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Abstract. During the period from January 2002 to March 2007, infections by melanized fungi were identified with greater frequency in aquarium-maintained leafy seadragons (Phycodurus eques) and weedy seadragons (Phyllopteryx taeniolatus), pivotal species to the educational and environmental concerns of the aquarium industry and conservation groups. The objective of this study was to characterize the pathology and identify fungi associated with phaeohyphomycotic lesions in these species. Samples from 14 weedy and 6 leafy seadragons were received from 2 institutions and included fresh, frozen, and formalin-fixed tissues from necropsy and biopsy specimens. Fresh and frozen tissues were cultured for fungi on Sabouraud dextrose agar only or both Sabouraud dextrose agar and inhibitory mold agar with gentamicin and chloramphenicol at 30uC. Isolates were processed for morphologic identification and molecular sequence analysis of the internal transcribed spacer region and D1/D2 domains of the large subunit ribosomal RNA gene. Lesions were extensive and consisted of parenchymal and vascular necrosis with fungal invasion of gill (11/20), kidney (14/20), and other coelomic viscera with or without cutaneous ulceration (13/20). Exophiala sp. isolates were obtained from 4 weedy and 3 leafy seadragons and were identified to species level in 6 of 7 instances, namely Exophiala angulospora (1) and a novel species of Exophiala (5), based on nucleotide sequence comparisons and phylogenetic analyses. Disseminated phaeohyphomycosis represents an important pathologic condition of both weedy and leafy seadragons for which 2 species of Exophiala, 1 a novel species, have been isolated.

A 14-y-old bay Quarter Horse gelding was presented with progressive neurologic signs, elevated rectal temperature, and icterus for 3 d prior to death. Postmortem examination revealed icterus, large amounts of serosanguineous fluid in the abdominal cavity, widespread petechiae and ecchymoses in several organs, and a large, pale, and well-demarcated focus of necrosis in the liver. Histologically, there was coagulative necrosis surrounded by a rim of inflammatory cells and large numbers of gram-positive rods, which were identified as Clostridium novyi by immunohistochemistry. Liver samples tested by PCR were positive for C. novyi type B flagellin and alpha toxin genes, but negative for Clostridium haemolyticum and other clostridia. Based on postmortem findings and ancillary tests, a definitive diagnosis of infectious necrotic hepatitis (INH) was made. Mostly a disease of ruminants, also known as black disease, INH has rarely been reported in horses, and a definitive etiologic diagnosis has not been achieved previously; the etiology of all cases reported to date was identified as C. novyi but the type was not determined. Animals are predisposed to clostridial hepatitis when hepatic anaerobiosis is established. Such conditions allow germination and proliferation of bacterial spores, resulting in production and release of toxins. INH, caused by C. novyi type B, and bacillary hemoglobinuria, caused by C. haemolyticum, are mechanistically and pathologically almost indistinguishable. Because these 2 microorganisms are closely related, differentiation requires molecular tools.

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