Taura Syndrome Virus of Penaeid Shrimp
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Category
Category 3 (Host Not in Canada)
Common, generally accepted names of the organism or disease agent
Taura syndrome virus, TSV, Taura syndrome, TS, Red tail disease (probably distinct from Red disease reported in penaeids from southeast Asia).
Scientific name or taxonomic affiliation
Taura syndrome virus has been tentatively classified as a picornavirus based on: its morphology (icosahedron of 30 - 32 nm diameter) and density of 1.337 g/ml; its cytoplasmic, Feulgen-negative sites of replication; its content of linear ssRNA of about 9 kb; and its having three major (49,36.8 and 23 kDa) and two minor (51.5 and 52.5 kDa) polypeptides in its capsid.
Geographic distribution
TSV appears to be limited to regions of the Americas: Ecuador; both coasts of Colombia; Peru; Gulf of Fonseca region of Honduran and El Salvador; Guatemala; northeast Brazil; Nicaragua; Mexican states of Sonora, Chiapas and Guerrero; United States states of Texas, Hawaii and Florida.
Host species
Penaeus vannamei, Penaeus stylirostris, and Penaeus setiferus. Experimental infections were produced in postlarval and juvenile Penaeus setiferus, postlarval Penaeus aztecus, and in juvenile Penaeus chinensis.
Impact on the host
TSV caused serious infections and high mortalities (cumulative losses of 80 to 95%) in cultured postlarvae (PL-12 and older) and juvenile P. vannamei. It is best known as a disease of nursery phase P. vannamei and usually occurs within about 14 to 40 days of stocking postlarvae into grow-out ponds or tanks. During early May 1995, a TSV epizootic crippled Texas shrimp aquaculture by causing large losses in coastal grow-out facilities. In contrast, P. stylirostris, though susceptible to infection, seemed to be highly resistant to the disease. Penaeus aztecus and P. duorarum may also be resistant to TSV disease. Until mid-1994, TSV was considered to have a toxic etiology because its initial discovery in the Taura region of Ecuador in 1992 was coincidental with the initiation of arial spraying of agricultural fungicides, some of which were sterols that were thought to mimic ecdysome, the sterol involved in crustacean molting. However, any link to the fungicides and TSV remains speculative and such a relationship has not been confirmed experimentally.
Diagnostic techniques
Gross Observations
TSV has grossly distinguishable acute and chronic/recovery phases. Acute phase: shrimp have a general pale reddish colouration with the tail fan and pleopods appearing distinctly reddish due to the expansion of the red chromatophores, typically the cutical is soft and the gut empty, and affected shrimp usually die during ecdysis. Chronic/recovery phase: shrimp may or may not have reddish colouration and soft cuticles but often show multifocal, melanized cuticular lesions typical of bacterial shell disease which are resolved after successful molting.
Wet Mounts
Appendages (uropod, antennal scale, pleopods, etc.) may show necrosis of the cuticular epithelium in postlarvae or juveniles in the acute phase of the disease.
Histology
Multifocal lesions in the cuticular epithelium of the general body surface, all appendages, gills, hindgut, esophagus and stomach. Frequently the subcuticular connective tissue and adjacent striated muscle fibers basal to the cuticular epithelial cells are also involved and rarely the antennal gland tubule epithelium is affected. The lesions consist of increased eosinophilia and generally spherical "bodies" (1 - 20 µm diameter, staining from eosinophilic to pale basophilic (with haematoxylin and eosin stain)) in the cytoplasm of infected cells and nuclear pykinosis and karyorrhexis which have a positive (for DNA) Feulgen reaction and are thus distinguishable from the cytoplasmic "bodies" which do not contain DNA. Absence of haemocytic infiltration or other signs of a significant host inflammatory response distinguishes the acute phase from the chronic/recovery phase of the disease.
Electron Microscopy
In the acute phase, the abundant spherical, intracytoplasmic inclusions consist of loosely to densely arranged electron lucent to electron dense aggregates of presumed TSV particles (uniformly sized at about 30 nm in section). Few to very abundant needle-like crystals of calcium phosphate are apparent in the cytoplasmic inclusions of TSV positive shrimp preserved with phosphate buffered fixatives. The presence of the calcium phosphate crystals is likely due to the disruption of calcium metabolism involved in decalcification and calcification of the cuticle during the molting process.
Bioassay
Juvenile P. vannamei fed on suspect shrimp carcases or inoculated with a prepared homogenate from suspect shrimp will develop gross signs and histopathology within 4 days and experience significant mortalities by 8 days (oral exposure) or begin to die within 24 to 48 hours (exposure by inoculation with high viral doses) if TSV is present. Details of the procedures involved were described by Lightner (1996).
DNA Probes
A cDNA probe for TSV provides excellent diagnostic sensitivity via the non-radioactive, DIG-labelled probe used in dot blot and in in situ hybridization assays. The DIG-labeled TSV probe is available from DiagXotics Inc. (27 Cannon Rd., Wilton, CT 06897, USA). Difficulties with the stability of the ssRNA genome of TSV during the dot blot assay process may limit the application of field kits based on DIG-labeled cDNA probes for this agent.
Methods of control
Information not available.
References
Hasson, K.W., D.V. Lightner, B.T. Poulos, R.M. Redman, B.L. White, J.A. Brock and J.R. Bonami. 1995. Taura syndrome in Penaeus vannamei: demonstration of a viral etiology. Diseases of Aquatic Organisms 23: 115-126.
Johnson, S.K. 1995. Taura virus hits Texas. World Aquaculture 26: 82-83.
Lightner, D.V. (ed.). 1996. A Handbook of Shrimp Pathology and Diagnostic Procedures for Disease of Cultured Penaeid Shrimp. World Aquaculture Society, Baton Rouge.
Citation Information
Bower, S.M. (1996): Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish: Taura Syndrome Virus of Penaeid Shrimp.
Date last revised: September 1996
Comments to Susan Bower
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