Invasive Species Compendium

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epizootic haematopoietic necrosis



epizootic haematopoietic necrosis


  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • epizootic haematopoietic necrosis
  • Overview
  • Epizootic haematopoietic necrosis (EHN) is a systemic iridovirus (Ranavirus) infection of redfin perch (Perca fluviatilis), rainbow trout (Oncorhynchus mykiss), sheatfish (Silurus glanis) and catfish (Ictalurus melas) (...

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Preferred Scientific Name

  • epizootic haematopoietic necrosis

International Common Names

  • English: epizootic hematopoietic necrosis; iridovirus of catfish disease; sheatfish iridovirus disease; systemic iridovirus diseases caused by ranaviruses

English acronym

  • EHN


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Epizootic haematopoietic necrosis (EHN) is a systemic iridovirus (Ranavirus) infection of redfin perch (Perca fluviatilis), rainbow trout (Oncorhynchus mykiss), sheatfish (Silurus glanis) and catfish (Ictalurus melas) (Ahne et al., 1989; Aubertin, 1991; Langdon et al., 1986; Pozet et al., 1992). The disease is caused by three similar viruses: epizootic haematopoietic necrosis virus (EHNV), European sheatfish virus (ESV) and European catfish virus (ECV) (Ahne et al., 1989; Hedrick et al., 1992; Langdon, 1989; Pozet et al., 1992; Reddacliff and Whittington, 1996). The geographical range of EHNV is currently restricted to Australia (Hyatt et al., 2000; Wolf, 1988). The ECV and ESV agents have only been detected among fish in Europe (Ahne et al., 1998; Ahne et al., 1989; Pozet et al., 1992). Although inducing similar diseases in their respective hosts, EHNV, ECV and ESV are distinct agents distinguished by molecular techniques (Hyatt et al., 2000; Mao et al., 1997; Tapiovaara et al., 1998).

EHN infection in redfin perch is generally lethal (Whittington et al., 1995). Rainbow trout are relatively resistant and only a small proportion of individuals become infected (Whittington et al., 1994; Whittington and Reddacliff, 1995; Whittington et al., 1999). Infections with ESV and ECV can induce high morbidity and mortality in their catfish hosts (Ahne et al., 1989, Pozet et al., 1992). The disease caused by all three iridoviruses is characterised by mortalities due to necrosis in the liver, spleen, haematopoietic tissue of the kidney and other tissues. Experimental exposure studies have shown that rainbow trout can be infected with ECV and ESV without showing morbidity and mortality (Ahne et al., 1998).

Iridoviridae of the genus ranavirus are becoming increasingly important as pathogens of feral, cultured and ornamental teleosts. They are endotheliotropic and can induce severe disease in susceptible fish species, characterized by necrotic lesions in vascular walls and visceral organs. The group consists of the epizootic haematopoietic necrosis virus (EHNV) (Langdon et al., 1986b; Eaton et al., 1991; Hedrick et al., 1992), isolates from two ictalurid fishes in Europe (Ahne et al., 1989; Pozet et al., 1992), turbot (Scophthalmus maximus) iridovirus-like agent (Bloch and Larsen, 1993), an isolate from two freshwater tropical ornamental species (Hedrick and McDowell, 1995) and largemouth bass virus (LMBV) (Plumb et al., 1996). The present discussion considers mainly diseases caused by EHNV and ictalurid viruses, which can cause 100% mortality in young susceptible warm-water hosts. The economic damage is rare but serious.

The type strain of ranavirus is the frog virus 3 (FV3) (Granoff et al., 1965; Essani and Granoff, 1989; Aubertin, 1991). Hedrick et al. (1992) suggested that EHNV and ictalurid isolates were strains of FV3. The amphibian group in ranavirus genus includes amphibian viruses from North America (Essani and Granoff, 1989), the European green frog virus (Fijan et al., 1991; Ahne et al., 1995) and the Australian Bohle (or burrowing frog) iridovirus (Speare and Smith, 1992; Hengstberger et al., 1993). The North American tadpole oedemavirus and the European frog virus are not pathogenic for fish tested in experiments (Wolf et al., 1968; Fijan et al., 1991), but the Bohle iridovirus induced 100% mortality in bath infected barramundi (Lates calcarifer) (Moody and Owens, 1994). The latter report indicates the possible importance of amphibian ranaviruses for finfish aquaculture.

