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Taura syndrome

The controversy

Taura syndrome (TS) 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 that a case of TS might have occurred on a shrimp farm in Colombia as early as 1990 and that 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 Penaeus vannamei is cultured. It has been estimated that the economic impact of TS in the Americas during that time might have exceeded 2 billion US dollars.

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. It was thought that the antifungicide Tilt (propiconazole,Ciba-Geigy) and Calixin (tridemorph, BASF) used to control black leaf, ran off into nearby ponds and were responsible for TS. Analytical data demonstrated propiconazole in water, sediments and hepatopancreas tissues of shrimp harvested from TS affected farms in Ecuador. No other pesticides were discovered.

An Ecuadorian shrimp farmer industry representative reported "According to the latest research work, it seems to us that this delicate [environmental] balance was lost with the growth of the banana industry and the measures taken in that sector to overcome sigatoka black leaf spot disease. With the application of fungicides, a critical mass of toxic substances was reached, producing Taura syndrome" . Other articles in the popular press described the toxic etiology of the disease . In his 1994 article, Wigglesworth mentions anomalies of the TS behavior with regard to a possible toxic etiology including higher resistance of wild post-larvae to the syndrome. The toxic etiology belief was strengthened by research performed by Intriago et al. (1997) and other groups. This was responsible for a controversy that lasted several years and might have contributed to the spread of the disease.

In January 1994, at the request of Ciba-Geigy, a TS workshop was held at the Aquaculture Pathology of the University of Arizona. Experts from seven countries with expertise in shrimp and insect pathology, shrimp nutrition, toxicology, myocology, water quality and farm management participated in the workshop. Industry representatives from Ecuador, Colombia, Switzerland, Belgium and the USA also participated. The group developed recommendations as to the standardization of the research on TS and suggested that studies be done to evaluate whether fungicide or an as-yet unrecognized agent was responsible for the syndrome.

James Brock first demonstrated the infectious etiology of the disease by feeding Taura victims to test shrimp. The dying test shrimp were then fed to a new set of shrimp who was dying at the same rate, precluding dilution of a toxic chemicals and suggesting the active replication of an infectious agent within the shrimp. Hasson et al. (1995) fulfilled the Rivers' postulates and proved the viral etiology of the syndrome. The basis for histopathological diagnosis of the disease was described by Lightner et al. (1995) and several diagnostic methods were later developed. The causative agent, Taura syndrome virus (TSV), of the disease has been designated has a notifiable disease by the Office international des Épizooties reflecting the serious and devastating impacts of the disease. The causal agent is referred by the name of Infectious cuticular epithelial necrosis virus (ICENV) by some authors.

Identification and description of the virus.

The causative agent of the disease, TSV, has been isolated and purified. Based on biological and physical characteristics, it was first classified as a possible member of the family Picornaviridae. It was later reclassified in the Dicistroviridae family, genus Cripavirus. It currently belongs to that same family, but it is unassigned to any genus.

TSV is a 32nm non-enveloped particle with an icosahedral morphology and a buoyant density of 1.338g/ml . Using light microscopic in situ hybridization (ISH) it was found that the binding of the probe was limited to the cytoplasm of infected cells, with no detectable signal within the nucleus (Hasson et al. 1999a). Srisuvan et al. (2006) used electron microscopic in situ hybridisation (EM-ISH) to evaluate the replication of the virus within the cell. They found that replicating TSV was associated with membranous structures within the cytoplasm. They observed eccentricity of the nuclei of infected cells, suggesting that TSV replication could take place in a defined region of the cell. In that study the nuclei were relatively free of hybridization signals, but a positive reaction was evident between the inner and outer nuclear membranes

TSV has a single-stranded positive-sense genome that consists of 10,205 nucleotides (excluding the 3' poly-A tail). There is a 377 nucleotides untranslated region at the 5' end followed by two open reading frames (ORF) separated by an intergenic region of 226 nucleotides. ORF1 has motifs characteristic of a helicase, a protease, an RNA-dependent-RNA-polymerase and a region of striking similarity with the baculovirus IAP repeat (BIR) domain at the N-terminal region. The capsid proteins CP1 (40kDa), CP2 (55kDa) and CP3 (24kDa) were mapped in ORF2 alongside a minor protein of 58kDa. It has been hypothesized that the minor protein is produced by different proteolytic cleavage of the capsid polyprotein and could be a precursor for other capsid proteins .

