Vesicular and Ulcerative Dermatopathy Resembling Superficial Necrolytic Dermatitis in Captive Black Rhinoceroses (Diceros bicornis)

Abstract

The histopathology, clinical presentation, and epidemiology of a cutaneous and oral mucosal disease affecting 40 black rhinoceroses ( Diceros bicornis) at 21 zoological parks (50% of the captive US population) were investigated. Twenty-seven biopsies were examined from recent lesions, and clinical information was available from 127 episodes. The cutaneous lesions began as plaques that progressed to vesicles, bullae, or ulcers. Lesions waxed and waned in individual cases. Lesions were predominantly bilaterally symmetrical, affecting pressure points, coronary bands, tips of the ears and tail, and along the lateral body wall and dorsum. Oral lesions were first noticed as ulcers and were present on the lateral margins of the tongue, palate, and mucocutaneous junctions of the lips. All recent lesions had similar histopathologic findings of prominent acanthosis, hydropic degeneration of keratinocytes in the stratum spinosum, spongiosis, intraepithelial vesicles, and parakeratosis without dermal inflammation. Chronic lesions were ulcerated. No pathogens were identified by culture or electron microscopy. Most episodes coincided with stress events (transportation, sudden cold temperatures, intraspecific harassment, estrus, advanced pregnancy) or concurrent diseases (toxic hepatopathy, hemolytic anemia, respiratory or urinary tract infections). Affected rhinoceroses usually were lethargic and had weight loss. Affected rhinoceroses also had lower hematocrit, serum albumin, and cholesterol values than captive healthy or wild rhinoceroses. The clinical patterns and histopathologic findings are similar to those of superficial necrolytic dermatitis in dogs and necrolytic migratory erythema in humans. The high prevalence of this skin disease in captive black rhinoceroses under many circumstances suggests that their epidermis is acutely sensitive to any disruption of metabolic homeostasis. We propose that metabolic changes secondary to a stress response from maladaptation or nutritional inadequacy of captive diets may contribute to the development of this disease in rhinoceroses without hepatopathies.