The Diagnostic Conundrum of Hypovitaminosis A

20/Jan/2014

Vitamin A is often implicated in diseases of reptiles, especially aquatic chelonians, and diseases such as palpebral oedema and aural abscesses are thought to be associated with hypovitaminosis A due to poor diet and husbandry (Boyer, 2006; Brown et. al., 2004). Some exotic pet practitioners believe that vitamin A supplementation is indicated for all sick chelonians, but that belief is slowly changing, in part because overzealous treatment of suspected hypovitaminosis A, can result in hypervitaminosis A leading to dry patches of skin and generalized sloughing of the epithelium.

The Diagnostic Conundrum of Hypovitaminosis A

A diagnosis of hypovitaminosis A is currently made on the basis of a dietary history indicating a lack of preformed vitamin A intake; clinical signs of hyperkeratosis, usually involving the eyelids, and general signs of lethargy, anorexia, weight loss and nasal/ocular discharge; and response to treatment with vitamin A supplementation (Boyer, 2006). A more definitive diagnosis involving vitamin A assays of liver or blood is usually not possible for several reasons. It may not be cost-effective and a liver biopsy would place the patient at risk. On the other hand, although a blood sample is relatively easy to collect, a vitamin A assay of the blood sample may not yield a meaningful result. This is because retinol binding proteins in blood tend to maintain blood levels of vitamin A at fairly stable levels unless liver stores are severely depleted or in cases of hypervitaminosis A (Schweigert et. al., 1991).

A lack of preformed vitamin A intake does not always mean that the reptile will suffer from hypovitaminosis A. There is generally no food intake at all during hibernation of reptiles in the wild, and komodo dragons (Varanus komodoensis) have been shown to still have large amounts of hepatic vitamin A despite not eating for six months (Jensen and With, 1939). This might indicate that a prolonged period of poor diet and husbandry might be required to produce clinical hypovitaminosis A. There are also a number of other causes of the more specific sign of hyperkeratosis of the eyelids, such as foreign bodies and bacterial infections (Lawton, 2006). Furthermore, vitamin A supplementation is seldom initiated without other improvements in diet and husbandry and other treatments such as ophthalmic antibiotic ointments are often prescribed, and it is very difficult to attribute resolution of clinical signs to vitamin A supplementation alone. However, there have been instances where dramatic improvement was reported after discontinuation of other treatments and single doses of vitamin A injections (Boyer, 2006), and these are probably the cases where a response to treatment can be used to retrospectively diagnose hypovitaminosis A.

Learning from the Past and Looking to the Future

Vitamin A appears to be a much maligned vitamin in reptilian diseases, but it has been acquitted before as illustrated in the following example. Vitamin A deficiency was implicated in upper respiratory tract diseases (URTD) of Desert Tortoises previously (Fowler, 1980), but it has since been proven that serum and liver vitamin A levels are not significantly different in healthy Desert Tortoises and Desert Tortoises with URTD (Jacobson et. al., 1991). Mycoplasma spp and Pasteurella spp are now the new suspects in this case (Jacobson et. al., 1991).

Very little additional information has become available since Elkan and Zwart (1967) published their comprehensive description of the clinical and histological changes in terrapins with suspected hypovitaminosis A. More research, especially prospective, laboratory-based controlled studies definitively linking hypovitaminosis A to the clinical signs that are thought to be associated with hypovitaminosis A are required to further the understanding of a relatively common syndrome in wild and captive reptiles.

References

  • Boyer T H, 2006. Hypovitaminosis A and Hypervitaminosis A. In Mader D R editor: Reptile Medicine and Surgery. Missouri. Saunders Elsevier.
  • Brown J D, Richard J M, Robertson J, Holladay S and Sleeman J M, 2004. Pathology of Aural Abscesses in Free-Living Eastern Box Turtles (Terrapene Carolina Carolina). Journal of Wildlife Diseases 40, 704-712.
  • Elkan E and Zwart P, 1967. The Ocular Disease of Young Terrapins Caused by Vitamin A Deficiency. Pathologia Veterinaria 4, 201-222.
  • Fowler M E, 1980. Comparison of Respiratory Infection and Hypovitaminosis A in Desert Tortoises. In Montali R J and Migaki G, editors: Comparative Pathology of Zoo Animals. Washington DC. Smithsonian Institute.
  • Jacobson E R, Gaskin J M, Brown M B, Harris R K, Gardiner C H, LaPointe J L, Adams H P, Reggiardo C, 1991. Chronic Upper Respiratory Tract Disease of Free Ranging Desert Tortoises ( Xerobates agassizii). Journal of Wildlife Diseases 27, 296-361.
  • Jensen H B and With T K, 1939. Vitamin A and carotenoids in The Liver of Mammals, Birds, Reptiles and Man, With Particular Regard to the Intensity of the Ultraviolet Absorption and the Carr-Price Reaction of Vitamin A. Biochemical Journal 33, 1771-1786.
  • Lawton M P C, 2006. Reptilian Opthalmology. In Mader D R editor: Reptile Medicine and Surgery. Missouri. Saunders Elsevier.

 

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