White spot syndrome

White spot syndrome
White spot syndrome
Virus classification
Group: Group I (dsDNA)
Family: Nimaviridae
Genus: Whispovirus

White spot Syndrome Baculovirus Complex

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]



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 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 and 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, 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.


  1. ^ "Non-Native Species Summaries: White Spot Syndrome Baculovirus Complex (WSBV)". Gulf States Marine Fisheries Commission. 2003. http://nis.gsmfc.org/nis_factsheet.php?toc_id=7. Retrieved June 30, 2005. 
  2. ^ Lightner, D. V. (1996). A handbook of shrimp pathology and diagnostic procedures for diseases of cultured penaeid shrimp. World Aquaculture Society, Baton Rouge, Louisiana, USA. 
  3. ^ Chen, S. N. (1995). "Current status of shrimp aquaculture in Taiwan.". In C. L. Browdy & J. S. Hopkins (Eds.). Swimming through troubled water. Proceedings of the special session on shrimp farming. Aquaculture ’95. World Aquaculture Society, Baton Rouge, Louisiana, USA. pp. 29–34. 
  4. ^ Huang, J., X. L. Song, J. Yu & C. H. Yang (1995). "Baculoviral hypodermal and hematopoietic necrosis: study on the pathogen and pathology of the explosive epidemic disease of shrimp". Marine Fisheries Research 16: 1–10. 
  5. ^ Nadala, E. C. B., Jr., L. M. Tapay & P. C. Loh (1998). "Characterization of a non-occluded baculovirus-like agent pathogenic to penaeid shrimp". Diseases of Aquatic Organisms 33 (3): 221–229. doi:10.3354/dao033221. PMID 9745719. 
  6. ^ Van Hulten, M. C. W., J. Witteveldt, S. Peters, N. Kloosterboer, R. Tarchini, F. Fiers, H. Sandbrink, R. K. Lankhorst & J. M. Vlak (2001). "The white spot syndrome virus DNA genome sequence". Virology 286 (1): 7–22. doi:10.1006/viro.2001.1002. PMID 11448154. 
  7. ^ Wang PH, Gu ZH, Wan DH, Zhang MY, Weng SP, Yu XQ, He JG (2011) The shrimp NF-κB pathway is activated by White Spot Syndrome Virus (WSSV) 449 to facilitate the expression of WSSV069 (ie1), WSSV303 and WSSV371. PLoS One 6(9):e24773.
  8. ^ a b c Wongteerasupaya, C., J. E. Vickers, S. Sriurairatana, G. L. Nash, A. Akarajamorn, V. Boonseang, S. Panyin, A. Tassanakajon, B. Withyachumnarnkul and T. W. Flegel (1995). "A non-occluded, systemic baculovirus that occurs in cells of ectodermal and mesodermal origin and causes high mortality in the black tiger prawn Penaeus monodon". Diseases of Aquatic Organisms 21: 69–77. doi:10.3354/dao021069. 
  9. ^ Wang, C. S., K. F. Tang, G. H. Kou & S. N. Chen (1997). "Light and electron microscopic evidence of white spot disease in the giant tiger shrimp, Penaeus monodon (Fabricius), and the kuruma shrimp, Penaeus japonicus (Bate), cultured in Taiwan". Journal of fish Diseases 20 (5): 323–331. doi:10.1046/j.1365-2761.1997.00301.x. 
  10. ^ Chen IT, Aoki T, Huang YT, Hirono I, Chen TC, Huang JY, Chang GD, Lo CF, Wang KC (2011) White spot syndrome virus induces metabolic changes resembling the Warburg effect in shrimp hemocytes in the early stage of infection. J Virol
  11. ^ Dhar, A. K., M. M. Roux, and K. R. Klimpel (2001). "Detection and Quantification of Infectious Hypodermal and Hematopoietic Necrosis Virus and White Spot Virus in Shrimp Using Real-Time Quantitative PCR and SYBR Green Chemistry". Journal of Clinical Microbiology 39 (8): 2835–2845. doi:10.1128/JCM.39.8.2835-2845.2001. PMC 88247. PMID 11474000. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=88247. 

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