Viral Diseases of Crayfish


Category 1 (Not Reported in Canada)

Common, generally accepted names of the organism or disease agent

  1. Cherax quadricarinatus bacilliform virus (CqBV), Cherax baculovirus.
  2. Astacus bacilliform virus (AaBV).
  3. Pacifastacus lenisculus bacilliform virus (PlBV).
  4. Cherax Giardiavirus-like virus (CGV).
  5. Cherax destructor bacilliform virus (CdBV).
  6. Cherax destructor systemic parvo-like virus (CdSPV).
  7. Cherax quadricarinatus putative gill parvovirus.
  8. Cherax quadricarinatus presumptive hepatopancreatic reovirus.
  9. Austropotamobius pallipes bacilliform virus (ApBV).
  10. Cherax quadricarinatus spawner-isolated mortality virus (SMV).
  11. White spot syndrome virus (WSSV or WSBV).
  12. Infectious pancreatic necrosis virus (IPNV), a birnavirus that causes acute disease in salmonids.

Scientific name or taxonomic affiliation

Various viruses as listed above. According to affiliations proposed by Evans and Edgerton (2002) the viruses of crayfish can be grouped as follows: CqBV, AaBV, PlBV, CdBV, ApBV and WSSV are similar in morphology and cytopathology and thus were grouped as intranuclear bacilliform viruses; CdSPV, the putative gill parvovirus of C. quadricarinatus and SMV are parvo-like viruses; and CGV is a Toti-like dsRNA virus.

Geographic distribution

  1. Northern Queensland and Northern Territory, Australia and has also been introduced into California, USA; Belize and Ecuador.
  2. Central Finland.
  3. California, USA.
  4. Initially detected in northern Queensland, Australia but is now known to be widespread in C. quadricarinatus in Australian aquaculture facilities. The lack of detection outside of Australia may be due to difficulties in diagnosis (Evans and Edgerton 2002).
  5. South Australia.
  6. Southern South Australia.
  7. Northern Queensland, Australia.
  8. Northern Queensland, Australia.
  9. South-eastern France.
  10. Northern Queensland, Australia.
  11. Associated with epizootic mortality in penaeid shrimp aquaculture throughout Asia and has been inadvertently introduced to various locations in North and South America.
  12. A wide geographical distribution, occurring in most major salmonid-farming countries of North and South America, Europe and Asia. However, infectivity to crayfish has been examined only in Germany.

Host species

  1. Cherax quadricarinatus, both wild and farmed populations and Pacifastacus lenisculus.
  2. Astacus astacus.
  3. Pacifastacus lenisculus.
  4. Cherax quadricarinatus in farmed and experimental juvenile populations.
  5. Cherax destructor.
  6. Cherax destructor.
  7. Cherax quadricarinatus.
  8. Cherax quadricarinatus.
  9. Austropotamobius pallipes.
  10. Initially known as a pathogen of Penaeus monodon, this parvo-like virus was detected in farmed Cherax quadricarinatus.
  11. Infects many penaeid shrimp species as well as many non-penaeid crustacea including freshwater crayfish from all three families (Edgerton et al. 2004). Specifically, mortalities associated with WSSV have been reported from Orconentes punctimanus and Procambarus sp. from southeastern USA and was experimentally transmitted to Procambarus clarkii by feeding them with infected Penaeus monodon (Wang et al. 1998, Edgerton et al. 2002a, Evans and Edgerton 2002); experimentally to Cherax quadricarinatus by injection of haemolymph from naturally infected Penaeus chinensis (Shi et al. 2000 - Note: Edgerton (2004, second last paragraph of Introduction) claims that the crayfish assayed by Shi et al. (2000) was Procambarus clarkii and not C. quadricarinatus); experimentally to Astacus leptodactylus and Orconectes limosus by injection and feeding on infected Penaeus monodon (Corbel et al. 2001); experimentally to Pacifastacus leniusculus by injection of isolates from P. monodon (Jiravanichpaisal et al. 2001); and experimentally to Cherax destructor albidus by injection with a Thai isolate of WSSV propagated in P. monodon but C. destructor albidus appeared less sensitive to infection when exposed by oral challenge (Edgerton 2004).
  12. Although a disease of salmon, this virus was experimentally transmitted to Astacus astacus by injection, feeding on infected salmon tissue and cohabitation with infected fry of rainbow trout (Oncorhynchus mykiss (=Salmo gairdneri))(Halder and Ahne 1988).

