Taura syndrome virus (TSV) lesion development and the disease cycle in thePacific white shrimp Penaeus vannamei

The Taura syndrome virus (TSV) disease cycle was redefined through histolog ical and gene probe analysis of experimentally infected specific pathogen-f ree (SPF) Penaeus vannamei sampled at timed intervals. The cycle consists o f 3 overlapping, but clinically and histologically distinct, phases: a simi lar to 7 d peracute to acute phase, a similar to 5 d transition phase (prev iously termed the chronic or recovery phase), and a definitive chronic phas e. The acute phase is characterized by the rapid development of severe, mul tifocal to diffuse cuticular epithelial necrosis and high mortalities. Usin g in situ hybridization analysis, infected pre-lytic cuticular epithelial c ells display very strong TSV-positive probe signals, and a total of 3 stage s of acute phase necrosis are described. Surviving P, vannamei then enter t he transition phase, which is distinguished histologically by multifocal me lanized lesions within regions of the cuticular epithelium (resolving acute phase lesions), focal active acute phase lesions, and the onset of lymphoi d organ (LO) spheroid development. Gene probe analysis of transitionally in fected shrimp reveals probe-positive foci of active acute phase lesions, a diffuse probe signal within the walls of morphologically normal LO tubules and/or focal probe signals within developing LO spheroids. Shrimp surviving this stage enter the chronic phase infection after ecdysis. The defining c haracteristics of the chronic phase include the cessation of mortalities, t he resumption of normal behavioral patterns, the complete absence of visibl e melanized lesions and acute phase histological lesions of the cuticular e pithelium, and marked LO hypertrophy directly resulting from the rapid deve lopment of numerous LO spheroids, some of which are TSV positive by in situ hybridization analysis.