The region separating the two non-overlaping ORFs contains an internal ribosome entry site (IRES) that directs the synthesis of the capsid proteins. Using northern blot analysis Robles-Sikisaka et al. (2001) suggested that although the genome of TSV contained more than 1 ORF the entire genome was transcribed as a single transcript, the capsid protein gene not being transcribed as subgenomic RNA.

Despite reports by Audelo-del-Valle (2003) that certain primate cell lines could be used to culture TSV. Pantoja et al. (2004) and Luo et al. (2004) demonstrated that their report was based on misinterpretated data. Hence, at the present time, there is no continuous cell line that supports the growth of TSV. Therefore, all virus amplifications require the use of live shrimp.

Variants of the virus

RNA viruses such as TSV have rates of spontaneous mutation in the order of 10-3 to 10-4 per incorporated nucleotide. 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 new genetic variants of the virus. Direct analysis of genetic variations has revealed initially two, and later three, clusters of geographic isolates . Four genetic clusters are currently recognised: Belize, America, South-east Asia and Venezuela. According to their mortality rate and reaction with available antibodies, five variants of the virus are recognized. Isolates representing what are essentially clusters of TSV genotypes and the year of collection are: TSV-HI94, TSV-SI98, TSV-BZ02, TSV-VZ05 and TSV-TH05. Hereafter referred to in this review as TSV-HI, TSV-SI, TSV-BZ, TSV-VE and TSV-TH.

The emergence of new strains could be caused by the rapid adaptation of the virus to new local environmental conditions following transfer. This produces adapted local substrains which facilitate infection of new hosts, resulting in the propagation of the new strain. It has been suggested that new strains such as TSV-SI could have had evolved as a result of its infection of Penaeus stylirostris, a new penaeid host for TSV. Species currently considered to be TSV tolerant might be at risk following the introduction of TSV into new areas.

Point mutations in TSV capsid proteins might provide specific isolate with selective advantages such as host adaptability, increased virulence or increased replication ability. Tang and Lightner (2005) noted that even small variations in the TSV genome can result in substantial differences in virulence. P. monodon infected with one isolate of TSV, isolated from brooders captured from Southern Taiwan coastal waters, showed no signs of active replication while another TSV isolate from Taiwan, isolated from a single Metapenaeus ensis specimen, was found to replicate freely within the shrimp .

Three variants were tentatively attributed to serotype according to their reaction with the then sole available Monoclonal antibody (MAb) 1A1. Serotype A: Hawaii, serotype B: Sinaloa (Mexico) and serotype C: Belize. Out of these, the Belize strain has consistently given higher mortality in bioassays and it is considered the most virulent. .

All TSV variants are similar in shape and size with light variations. The average size of TSV-BZ virus particles is 32.693+/- 1.834nm compared to TSV-HI with a size of 31.485 +/- 1.187 nm. The region of highest genetic difference is within CP2 with pairwise comparison of nucleotide showing a 0 to 3.5% difference amongst isolates while the difference for CP1 is 0 to 2.4%. Tang et al. (2005) reported up to 5.6% difference in CP2 using a larger group of isolates collected over a longer time span (11 vs 1 year for Robles-Sikisaka et al. 2002). 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.