Impact on the host

The relationship between infection and disease remains obscure for the majority of crayfish viruses. Depending on the virus involved and whether or not there is synergism with other viruses or pathogens, the effects on the host may be lethal, relatively benign or even unknown. Some viral infections may become patent only when crayfish have been exposed to stress factors such as captivity, crowding, or a degraded environment. Disease associated with viruses in crayfish were reported as follows:

  1. Although CqBV has been associated with mortalities in experimental and farmed populations of C. quadricarinatus, it is considered to have low virulence because serious mortalities have not been observed in farms that have a high prevalence of infected crayfish (Edgerton and Owens 1999, Evans and Edgerton 2002). Also, there was no external or internal signs of disease in captive reared C. quadricarinatus in California but animals submitted for a routine health examination had poorer than expected growth with no associated mortalities (Groff et al. 1993). However, Edgerton and Owens (1997) demonstrated that juvenile crayfish (2 weeks after moulting into stage 3) were susceptible to infection which increased in prevalence with time, but pathogenicity could not be assessed because of cannibalism.
  2. AaBV was not associated with clinical disease but the high intensity of infection in some crayfish suggested possible pathogenicity to A. astaci (Edgerton et al. 1996).
  3. PlBV has been reported on only one occasion and the potential for associated disease is not known (Edgerton et al. 2002a).
  4. CGV is very common in farmed C. quadricarinatus and prevalence of infection increases dramatically among juvenile crayfish following moulting into stage 3 (first feeding stage) suggesting oral transmission. Although not known to cause disease in adult C. quadricarinatus, intense infections may result in juvenile morbidity (Edgerton and Owens 1999, Edgerton et al. 2002a). Also, infection was associated with mortalities among juvenile crayfish held in experimental aquaria (Edgerton et al. 1994). Thus, CGV may be a significant pathogen of juvenile C. quadricarinatus (Evans and Edgerton 2002).
  5. Few C. destructor infected with CdBV have been detected, thus nothing is known about its prevalence, transmission or potential host range (Edgerton et al. 2002a).
  6. CdSPV has been observed in only one moribund C. destructor from a farm crayfish culture pond. Because no other studies have been conducted, the distribution and prevalence of this virus is not known (Edgerton et al. 2002a).
  7. Putative gill parvovirus was associated with chronic mortalities in C. quadricarinatus that were obtained from a farm as sub-adults and employed in laboratory disease transmission trials (Edgerton et al. 2000).
  8. Presumptive hepatopancreatic reovirus of C. quadricarinatus was associated with chronic mortalities in C. quadricarinatus from one farm (Edgerton et al. 2000).
  9. ApBV was associated with an epizootic mortality of A. pallipes in the Nant watershed, Ardéche, France in the summer of 2000 (Edgerton et al. 2002b). Since 2000, ApBV has been found in a high proportion (73% to 100%) of A. pallipes from other rivers in south-eastern France without obvious mortalities but some sampled crayfish from one river were moribund and all had low lipid stores and frequent melanitic lesions in the gills suggestive of stressed populations (Edgerton 2003).
  10. SMV was associated with reduced tolerance to stress in C. quadricarinatus with high mortalities associated with handling (capture and transport) and a significant reduction in yield at harvest (Owens and McElnea 2000).
  11. WSSV causes severe disease in many species of penaeid shrimp and significant mortalities in some experimentally exposed crayfish populations (Wang et al. 1998, Edgerton et al. 2002a). In P. leniusculus injected with WSSV, the virus had a significant effect on the proportion of different haemocyte types and all experimental crayfish were dead by 10 days post-injection (Jiravanichpaisal et al. 2001).
  12. Although it was not demonstrated that IPNV replicated in A. astacus, this crayfish served as a mechanical vector of infection and IPNV was isolated from A. astacus haemolymph up to 1 year post exposure by injection, oral and cohabitiation - waterborne routes (Halder and Ahne 1988).

Diagnostic techniques

Gross Observations: Gross signs of infection have been reported only for three of the viruses reported from crayfish:

  1. Crayfish with heavy CqBV are lethargic, have a weak or failed tail-flick response and are unable to right themselves when placed up-side-down.
  2. The one crayfish with CdSPV was moribund and had patches of opaque musculature observed through the translucent cuticle of the ventral surface of the abdomen (Edgerton et al. 1997).
  3. Clinical signs of WSSV in O. punctimanus and Procambarus sp. included discoloration and mottling of the exoskeleton primarily on the carapace and occasionally on the chelipeds (Edgerton et al. 2002a). Clinical signs in Pacifastacus leniusculus included reddish haemolymph that had a significant delay in clotting time and a reduction in activity and locomotion including a weak response to stimulation but not the appearance of white spots on the cuticle and overall reddish body coloration typically observed in WSSV infected penaeid shrimp (Jiravanichpaisal et al. 2001).


