially lighting, when developing supplementation protocols. For example those animals that receive large amounts of natural sunlight exposure do not need to be supplemented with large amounts of Vitamin D. If an animal receives large amounts of natural sunlight plus a large amount of dietary Vitamin D, hypervitaminosis D can easily occur. Generally speaking, the author suggests that insect diets be supplemented with fat soluble vitamins 1-2 times weekly. Minerals and water soluble vitamins can be supplemented daily if desired.
A good rule to remember is that it is very difficult to maintain a healthy, robust captive insectivorous reptile without feeding it a varied diet of healthy, robust prey animals!
Most veterinarians who have any experience working with reptiles are familiar with conditions involving vitamin D and/or calcium deficiency. Commonly referred to as "metabolic bone disease", the condition of nutritional secondary hyperparathyroidism (NSHP) occurs most frequently in young, growing insectivorous or herbivorous reptiles. The insects most frequently fed to captive reptiles are deficient in vitamin D and calcium. Thus, without exposure to adequate UVB for creation of active vitamin D or proper supplementation malnutrition is likely to occur.6,7,8
Gut loading insects with diets containing large amounts of calcium can drastically increase the calcium content prior to feeding. Unfortunately, gut loading with high calcium diets inevitably leads to the death of the insect after a few days due to constipation.5 The author prefers to offer feeder insects a complete diet that encourages growth and reproduction, and supplement via dusting with a calcium supplement if needed.
Treatment of NSHP consists of normalizing circulating calcium levels and halting the resorption of existing bone and promoting the formation of new, normal bone. Serial measurement of blood calcium levels (preferably total and ionized) is critical in the initial management of these cases. In animals that are clinically hypocalcemic, calcium gluconate at a dose of 10-50 mg/kg can be administered intramuscularly. It is recommended to dilute the calcium gluconate if possible and limit the number of injections received by the animal as it can be very irritating to tissues. Many practitioners routinely use calcitonin when treating NSHP, and the author has had great success with this approach. Calcitonin is administered at 50 IU/kg IM twice 14 days apart. It is paramount that blood calcium levels are normal prior to administration of calcitonin, otherwise fatal acute hypocalcemia can occur. Vitamin D3 can be administered at 200-400 IU/kg IM at 14 day intervals.2,8 In human medicine, some recommend concurrent administration of Vitamin A and Vitamin K to protect against potential adverse effects of Vitamin D.9 Remember that all the treatments in the world will do little good if the animal continues to live in suboptimal conditions and receive an inappropriate diet.
If oversupplementation with Vitamin D occurs, severe hypercalcemia and consequently mineralization of viscera can occur. Clinical signs vary according to the organ system most affected. Most animals that succumb to acute vitamin D toxicosis die of renal failure. Treatment of hypervitaminosis D is generally unrewarding as the damage is typically too great by the time the problem is detected. Diuresis (0.9% saline +/- furosemide) and glucocorticoid administration can be attempted in an effort to salvage these animals. Calcitonin can also be used in these cases in an effort to bring calcium levels down. It is important to realize that when an animal has exposure to large amounts of natural sunlight and/or artificial UVB the requirement for vitamin D in the diet decreases. The cases of hypervitaminosis D that the author has seen have all resulted from heavily supplementing animals that receive a large amount of UV exposure.
Hypovitaminosis A was classically seen as a disorder of aquatic turtles in the past. These turtles were typically fed diets consisting of dried insects and skeletal muscle meat, both of which contain very low if any vitamin A. External clinical signs usually consisted of swollen and infected conjunctiva; the end result of squamous metaplasia of the periocular glands.1 Currently, vitamin A malnutrition is receiving much attention as a cause of disease and reproductive failure in other species of reptiles.
