Joerg Mayer is associate professor in zoological medicine at the University of Georgia. He received his doctoral degree from the University of Budapest/Hungary; completed an internship in zoological medicine and surgery at the Roger Williams Park Zoo in Providence, Rhode Island; and completed a Master of Science degree in wild animal health from the Royal Veterinary College in London, England. He also served as a clinical associate professor and head of the clinical service for exotic animals for 10 years at Tufts University in Boston, Massachusetts. In 2013, he received the Exotic Speaker of the Year award by the NAVC. In 2016, he received the Oxbow/AEMV Exotic Mammal Health Award, an annual award to recognize excellence and innovation in the field of exotic mammal healthRead Articles Written by Joerg Mayer
Joyce Huang is a recent graduate from the University of Georgia College of Veterinary Medicine and is currently working in a small animal private practice. She received her bachelor degree in Wildlife Sciences at UGA. Her clinical interests include zoological medicine, wildlife medicine, surgery, and anesthesia.Read Articles Written by Joyce Huang
Hypervitaminosis A is a nutritional disorder, an overload of vitamin A, which in reptiles can be iatrogenically induced by injection of vitamin A to reptiles suspected of having hypovitaminosis A.1-3 Vitamin A is a fat-soluble vitamin, meaning that it dissolves in fats and oils, and is a major part of commercially prepared diets. Vitamin A supplements are often given presumptively to reptiles because hypovitaminosis A is a known nutritional problem that often results from unbalanced diets.2,4
The safe dose for vitamin A administration is 5000-10,000 IU/kg, and a toxic dose is roughly 100 times higher (50,000 to 100,000 IU/kg).1,2 The risk for overdosing can be decreased by administering vitamin A in an oral, rather than injectable, formulation.3 However, hypervitaminosis A can still be induced, even when a “safe dose” of supplement is given as an injection and an increased amount of vitamin A is consumed as part of the diet for a prolonged period.2
Vitamin A plays an important role in maintaining normal epithelial tissues and is vital for vision, growth, reproduction, and immune function; it is stored in the liver.2 Excess levels of vitamin A (i.e., toxicity) overwhelm the hepatic function and storage capabilities and lead to tissue damage, which then is clinically seen initially as dry, flaky skin.1,4
Herbivorous reptiles typically do not experience vitamin A deficiency because of their plant-based diet and their ability to synthesize vitamin A.1,2 Plants, which contain vitamin A precursors called carotenoids (beta-carotene, lutein, and canthaxanthin are the most essential), include leafy greens, orange and yellow vegetables, and fruits.2 However, some reptiles, such as carnivorous turtles and other carnivorous reptiles (e.g., box turtles), are not able to synthesize beta-carotene well. In reptiles, conversion occurs in the intestines or liver, where it is later stored.4 Vitamin A toxicity from dietary intake is unlikely to occur in herbivorous reptiles. For omnivorous or carnivorous reptiles, a diet including liver can cause dietary hypervitaminosis.
Reptiles typically affected by this disease are carnivorous or omnivorous tortoises, such as box turtles and aquatic turtles.1 There is no age or sex predisposition.
In reptiles, the clinical signs of hypervitaminosis A are typically manifested in the skin.2 The signs are dry, scaly skin; skin ulceration and/or sloughing to various degrees; depression; lethargy; anorexia; weight loss; and/or dehydration (FIGURES 1 AND 2).1-3 The areas of skin that tend to be the most affected are the areas of loose skin near the front legs and neck; those tissues eventually become swollen because of cell damage (when water-soluble vitamin A has been administered).1,4 In reptiles with severe hypervitaminosis, the dermis and muscle can become exposed and they can die of secondary dehydration.1 Commonly associated with skin lesions is secondary infection (bacteria or fungal), which can lead to sepsis.1,2 In chameleons specifically, excess vitamin A can potentially lead to nutritional metabolic bone disease because of vitamin D interference.5
History and clinical findings are extremely important for diagnosing hypervitaminosis A, especially if vitamin A was administered weeks or months before you examine the animal.1-3 The history should provide information about the patient’s dietary intake of vitamin A (such as raw liver).2 Information from liver biopsy results and serum vitamin A levels is also helpful;2 however, although liver biopsy results can be considered more accurate, biopsy sample collection is obviously more invasive than blood collection. Skin biopsy results can help you determine primary or secondary causes, and culture and sensitivity should be considered for determining medical treatment.1 Ideally, you can collect biopsy samples endoscopically or grossly (e.g., wedge biopsy) because fine-needle aspiration may not be diagnostic. Several laboratories can test for vitamin A; you can send serum samples to IDEXX Laboratories, Inc., the Animal