Epizootic haematopoietic necrosis and EHNV were reviewed by Wolf (1988) and McAllister (1993a). This datasheet describes EHN in redfin perch.

Topics for Further Studies

The development of methods for distinguishing ranavirus isolates requires further attention. Such methods are needed to study epizootiology and taxonomy. Surveys of sheatfish, bullhead, ornamental and other fish production sites for ranaviruses in fish and amphibians are needed to assess the range, extent and significance of currently known and possible other diseases in this group. Studies on host ranges and reciprocal pathogenicity of fish and amphibian ranaviruses for early life stages could help to detect virus sources and reservoirs.

[Based upon material originally published in Woo PTK, Bruno DW, eds., 1999. Fish diseases and disorders, Vol. 3 Viral, bacterial and fungal infections. Wallingford, UK: CABI Publishing.]

Hosts/Species Affected

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Members of the ranavirus genus were isolated from freshwater fishes on three continents. Epizootic haemopoietic necrosis virus affects redfin perch (Percafluviatilis) and rainbow trout (Langdon et al., 1986a, b, 1988; Langdon and Humphrey, 1987) in Australia (Victoria, New South Wales, and South Australia).Sheatfish iridovirus (or IW for iridovirus wels) was isolated in Germany (Ahne et al., 1989). Black bullhead iridovirus (or ICF for iridovirus of catfish) caused mortality of Ameiurus melas (syn. Ictalurus melas) in France (Pozet et al., 1992) and in Italy (Bovo et al., 1993). Iridovirus of ornamental tropical fish (IOTF) was isolated from imported guppy (Poecilia reticulata) and doctor fish (Labroides dimidatus) in California, USA (Hedrick and McDowell, 1995).Largemouth bass virus was isolated from a mortality among adult largemouth bass in a reservoir in South Carolina, USA (Plumb et al., 1996).

The redfin perch and rainbow trout isolates of EHNV are serologically indistinguishable. Langdon (1989) experimentally infected 11 teleosts. The mosquito fish (Gambusia affinis) is the only species besides redfin perch which is susceptible to horizontal transmission. Four native species are highly susceptible to the virus and at least one of them (Macquarie perch, Macquaria australasia) is in decline. Atlantic salmon (Salmo salar) develops clinical disease but the infection is not lethal. Barramundi is refractory and so are two exotic cyprinids, which do not seem to be the original host (Langdon, 1989). Whittington et al. (1996) demonstrated the spread of EHN in redfin perch to river systems and impoundments in Australia. In outbreaks of sheatfish and black bullhead diseases (Ahne et al., 1989; Pozet et al., 1992), the water environment contained several other warm-water species, including cyprinids, pike and perch, but they remained unaffected. The ornamental fish strain is pathogenic for rainbow trout (Hedrick and McDowell,1995). Largemouth bass virus has not induced mortality in infected adult largemouth bass (Plumb et al., 1996).

The factors modulating the susceptibility of fish to EHNV, ESV and ECV infection are poorly understood. Clinical outbreaks due to EHNV are associated with poor water quality. In rainbow trout, infection occurs naturally at water temperatures from 11 to 17°C and experimentally from 8 to 21°C (Whittington et al., 1994). Disease in redfin perch does not occur at temperatures below 12°C. The following fish species were found to be susceptible to EHNV following bath exposure: redfin perch, rainbow trout, Macquarie perch (Macquaria australasica), mosquito fish (Gambusia affinis), silver perch (Bidyanus bidyanus) and mountain galaxias (Galaxias olidus) (Langdon, 1989). Both juvenile and adult redfin perch may be affected in outbreaks, but juveniles may be more susceptible to the disease. EHNV has now been detected in diseased rainbow trout ranging from hatchery fry to table-sized fish, although mortalities are most often seen in 0+ fish up to 125 mm fork-length.


