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

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 LO tubules and/or focal probe signals within developing LO 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 complete absence of visible melanized lesions and acute phase histological lesions of the cuticular epithelium, and marked LO hypertrophy directly resulting from the rapid development of numerous LO spheroids, some of which are TSV positive by in situ hybridization analysis.