  1. qBV typically infects the senescent proximal hepatopancreatocytes in a proximal to medial position in the hepatopancreatic tubules and less frequently the epithelail cells of the antechamber, midgut and proximal midgut caecum. Bacteraemia is common in crayfish with intense infections. Necrosis and atrophy of infected tissues has been observed in acute cases (Edgerton 1996). Infected nuclei are often hypertrophied, with chromatin and nucleolus margination and contain a single granular eosinophilic inclusion giving them a signet ring appearance. The inclusion may contain fine strands of chromatin or have a haloed appearance if fixation resulted in shrinkage. The cytoplasm may have increased basophilia. Early infections are characterised by small, haloed eosinophilic intranuclear inclusions is susceptible cells.
  2. AaBV infects the epithelial cells of the digestive tract in which it causes mildly hypertrophic, irregular-shaped nuclei. Affected nuclei have emarginated chromatin and contain amorphous eosinophilic inclusions that are often darker towards the centre, haloed or compartmentalised by strands of chromatin. The nucleolus was not apparent in late infections and the cytoplasm of infected cells may be deeply basophilic. Infected cells were routinely observed sloughing into the gut lumen and on occasion, the midgut, the midgut caecum or hepatopancreatic tubules were necrotic and encapsulated by haemocytes (Edgerton et al. 1996).
  3. PlBV infects epithelial cells of the hepatopancrease which may detach from the tubule basement membrane. Infected cells have hypertrophic nuclei with emarginated chromatin which contain a granular eosinophilic inclusion.
  4. CGV is confined to the R, F and B epithelial cells (but not E cells) of the hepatopancrease and infected cells do not usually slough into the hepatopancreatic tubule lumen. Infection causes negligible to mild nuclear hypertrophy but infected nuclei have emarginated and clumped chromatin and contain multiple purple-red (with haematoxylin and eosin staining) well-developed inclusions. In late infections, the inclusions coalesce thus becoming fewer in number and larger in size. Various staining properties of infected nuclei and nuclease digestion of histological material confirmed the predominance of double-stranded RNA in the inclusions (Edgerton et al. 1994).
  5. CdBV infects the nucleus of hepatopancreatic epithelium (hepatopancreatocytes) resulting in their lysis and sloughing into the tubule lumen. Infected nuclei are markedly hypertrophic, have emarginated chromatin and contain an amorphous eosinophilic inclusion. The cytoplasm of infected cells is often more basophilic than uninfected cells.
  6. The one crayfish with CdSPV had extensive necrosis in several major organs including the gills, hepatopancrease and muscle. However, cytopathic lesions characteristic of a viral infection were only observed in the gills, epicardium and spongy connective tissue. The nuclei of infected cells were markedly hytertrophic with emarginated chromatin and contained Cowdry type A intranuclear inclusions.
  7. The only consistent lesion associated with the putative gill parvovirus in C. quadricarinatus was multifocal hypertrophic nuclei with emarginated chromatin in the gill epithelium. There was associated haemocyte infiltration in one moribund crayfish and occasionally the majority of gill epithelial nuclei in a longitudinal section of a lamella were infected. The epithelium of heavily infected lamellae were more basophilic (with haematoxylin and eosin stain) and had shrunken away from the cuticle (Edgerton et al. 2002a).
  8. The one C. quadricarinatus infected by the presumptive hepatopancreatic reovirus had eosinophilic, cytoplasmic inclusions in the cytoplasm of hepatopancreatocytes at or near the distal tips of tubules throughout the hepatopancrease. The inclusions were in cytoplasmic vacuoles and some were closely associated with the nucleus. There was a marked demarcation between affected and unaffected epithelia in longitudinally section tubules as affected tubules displayed significantly less lipid vacuolation than normal epithelia and were flattened. Also, affected tubules were surrounded by haemocyte accumulations (Edgerton et al. 2000).
  9. ApBV infects the epithelial cells of the hepatopancrease (usually in the antechamber and main collection ducts but never in the apical tips of the tubules), midgut and midgut caecum with the intensity of infection in most cases higher in the midgut and/or midgut caecum. Infected cells had hypertrophic nuclei which contain emarginated chromatin and eosinophilic, granular inclusions. Affected nuclei frequently occurred in the apex of the epithelial cell (Edgerton et al. 2002b). Infected cells were observed sloughing into the gut lumen (Edgerton 2003).
  10. No specific evidence of the disease was observed by routine histopathological examination (using heamatoxylin and eosin stain). However, tissue sections stained by in situ hybridisation with a DIG labeled SMV probe gave positive signals in the nuclei of many organs of 75% of the moribund C. quadricarinatus (Owens and McElnea 2000).
  11. WSSV infects the haemocytes and other cells of mesodermal and ectodermal origin, especially the cuticular epidermis. The nuclei of infected cells are hypertrophic, have emarginated chromatin and contain single lightly esoinophilic to deeply basophilic inclusions. In P. leniusculus, histopathological observations in various tissues of infected crayfish were similar to those of WSSV infected penaeid shrimp (Jiravanichpaisal et al. 2001).
  12. No histopathology was observed in crayfish tissues after experimental exposure but IPNV was isolated from various tissues by virus in vitro culture in fish cells.