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The reported geographical ranges of fish ranaviruses are so far restricted to respective continents of isolation. However, that from exotic ornamental fish is suspected to be a part of putative transcontinental transmission (Hedrick and McDowell, 1995). The Bohle iridovirus, which is present only in Queensland, is geographically distinct from EHNV (Speare and Smith, 1992).

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes


AfghanistanNo information availableOIE, 2009
ArmeniaDisease never reportedOIE, 2009
AzerbaijanDisease never reportedOIE, 2009
BahrainDisease never reportedOIE, 2009
BangladeshDisease never reportedOIE, 2009
BhutanNo information availableOIE, 2009
Brunei DarussalamDisease not reportedOIE Handistatus, 2005
CambodiaNo information availableOIE, 2009
ChinaDisease never reportedOIE, 2009
-Hong KongDisease never reportedOIE, 2009
Georgia (Republic of)Disease never reportedOIE Handistatus, 2005
IndiaNo information availableOIE, 2009
IndonesiaDisease not reportedOIE, 2009
IranDisease never reportedOIE, 2009
IraqDisease never reportedOIE, 2009
IsraelDisease never reportedOIE, 2009
JapanDisease never reportedOIE, 2009
JordanNo information availableOIE, 2009
KazakhstanDisease not reportedOIE, 2009
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofNo information availableOIE, 2009
KuwaitDisease not reportedOIE, 2009
KyrgyzstanDisease not reportedOIE, 2009
LaosNo information availableOIE, 2009
LebanonNo information availableOIE, 2009
MalaysiaDisease never reportedOIE, 2009
-Peninsular MalaysiaDisease never reportedOIE Handistatus, 2005
-SabahNo information availableOIE Handistatus, 2005
-SarawakNo information availableOIE Handistatus, 2005
MongoliaNo information availableOIE, 2009
MyanmarNo information availableOIE, 2009
NepalNo information availableOIE, 2009
OmanNo information availableOIE, 2009
PakistanNo information availableOIE, 2009
PhilippinesNo information availableOIE, 2009
QatarNo information availableOIE, 2009
Saudi ArabiaNo information availableOIE, 2009
SingaporeDisease never reportedOIE, 2009
Sri LankaNo information availableOIE, 2009
SyriaNo information availableOIE, 2009
TaiwanDisease never reportedOIE Handistatus, 2005
TajikistanNo information availableOIE, 2009
ThailandNo information availableOIE, 2009
TurkeyNo information availableOIE, 2009
TurkmenistanDisease not reportedOIE Handistatus, 2005
United Arab EmiratesNo information availableOIE, 2009
UzbekistanDisease never reportedOIE Handistatus, 2005
VietnamNo information availableOIE, 2009
YemenNo information availableOIE, 2009


