Spring Viraemia of Carp

Also Known As: SVC -— Swim Bladder Inflammation -- SBI

Caused By: Spring Viraemia of Carp Virus –- SVCV –- Rhabdovirus Carpio –- RVC

Introduction

Spring Viraemia of Carp is caused by a bullet shaped Rhabdovirus. It is also known as Rhabdovirus carpio and it causes an acute, systemic, contagious disease primarily affecting carp. The effects of the virus further down the food chain (in predators) is unknown.

The disease is not zoonotic.

Distribution

Europe, North and South America, USSR and Asia.

Spring Viraemia of Carp is passed mainly horizontally, being shed in faecal casts, urine and gill mucus. It is also transmitted by louse, leech, crustacean and annelid vectors. It usually enters via the gills and replicates here before dissipating to the swim bladder. Vertical transmission is possible but infrequent.

Signalment

Carp are mainly affected, although goldfish and other species have also been found with the disease. Carp of all four varieties can be infected. There is no age susceptibility, although seasonality produces trends at 9-12 and 21-24 months old.

Feral carp are more vulnerable than farmed varieties.

Disease typically occurs in water <18⁰C so is predominantly in the Spring.

Clinical Signs

The virus causes haemorrhage and inflammation of the swim bladder leading to abdominal distension, lethargy, imbalance, swimming on their side and sinking. Affected fish may also appear pale, with darkening of the skin and fins +/- pin point haemorrhages. They may congregate in slow moving areas of their habitat.

Mortalities are common.

Where fish can be easily visualised, long thick mucoid casts from the vent will be noticed . Fish are often anaemic due to viral invasion and multiplication within haematopoietic tissues.

Diagnosis

Definitive diagnosis can be achieved by virus isolation or direct immunofluorescence (IF) or ELISA. Ideally, IF or ELISA diagnosis should be confirmed by virus isolation (VI). Decomposed carcasses however will seldom produce results. Virus neutralisation can be used as an alternative or accompaniment to virus isolation. Nested PCR and RT-PCR are available of which the former is the more sensitive.

Identification of SVCV is also possible by molecular biology methods such as ribonuclease protection assays, which are more reliable but more advanced and less widely available.

Fish for necropsy should be transported under refrigeration or on ice but never frozen. All organs and the encephalon should be immediately sent from fish 4-6cm in size or kidney, spleen and encephalon from fish over 6cm. Virus isolation should be performed in under 24 hours.

Necropsy of infected fish reveals splenomegaly with reticuloendothelial hyperplasia and enlarged melanomacrophage centres. The liver is hyperaemic with multifocal necrosis and degeneration. Kidney tubules are often clogged with casts and cells are vacuolated and degenerate due to multiplication of viral cells within them. Pericarditis is also seen. Haemorrhage and organ swelling with oedema is a cardinal feature and may be present throughout. There may be white-grey patches of tissue and organ necrosis. Blood vessels throughout show oedematous perivasculitis.

The swim bladder lamina changes into a discontinuous monolayer with dilated vasculature and lymphocyte infiltration. Electron microscopy reveals virus particles in the nuclei of the cells.

Treatment

There is no treatment once infected.

Control

The virus is inactivated by lipid solvents, heating >60⁰ for 15 minutes, glycerol, ozone, gamma radiation, UV light, extremes of pH, formalin and both acid and alkaline solvents. Virus infectivity is retained in tap water and mud for 6 weeks.

Regular physical and chemical disinfection of equipment, careful handling of fish to reduce stress and safe disposal of dead fish can reduce the severity of outbreaks.

Spring Viraemia of Carp Learning Resources
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References

Sano, M., Naki, T. and Fijan, N. (2011) Viral Diseases and Agents of Warmwater Fish. In: Fish Diseases and Disorders, Volume 3: Viral, Bacterial and Fungal Infections, 2nd edition (eds. Woo, P.T.K. and Bruno, D.W.), CABI, Wallingford, UK. Pp. 166-244.

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 6 July 2011.