Viral Haemorrhagic Septicaemia

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Caused By: Viral Haemorrhagic Septicaemia Virus — VHSV — Egtved virus


Viral Haemorrhagic Septicaemia is an economically important haematological disease of fish, primarily salmonids, caused by a bullet shaped, enveloped RNA rhabdovirus. The virus is a member of the genus Novirhabdovirus and they share a common and distinctive feature – the presence of an additional non-virion protein encoding gene.

There are three known serotypes of VSHV with some cross-immunity between them. Based on phylogenetic analyses of nucleotide sequences the virus has been shown to have four genotypes and they are related to geographical distribution rather than host specficity.

This disease is not zoonotic.


Widespread across continental Europe; also present in Korea, Japan and the USA.

The virus has been isolated from free living wild fish across the Pacific and Atlantic Oceans, Baltic Sea and North Sea.

Type 1 and Type 2 VHSV serotypes were first found in Denmark and Type 3 from brown trout in France.

VHS is transmitted both by clinically affected fish and covert carriers of the virus. Virus is shed in large amounts in urine.


Grass carp, rainbow trout, brown trout, grayling, pike, bass, Japanese flounder, turbot, pike, chinook salmon and Atlantic salmon can be infected by VHSV.

The number of wild species in which the virus is isolated is large and growing and they include both freshwater and marine fish.

Younger fish are more susceptible to disease than adults, but this is not exclusive.

Water temperature is also important; disease generally occurs only between 4 and 14⁰C. Low temperatures of 1-5⁰C often create a disease profile with an extended course and high accumulated mortality. Higher temperatures (15-18⁰C) generally produce a short course of disease with lower mortality. Stress is also a predisposing factor and disease can remain latent until stress and/or immunosuppression facilitate its pathogenicity.

Disease is most common in springtime when water temperature is most unstable.

Rainbow trout are especially susceptible to VHS, particularly first feeding fry.

Clinical Signs

VHS replicates in the vascular endothelial cells, haematopoietic tissues, nephrons and the leucocytes themselves. It then crosses into the blood, accessing and damaging major internal organs. This causes impairment of osmotic balance, haemorrhage and death of the fish.

VHS is the most important viral disease of farmed rainbow trout, causing lethargy, darkening of the skin, disorientation and erratic swimming behaviour such as flashing and cork screwing. Fish may congregate together in still areas or on the bottom of the tank. Exophthalmia is often a feature. Haemorrhages may be visible in the musculature and around the orbit or fish may have a pot bellied appearance due to internal bleeding and/or ascites. The gills become markedly pale due to anaemia.

There are three forms of disease:

acute which causes clinical signs, behavioural changes and moribund fish
chronic which produces few or no external signs but has visceral pathology and haematological suppressive effects
nervous, which causes constant flashing, tail chasing and spiralling behaviour due to its marked tropism for the brain

VHS causes significant mortality in turbot and Japanese flounder in aquaculture.

It has also causes significant mortality in wild herring and pilchards in American waters.


Virus can be isolated from cell cultures and confirmed immunologically by virus neutralisation, immunofluorescence, ELISA, immunoperoxidase staining or reverse transcriptase PCR (RT-PCR) . Of these, the serological methods such as neutralisation and PCR may be more important for detection of carrier fish, while the others are useful for fish with overt disease.

On necropsy, widespread haemorrhages are seen in the liver, in the adipose tissue and within the musculature. Systemic haemorrhage may involve the eyes and viscera. The kidneys may be red and swollen if in early stages of disease or pale and necrotic with white-grey patches visible later on. The intestines are often full of stringy mucus and no food is present.

Histopathologically, necrosis begins in the haematopoietic tissues where lysis of melanomacrophages causes granule release and necrosis, which becomes generalised. Widespread focal necrosis, nuclear degeneration (pyknosis and karyolysis) and chromatin granulation is seen in the liver of affected rainbow trout. In turbot, marked necrosis of the ventricular fibres of the heart is seen.

The immunity granted to recovered fish varies in nature and duration; some fish become covet carriers and continue to infect other susceptible individuals.


There is no treatment for infected fish.


Official health surveillance and control policies are in place and have successfully eradicated the disease from several parts of Europe.

Disinfectants, such as chlorine, hypochlorite and iodophors are effective against rhabdoviruses and will prevent the spead of the virus from farm to farm via transport tanks and equipment.

Genetic selection and vaccination are in their experimental stages.

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Smail, D.A., Snow, M. (2011). Viral Haemorrhagic Septicaemia. In: Fish Diseases and Disorders, Volume 3: Viral, Bacterial and Fungal Infections, 2nd edition (eds. P.T.K Woo and D.W. Bruno), CABI, Wallingford, U.K. pages 110-142.


This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on 31 July 2011.

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