Aquatic Animal Diseases Significant to Australia: Identification Field Guide 4th Edition

Aquatic Animal Diseases Significant to Australia:
Identification Field Guide 4th Edition

Viral haemorrhagic septicaemia (VHS)

EXOTIC DISEASE

VHS in rainbow trout (Oncorhynchus mykiss); note pale colour of stomach region, pinpoint haemorrhages in fatty tissue and pale gills Source: T Håstein

VHS in rainbow trout (Oncorhynchus mykiss); note swollen stomach and ‘popeye’ Source: T Håstein

Signs of disease

Disease outbreaks are seen in farmed trout and other salmonids, as well as in farmed turbot and Japanese flounder.

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  rapid onset of high mortality
  
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  lethargic swimming
  
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  separation from shoal
  
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  loss of appetite
  
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  crowding at pond edges.
  

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  significant cumulative mortality (protracted)
  
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  uncoordinated swimming (ataxia) with rotating movement around body axis (i.e. spinning).
  

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  low mortality
  
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  severe abnormal swimming behaviour (flashing and spiralling).
  

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  exophthalmos (popeye)
  
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  haemorrhaging under the skin, around the base of pectoral and pelvic fins and in the eyes
  
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  swollen abdomen
  
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  pale gills, with or without petechial (pinpoint) haemorrhages.
  

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  slight darkening of the body colour
  
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  exophthalmos (popeye)
  
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  bleeding around the eyes
  
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  bleeding under the skin around the base of the pectoral and pelvic fins
  
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  skin ulceration
  
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  swollen abdomen
  
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  pale gills with pinpoint haemorrhages
  
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  ascites (fluid in the abdominal cavity)
  
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  petechial (pinpoint) haemorrhages in the fatty tissue, intestine, gonads, liver, swim bladder and muscle
  
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  dark-red kidneys.
  

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  often an absence of external signs
  
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  intense darkening of the skin
  
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  exophthalmos (popeye)
  
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  pale gills (anaemic)
  
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  pale abdominal organs
  
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  pale and mottled liver (evidence of haemorrhages on surface)
  
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  pale gastrointestinal tract that is empty of food.
  

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  accumulation of erythrocytes in skeletal muscle fibres
  
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  extensive focal necrosis in the liver, kidney and spleen
  
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  VHS virus-positive endothelial cells in vascular system evident from immunohistochemistry.
  

Disease agent

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  type I, continental Europe—freshwater group, trout farms (highly pathogenic to rainbow trout)
  
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  type II, European marine strain (Baltic sea)—marine strain affecting wild and cultured marine and freshwater species (has low pathogenicity in rainbow trout)
  
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  type III, north Atlantic marine group (North sea near the British Isles)
  
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  type IVa, west coast of north America and east Asian group—marine group affecting a range of free-living marine and cultured species (highly pathogenic in Pacific herring; however, rainbow trout appear refractory to infection with this genotype)
  
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  type IVb, Great lakes region—significant mortalities in wild freshwater species in the Great lakes.
  

Host range

Species known to be susceptible to VHS are listed below.

Presence in Australia

EXOTIC DISEASE—not present in Australia.

Epidemiology

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  Variant strains of the virus are responsible for disease in different geographical locations.
  
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  Marine and freshwater species are susceptible to VHS virus infection. Younger fish are generally more susceptible to disease.
  
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  Rainbow trout appear to be less susceptible to infection by marine strains of the virus.
  
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  Water temperatures in an outbreak are generally near 10 °C. At water temperatures between 15 °C and 18 °C, the disease generally takes a shorter course with a modest accumulated mortality, but transmission can occur at water temperatures up to 22 °C. Mortality and morbidity have rarely been documented when water temperatures are above 18 °C, although VHS virus genotype IV has caused at least one fish kill at 20–22 °C, and some isolates can replicate in vitro at temperatures up to 25 °C.
  
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  Transmission is horizontal directly through the water, from virus shed in faeces, urine (predominantly) and sexual fluids of clinically infected or carrier fish. The virus can also be spread by birds that have consumed infected fish, via blood-feeding vectors such as leeches, and on equipment that has been in contact with water from infected fish. The virus gains entry via the gills, skin wounds, oral exposure (predation) and possibly through the skin.
  
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  Once infected, survivors are lifelong carriers of the virus; however, shedding is intermittent.
  
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  Stressors including overcrowding, extreme temperatures and overfeeding will greatly reduce an animal’s resistance to infection.
  
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  Mortality rate can range from 10% to 80%, depending on the VHS virus isolate, environmental variables (temperature), age, species, route of exposure and presence of additional stressors (highest mortality rates occur with acute infection, and lowest mortality rates in the neurological form).
  

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  VHS virus is thought to have existed in the marine environment before its apparent transfer to fresh water, where it first became virulent in trout.
  

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  It has been suggested that the European freshwater strains of VHS virus originated from fish in the northern Pacific and Atlantic oceans. The mechanism of transfer was possibly through the feeding of marine fish to cultured freshwater species.
  

Differential diagnosis

Similar diseases

Sample collection

Emergency disease hotline

Further reading

For more information on VHS virus isolates, refer to the European Community Reference Laboratory for Fish Disease at www.fishpathogens.eu/vhsv.