VESICULAR AND ULCERATIVE DERMATOPATHY RESEMBLING SUPERFICIAL NECROLYTIC DERMATITIS IN CAPTIVE BLACK RHINOCEROSES (DICEROS-BICORNIS)

The histopathology, clinical presentation, and epidemiology of a cutan eous and oral mucosal disease affecting 40 black rhinoceroses (Diceros bicornis) at 21 zoological parks (50% of the captive US population) w ere investigated. Twenty-seven biopsies were examined from recent lesi ons, and clinical information was available from 127 episodes. The cut aneous lesions began as plaques that progressed to vesicles, bullae, o r ulcers. Lesions waxed and waned in individual cases. Lesions were pr edominantly bilaterally symmetrical, affecting pressure points, corona ry bands, tips of the ears and tail, and along the lateral body wall a nd dorsum. Oral lesions were first noticed as ulcers and were present on the lateral margins of the tongue, palate, and mucocutaneous juncti ons of the lips. All recent lesions had similar histopathologic findin gs of prominent acanthosis, hydropic degeneration of keratinocytes in the stratum spinosum, spongiosis, intraepithelial vesicles, and parake ratosis without dermal inflammation. Chronic lesions were ulcerated. N o pathogens were identified by culture or electron microscopy. Most ep isodes coincided with stress events (transportation, sudden cold tempe ratures, intraspecific harassment, estrus, advanced pregnancy) or conc urrent diseases (toxic hepatopathy, hemolytic anemia, respiratory or u rinary tract infections). Affected rhinoceroses usually were lethargic and had weight loss. Affected rhinoceroses also bad lower hematocrit, serum albumin, and cholesterol values than captive healthy or wild rh inoceroses. The clinical patterns and histopathologic findings are sim ilar to those of superficial necrolytic dermatitis in dogs and necroly tic migratory erythema in humans. The high prevalence of this skin dis ease in captive black rhinoceroses under many circumstances suggests t hat their epidermis is acutely sensitive to any disruption of metaboli c homeostasis. We propose that metabolic changes secondary to a stress response from maladaptation or nutritional inadequacy of captive diet s may contribute to the development of this disease in rhinoceroses wi thout hepatopathies.