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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Since 1993 non-occluded baculoviruses, associated with a syndrome with high mortalities, have been reported in cultured penaeid shrimp from Asia and the Indo-Pacific region. Infections are typically accompanied by the presence of white spots on the cuticle. Numerous names were given to the virus(es) in early reports on the disease, but the syndrome is increasingly known as White Spot Syndrome (\YSS) and its viral agent(s) as White Spot Syndrome Baculovirus (WSSV). The \YSS virion is a stocky rod-shaped particle w~t h an apical envelope extension. The nucleocdpsid is cylindr~cal with asymmetric ends, and has a superfic~al segmented appearance. The pattern of degradat~on confirms that the nucleocapsid is a cylinder formed by stacks of rlngs, which are in turn composed of 2 robvs of regularly spaced subunits. WSSV replication takes place in the nucleus and is f~rst indicated by chromatin margination and nuclear hypertrophy. Viral morphogenesis begins by the formation of membranes d e novo in the nucleoplasm and by the elaboration of segmented, empty, long tubules.These tubules break into fragments to form naked empty nucleocapsids. After that, membranes envelop the capsids leavlng an open extremity. The nucleoproteins, which have a filamentous appearance, enter the capsid through this open end. When the core is completely formed, the envelope narrows at the open end and forms the apical tail of the mature virion.

During mortality outbreaks in hatchery-reared Macrobrachium rosenbergii postlarvae (PL) in Guadeloupe Island (French West Inbes) during 1997, an associated viral disease was discovered and the agent was subsequently isolated. The clinical signs presented by severely affected PL consisted essentially of an opaque whitish appearance of the abdomen. Histopathological changes in affected PL were characterized predominantly by pale to darkly basophilic, often reticulated, cytoplasmic inclusions in the connective tissue cells of most organs and tissues. The isolated virus was approximately 30 nm in diameter as observed with an electron microscope by negative staining. By its location, structure and size it could be related to different families of the small RNA cytoplasmic viruses such as the Picornaviridae or the Nodaviridae. Its characterization is in progress.

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