Taura syndrome

Taura syndrome is one of the more devastating diseases affecting the shrimp farming industry worldwide. Since its first description in Ecuador, it has spread to all shrimp-growing countries of the Americas and outbreaks have been described in many South-East Asian regions. It was first thought that the disease had a toxic etiology and was caused by pesticides used on nearby banana plantations. The infectious cause of the disease is now widely accepted. Taura syndrome is recognized as a notifiable disease by the Office International des Epizooties.

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The disease has three distinct but overlapping phases, namely acute, transition and chronic. The disease cycle has been characterized in detail in Litopenaeus vannamei. L. vannamei is particularly susceptible to this disease. After infection either by cannibalism or water-borne exposure, the acute phase develops. Clinical signs can occur as early as seven hours after infection in some individuals. Infected shrimp display anorexia, lethargy, erratic swimming behavior, opacification of the tail musculature, soft cuticle and, in naturally occurring infection, chromatophore expansion (red tail). Histologically, this phase is characterized by nuclear pyknosis/karyorrhexis and numerous cytoplasmic inclusion bodies in the subcutis and cuticular epithelium within the appendages, foregut, hindgut, general body cuticle and the gills. The inclusions give a buckshot appearance to the tissue and are considered pathognomonic for the disease. The acute phase can last up to 7 days and mortality rates up to 95% can occur.

Shrimp that survive this first phase move into a transitional phase (roughly day 5 to 8 post-exposure). Characteristic of this phase are variably shaped and sized melanized lesions that can be seen on the head and the tail of the shrimp. If the shrimp undergoes another successful molt following this phase it will cast off the melanized lesions and enter the chronic phase. The chronic phase is characterized histologically by the absence of acute lesions and the presence of lymphoid organ spheroids (LOS) of successive morphogeny. Lymphoid spheroids are not by themselves characteristic of Taura syndrome infection and can be seen in other viral disease of shrimp such as infection with white spot syndrome virus. The chronic phase is first seen 6 days post infection and can persist for an undetermined period of time, at least 8 months under experimental conditions. Diagnosis of the disease during this phase is problematic as shrimp do not display any outward signs of the disease. Shrimp surviving outbreak of TSV seem to be refractory to reinfection while remaining infectious.

A presumptive diagnosis can be established by seeing dead or dying shrimp in nets used for routine evaluation. Predatory birds are attracted to diseased ponds and feed heavily on the dying shrimp contributing to the dispersal of the disease throughout a farm or a shrimp-farming region. The unique signs of infection caused by Taura syndrome such as the cuticular melanized spots can provide a strong presumptive diagnosis, but care must be taken as these can be confused with other forms of shell diseases such as bacterial shell disease. In general, pathognomonic histopathological lesions are the first step in confirmatory diagnosis. In situ hybridization, reverse transcription polymerase chain reaction and specific MAbs can also be used for diagnosis.

Management strategies for the disease have included raising of more resistant species such as L. stylirostris and stocking of specific pathogen free (SPF) or specific pathogen resistant (SPR) shrimp. Stocking of post-larvae at higher density has also been advocated. Other techniques used with limited efficacity have been the polyculture of shrimp with Tilapia, immunostimulants, provided in feed or water, and pond liming.^[1]

Taura syndrome virus (TSV) is a member of the Discistroviridae family, genus Cripavirus. This intracytoplasmic virus is a 32 nm non-enveloped particle having an icosahedral morphology. Its single positive stranded genome consists of 10,205 nucleotides (excluding the 3' poly-A tail). There is a 377-nucleotide untranslated region at the 5' end followed by two open reading frames (ORF) separated by an intergenic region of 226 nucleotides. ORF1 revealed motifs characteristic of a helicase, a protease and an RNA-dependent RNA polymerase. Capsid proteins (55, 40 and 24 kDa) were mapped in the ORF2.^[2]

References

1. ^ Gulf States Marine Fisheries Commission: Non-Native Species Summaries: Taura Syndrome Virus (TSV), 2003. Accessed June 30, 2005.
2. ^ World Organization for Animal Health (OIE): Aquatic Manual, 4th Ed., 2003. Section 4.1.1. ISBN 92-9044-563-7.

• Jimenez R. (1992) Sindrome de Taura (resumen) Pages 1-16 in: Aquacultura del Ecuador. Camara Nacional de Acuacultura, Guayaquil, Ecuador
• Hasson K.W., Lightner D.V, Poulos B.T., Redman R.M., White B.L., Brock J.A. and Bonami J.-R. (1995) Taura syndrome in Penaeus vannamei: demonstration of a viral etiology. Diseases of Aquatic Organisms 23: 115-126
• Lightner D.V., Redman R.M., Hasson K.W. and Pantoja C.R. (1995) Taura syndrome in Penaeus vannamei (Crustacea: Decapoda): gross signs, histopathology and ultrastructure. Diseases of Aquatic Organisms. 21: 53-59
• Mari J., Poulos B.T., Lightner DV.. and Bonami J.-R. (2002) Shrimp Taura syndrome virus: genomic characterization and similarity with members of the genus Cricket paralysis-like viruses. Journal of General Virology. 83: 915-926