Details | OIE data | Non-OIE data | All

Details for White Sturgeon Iridoviral Disease

Occurence category:

Previously listed diseases

Species affected:




Viral disease; Iridovirus; White sturgeon iridovirus

Summary from the OIE Diagnostic Manual (4th ed.): Chapter 2.1.16.

The white sturgeon iridoviral disease ( WSIVD ) is a significant cause of mortality among farm-raised juvenile white sturgeon (Acipenser transmontanus) in North America and among Russian sturgeon (A. guldenstadi) in Europe ( 1, 2, 4 ) . White sturgeon are the host from which the causative agent, the white sturgeon iridovirus ( WSIV ) was first isolated. Lake sturgeon (A. fluvescens) have been experimentally infected with the WSIV, but the susceptibility of other sturgeon is currently unknown ( 3 ) .

The original description of white sturgeon iridovirus was among the first hatchery-raised white sturgeon in North America. The source of the virus was assumed to originate from captive wild sturgeon adults collected from the Sacramento River in California, United States of America ( USA ) for use as broodstock ( 2 ) . The WSIV has also been detected in cultured white sturgeon from the lower Columbia River in Oregon and Washington states of the USA, the Snake River in the southern region of the State of Idaho and the Kootenai River in northern Idaho, USA ( 4, 5 ) . These cultured white sturgeon were all progeny originating from captured wild adult white sturgeon. The virus has been detected among wild juvenile white sturgeon collected from the lower Columbia River and the virus is potentially enzootic in wild white sturgeon populations throughout the Pacific Northwest of North America ( 4 ) . An iridovirus similar to WSIV has been identified in Russian sturgeon from Northern Europe where it may be enzootic among cultured populations of several species of sturgeon ( 1 ) .

The WSIV is an epitheliotropic virus infecting the skin, gills, and upper alimentary tract. Infections of the oral mucosa and olfactory organ epithelium are presumed causes of the cessation of feeding that leads to a progressive emaciation or starvation of the fish - the principal external sign of the disease ( 6 ) . Cumulative mortality of up to 95% has been reported among groups of infected fish in the hatchery and secondary infections with external protozoa or bacteria often contribute to the overall mortality ( 2 ) . Infected fish with moderate to severe emaciation began dying 2-3 weeks following exposure to the virus at water temperatures of 17-19°C ( 7 ) . Haemorrhages on the abdomen and the ventral scuta may be present, but these are not specific for WSIVD. There are no specific internal signs of infection as the virus does not invade systemically. Viral infection is evident on microscopic observation of stained tissue sections from infected fish. Areas of the integument and particularly the skin may show a focal to diffuse hyperplasia with characteristic amphophilic to basophilic enlarged Malpighian cells ( 6 ) . These cells are filled with virus particles as demonstrated by electron microscopy. The virus can be isolated, but with some difficulty, from infected fish using sturgeon cell lines.

The modes of transmission of WSIV are not completely understood but horizontal transmission via the water has been demonstrated in the hatchery and experimentally in the laboratory ( 3 ) . There is strong circumstantial evidence from epidemiological investigations at the hatchery that the virus is transmitted vertically from adult broodstock, but the virus has never been isolated or observed in adult fish.

There appears to be little antigenic relationship of WSIV to the systemic iridoviral agents represented by epizootic haematopoietic necrosis virus or the red sea bream iridovirus. The larger size and inner membrane structure of WSIV virion, host cell-line specificity, type of cytopathic effect, and location of target host cells ( epitheliotropic and not systemic ) distinguish the agent from other groups of fish iridoviruses. Although lymphocystivirus ( LCDV ) has a similar virion morphology, LCDV infects fibroblasts and not Malpighian cells as in WSIV infections, and the cell line specificity and types of cytopathic effects are clearly different between the two agents.

The principal diagnostic methods for WSIV include microscopic observation of characteristic infected cells in stained tissue sections of the oral mucosa, gills and skin, or isolation of the virus in sturgeon cell lines ( 3 ) . Neutralising polyclonal antibodies and binding monoclonal antibodies recognise WSIV, but not the systemic iridoviral agents. These antibodies can also be used in indirect immunofluorescence tests or for immunohistochemical staining of infected cells in tissue culture and sections of infected tissues.

Control methods currently rely on avoidance of the agent where possible. Because there are currently no methods for detecting the virus in adult broodstocks, quarantine and investigation of juveniles suffering mortality are the principal means to detect WSIV in young fish. Methods to detect the virus in broodstock are currently under development.

© Crown Copyright 2011
Data Last Updated: 05 February 2016