A new emerging disease in shrimp, first reported in 2009, was initially named early mortality syndrome (EMS). In 2011, a more descriptive name for the acute phase of the disease was proposed as acute hepatopancreatic necrosis syndrome (AHPNS). Affecting both Pacific white shrimp Penaeus vannamei and black tiger shrimp P. monodon, the disease has caused significant losses in Southeast Asian shrimp farms. AHPNS was first classified as idiopathic because no specific causative agent had been identified. However, in early 2013, the Aquaculture Pathology Laboratory at the University of Arizona was able to isolate the causative agent of AHPNS in pure culture. Immersion challenge tests were employed for infectivity studies, which induced 100% mortality with typical AHPNS pathology to experimental shrimp exposed to the pathogenic agent. Subsequent histological analyses showed that AHPNS lesions were experimentally induced in the laboratory and were identical to those found in AHPNS-infected shrimp samples collected from the endemic areas. Bacterial isolation from the experimentally infected shrimp enabled recovery of the same bacterial colony type found in field samples. In 3 separate immersion tests, using the recovered isolate from the AHPNS-positive shrimp, the same AHPNS pathology was reproduced in experimental shrimp with consistent results. Hence, AHPNS has a bacterial etiology and Koch's Postulates have been satisfied in laboratory challenge studies with the isolate, which has been identified as a member of the Vibrio harveyi clade, most closely related to V. parahemolyticus.

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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~,

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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