Taura syndrome ( TS ) , caused by TS virus ( TSV ) , has resulted in serious disease epizootics throughout the shrimp-growing regions of the Western Hemisphere ( 1, 3-6, 10-23, 27, 33 ) . The virus has recently been introduced into Asia with infected imported Pacific white shrimp, Penaeus vannamei, from Central and South American sources ( 30, 32 ) .
Although it is not listed in the most recent report of the International Committee on Nomenclature of Viruses ( 31 ) , TSV has been characterised and tentatively assigned to the family Picornaviridae ( 2, 12, 24, 29 ) . TSV was recently placed in the genus 'Cricket paralysis-like viruses' ( 25 ) . The virus replicates in the cytoplasm of host cells. TSV particles are 32 nm, nonenveloped icosahedrons with a buoyant density of 1.338 g/ml. The genome of TSV consists of a linear, positive-sense single-stranded RNA of 10,205 nucleotides, excluding the 3' poly-A tail, and it contains two large open reading frames ( ORFs ) . ORF 1 contains the sequence motifs for nonstructural proteins, such as helicase, protease and RNA-dependent RNA polymersae. ORF 2 contains the sequences for TSV structural proteins, including the three major capsid proteins VP1, VP2 and VP3 ( 55, 40, and 24 kDa, respectively )( 2, 24, 25 ) .
The principal host for TSV is the Pacific white shrimp, P. vannamei , although other species can be infected and present disease ( 1, 11, 17, 27, 29 ) . Cumulative mortalities due to TSV epizootics have ranged from 40 to >90% in cultured populations of postlarval ( PL ) , juvenile, and subadult P. vannamei . Survivors of TSV infections may carry the virus for life ( 4, 11, 15, 16, 22 ) . TSV has been demonstrated to remain infectious in the faeces of sea gulls that have ingested infected shrimp carcasses, which may implicate birds as being an important route of transmission of the virus within affected farms or farming regions ( 8, 17 ) .
TSV can also infect other Western Hemisphere penaeid species ( i.e. P. stylirostris, P. setiferus , and P. schmitti) , sometimes resulting in disease and mortalities in PL or yearly juvenile stages, but also in asymptomatic persistent infections ( 4, 27 ) . Other Western Hemisphere penaeids (P. aztecus and P. duorarum) and Eastern Hemisphere penaeids (P. chinensis, P. monodon , and P. japonicus) have been experimentally infected with TSV ( 4, 15, 16, 27 ) .
Following its recognition in 1992 as a distinct disease of cultured P. vannamei in Ecuador ( 1, 3, 4, 13, 15, 16, 20 ) , TS has spread rapidly throughout many of the shrimp-farming regions of the Americas through shipments of infected PL and broodstock ( 3-6, 10, 15 ) . Within the Western Hemisphere, TS and TSV have been reported from virtually every penaeid shrimp-growing region in the Americas and Hawaii ( 1, 16, 19, 29, 33 ) . TSV is enzootic in cultured penaeid shrimp stocks on the Pacific coast of the Americas from Peru to Mexico, and it is occasionally found in some wild stocks of P. vannamei from the same region ( 15-17, 19 ) . TSV has also been reported in cultured penaeid stocks from the Atlantic, Caribbean, and Gulf of Mexico coasts of the Americas, but it has not been reported in wild stocks from the these regions ( 10, 16 ) . Until the recent reports of an introduction of the disease to Taipei China with imported P. vannamei from Central America, TSV had not been confirmed to occur in wild or cultured penaeid shrimp stocks outside of the Western Hemisphere ( 30, 32 ) .
During the 1999-2000 shrimp farming seasons, a new stain of TSV emerged in Mexico that caused high mortalities ( as high as 90% ) in stocks of Pacific blue shrimp, P. stylirostris, that were previously resistant to TS ( 17, 33 ) . What may be a second newly emerged strain of TSV appeared in 2001 in Central America where it caused similarly high mortalities in selected stocks of P. vannamei that had been selected because of demonstrated resistance to TSV ( 7 ) . The new Mexican strain of TSV may be distinguished with antibody-based methods from the reference ( Hawaiian 1994 ) isolate of TSV ( 2, 12, 25 ) , and from other ( but otherwise indistinguishable ) geographic and temporal isolates of the virus ( 7 ) .
Standard histological and molecular methods are the surveillance methods for TSV in penaeid shrimp ( 13, 14, 19, 24 ) . With standard histological methods, diagnostic lesions during the acute phase of the disease are demonstrated in specific target tissues, especially the cuticular epithelium. In chronic-phase infections, lymphoid organ spheroids are the only lesion apparent in shrimp with persistent TSV infections. In some circumstances, molecular methods may be more effective for surveillance than routine histology. Specific cDNA probes applied to in-situ hybridisation assays with paraffin sections provide the greatest diagnostic certainty of this agent ( 9-12, 16, 17, 19 ) . The use of specific primer sets in reverse-transcription polymerase chain reaction assays for TSV provides the advantages of larger sample sizes and nonlethal sampling of broodstock ( 19, 26 ) . A variety of other diagnostic methods can be used to provide presumptive and confirmatory diagnoses of TSV infections. Among these methods are live shrimp bioassay ( 3--5, 8, 12, 15 ) and antibody-based methods with monoclonal antibodies ( 28 ) .
Eradication methods for TSV have been successfully applied to certain aquaculture situations. These methods are dependent on the total depopulation of infected stocks, disinfection of the culture facility, avoidance of re-introduction of the virus ( from other nearby culture facilities, wild shrimp, etc. ) , and re-stocking with TSV-free postlarvae that have been produced from TSV-free broodstock ( 6, 17, 18 ) .