AlgeriaNo information availableOIE, 2009
AngolaNo information availableOIE, 2009
BeninNo information availableOIE, 2009
BotswanaNo information availableOIE, 2009
Burkina FasoNo information availableOIE, 2009
BurundiDisease never reportedOIE Handistatus, 2005
CameroonDisease never reportedOIE Handistatus, 2005
Cape VerdeDisease not reportedOIE Handistatus, 2005
Central African RepublicDisease not reportedOIE Handistatus, 2005
ChadNo information availableOIE, 2009
CongoNo information availableOIE, 2009
Congo Democratic RepublicDisease not reportedOIE Handistatus, 2005
Côte d'IvoireNo information availableOIE Handistatus, 2005
DjiboutiNo information availableOIE, 2009
EgyptNo information availableOIE, 2009
EritreaNo information availableOIE, 2009
EthiopiaNo information availableOIE, 2009
GambiaNo information availableOIE, 2009
GhanaNo information availableOIE, 2009
GuineaNo information availableOIE, 2009
Guinea-BissauNo information availableOIE, 2009
KenyaNo information availableOIE, 2009
LesothoDisease never reportedOIE, 2009
LibyaNo information availableOIE Handistatus, 2005
MadagascarNo information availableOIE, 2009
MalawiNo information availableOIE, 2009
MaliNo information availableOIE, 2009
MauritiusNo information availableOIE, 2009
MoroccoNo information availableOIE, 2009
MozambiqueDisease not reportedOIE, 2009
NamibiaNo information availableOIE, 2009
NigeriaNo information availableOIE, 2009
RéunionNo information availableOIE Handistatus, 2005
RwandaNo information availableOIE Handistatus, 2005
Sao Tome and PrincipeNo information availableOIE Handistatus, 2005
SenegalNo information availableOIE, 2009
SeychellesNo information availableOIE Handistatus, 2005
SomaliaNo information availableOIE Handistatus, 2005
South AfricaNo information availableOIE, 2009
SudanDisease never reportedOIE, 2009
SwazilandNo information availableOIE, 2009
TanzaniaNo information availableOIE, 2009
TogoNo information availableOIE, 2009
TunisiaDisease not reportedOIE, 2009
UgandaNo information availableOIE, 2009
ZambiaNo information availableOIE, 2009
ZimbabweNo information availableOIE, 2009

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaDisease never reportedOIE, 2009
GreenlandDisease never reportedOIE, 2009
MexicoDisease not reportedOIE, 2009
USADisease never reportedOIE, 2009
-CaliforniaPresentHedrick and McDowell , 1995
-South CarolinaPresentPlumb and et al. , 1996

Central America and Caribbean

BarbadosDisease never reportedOIE Handistatus, 2005
BelizeDisease never reportedOIE, 2009
British Virgin IslandsDisease never reportedOIE Handistatus, 2005
Cayman IslandsDisease never reportedOIE Handistatus, 2005
Costa RicaDisease never reportedOIE, 2009
CubaDisease never reportedOIE, 2009
CuraçaoNo information availableOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicDisease never reportedOIE Handistatus, 2005
El SalvadorNo information availableOIE, 2009
GuadeloupeNo information availableOIE, 2009
GuatemalaDisease never reportedOIE, 2009
HaitiNo information availableOIE, 2009
HondurasNo information availableOIE, 2009
JamaicaNo information availableOIE, 2009
MartiniqueNo information availableOIE, 2009
NicaraguaDisease never reportedOIE, 2009
PanamaNo information availableOIE, 2009
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease not reportedOIE Handistatus, 2005
Trinidad and TobagoDisease never reportedOIE Handistatus, 2005

South America

ArgentinaDisease never reportedOIE, 2009
BoliviaNo information availableOIE, 2009
BrazilDisease never reportedOIE, 2009
ChileDisease never reportedOIE, 2009
ColombiaDisease never reportedOIE, 2009
EcuadorNo information availableOIE, 2009
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaDisease not reportedOIE, 2009
GuyanaDisease never reportedOIE Handistatus, 2005
ParaguayDisease never reportedOIE Handistatus, 2005
PeruNo information availableOIE, 2009
UruguayNo information availableOIE, 2009
VenezuelaDisease never reportedOIE, 2009


