| White spot syndrome | |
|---|---|
| Virus classification | |
| Group: | Group I (dsDNA) |
| Family: | Nimaviridae |
| Genus: | Whispovirus |
| Species | |
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White spot Syndrome Baculovirus Complex |
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White spot syndrome (WSS) is a viral infection of penaeid shrimp. The disease is highly lethal and contagious, killing shrimps quickly. Outbreaks of this disease have wiped out within a few days the entire populations of many shrimp farms throughout the world.
The disease is caused by a family of related viruses subsumed as the white spot syndrome baculovirus complex (WSSV) [1] and the disease caused by them as white spot syndrome (WSS).[2]
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The first reported epidemic due to this virus is from Taiwan in 1992;[3] however, reports of losses due to white spot disease came from China in 1993,[4] where it led to a virtual collapse of the shrimp farming industry. This was followed by outbreaks in Japan and Korea in the same year, Thailand, India and Malaysia in 1994, and by 1996 it had severely affected East Asia and South Asia. In late 1995, it was reported in the USA, 1998 in Central and South America, 1999 in Mexico and in 2000 in the Philippines. Currently, it is known to be present in all shrimp-growing regions except Australia.
WSSV is a rod-shaped, double-stranded, DNA virus, and the size of the enveloped viral particles have been reported to be 240–380 nm long and 70–159 nm in diameter and nucleocapsid core is 120–205 nm long and 95–165 nm in diameter. The virus has an outer lipid bilayer membrane envelope, sometimes with a tail like appendage at one end of the virion. The nucleocapsid consists of 15 conspicuous vertical helices located along the long axis, each helix has two parallel striations, composed of 14 globular capsomers, each of which is 8 nm in diameter.[5]
The complete DNA sequence of WSSV genome has been assembled into a circular sequence of 292,967 bp.[6] It encodes 531 putative open reading frames.
One of the proteins – WSSV449 – has some similarity to host protein Tube and can function like Tube by activating the NF-κB pathway.[7]
Transmission of the virus is mainly through oral ingestion and water-borne routes in farms (horizontal transmission) and vertical transmission (from infected mother prawns) in the case of shrimp hatcheries. The virus is present in the wild stocks of shrimp, especially in the coastal waters adjacent to shrimp farming regions in Asian countries, but mass mortalities of wild shrimps are yet to be observed.
The virus has a wide host range, is highly virulent and leads to mortality rates of 100% within days in the case of cultured penaeid shrimps. Most of the cultured penaeid shrimps (Penaeus monodon, Marsupenaeus japonicus, Litopenaeus vannamei, and Fenneropenaeus indicus) are natural hosts of the virus. Several non-penaeid shrimps were also found to be severely infected during experimental challenges. Many crustaceans like crabs (Scylla spp., Portunus spp.), spiny lobsters (Panulirus spp.), crayfish (Astacus spp., Cherax spp.) and freshwater shrimp (Macrobrachium spp.) are reported to be infected with variable severities depending on the life stage of the host and presence of external stressors (temperature, salinity, bacterial diseases, pollutants).
Clinical signs of WSSV include a sudden reduction in food consumption, lethargy, loose cuticle and often reddish discolouration, and the presence of white spots of 0.5 to 2.0 mm in diameter on the inside surface of the carapace, appendages and cuticle over the abdominal segments.
In the host, WSSV infects a wide variety of cells from ectodermal and mesodermal origin. Histological changes are seen in the gill epithelium, antennal gland, haematopoeitic tissue, nervous tissue, connective tissue and intestinal epithelial tissue. Infected cells have prominent intranuclear occlusions that initially stain eosinophilic, but become basophilic with age; hypertrophied nuclei with chromatin margination; and cytoplasmic clearing.[8] Pathogenesis involves widespread tissue necrosis and disintegration.
White spots on the shell of infected shrimp under scanning electron microscope appear as large, dome-shaped spots on the carapace measuring 0.3 to 3 mm in diameter. Smaller white spots of 0.02 to 0.1 mm appear as linked spheres on the cuticle surface. Chemical composition of the spots is similar to the carapace, calcium forming 80–90% of the total material and it is suggested to have derived from abnormalities of the cuticular epidermis.[9]
A number of biochemical changes have been reported after infection with this virus:[10] glucose consumption and plasma lactate concentration increase, glucose 6 phosphate dehydrogenase activity increases and triglyceride concentration decreases. The voltage dependent anion channel of the mitochondrion is also up regulated.
Infection with WSSV differs from other described penaeid infections Yellowhead virus (YHV) and Infectious Hypodermal and Hematopoietic Necrosis virus (IHHNV) in the described histological findings as YHV has a reduced tissue specificity, infecting only the intestinal epithelial tissues and IHHNV causes intranuclear occlusions that stain eosinophillic but do not change over the course of the infection.[8]
Rapid and specific diagnosis of the virus can be accomplished using nested[8] or real-time polymerase chain reaction (PCR).[11]
There are no available treatments for WSS.
A large number of disinfectants are widely used in shrimp farms and hatcheries to prevent an outbreak. Stocking of uninfected shrimp seeds and rearing them away from environmental stressors with extreme care to prevent contamination are useful management measures.
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