epizootic haematopoietic necrosis

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

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, 1999; 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, 1999), 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.]

EHN

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).

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).

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).

This species is not a zoonosis.