Abstract
Fungal dermatoses have been reported in a variety of reptiles.1-6 Organisms which have been isolated include Aspergillus, Basidobolus, Fusarium, Geotrichium, Microsporum, Mucor, Oospora, Penicillum, Prototheca, Saprolegnia, Trichoderma, Trichophyton, Trichosporan and Candida.6 Typical lesions mimic bacterial dermatitis and consist of blisters, ulcers, nodules, crusts and granulomas.
Although disease in sea snakes is rarely reported, in this instance a female snake was housed in the Waikiki Aquarium after being found washed up on the beach. She was lethargic and was undergoing a prolonged ecdysis primarily around the head and lower body. Multiple proliferative skin pustules developed. Pseudomonas aeruginosa was cultured from the skin lesions and the snake was treated with injectable enrofloxacin IM 1.63 mg/kg q24 hours. She was also soaked once overnight in Nitrofurazone at 10 mg/L. The skin lesions appeared to be slowly healing but she had not eaten or drunk fresh water since capture and died unexpectedly. On gross examination, the snake was severely dehydrated and had multiple open skin wounds, swellings and healing lesions. The internal organs appeared normal and there was fluid, feces and urates in the colon. No parasitic ova were identified on fecal examination.
The primary lesions were multifocal, erosive and ulcerative with pustules occurring within the overlying epithelium. The pustules were characterized by aggregates of heterophils with associated hemorrhage, fibrin and edema separating the layers of the stratified squamous epithelium. Within foci, there were large numbers of proliferating fungal organisms. Nonparallel cell walls, irregular internal septations and dichotomous branching characterized fungal hyphae. Fungal hyphae infiltrated into the dermis in the areas of ulceration. Proliferations of small coccobacillus organisms also occurred randomly throughout the ulcerative lesions.
Underlying and/or contributing lesions were not identified in the remaining organs. Death was likely due to a combination of factors including the dermatitis, anorexia, and dehydration.
The paraffin tissue blocks of the skin lesions were submitted for DNA sequencing to identify the fungal organisms. A section of the 28S ribosomal DNA was amplified from the fixed tissue block. The sequence from this sample's amplification product closely matched that of Fusarium solani and F. lichenicola (98% sequence identity), as well as other members of the genus Fusarium.
Fusarium species are common soil saprophytes and plant pathogens. In one report, Fusarium solani was determined to be the agent of a cutaneous infection in an injured loggerhead sea turtle (Caretta caretta L.). The turtle was treated topically with a 10% solution of iodine in alcohol and with systemic ketoconazole. The lesions regressed after 6 months.2 In a series of six snakes with mycotic dermatitis, four had concurrent Pseudomonas bacteria isolated from the skin lesions.5 The fungal organisms were suspected to be environmental contaminates and suboptimal environmental temperature a contributing factor in the development of disease.
Acknowledgments
The authors thank Dr. Oaks and staff of the Washington Animal Disease Diagnostic Lab for work on the fungal identification. We also thank Dr. Piccoli for editorial comments.
References
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