AlbaniaNo information availableOIE, 2009
AndorraDisease never reportedOIE Handistatus, 2005
AustriaNo information availableOIE, 2009
BelarusDisease never reportedOIE, 2009
BelgiumNo information availableOIE, 2009
Bosnia-HercegovinaDisease not reportedOIE Handistatus, 2005
BulgariaNo information availableOIE, 2009
CroatiaDisease never reportedOIE, 2009
CyprusDisease never reportedOIE, 2009
Czech RepublicDisease never reportedOIE, 2009
DenmarkDisease never reportedNULLBloch and Larsen , 1993; OIE, 2009
EstoniaNo information availableOIE, 2009
FinlandDisease not reportedOIE, 2009
FranceDisease not reportedNULLPozet and et al. , 1992; OIE, 2009
GermanyDisease not reported2006Ahne and et al. , 1989; OIE, 2009
GreeceNo information availableOIE, 2009
HungaryDisease never reportedOIE, 2009
IcelandDisease never reportedOIE, 2009
IrelandDisease never reportedOIE, 2009
Isle of Man (UK)Disease never reportedOIE Handistatus, 2005
ItalyNo information availableNULLBovo and et al. , 1993; OIE, 2009
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease never reportedOIE, 2009
LiechtensteinNo information availableOIE, 2009
LithuaniaDisease never reportedOIE, 2009
LuxembourgNo information availableOIE, 2009
MacedoniaNo information availableOIE, 2009
MaltaNo information availableOIE, 2009
MoldovaDisease never reportedOIE Handistatus, 2005
MontenegroNo information availableOIE, 2009
NetherlandsDisease never reportedOIE, 2009
NorwayDisease never reportedOIE, 2009
PolandDisease never reportedOIE, 2009
PortugalDisease not reportedOIE, 2009
RomaniaNo information availableOIE, 2009
Russian FederationNo information availableOIE, 2009
SerbiaNo information availableOIE, 2009
SlovakiaDisease not reportedOIE, 2009
SloveniaDisease not reportedOIE, 2009
SpainDisease never reportedOIE, 2009
SwedenDisease never reportedOIE, 2009
SwitzerlandDisease not reportedOIE, 2009
UKDisease never reportedOIE, 2009
-Northern IrelandDisease never reportedOIE Handistatus, 2005
UkraineDisease not reportedOIE, 2009
Yugoslavia (former)No information availableOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)No information availableOIE Handistatus, 2005


AustraliaDisease not reported2004Langdon and et al. , 1986a; Langdon and et al. , 1986b; Langdon and Humphrey , 1987; Langdon and et al. , 1988; OIE, 2009
-New South WalesFijan , 1999
-QueenslandPresentSpeare and Smith , 1992
-South AustraliaFijan , 1999
-VictoriaFijan , 1999
French PolynesiaDisease never reportedOIE, 2009
New CaledoniaDisease not reportedOIE, 2009
New ZealandDisease never reportedOIE, 2009
SamoaNo information availableOIE Handistatus, 2005
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005


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Focal necrosis is a consistent finding in haematopoietic kidney and liver of naturally and experimentally infected fish. In the spleen and pancreas, this sign is variable. Necrotic haemopoietic cells are disseminated in all vessels. Lesions in other susceptible species are inconstant (Langdon, 1989). The most consistent is the necrosis in haemopoietic kidney and liver. A description of gross lesions in redfin perch by Reddacliff and Whittington (1996) includes haemorrhage around bases of fins, focal haemorrhage in gills, oedema and multiple necrotic foci in liver. Microscopic changes consist of focal to extensive necrosis in haematopoietic kidney, liver, spleen, heart, pancreas and lamina propria of the intestine. Thrombosis, haemorrhage and fibrinous exudate are common in gills. Lesions in rainbow trout are similar but milder.

Sheatfish Iridovirus Disease

Histopathology and electron microscopy in experimentally infected sheatfish of 4-5 cm revealed alterations in all organs (Ogawa et al., 1990). Endothelium and reticuloendothelial cells are the main target. Periarteriolar necrosis of the haemopoietic tissue and degeneration of tubular and duct epithelia are prominent in kidneys. Gill epithelium and chloride cells are hyperplastic and oedematous. The lumen of the circulatory system is congested and the proliferating cells contain eosinophilic inclusions. Alterations in the skin include proliferation and necrosis of epithelial cells, hyperplasia of monocellular glands and zonal haemorrhage in hypodermis. Myocarditis and endocarditis are diffuse. Small necrotic foci are seen in the liver and spleen. Glial proliferation and spongiosis in the brain are also pronounced. The pathology and incubation most closely resemble those of EHN.

Iridovirus of Catfish Disease

The kidney is the principal target organ and both the haematopoietic and the excretory part are severely altered. Blood vessel walls are damaged. Necroses in the spleen and kidney can be severe. Interlamellar spaces in gills are obliterated and lamellar fusion is evident (Pozet et al., 1992).