Health Diagnostic Center at Cornell University, and the veterinary diagnostic laboratories at Michigan State University or Iowa State University. Before transport, the serum needs to be separated from the clot, kept refrigerated, and kept away from light. Turnaround times range from 3 to 7 business days after sample receipt (varying according to laboratory). Serum levels can vary significantly compared with hepatic vitamin A levels, and serum levels might therefore not be practical for a diagnosis because of these normal fluctuations.4 Vitamin A levels in the blood can also be assessed through plasma retinol values. In captive aquatic turtles, plasma retinol levels are 0.03 to 0.364 mg/mL and in tortoises, 0.034 to 0.415 mg/mL. Plasma retinol levels in lizards and snakes have been reported between 0.049 to 0.372 mg/mL and 0.012 to 0.049 mg/mL.2 Differential diagnoses for skin lesions in reptiles are infection (bacterial, fungal, viral, parasitic) and/or trauma.1
Unfortunately, prior administration of vitamin A cannot be reversed.2 Therefore, the treatment of hypervitaminosis A is typically supportive and includes prevention of secondary skin infections (FIGURES 3 AND 4). Decreasing and potentially discontinuing vitamin A intake/usage are important.2,3,6,7
Reptiles with acute hypervitaminosis A require supportive care and fluid therapy (10 to 30 mL/kg/day).2 Skin lesions can be treated with hydrotherapy, antiseptic solution soaks, systemic antimicrobials, and pain medication as needed.1,2 Skin lesions should be treated like burn wounds; prevent secondary infections and relieve pain. Therapeutic laser therapy (photobiomodulation) is a newer form of wound management that has shown some promising results in iguanas when used at 10 Joules/cm2.8 Morphine can be used in chelonians (1.5 mg/kg IM or SC) and lizards (10 mg/kg IM or SC) or meloxicam can be used at 0.2 to 0.3 mg/kg PO or IM q24h, but the patient must be carefully monitored for respiratory depression.1 Nutritional support, with or without a feeding tube, may also be indicated.1,2 Treatment should continue until wounds have healed, which can take 4 to 6 months.1,2,4
Reptiles with chronic hypervitaminosis A require long-term support and wound management as well as routine check-ups.1
If vitamin A supplementation is warranted, it is better to give a fat-soluble than a water-soluble formulation because water-soluble vitamin A can be absorbed more quickly and thus potentially be more toxic.4
The prognosis for patients with hypervitaminosis A depends on the extent of skin lesions, amount and form of vitamin A given, clinical signs, prior health of the animal, chronicity of the disease, and aggressiveness of treatment.1-4 The prognosis for lesions is fairly good, unless there are large areas of sloughing.1
It is easy to oversupplement reptiles with vitamin A. Before administering vitamin A, you should perform a physical examination, review the diet, and analyze blood test results.1,4 If the patient is showing signs of hypovitaminosis, rather than directly administering an injectable formulation, consider providing oral medication and changing the diet to include more vegetables with vitamin A.1,6 Typically, this regimen will help treat hypovitaminosis A and is unlikely to cause hypervitaminosis A, which, again, is often iatrogenically induced.6 Vitamin A from natural foods rarely leads to an overdose.1 The best ways to avoid and under- and oversupplementation of vitamin A are to provide oral supplementation such as gut-loading insects (feeding insects nutritious diets prior to feeding the reptile), dietary supplementation, and/or vitamin A-rich vegetables.
Client Key Points
- Hypervitaminosis A typically affects carnivorous or omnivorous reptiles; herbivorous reptiles are less affected because of their diet.
- Treatment is mainly supportive, so resolution may several weeks to months.
- Any skin lesions should be treated with antimicrobials and pain medications.
- The key to treating and preventing hypervitaminosis A is to ensure the reptiles are fed a well-balanced diet.
- Stahl SJ. Hypervitaminosis A. In: Stahl SJ, ed. Clinical Veterinary Advisor: Birds and Exotics Pets; 2015.
- Mans C, Braun J. Update on common nutritional disorders of captive reptiles. Vet Clin North Am Exot Anim Pract 2014;17(3):369-395.
- Hoppmann E, Barron HW. Dermatology in reptiles. J Exot Pet Med 2007;16(4):210-224.
- Boyer TH. Hypovitaminosis A and hypervitaminosis A. In: Mader DR, ed. Reptile Medicine and Surgery. St. Louis, Missouri: Elsevier; 2006:831-835.
- Donoghue S. Nutrition. In: Mader DR, ed. Reptile Medicine and Surgery. St. Louis, Missouri: Elsevier; 2006:251-298.
- Harkewicz KA. Dermatologic problems of reptiles. Semin Avian Exot Pet Med 2002;11(3):151-161.
- Zwart P. Papers presented at the European Zoo Nutrition Conferences 2000. https://www.researchgate.net/publication/46628162_Nutrition_of_chelonians. Accessed October 2018.
- Cusack L, Mayer J, Cutler D, et al. Gross and histologic evaluation of photobiomodulation, silver sulfadiazine, and a topical antimicrobial wound application on experimental, full thickness skin wounds in the green iguana (Iguana iguana). Am J Vet Res 2018;79:465-473.