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Members of the genus Nannizziopsis are emerging fungal pathogens of reptiles that have been documented as the cause of fatal mycoses in a wide range of reptiles in captivity. Cases of severe, proliferative dermatitis, debility and death have been detected in multiple free-living lizard species from locations across Australia, including a substantial outbreak among Eastern water dragons (Intellagama lesueurii) in Brisbane, Queensland. We investigated this disease in a subset of severely affected lizards and identified a clinically consistent syndrome characterized by hyperkeratosis, epidermal hyperplasia, dermal inflammation, necrosis, ulceration, and emaciation. Using a novel fungal isolation method, histopathology, and molecular techniques, we identified the etiologic agent as Nannizziopsis barbatae, a species reported only once previously from captive lizards in Australia. Here we report severe dermatomycosis caused by N. barbatae in five species of Australian lizard, representing the first cases of Nannizziopsis infection among free-living reptiles, globally. Further, we evaluate key pathogen and host characteristics that indicate N. barbatae-associated dermatomycosis may pose a concerning threat to Australian lizards.

An 11-yr-old captive-born male Everglades ratsnake (Elaphe obsoleta rosalleni) presented with dysecdysis, hyperkeratosis, and inappetance. Two skin biopsies demonstrated a diffuse hyperkeratosis with both a bacterial and fungal epidermitis. Fusarium oxysporum was cultured from both biopsies and considered an opportunistic infection rather than a primary pathogen. Medical management was unsuccessful, and the snake was euthanized. Histologic findings included a pituitary cystadenoma arising from the pars intermedia, severe intestinal lipidosis, generalized epidermal hyperkeratosis, and lesions consistent with sepsis. It is hypothesized that endocrine derangements from the pituitary tumor may have caused the skin and intestinal lesions.

The Chrysosporium anamorph of Nannizziopsis vriesii (CANV), a keratinophilic fungus that naturally and experimentally causes severe and often fatal dermatitis in multiple reptile species, was isolated in pure culture from skin samples of three inland bearded dragons (Pogona vitticeps) with deep granulomatous dermatomycosis. The first animal presented with a focal maxillary swelling involving the skin and gingiva. This lizard died while undergoing itraconazole and topical miconazole therapy. The second presented with focally extensive discoloration and thickening of the skin of the ventrum and was euthanized after 10 weeks of itraconazole therapy. A third lizard presented with hyperkeratotic exudative dermatitis on a markedly swollen forelimb. Amputation and itraconazole therapy resulted in a clinical cure. Histopathology of tissue biopsies in all cases demonstrated granulomatous dermatitis with intralesional hyphae morphologically consistent with those produced by the CANV. The second lizard also had granulomatous hepatitis with intralesional hyphae. Evidence in this report suggests that the CANV is the etiologic agent of an emerging condition in captive bearded dragons that has been called 'yellow fungus disease'.

A case of primary cutaneous zygomycosis caused by Mucor circinelloides is described. Histopathology showed typical hyphae along with chlamydospores. The isolate was identified by molecular and phenotypic methods. The utility of sequence analysis of the internal transcribed spacer region is highlighted; however, further studies are needed to assess species genetic heterogeneity.

The fungus Chrysosporium anamorph of Nannizziopsis vriesii was identified as the cause of fatal, multifocal, heterophilic dermatitis in four freshwater aquatic captive-bred tentacled snakes (Erpeton tentaculatum). Pale, 1- to 4-mm focal lesions involving individual scales, occurred primarily on the head and dorsum. Histology showed multifocal coagulation necrosis of the epidermis, with marked heterophilic infiltration without involvement of the underlying dermis. Septate, irregularly branched hyphae, and clusters of 4- to 8- by 2- to 3-microm rod-shaped cells (arthroconidia) were present within the lesions and in a superficial crust. Failure to maintain an acidic environment was likely a predisposing factor in the development of these lesions.