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Fish ranaviruses are endotheliotropic and cause haemorrhagic diathesis, oedema and peripheral circulatory failure.


Epizootic haematopoietic necrosis appeared during the spring of 1984 in a lake and caused severe mortality among juvenile redfin perch. The disease is less serious in farmed rainbow trout. Experimentally infected 35-45-day-old redfin perch develop depression, skin darkening and erratic swimming and die after 4-5 days (Langdon, 1989). Some have erythema around the brain and nostrils. Clinical signs in disease outbreaks described by Langdon and Humphrey (1987) are identical, except for skin ulcers invaded by fungus in some fish.

Sheatfish Iridovirus Disease

The sheatfish iridovirus disease (iridovirous wels disease (IWD)) is characterized by loss of appetite, apathy, ataxia (including rapid spiral swimming), petechial haemorrhage in skin and internal organs and generalized destruction of haematopoietic tissues in the kidney and spleen. The cumulative fry mortality in a recirculation system was 100% (Ahne et al., 1989). Fry infected by bath in virus suspension and by cohabitation also succumbed to high mortality within 8 and 11 days, respectively (Ahne et al., 1990). Adult fish are also susceptible but mortality does not exceed 30% (Ahne et al., 1991).

Iridovirus of Catfish Disease

Iridovirus of ornamental tropical fish was isolated from carriers but the experimental infection of rainbow trout induced low mortality, considerable lesions in the kidney and spleen and virus titres greater than 108 TCID50 g-1 (Hedrick and McDowell, 1995).

Experimental infection of barramundi with Bohle iridovirus resulted in mortality and focal necrosis in the liver (Moody and Owens, 1994).

Procedures recommended by the OIE Manual (1995b) for EHNV are applicable to other viruses in the ranavirus group considered in this chapter. Presumptive diagnosis is based on clinical signs, virus isolation in BF-2 or other susceptible cells and electron microscopy. Identification of EHNV is based on IFAT or ELISA tests (OIE Manual, 1995b) and PCR (Gould et al., 1995). Other viruses in the group show antigenic relatedness to EHNV and FV3 demonstrable by IFAT (Hedrick et al., 1992; Ahne et al., 1995; Hedrick and McDowell, 1995), Western blotting and nucleic acid hybridization (Hedrick and McDowell, 1995).

Epizootic haematopoietic necrosis virus is detectable by ELISA, immunohistochemistry and electron microscopy (Hyatt et al., 1991). An improved antigen-capture ELISA (Whittington and Steiner, 1993) can recognize EHNV in clarified fish tissue and in cell-culture supernatant. The lowest detectable level of the virus in supernatant is 103.5 TCID50 ml-1. Sensitivity and specificity of this method for tissue samples are about 81 and 99%, respectively, and for cellculture supernatant 96 and close to 100%. Manual grinding with a pestle in a tube, followed by vortexing in the same tube with 3 mm glass beads and clarification in a microcentrifuge, is the most efficient method for releasing EHNV from tissue samples (Whittington and Steiner, 1993).

The viruses do not induce differentiating neutralising antibodies in mammals or fish (Hyatt et al., 2000). The viruses can be identified by immunofluorescence, enzyme-linked immunosorbent assays (ELISAs) or immunoelectron microscopy (Hedrick et al., 1992; Hengstberger et al., 1993; Hyatt et al., 1991; Hyatt et al., 2000; Steiner et al., 1991). EHNV has several antigens in common with ESV and ECV from Europe and at least one antigen in common with the amphibian iridoviruses from North America (frog virus 3) and Australia (Bohle iridovirus) (Ahne et al., 1995; Hedrick et al., 1992; Hengstberger et al., 1993). Antigen-detection tests with polyclonal antibodies against EHNV detect each of these viruses. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE), Western blotting and polymerase chain reaction (PCR) can differentiate to varying degrees between the different viruses (Hyatt et al., 2000; Mao et al., 1997).