Geographic distribution

TSV has been reported from virtually all shrimp-growing regions of the Americas including Ecuador, Columbia, Peru, Brazil, El Salvador, Guatemala, Honduras, Belize, Mexico, Nicaragua, Panama, Costa Rica, Venezuela as well as from the States of Hawaii, Texas, Florida and South Carolina . In 1997 the virus had spread to virtually all shrimp growing regions in the Americas, but had not yet been described in Asia and other part of the world. Until 1998, it was considered to be a Western Hemisphere virus. The first Asian outbreak occurred in Taiwan. It has more recently been identified in Thailand, Myanmar, China, Korea and Indonesia where it has been associated with significant epizootics in farmed Penaeus vannamei and P. monodon.

The wide distribution of the disease has been attributed to the movement of host stocks for aquaculture purposes. This might have been helped by the highly stable nature of the virus. It is thought that importation of TSV-infected P. vannamei from the Western Hemisphere was at the origin of the outbreak in Taiwan. This was further suggested by the genomic similarity of the Taiwan and Western Hemisphere isolates. TSV appeared in Thailand in 2003. Due to the similarities in deduced VP1 protein sequence and the chronology of the disease outbreaks in relation to imported stocks it is likely that at least some of the Thai isolates originated from Chinese stocks.

Species of shrimp susceptible

TSV is known to affect many penaeid shrimp species. It causes serious diseases in the postlarval (PL), juvenile and adult stages of Penaeus vannamei, the most susceptible target host with up to 50-90% mortality in non-selected population. It also affects severely P. setiferus, P. stylirostris, P. schmitt, Metapenaeus ensis. Srisuvan et al. (2005) demonstrated the disease in P. monodon, a species previously thought to be resistant. Other species such as P. chinensis (experimentally) present mortality. P. aztecus, P. duorarum and P. Japonicus have also been shown to be hosts for TSV in natural and experimental infections. P. aztecus and P. duorarum were relatively tolerant to the virus and were not killed by TS.

TSV infection has no known impact on nauplii through the early postlarval stages. Postlarval to adult sizes are susceptible to infection by TSV but seem to show increasing TS resistance with increase in size (Brock 1997; Brock et al. 1997). The size of shrimp affected with TS in Sinaloa, Mexico, has been reported as ranging from 0.063g to 15.0g. Laboratory results have, however, failed to find significant differences supporting the hypothesis that P. vannamei increase its tolerance to TSV as it increases in size to up to 30g. Lotz (1997) noted a consistent trend for larger shrimp to be more likely to succumb infection. The discrepancy between these findings and what is commonly observed in the field might be due to the larger shrimp being more likely to have previously been exposed and therefore having acquired resistance. The likelihood of infection and mortality from TSV is also dependent on the initial dose. For both per os and water route of transmission the dose of TSV per g of shrimp will decrease as the shrimp increase in size (Lotz 1997). There is variation within species and TSV-resistant strains of shrimp have been developed (Argue et al. 2002). Wild stocks are showing increased resistance, perhaps through intense natural selection (Laramore 1997; Lightner et al. 1997b; Lightner 1999). Reports of TS in the wild are limited, but in February 1995, the Mexican Fisheries Ministry reported the presence of TSV in wild-type shrimp captured on the border of Mexico and Guatemala (reported in Zarain-Herzberg and Ascencio-Valle 2001). Investigators have also reported the occurrence of TS in wild post-larvae from the Gulf of Guayaquil, Ecuador during mid-1993 and in adult P. vannamei collected from the Pacific Coast of Honduras and El Salvador (reported in Lightner et al. 1997b). There are no confirmed reports indicating that TSV is infectious to other groups of decapod or non-decapod crustaceans (Brock 1997).

As a RNA virus, TSV has shown rapid sequence evolution. This could be related to adaptation to new hosts. According to Phalitakul et al. (2006) the sequence divergence of an isolate of TSV from Thailand suggested adaptation to P. monodon as a new host species. Adaptation of the virus to new host has also been suggested in the case of P. stylirostris and TSV-SI (Erickson et al. 2002; Robles-Sikisaka et al. 2002).

