All content in this area was uploaded by Shangzhe Xie on Oct 03, 2016
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All content in this area was uploaded by Shangzhe Xie on Oct 03, 2016
Content may be subject to copyright.
Vitamin A Balance in Reptiles
Shangzhe Xie1, BSc/BVMS, MVS (Conservation Medicine); Ji Zhen Low2, BSc/BVMS
1School of Animal and Veterinary Sciences, The University of Adelaide, Adelaide,
SA, Australia; 2St. Bernards Road Veterinary Clinic, Magill, SA, Australia
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 (Brown et al. 2004; Boyer 2006). At the other end of the spectrum,
hypervitaminosis A, sometimes as a result of overzealous treatment of
suspected hypovitaminosis A, can result in dry patches of skin and generalized
sloughing of the epithelium.
VITAMIN A FUNCTIONS
Vitamin A has been shown to serve crucial biological functions in animals,
including reptiles. One of these functions is as a visual pigment in
photoreceptors (rods and cones) and this has been measured in reptilian
species including Pseudemys scripta, Chelonia mydas (Liebman, Granda
1971), Podarcis sicula, and Anolis carolinensis (Provenico et al. 1992). Vitamin A
also encourages the formation of mucus-secreting cells at the expense of
keratinized cells to synthesise glycoproteins (Moore 1957), that is, it acts as a
hormone regulating epidermal growth (Vershinin 1999). This effect becomes
obvious when there is insufficient vitamin A, resulting in hyperkeratosis (Moore
CAUSES OF HYPOVITAMINOSIS A
In captivity, hypovitaminosis A is most commonly caused by a lack of dietary
intake of preformed vitamin A. Insects are poor sources of preformed vitamin A,
that is, retinoids, because invertebrates in general do not convert carotenoids to
retinol (Moore 1957) and the majority of retinoids are found in the insects' eyes
(Finke 2003). Whole vertebrate prey, in general, contain sufficient preformed
vitamin A in their livers (Douglas et al. 1994), which may explain why there are
less reports of hypovitaminosis A in reptiles consuming such prey (e.g., snakes).
Some reptiles may be able to convert carotenoids to retinol, and Dierenfeld et al.
(2002) quoted unpublished information from Ferguson GW, that suggested that
Panther chameleons (Furcifer pardalis) might be one such species. Ferguson et al.
(1996) quoted unpublished information from Talent LG, suggesting that
insectivorous lizards can utilize beta carotene to overcome vitamin A deficiency,
but more definitive information does not seem to be available. Another study
involving juvenile green iguanas (Iguana iguana) found that polar xanthophyll,
not beta-carotene, was selectively accumulated by iguanas fed different
carotenoids after 56 days of carotenoid deficiency (Raila et al. 2002), indicating
that in some reptilian species, there may not even be absorption/digestion of
dietary carotenoids. In this study, there was also no change found in plasma
retinol levels after carotenoids were fed to the iguanas (Raila et al. 2002).
Environmental contamination with organochlorine compounds and
subsequent chronic exposure to these compounds is a possible cause of
hypovitaminosis A in wild reptiles (Holladay et al. 2001; Brown et al. 2004;
Sleeman et al. 2008). A study of aural abscesses in wild box turtles (Terapine
carolina) reported mucosal hyperplasia and squamous metaplasia of the
conjunctiva, pharynx, trachea, and auditory tubes, and that there was a
nonsignificant trend of decreased serum and hepatic vitamin A levels in the
turtles (Holladay et al. 2001). Brown et al. (2008) found that the histopathologic
changes were more severe in box turtles with aural abscesses and sometimes
involved bacterial infections. Sleeman et al. (2008) went one step further to
assign scores to the histopathologic changes and found that these scores were
positively correlated with o,p-DDT and vitamin A levels but no correlation with
total hepatic organochlorine compound concentrations. The positive correlation
between pathologic scores and vitamin A levels were unexpected, but possibly
explained by the initial increase in vitamin A levels as organochlorine
concentration increased (Sleeman et al. 2008). Laboratory-based studies may
produce more convincing results linking hypovitaminosis A to aural abscesses
but none have been reported to date.
THE DIAGNOSTIC CONUNDRUM
Diagnoses of hypovitaminosis A are 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, 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
signs 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
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 by the following example. Vitamin A
deficiency has been 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).
This paper may have raised more questions than answers, but maybe the
point to take home is that thinking more critically about common diagnoses and
treatments of reptilian diseases may lead to new studies and discoveries that
are important in expanding the field of reptilian medicine. 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.
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Ji Zhen Low, BSc/BVMS
St. Bernards Road Veterinary Clinic
Magill, SA, Australia
Shangzhe Xie, BSc/BVMS, MVS (Conservation Medicine)
School of Animal and Veterinary Sciences
The University of Adelaide
Adelaide, SA, Australia