The screening and diagnostic procedures for EHNV, ESV and ECV are based on isolation of virus in cell culture, ELISA, indirect fluorescent antibody tests (IFAT), and electron microscopy (Ahne et al., 1989; Eaton et al., 1991; Hedrick et al., 1992; Hyatt et al., 1991; Langdon et al., 1986; Pozet et al., 1992; Steiner et al., 1991). Antigen-capture ELISA has a sensitivity of 60-80% depending on the stage of infection when used to test tissues from both rainbow trout and redfin perch (Hyatt et al., 1991; Steiner et al., 1991; Whittington et al., 1995; Whittington and Steiner, 1993). Antigen-capture ELISA is the method of choice for confirming the cause of cytopathic effect in cell culture; IFAT and electron microscopy are also useful. IFAT or immunoperoxidase staining may also be used for diagnosis on formalin-fixed tissues. PCR may be used to detect Ranavirus DNA in infected tissues (6). Western blots, SDS-PAGE and PCR sequencing can be used to specifically identify EHNV, ESV and ECV (Hyatt et al., 2000; Mao et al., 1997).

The diagnosis of epizootic haematopoietic necrosis (EHN) is based on direct methods that are either the isolation of virus (epizootic haematopoietic necrosis virus [EHNV], European sheatfish virus [ESV] and European catfish virus [ECV]) in cell culture followed by its immunological identification (conventional approach), or the immunological demonstration of virus antigen in infected fish tissues.

Due to insufficient knowledge of the serological responses of fish to virus infections, the detection of fish antibodies to viruses has not thus far been recognised as a valuable diagnostic method for assessing the virus status of fish populations. In the case of EHNV, preliminary investigations using enzyme-linked immunosorbent assay (ELISA) in known infected rainbow trout populations have revealed up to 1% prevalence of seropositive fish in adult age classes. Further investigation of the epidemiology of EHNV in rainbow trout is needed before serological results can be interpreted.

List of Symptoms/Signs

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SignLife StagesType
Finfish / Cessation of feeding - Behavioural Signs Aquatic:Adult Sign
Finfish / Cessation of feeding - Behavioural Signs Aquatic:Adult Sign
Finfish / Corkscrewing - Behavioural Signs Aquatic:Adult Sign
Finfish / Darkened coloration - Skin and Fins Aquatic:Fry Sign
Finfish / Generalised lethargy - Behavioural Signs Aquatic:Adult Sign
Finfish / Generalised lethargy - Behavioural Signs Aquatic:Adult Sign
Finfish / Haemorrhagic lesions - Skin and Fins Aquatic:Adult Sign
Finfish / Haemorrhagic lesions - Skin and Fins Aquatic:Adult Sign
Finfish / Kidney - white-grey patches (haemorrhage / necrosis / tissue damage) - Organs Aquatic:Adult Sign
Finfish / Kidney - white-grey patches (haemorrhage / necrosis / tissue damage) - Organs Aquatic:Adult Sign
Finfish / Kidney - white-grey patches (haemorrhage / necrosis / tissue damage) - Organs Aquatic:Adult Sign
Finfish / Kidney - white-grey patches (haemorrhage / necrosis / tissue damage) - Organs Aquatic:Adult Sign
Finfish / Liver - white / grey patches (haemorrhage / necrosis / tissue damage) - Organs Aquatic:Adult Sign
Finfish / Liver - white / grey patches (haemorrhage / necrosis / tissue damage) - Organs Aquatic:Adult Sign
Finfish / Mortalities -Miscellaneous Aquatic:Fry Sign
Finfish / Mortalities -Miscellaneous Aquatic:All Stages Sign
Finfish / Mortalities -Miscellaneous Aquatic:Fry Sign
Finfish / Skin erosion - Skin and Fins Aquatic:Fry Sign
Finfish / Spleen white-grey patches (haemorrhage / necrosis / tissue damage) - Organs Aquatic:Adult Sign
Finfish / Spleen white-grey patches (haemorrhage / necrosis / tissue damage) - Organs Aquatic:Adult Sign
Finfish / Ulceration - Skin and fins Aquatic:Fry Sign

Disease Course

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Adult redfin perch is extremely susceptible to EHNV infection by bath and i.p. inoculation. As little as 0.08 TCID50 ml-1 was lethal at 19-21°C. The incubation period at this temperature is 11 days and at 13-19°C up to 28 days. Disease does not develop below 12°C (Whittington and Reddacliff, 1996). Virus replication in endothelial cells results in necrosis and consequent haemorrhage.