Pathology and disease cycle

In farm situations, TS often causes high mortality during the first 40 days of stocking into shrimp ponds (Brock 1997). The course of infection may be acute (5-20 days) to chronic (more than 120 days) at the pond level (Brock et al. 1997).

The disease has three distinct but overlapping phases: acute, transition and chronic. The disease cycle has been characterized in detail in Penaeus vannamei. Lotz et al. (2003) have developed mathematical model for epidemics of TSV in closed population. This model included the three phases described previously into five compartments: uninfected susceptible, prepatently infected, acutely infected, chronically infected and dead infected shrimp.

After the initial infection, the acute phase develops. Clinical signs can occur as early as 7 hours post-infection in some individuals and last for about 4-7 days. Infected shrimp display [anorexia], lethargy and erratic swimming behavior. They also present opacification of the tail musculature, soft cuticle and, in naturally occurring infection, a red tail due to the expansion of chromatophores (Hasson et al. 1999a). Focal necrosis of the tail cuticular epithelium can be seen with a 10X hand lens (Lightner 1996; Flegel 2006). Mortality during this phase can as high as 95% (Brock 1997).

The acute phase is characterized histologically by multifocal areas of nuclear pyknosis/karyorrhexis and numerous cytoplasmic inclusion bodies in the cuticular epithelium and the subcutis of the general body surface, all appendages, gills, hindgut, esophagus and stomach (Lightner et al. 1995; Hasson et al. 1999b). The pyknosis and karyorrhexis give a “buckshot” appearance to the tissue and are considered pathognomonic for the disease (Lightner et al. 1995). In severe infections the antennal gland tubule epithelium, the hematopoietic tissues and the testis are also affected (Hasson et al. 1995; Lightner et al. 1995). This occurs mainly in severe infection following injection of viral particles and has not been reported from naturally infected P. vannamei (Hasson et al. 1999b).

Transmission electron microscopic (TEM) evaluation of affected cells has allowed the observation of the inclusion bodies occupying a large area within the cytoplasm of infected cells. The inclusion bodies are composed of an amorphous, granular, electron-dense matrix reacting with TSV by ISH using TSV specific cDNA probes. In early TEM studies, it was found that the inclusion bodies often contained needle-like crystals that were presumed to be made of calcium phosphate and associated to a disruption of the calcium metabolism and the calcification process of the exoskeleton . It has later been stated that these crystalline deposits were a variable finding that could reflect an artefact from the use of phosphate buffered glutaraldehyde fixation (reported in Brock et al. 1997).

Shrimp that survive the acute stage enter a transitional stage and show randomly distributed melanized (brownish/black) lesions within of the cuticle of the cepahlothorax and tail region (Hasson et al. 1999b) These foci are the sites of acute lesions which have progressed onto subsequent stages of hemocytic inflammation, cuticular epithelium regeneration and healing (Brock 1997), and which might be secondarily infected with bacteria (Hasson et al. 1999b). These foci are negative for TSV by ISH (Hasson et al. 1999b). Shrimp in the transition phase are lethargic and anorexic, possibly because of the redirection of all their resources toward wound repair and recovery (Dhar et al. 2004). Histologically these shrimp present focal active acute lesions and the onset of lymphoid organ spheroids (LOS) development. By ISH with TSV specific probes a diffuse positive signal can be observed within the walls of LO of normal appearance with or without focal probe signals within developing LOS (Hasson et al. 1999b).

If the shrimp undergo another successful moult following the transitional phase they will cast off the melanized lesions (Hasson et al. 1995) and enter the chronic phase. The chronic phase is first seen 6 days post-infection and can persist for an undetermined period of time, at least 12 months under experimental conditions (Hasson et al. 1999b; Poulos et al. 2008). The chronic phase is characterized histologically by the absence of acute lesions and the presence of LOS of successive morphologies (Hasson et al. 1999c). These LOS are positive by ISH for TSV (Poulos et al. 2008). A low prevalence of ectopic spheroids can also be observed in some cases (Hasson et al. 1999c). LOS are not by themselves characteristic of TSV infection and can be found in other viral diseases of shrimp such as lymphoid organ vacuolization virus (LOVV), lymphoid parvo-like virus (LPV), lymphoid organ virus (LOV), rhabdovirus of penaeid shrimp (RPS) and yellow head virus (YHV) (Hasson et al. 1999c).

