In Taiwan, high mortality of cultured Pacific white shrimp Penaeus vannamei juveniles occurred within 3 days of disease onset in March, 1999. Moribund juveniles were anorexic and lethargic, exhibited ataxic swimming behavior, and had opaque musculature, a soft shell and a pale reddish coloration that made the tail fan and pleopods distinctly red. Survivors were found with multifocal, melanized, cuticle lesions on the cephalothorax and abdominal exoskeleton. Necrosis of the cuticular epithelium was found upon histopathological examination of moribund shrimp. Prominent necrosis in the cuticular epithelium and subcutis were found throughout the appendages, cephalothorax and foregut. The necrotic cells had pyknotic nuclei and cytoplasmic spherical inclusions, which ranged from eosinophilic to darkly basophilic. The cytoplasmic inclusions, and pyknotic and karyorrhectic nuclei gave lesions a peppered, or buckshot-riddled, appearance. In situ hybridization analyses using Taura syndrome virus (TSV)-specific CDNA probes showed that 87% of the juveniles examined were TSV positive and that cuticular epithelium was the target tissue. Negative staining of the purified viral preparations revealed the presence of icosahedral particles, 28 to 31 nm in diameter. These results indicate that TSV, or a very similar strains of the same virus, is responsible for the acute mortality of white shrimp in Taiwan. TSV may have been introduced to Southeast Asia with chronically infected brooders or asymptomatic carriers imported from the Western Hemisphere.