The immunological response in fish and rabbits does not generally include neutralizing antibodies. One survivor of ICFD had neutralizing antibodies (Pozet et al., 1992). However, rabbits react to these viruses by producing antibodies suitable for IFAT and ELISA. Redfin perch survivors from natural disease outbreaks are resistant to challenge with EHNV (Langdon, 1989). The epizootiology of EHN in rainbow trout suggests that this species is incapable of developing long-lasting resistance (OIE Manual, 1995b).


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The epidemiology of EHNV in rainbow trout is incompletely understood (Whittington et al., 1994; Whittington and Reddacliff, 1995; Whittington et al., 1999). Due to their extreme susceptibility, it is unlikely that redfin perch are a natural host (Whittington and Hyatt, 1996; Whittington et al., 1995). Infection may recur annually at a rainbow trout production site and this may be due to reinfection from wild redfin perch in the catchment area. A carrier state in naturally infected rainbow trout appears to be very uncommon as neither EHNV antigen nor anti-EHNV antibody are routinely detected in rainbow trout surviving an outbreak (Whittington et al., 1980; Whittington et al., 1999). However, the disease can occur at a very low frequency in an infected population, and mortalities may not exceed the usual background rate. Thus infected fish could easily be included in batches of healthy translocated fish and there is good evidence that this has occurred. No epidemiological data are available for ESV or ECV.

Natural epizootics of EHN in early summer among young redfin perch last for 2-3 weeks. They are recurrent in several major waterways in Victoria, Australia (Langdon, 1989). Adults are rarely affected. Virus isolation from juveniles and adults immediately after an epizootic is infrequent (Langdon and Humphrey, 1987). 100-day-old survivors of disease outbreaks are resistant to challenge (Langdon, 1989). Redfin perch carriers were not detected and there is no evidence for vertical transmission. An unknown reservoir and carrier host are suspected. Silver gulls (Larus novaehollandiae) and great cormorants (Phalacrocorax carbo) can spread EHNV by the regurgitation of ingested material (Whittington et al., 1996). Other means of spread include transportation of fish by humans, transfer on boats, nets and other equipment as well as water flow and migration of carrier fish in a catchment area (Whittington et al., 1996). The epizootiology of other diseases in the group was not studied.

The close relatedness of fish and amphibian ranaviruses and the pathogenicity of Bohle iridovirus for barramundi should be kept in mind in programmes for avoidance of pathogens in aquaculture (Hedrick et al., 1992; Ahne et al., 1995). Frogs are ubiquitous on large farms for warm-water fishes. These could be reservoirs and vectors of fish pathogens. Hedrick et al. (1992), Hedrick and McDowell (1995) and Hedrick (1996) consider transcontinental movements of amphibians and exotic ornamental fish as possible reasons for the appearance of similar viruses in Australia and Europe. It was suggested that control be extended to aquatic amphibians and tropical aquarium fishes (Ahne et al., 1995; Hedrick, 1996).

Impact Summary

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Fisheries / aquaculture Negative

Zoonoses and Food Safety

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This species is not a zoonosis.


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Langdon JS, 1989. Experimental transmission and pathogenicity of epizootic haematopoietic necrosis virus (EHNV) in redfin perch, Perca fluviatilis L., and 11 other teleosts. Journal of Fish Diseases, 12(4):295-310.

Langdon JS; Humphrey JD, 1987. Epizootic haematopoietic necrosis, a new viral disease in redfin perch, Perca fluviatilis L., in Australia. Journal of Fish Diseases, 10(4):289-297.

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