Posters Session - Proceedings of European Association of Zoo and Wildlife Veterinarians - Ebeltoft, 2004

A recent study found aural abscessation to be a significant cause of morbidity and mortality in free-living eastern box turtles (Terrapene carolina carolina) in Virginia (1). Though its etiology remains unknown, hypovitaminosis A has been suggested based on a similar lesion occurring in captive chelonia fed diets deficient in vitamin A (4). This hypothesis was supported by significantly greater body burdens of organochlorine compounds, a reported disruptor of vitamin A metabolism (5), and a non-significant trend toward lower serum and vitamin A levels found in free-living box turtles with this lesion (3). The tympanic epithelium was evaluated in twentyseven turtles (ten with aural abscessation and seventeen without) in order to describe the pathology of this lesion. Pathological changes to the tympanic epithelium of turtles with aural abscessation included: hyperplasia, squamous metaplasia, hyperemia, cellular sloughing, desquamation, granulomatous inflammation, and bacterial infection. These changes were more severe in box turtles with aural abscesses as opposed to those without, and were greater in tympanic cavities containing an abscess as opposed to one without (when the lesion was unilateral). The epidemiology of 46 cases of aural abscessation in free-living eastern box turtles admitted to the Wildlife Center of Virginia (WCV, Virginia, USA) from 1991 to 2000 was also evaluated using univariate analysis followed by multivariable logistic regression. County human population density, year and season of admission, weight, and gender were not associated with an increased risk for box turtles developing aural abscesses. Spatial location of cases (based on county) was analyzed for clustering by Grimson’s method (2). Counties with cases of aural abscessation were not randomly distributed, but rather were clustered into two multi-county regions. The histopathological changes in box turtles with aural abscessation and the epidemiological profile are consistent with a syndrome that may involve hypovitaminosis A and/or environmental organochlorine compound exposure, and is being further investigated.