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.

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.

[1] Analytical data demonstrated propiconazole in water, sediments and hepatopancreas tissues of shrimp harvested from affected farms in Ecuador.

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.

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.

Taura syndrome virus was first classified as a possible member of the family Picornaviridae based on biological and physical characteristics.

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.

TSV has been reported from virtually all shrimp-growing regions of the Americas, including Ecuador, Colombia, Peru, Brazil, El Salvador, Guatemala, Honduras, Belize, Mexico, Nicaragua, Panama, Costa Rica, and Venezuela, as well as from the states of Hawaii, Texas, Florida and South Carolina.

Shrimp in the transitional phase show randomly distributed, melanized (brownish/black) lesions within of the cuticle of the cephalothorax and tail region.

These foci are the sites of acute lesions which have progressed onto subsequent stages of hemocytic inflammation,[9] cuticular epithelium regeneration and healing and which might be secondarily infected with bacteria.

Histologically, these shrimp present focal active acute lesions and the onset of lymphoid organ spheroids (LOSs) development.

These shrimp will be lethargic and anorexic, possibly because of the redirection of their energy and metabolic resources toward wound repair and recovery.

[12] A 2011 study by Laxminath Tumburu looked at the relationship between an environmental stressor (pesticide endosulfan) and Taura syndrome virus (TSV) and their interactions on the susceptibility and molting of marine penaeid shrimp L. vannamei and found the interference of endosulfan-associated stress led to increasingly higher susceptibility at postmolt stage during the acute phase of the TSV disease cycle.

[14] Infectious TSV has been found in the feces of laughing gulls that fed on infected shrimp during an epizootic in Texas.

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.

It has been hypothesized that TSV was introduced to Southeast Asia with chronically infected shrimp imported from the Western Hemisphere.

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.

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.

An alternative for virus detection is the use of specific monoclonal antibodies (MAbs) directed against the relatively stable proteins in the viral capsid.

Rapid diagnostic tests using MAbs are now in common use for white spot syndrome virus and are being marketed under the commercial name of Shrimple.

Relatively simple laboratory challenges can be used to predict the performance of selected stocks in farms where TSV is enzootic.

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.

Other techniques used with limited efficacy have been the polyculture of shrimp with tilapia [21] and maintenance of near-optimal water quality conditions in the grow-out ponds with reduction of organic loading.