Taura syndrome (TS) is one of the more devastating diseases affecting the shrimp farming industry worldwide. It was first described in Ecuador during the summer of 1992. In March 1993, it returned as a major epidemic and was the object of extensive media coverage. Retrospective studies have suggested a case of Taura syndrome might have occurred on a shrimp farm in Colombia as early as 1990 and the virus was already present in Ecuador in mid-1991. Between 1992 and 1997, the disease spread to all major regions of the Americas where whiteleg shrimp (Litopenaeus vannamei) is cultured. The economic impact of TS in the Americas during that period might have exceeded US$2 billion by some estimates.
Overview
The 1992 Ecuadorian TS epidemic occurred concurrently with an outbreak of black leaf wilt disease in banana plantations. The outbreak of black leaf disease led to an increase in fungicide usage within the Taura River basin district near the city of Guayaquil. The fungicides propiconazole (Tilt, Ciba-Geigy) and tridemorph (Calixin, BASF) used to control black leaf, ran off into nearby ponds and were initially thought to be responsible for the disease. Analytical data demonstrated propiconazole in water, sediments and hepatopancreas tissues of shrimp harvested from affected farms in Ecuador. No other pesticides were discovered. In January 1994, at the request of Ciba-Geigy, a workshop on Taura syndrome was held at the Aquaculture Pathology Laboratory of the University of Arizona. Experts from several countries with expertise in shrimp and insect pathology, shrimp nutrition, toxicology, mycology, water quality and farm management participated in the workshop. Industry representatives also participated. The group developed recommendations as to the standardization of the research on TS and suggested that studies be done to evaluate whether fungicides or as-yet unrecognized agents were responsible for the syndrome. Dr. Jim Brock, the aquatic disease specialist for the State of Hawaii during this period, first demonstrated the disease could be transmitted by feeding Taura victims to healthy shrimp in early 1994. The dying test shrimp were then fed to a new set of shrimp, which was dying at the same rate. Rivers' postulates were fulfilled in 1994 by Dr. Ken Hasson and co-researchers at the University of Arizona. This proved the viral etiology of the syndrome. The virus was named Taura syndrome virus, often referred to as TSV. The virus is referred to by the name infectious cuticular epithelial necrosis virus (ICENV) by some authors in Latin America. Taura syndrome is a notifiable disease by the Office international des Épizooties (OIE), which reflects the serious nature and devastating impact of the disease.
Identification and description of the virus Taura syndrome virus was first classified as a possible member of the family Picornaviridae based on biological and physical characteristics. It was later reclassified in the Dicistroviridae family, genus Cripavirus. It has since been reassigned to a second genus in the same family – the Aparavirus. TSV is a 32 nm nonenveloped particle with an icosahedral morphology and a buoyant density of 1.338 g/ml. The genome is single-stranded positive-sense and has 10,205 nucleotides (excluding the 3' poly-A tail). The capsid consists of three major proteins: CP1 (40 kDa), CP2 (55 kDa) and CP3 (24 kDa) alongside a minor protein of 58 kDa. Audelo-del-Valle in 2003 reported certain primate cell lines could be used to culture TSV. Later studies demonstrated their report was based on misinterpreted data. TSV does not appear to be a potential zoonosis. All virus amplifications require the use of live shrimp, as there is no continuous cell line that supports the growth of shrimp viruses.
Variants of the virus RNA viruses such as TSV have high rates of spontaneous mutation. These very high rates might be due to the lack of proofreading function of the RNA-dependent RNA polymerase and have resulted in the emergence of several genetic variants of the virus. As of May 2009, four genetic clusters are recognized: Belize (TSV-BZ), America (TSV-HI), Southeast Asia and Venezuela. The Belize strain is considered the most virulent. Point mutations in TSV capsid proteins might provide specific isolates with selective advantages such as host adaptability, increased virulence or increased replication ability. Even small variations in the TSV genome can result in substantial differences in virulence. All TSV variants are similar in shape and size, with light variations. The average size of TSV-BZ virus particles is 32.693+/- 1.834 nm compared to TSV-HI with a size of 31.485 +/- 1.187 nm. The region of highest genetic difference is within the capsid protein CP2, with pairwise comparison of nucleotide showing a 0 to 3.5% difference amongst isolates. The most variations in CP2 occur at the 3'-terminal sequence; this may be because it is less constrained by structural requirements and more exposed than other regions of the protein.
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