Diagnosis of the disease during the chronic phase is problematic as shrimp do not display any outward signs of the disease and do not show mortality from the infection (Brock et al. 1997; Hasson et al. 1999c). It has been suggested that shrimp with chronic TSV infection were not as vigorous as uninfected shrimp, as demonstrated by their inability to tolerate a salinity drop as well as uninfected shrimp (Lotz et al. 2005).

Cellular biology of the disease

Little is known regarding the effect of the virus at the cellular level. Lamr/p40 type receptor has been proposed as a putative attachment site for the virus CP2 (Senapin and Phongdara 2006). Cevallos and Sarnow (2005) have hypothesized that the virus might counteract phosphorylation of eIF2 by kinase of the innate immune system by initiating translation without requirement for initiator-tRNAmet. They also suggested the alternative hypothesis that the replication of the virus on cellular membranes may cause stress resulting in the activation of eIF2 kinase and an overall inhibition of initiator-tRNAmet-dependent translation.

Viral particles have been detected in the hemolymph of infected shrimp (Bonami et al. 1997). These had the same morphology as virus purified from tissue. This indicates the systemic nature of the acute phase infection and that the whole virion is transported by the hemolymph. The expression of protein in the hemocytes of acutely infected shrimp has been evaluated using two-dimensional gel electrophoresis. It showed that 11 forms of eight proteins were significantly up regulated whereas nine forms of five proteins that were down regulated. The up regulated proteins were 14-3-3 Zeta protein, tubulin beta-2 chain, beta-actin, acetylglucosamine, hemocyanin, protein disulfide isomerase precursors, catalase, carboxylesterase and one unknown protein. The down regulated proteins were TM, transglutaminase, the light chain of myosin, glutathione transferase and hemocyacin. Only hemocyanin fragments (either C or N terminal) were altered, not the full-length protein. These fragments could have a functional significance during the molecular response of shrimp hemocytes to TS (Chongsatja et al. 2007).

Routes of transmission

The most likely route for transmission of TSV is cannibalism of dead infected shrimp. The virus can be spread from one farm to another by seagulls and aquatic insects, such as the water boatman, Trichocorixa reticulata (Lightner and Redman 1998). Shrimp farmers from Ecuador, Honduras and Columbia have reported numbers of these insects in TSV-infected ponds (reported by Hasson et al. 1995). ISH assays run on histological sections of water boatman collected from ponds in which severe TS outbreaks were on-going showed several individuals with TSV positive gut contents. There was, however, no indication that the virus was infecting or replicating in the insect (Lightner et al 1997b). Infectious TSV has been found in the feces of laughing gulls, Larus atricilla, that fed on infected shrimp during an epizootic in Texas (Garza et al. 1997). Controlled laboratory studies have documented that TSV remains infectious for up to one day after passage through the gut of white leghorns chicken, Gallus domesticus, and laughing gulls . Vertical transmission of TSV is thought to occur based on anecdotal information, but this has not been experimentally confirmed (Lightner and Redman 1998; Dhar et al. 2004).

