Abstract

The organism responsible for causing viral nervous necrosis (VNN) or viral encephalopathy and retinopathy (VER) has been demonstrated to belong to the group Nodaviridae [K. Mori, et al., 1992] [M. Comps, et al., 1994]. Since its initial identification in 1990 by Yoshikoshi and Inoue (1990), in Japanese parrotfish, its distribution and/or identification has become global. Methods of identification developed and results from outbreaks of VNN in white seabass between 1992 and 1999 have been published in Curtis et al. (2001). The white seabass cultured at the Hubbs-SeaWorld Research Institute's hatchery in Carlsbad California (CBD), have experienced VNN, of varying severity, since 1992. Disease in 1992 was thought to be due to a picrona-like virus but the indirect fluorescent antibody technique (IFAT) performed in 1999 on samples from 1992, indicated the same nodavirus was responsible. Confirmation of the nodavirus in white seabass was done using IFAT, reverse transcription-polymerase chain reaction (RT-PCR), electron microscopy and virus isolation via cell culture. The strain of nodavirus isolated from white seabass was shown to be similar to that recovered from redspotted grouper in Japan. The most serious and extensive outbreak experienced in white seabass at CBD extended from August of 2002 to May 2003. Since 1999 a concerted effort has been made to further the understanding of VNN epidemiology in white seabass. Recently, enzyme linked immunosorbant assays (ELISA) performed on sera samples from wild fish have demonstrated VNN exposure in wild juvenile white seabass. With the apparent lack of species specificity of VNN and its global distribution, continued devastating impacts on new marine species development are a distinct possibility. Along with cooperative measures for identification and epidemiology, there needs to be a drive towards development of preventative husbandry protocols and methods of prophylaxis.

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