Abstract

“Short tongue syndrome” (STS) is an acquired condition first recognized in the endangered Wyoming toad (Bufo baxteri). Despite vigorous efforts, toads with STS have a diminished ability to apprehend prey and may eventually require hand feeding. Histologically, a commonly observed change is transformation of mucus-producing lingual epithelium to stratified squamous keratinizing epithelium (squamous metaplasia). In other cases, there are significantly decreased amounts of cytoplasmic mucus in lingual epithelial cells without overt squamous metaplasia. Review of necropsy records submitted to the Wyoming toad SSP between 1999–2003 showed that 22/41 (54%) animals in which tongue was examined histologically had some degree of lingual squamous metaplasia. Because squamous metaplasia of mucus-producing epithelia is commonly associated with hypovitaminosis A in other species, investigation of vitamin A status in affected toads was pursued. Captive Wyoming toads with squamous metaplasia (n=11) had significantly decreased hepatic retinol (mean 1.6 µg/g) when compared to free-ranging Wyoming toads (n=10; mean 104.6 µg/g). The combination of squamous metaplasia and decreased hepatic retinol is highly suggestive of hypovitaminosis A. Similar clinical signs and histologic changes have subsequently been observed in other captive toads including Rocky Mountain boreal toads (Bufo boreas boreas) and Woodhouse’s toads (Bufo woodhousii). Possible contributory factors to the development of hypovitaminosis A include inadequate supplementation of insect-based diets, use of outdated supplements and unique species requirements for vitamin A or vitamin A precursors.