Shrimp surviving an outbreak of TSV seem to be refractory to reinfection (Ken Hasson reported by anon 1995) albeit remain carriers and are source for infection of susceptible animals (Vincent et al. 2004). It has been hypothesized that TSV was introduced to Southeast Asia with chronically infected shrimp imported from the Western Hemisphere (Yu and Song 2000). The ability of TSV to remain at least partly infectious after one or several freeze-thaw cycles might be a contributing factor facilitating its spread in the international commerce of frozen commodity products (Lightner 1995). TSV is however easily degraded by multiple freeze-thaw cycles when in purified or pre-purified form (Bonami et al. 1997). Mechanisms by which infected frozen shrimp could spread the virus include: reprocessing of shrimp at processing plants with release of infectious liquid wastes, disposal of solid wastes in landfills where seagulls could acquire the virus and then spread it, the use of shrimp as bait by sport fishermen and the use of imported shrimp as fresh food for other aquatic species (Lightner et al. 1997a). The latter was practiced at the National Zoo in Washington when freshwater crayfish became infected with another exotic virus of shrimp White spot syndrome virus (WSSV) (reported in Lightner et al. 1997a). The importation of infected commodity shrimp might therefore present a risk of accidental contamination of wild and cultured stocks (Lightner et al 1997a). The disease has potential to become established in wild stock and its long-term effects on commercial penaeid fisheries or on the culture of native species are unknown (Lightner et al. 1997a; Flegel 2006).

TS can spread rapidly when introduced in news areas. A shrimp farmer described the 1995 outbreak in Texas as " This thing spread like a forest fire... There was not stopping it. I just sat there and watched it, and in a matter of three days, my shrimp were gone. Dead!" (reported in Rosenberry 1995).

Diagnostic methods

A presumptive diagnosis of acute TSV infection can be established by the presence of dead or dying shrimp in cast nets used for routine evaluation. Predatory birds are attracted to diseased ponds and feed heavily on the dying shrimp, contributing to the dispersion of the disease throughout a farm or a shrimp farming region. The unique signs of infection caused by TS such as the cuticular melanized spots can provide a strong presumptive diagnosis, but care must be taken as these can be confused with other diseases such as bacterial shell disease. In general pathognomonic histopathological lesions are the first step in confirmatory diagnosis. Discrete foci of pyknotic and karyorhectic nuclei and inflammation are seen within the cuticular tissues. The lymphoid organ might display spheroids, but is otherwise unremarkable.

The genome of the virus has been cloned and specific cDNA probes are available for diagnosis . ISH analysis of acute phase lesions has demonstrated that gene probe positive signals are strongest within intact cuticular cells in the early stages of infection. It is believed that, following cell lysis, the virus is rapidly dispersed by the hemolymph resulting in a weakly positive to negative probe signal to the remaining cellular (e.g. pyknotic or karyorhectic nuclear fragments) components.

Reverse transcriptase polymerase chain reaction (RT-PCR) methods have been developed for detection of TSV and have a detection limit of 104 copies/µg of RNA. Real-time RT-PCR using either a Taq Man assay or SYBR green has a lower detection limit of 102 copies/µg of RNA . Real-time techniques allow for quantification of the virus. The IQ2000TM TSV detection and prevention system, a RT-PCR method, is said to have a detection limit of 10 copies per reaction .

RNA-based methods are specific and sensitive and have proven to be very helpful in research and as diagnostic reagents. However, they are relatively expensive to perform and require specific equipment and highly trained personnel. They are also limited by the relative fragility of the viral RNA. Prolonged fixation in Davidson's fixative might result in RNA degradation due to fixative-induced acid hydrolysis (Hasson et al. 1997; Lien et al. 2002). The complexity of these approaches has limited their practical “field” applications (Poulos et al. 1999). An alternative for virus detection is the utilization of specific monoclonal antibodies, MAbs, directed against the relatively stable proteins in the viral capsid. Because of their speed, versatility and reasonably good sensitivity MAbs-based tests could be potentially very useful as routine diagnostic test for the screening of a large number of samples at a relatively low cost and with minimum requirement of technical expertise (Poulos et al. 1999).

Such rapid diagnostic tests are now in common use for WSSV and are being marketed under the commercial name of Shrimple® (Enbio Tech, Tokyo. Japan). Similar tests for TSV, Yellow head virus (YHV) and IHHNV are currently under development. These tests are based on the principle of the sandwich immuoassay, no special tissue preparation is required and results can be obtained readily (Takahashi et al. 2003).

