Abstract
Mass mortality of cultured white shrimp in southern Taiwan was diagnosed as an outbreak of Taura syndrome (TS). From late 1998 to early 1999, 90% of the shrimp ponds were abandoned at 30 to 45 d after stocking post larvae from Ecuador and elsewhere. The shrimp began to die within 2 to 3 d after they stopped feeding. There were no other gross signs, except that some affected shrimp had reddened tails. Histologically, multifocal necrosis of the cuticular epithelium was the main lesion. The necrotic foci contained pyknotic and karyorrhectic nuclei, and many lightly and densely stained intracytoplasmic and intercellular, spherical inclusions. By transmission electron microscopy, small, icosahedral, picornalike virus particles 30 nm in diameter were seen. Taken together, the observations resembled those for outbreaks caused by Taura syndrome virus (TSV). It is assumed that TSV was transferred to Taiwan via contaminated post larvae and spawners from epizootic areas. This is the first report of a TS outbreak in Taiwan. this newly introduced species. By early 1998, P. vannarnei became the most popular and highest-yield cultured shrimp in southern Taiwan. However, from late 1998 to early 1999, due to high mortality, shrimp production dropped sharply to as little as 10% of the production in early 1998. Based on the gross signs of disease, histopathological changes and evidence from transmission electron microscopy, we report in this paper that Taura Syndrome Virus (TSV) was responsible for the high shrimp mortality. Materials and methods. Moribund shrimp collected from cultivation ponds experiencing high mortality were fixed by Davison's fixative and processed as described in Bell & Lightner (1988). For electron microscopy, whole moribund shrimp were mixed with
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