Abstract
The clown knifefish (Chitala chitala) is a popular species that can be seen in aquariums worldwide and is considered as near threatened in the wild. Populations have declined due to overexploitation and the deterioration of water quality in their habitats.1 Six Chitala chitala from a public aquarium died with nonspecific clinical signs. These individuals were submitted to the Fish Pathology Unit of the Institute of Animal Health and Food Safety (IUSA) of the ULPGC for further analysis. Complete and systematic necropsies were performed for diagnostic purposes. The main findings were extensive yellowish multifocal lesions distributed throughout the subcutaneous tissue, musculature, and perivisceral fat, including locations such as the aortic bulb, central nervous system, and retrobulbar fat. Additionally, some animals presented with mild exophthalmia, and one specimen had a tongue deformity due to presence of lesions at the base of the tongue. Histopathological examination revealed foci of necrosis in the fat tissue, where adipocytes appeared degenerated with proliferation of connective tissue and inflammatory cells. The presence of calcified areas and the formation of granuloma-like aggregates were also observed, as well as the presence of ceroid pigment and melanomacrophage aggregates. Massive fatty infiltration was identified in different organs, such as spleen, liver, and cardiac muscle fibers. The occurrence of fat necrosis in other species has been associated with vitamin E deficiency.2-4 Given the chronic nature of this condition and the fact that more than one individual was affected, vitamin E deficiency emerged as the primary suspicion. In response to this concern, dietary supplementation with a vitamin E complex was started. Since the diet modification, there have been no further mortalities. To the authors’ knowledge, this is the first report of fat necrosis in Chitala chitala, and the positive response to dietary supplementation is suggestive that this species is highly sensitive to vitamin E deficiencies.
*Presenting author
Literature Cited
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