Taura syndrome (TS) was hypothesized to be caused by a virus and proven experimentally by meeting the criteria of Rivers' postulates. This was accomplished through 3 serial infectivity studies utilizing specific-pathogen-free Penaeus vannamei as the host for the TS virus (TSV). Test animals were infected via intramuscular injection with either a crude or cell-free suspension of the virus. The source of the crude homogenate was TSV-infected Ecuadorian P. vannarnel, which were collected during August 1993. Both types of viral inocula caused cumulative mortalities of 73 to 87'.';, among treatment groups. Diagnosis of TS was based on histological analysis of moribund shrimp collected during each experiment. All moribund shrimp, collected between 1 to 3 d post-injection, demonstrated moderate to severe pathognomonic TS les~ons. Both gross external and histological lesions, characteristic of chronic phase TS, were observed In 25 to 100"t, of all survivors. Virions with a buoyant density of approximately 1.337 g m1 ', lcosahedral morphology, and a diameter of 31 to 32 nm, characteristics which suggest that TSV is a member of either the Picornaviridae or Nodaviridae, were recovered from the dead shrimp collected during each of the 3 infectivity studies. Comparisons of TSV samples isolated from naturally infected P. vannamei from Hawaii (USA) and Ecuador indicate that the same virus was responsible for the TS epizootics in both of these shrimp growing regions.

Role of lymphoid organ spheroids in chronic Taura syndrome virus (TSV) infections in Penaeus vannamei Kenneth W. asso on'^', Donald V. ~i g h t n e r~, Leone L. ~o h n e y~, Rita M. ~e d m a n~,

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The Taura syndrome virus (TSV) disease cycle was redefined through histological and gene probe analysis of experimentally infected specific pathogen-free (SPF) Penaeus vannamei sampled at timed intervals. The cycle consists of 3 overlapping, but clinically and histologically distinct, phases: a -7 d peracute to acute phase, a -5 d transition phase (previously termed the chronic or recovery phase), and a definitive chronic phase. The acute phase is characterized by the rapid development of severe, multifocal to diffuse cuticular epithelial necrosis and high mortalities. Using in situ hybridization analysis, infected pre-lytic cuticular epithelial cells display very strong TSV-positive probe signals, and a total of 3 stages of acute phase necrosis are described. Surviving P. vannamei then enter the transition phase, which is distinguished histologically by multifocal melanized lesions within regions of the cuticular epithelium (resolving acute phase lesions), focal active acute phase lesions, and the onset of lymphoid organ (LO) spheroid development. Gene probe analysis of transitionally infected shrimp reveals probe-positive foci of active acute phase lesions, a diffuse probe signal within the walls of morphologically normal L 0 tubules and/or focal probe signals within developing L 0 spheroids. Shrimp surviving this stage enter the chronic phase infection after ecdysis. The defining characteristics of the chronic phase include the cessation of mortalities, the resumption of normal behavioral patterns, the con~plete absence of v~sible melanized lesions and acute phase histological lesions of the cuticular epithelium, and marked L 0 hypertrophy directly resulting from the rapid development of numerous L 0 spheroids, some of which are TSV positive by in situ hybridization analysis.

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