Taura Syndrome - Pathology and Disease Cycle

Pathology and Disease Cycle

In farm situations, TS often causes high mortality during the first 15 to 40 days of stocking into shrimp ponds. The course of infection may be acute (5–20 days) to chronic (more than 120 days) at the pond and farm level. The disease has three distinct phases that sometimes overlap: acute, transition and chronic. The disease cycle has been characterized in detail in P. vannamei.

After the initial infection, the acute phase develops. Clinical signs can occur as early as 7 hours after 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 the red chromatophores. Mortality during this phase can be as high as 95%. 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. The pyknosis and karyorrhexis give a “buckshot” appearance to the tissue and are considered pathognomonic for the disease. In severe infections the antennal gland tubule epithelium, the hematopoietic tissues and the testis are also affected. This occurs mainly in severe infection following injection of viral particles and has not been reported from naturally infected P. vannamei. Shrimp that survive the acute stage enter a transitional stage.

Shrimp in the transitional phase show randomly distributed, melanized (brownish/black) lesions within of the cuticle of the cepahlothorax and tail region. These foci are the sites of acute lesions which have progressed onto subsequent stages of hemocytic inflammation, cuticular epithelium regeneration and healing and which might be secondarily infected with bacteria. These foci are negative for TSV by in situ hybridization (ISH) using a TSV-specific cDNA probe. Histologically, these shrimp present focal active acute lesions and the onset of lymphoid organ spheroids (LOSs) development. By ISH with TSV-specific probes, a diffuse positive signal can be observed within the walls of the lymphoid organ of normal appearance with or without focal probe signals within developing LOSs. These shrimp will be lethargic and anorexic, possibly because of the redirection of their energy and metabolic resources toward wound repair and recovery. If the shrimp undergo another successful moult following the transitional phase, they will cast off the melanized lesions and enter the chronic phase.

The chronic phase is first seen six days after infection and persist for at least 12 months under experimental conditions. This phase is characterized histologically by the absence of acute lesions and the presence of LOS of successive morphologies. These LOSs are positive by ISH for TSV. A low prevalence of ectopic spheroids can also be observed in some cases. LOSs 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 yellowhead virus (YHV). 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. Survivors may become carriers for life. Shrimp with chronic TSV infection are not as vigorous as uninfected shrimp, as demonstrated by their inability to tolerate a salinity drop as well as uninfected shrimp. 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.