Category
| Common Name | Scientific Name | Distribution | Host SpeciesCategory 3 (Host Not in Canada)
Taura syndrome virus, TSV, Taura syndrome, TS, Red tail disease (probably distinct from Red disease reported in penaeids from southeast Asia).
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.
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.
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.
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.
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.
Information not available.
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.
Bower, S.M. (1996): Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish: Taura Syndrome Virus of Penaeid Shrimp.
URL: http://www.pac.dfo-mpo.gc.ca/science/species-especes/shellfish-coquillages/diseases-maladies/pages/tsvsp-eng.htm
Date last revised: September 1996
Comments to
Susan Bower