Some animals possess enzymes that are capable of converting carotenoid precursors into retinol or retinal, both of which have Vitamin A activity. Animals that don't possess these enzymes required pre-formed Vitamin A in their diet. It seems that some insectivorous lizards are capable of converting carotenoids into active Vitamin A; however it is dangerous to assume that all species are the same. For this reason the best approach may be to provide a diet with a combination of vitamin A and carotenoids. Preformed vitamin A is only found in animal tissue but is ultimately derived from carotenoids contained in plant material. Extra vitamin A is stored in the liver, and serves as a deposit for regulation of vitamin A levels when the diet is not alone sufficient to maintain them.1,3,10
Vitamin A is essential for growth and reproduction. Proper vitamin A levels are responsible for morphogenesis, cell growth and differentiation and development of the retina. Appropriate maternal vitamin A levels are critical for successful reproduction.3
In mature animals hypovitaminosis A can cause squamous metaplasia of epithelial tissues and affect all organs where this type of tissue is found. External lesions can include conjunctivitis, corneal ulceration, stomatitis, adenitis, and dermal ulceration especially in weight-bearing regions. Epithelium is present in many internal organs and hypovitaminosis A frequently affects the liver and kidneys.1 This is important to remember when the clinician is asked to offer a prognosis for an affected patient.
Treatment of hypovitaminosis A consists of addressing any secondary infections of affected tissues, supportive care if organ dysfunction is present, and correction of the vitamin A levels. In treatment of hypovitaminosis A, water-miscible vitamin A palmitate can be given SC or IM at doses ranging from 200 IU/kg to 5000 IU/kg.2 In order to avoid possible toxicity, the author prefers to dose in the 500-1000 IU/kg range. This dose can be repeated every 7-10 days for 2-3 treatments. Concurrent dietary supplementation is also recommended.
Hypervitaminosis A can result in edema, skin sloughing and deficiencies of other fat soluble vitamins. Dietary oversupplementation with preformed vitamin A can result in hypervitaminosis A, but it more frequently occurs with parenteral dosing of vitamin A preparations. Careful attention needs to be paid when figuring doses of parenteral vitamin A, and it should be understood that not all vitamin A preparations behave the same. Water soluble preparations, such as vitamin A palmitate, can result in toxicity when administered at the same doses recommended for fat soluble forms.1 The author has personally seen many cases of vitamin A toxicity in chelonians, but none in insectivorous lizards.
1. Boyer, T.H. 2006. Hypovitaminosis A and hypervitaminosis A. In: Mader, D.R.(ed.) Reptile medicine and surgery. Saunders/Elsevier. St. Louis, MO. Pp. 831-835.
2. Carpenter, J.W. 2005. Exotic animal formulary (3rd ed.). Saunders/Elsevier. St. Louis, Mo.
3. Dierenfeld, E.S., E.B. Norkus, K. Carroll, and G.W. Ferguson. 2002. Carotenoids, vitamin A, and vitamin E concentrations during egg development in panther chameleons (Furcifer pardalis). Zoo Biol. 21:295-303.
4. Donoghue, S. 2006. Nutrition. In: Mader, D.R.(ed.) Reptile medicine and surgery. Saunders/Elsevier. St. Louis, MO. Pp. 251-298.
5. Finke, M.D. 2003. Gut loading to enhance the nutrient content of insects as food for reptiles: a mathematical approach. Zoo Biol. 22:147-162.
6. Gehrmann, W.H. 2006. Artificial lighting. In: Mader, D.R.(ed.) Reptile medicine and surgery. Saunders/Elsevier. St. Louis, MO. Pp. 1081-1084.
7. Laing, C.J., and D.R. Fraser. 1999. The vitamin D system in iguanian lizards. Comp. Biochem. Physiol. Part B. 00:373-379.
8. Mader, D.R. 2006. Metabolic bone diseases. In: Mader, D.R.(ed.) Reptile medicine and surgery. Saunders/Elsevier. St. Louis, MO. Pp. 841-851
9. Masterjohn, C. 2007. Vitamin D toxicity redefined: vitamin K and the molecular mechanism. Medical Hypothesis. 68(5):1026-1034.
10. Raila, J., A. Schuhmacher, J. Gropp, and F.J. Schweigert. 2002. Selective absorption of carotenoids in the common green iguana (Iguana iguana). Comp. Biochem. Physiol. Part A. 132:513-518.