Polyclonal antibodies against TSV have been made (Poulos et al. 1999; Chaivisuthangkura et al. 2006) and rabbit anti-TSV PAbs are commercially available (Abcam, Cambridge, MA). Polyclonal antibodies react with a wide range of epitopes and do not present the reactional stability of MAbs. PAbs also require a constant use of animals, whether mice, rabbits or chickens, with possible lot-to-lot variation. Monoclonal antibodies against TSV CP2 have been developed (Poulos et al. 1999). However they do not recognize three of the five recognized strains of the virus: TSV-SI, TSV-BZ and TSV-VE (Erickson et al. 2002; Erickson et al. 2005; Cote et al. this thesis). There is a definite need to produce monoclonal antibodies against these strains, which could be used in rapid diagnostic tests and other assays for virus characterization (Erickson et al. 2003). Monoclonal antibodies recognising the more conserved CP3 have been developed (Longyant et al. 2008). Targeting this protein could prove to be an interesting avenue for diagnosis.

Prior et al. (2003) have developed a controlled bioassay system for the determination of lethal infective dose of tissue homogenate containing TSV. Their bioassay system uses individual flasks to house TSV challenged indicator shrimp to eliminate the possibility of viral dose magnification during the challenge due to cannibalism or the shedding of infectious particles in the water by infected shrimp.

Methods of control

Management strategies for the disease have included raising more resistant species such as Penaeus stylirostris and stocking of specific pathogen free (SPF) or specific pathogen resistant (SPR) shrimp. Relatively simple laboratory challenges can be used to predict the performance of selected stocks in farm where TSV is enzootic. TSV-resistant shrimp are susceptible to infection but have high survival following challenge with at least four variants of TSV (HI, BZ, VE, TH). In challenge assays there was no significant difference between the survival of TSV-resistant lines. The author stated that resistant lines have reached nearly complete resistance to TSV-HI and TH and further improvement due to breeding for TSV-resistance should be minor . Significant improvements in TSV survival were made through selective breeding despite low to moderate heritability for this trait.

A management strategy used to reduce the impact of TS has been the practice of stocking PLs at increased stocking density (Laramore 1997). Following this strategy, farms would experience mortality due to TS at an early stage of the production cycle, before substantial feeding had begun, and the surviving shrimp would be resistant to further TSV challenges (Lightner and Redman 1998). Other techniques used with limited efficacy have been the polyculture of shrimp with tilapia and maintenance of near optimal water quality conditions in the grow-out ponds with reduction of organic loading (Chamberlain 1994; Brock 1997). Transgenic shrimp expressing an antisense TSV coat protein (TSV-CP) exhibited increased survival in TSV challenges (Lu and Sun 2005). The public perception of transgenic animals as well as current technical limitations, limit the use of transgenic animals as a mean of disease control (Einsiedel 2005).

There is one instance where TSV was successfully eradicated from one shrimp farming country (Belize). This required strict disinfection and quarantine protocols and was helped by the relative isolation and the relatively small size of the Belize shrimp farming industry (Dixon and Dorado 1997). TSV has since reappeared in Belize and eradication is now not considered a viable option for control of the disease, rather control by using TSV-resistant shrimp stocks (Erickson et al. 2005; Argue et al. 2002). The virus has been eradicated from the Hawaii islands and has not been detected in Hawaii during the period from 1994 to 2006 (Lightner et al. 2007). A case of TSV occurred in one Hawaiian farm and was confirmed on the 4/18/2007 (OIE, 2007). TSV was thereafter re-eradicated from the State of Hawaii.

References

Tang, K.F.J., and D.V. Lightner. 2005. Phylogenetic analysis of Taura syndrome virus isolates collected between 1993 and 2004 and virulence comparison between two isolates representing different genetic variants. Virus Research 112: 69-76.

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