Electron Microscopy:

  1. CqBV virions (about 262 x 102 nm) are rod-shaped with a cylindrical nucleocapsid (212 x 53 nm) surrounded by a loose trilaminar envelope that has a slight unilateral bulge to accommodate a reflexed tail-like structure at one end (Edgerton 1996). Virons accumulate in the nucleus within a granular viroplasm and rounded putative nucleolar remnants are common within the infected nucleus.
  2. AaBV virions (343 x 71 nm) have a cylindrical rod-shaped nucleocapsid (261 X 51 nm) surrounded by a closely applied trilaminar envelope that has a unilateral expansion at one end that appears to accommodate a reflexed tail-like structure. The virions were often arranged in rows and often associated with nucleolar remnants. They were only present in the cytoplasm of infected cells following lysis of the nucleus (Edgerton et al. 1996).
  3. PlBV virions are rod-shaped and enveloped (240 x 66 nm) with a nucleocapsid (189 x 44 nm) and accumulate in the nucleus.
  4. CGV virions (about 25 nm in diameter) are icosahedral, and non-enveloped. Nuclear inclusions are entirely composed of virions in paracrystalline arrays.
  5. CdBV virions (304 x 68 nm) are rod-shaped and have a cylindrical nucleocapsid (263 x 50 nm) that is slightly to markedly bent within a closely applied trilaminar envelope. The envelope expands laterally in the bent region and accommodates a tail-like structure that arises from the end of the nucleocapsid. Virions are scattered throughout the viroplasm and accumulate at the nuclear membrane. The viroplasm contains abundant putative ribosomal precursor particles and membrane fragments that often form circles (Edgerton 1996).
  6. CdSPV virions (about 21 nm in diameter) are icosahedral. Aggregates of viral particles were observed between the viroplasm and the inner nuclear membrane. The nucleolus was closely associated with the developing viroplasm and was often hypertrophied. The intranuclear inclusions consisted mainly of empty capsids and microfilaments.
  7. Cherax quadricarinatus putative gill parvovirus (about 20 nm in diameter) were rounded with angular profiles. These virus-like particles were scattered throughout the interior of the nucleus and surrounded by the emarginated chromatin and nucleoli of the hypertrophied nucleus. The mitochondria of infected cells were swollen and displayed irregular profiles, and the cytoplasm was more electron dense than uninfected cells.
  8. Cherax quadricarinatus presumptive hepatopancreatic reovirus virions (35 to 40 nm) were non-enveloped, with an angular appearance and irregular in shape (hexagonal and pentagonal forms), and were regularly spaced in the virogenic stroma near paracrystaline arrays in the cell cytoplasm. Although the cytoplasmic inclusions were intimately associated with the nucleus, the nucleus appeared unaltered (Edgerton et al. 2000).
  9. ApBV virons (about 258 x 63 nm) with a cylindrical nucleocapsid (225 x 52 nm) surrounded by a trilaminar envelope that was snugly applied at one end and with a unilateral expansion at the other (Edgerton et al. 2002b).
  10. Not described from crayfish, but in Penaeus monodon, the virions (about 20 nm in diameter) were hexagonally shaped suggesting icosahedral symmetry (Fraser and Owens 1996).
  11. WSSV virions (350 x 100 nm) in crayfish are rod-shaped to elliptical.
  12. No cytopathology was observed in crayfish tissues after experimental exposure to IPNV but virions were observed in haemocyte granules.

DNA Probes: Several molecular tools including PCR and in situ hybridization assays have been developed to detect WSSV and IPNV. SMV was first detected in crayfish by in situ hybridisation (DIG-labeled probe) developed for the diagnosis of this disease in Penaeus monodon (Owens and McElnea 2000). No molecular tools are available to detect the other viruses of crayfish.

Methods of control

Some diseases may be avoided or severity reduced by minimizing stress in captive crayfish. Disease or at least large-scale mortalities may be prevented in aquaculture situations by proper husbandry. To prevent CqBV and CGV infections in aquaculture and inadvertent translocations of these viruses through aquaculture activities, Edgerton and Owens (1997) recommended the production of presumptive virus-free juvenile C. quadricarinatus by employing suitable hatchery and grow-out technology. This approach is feasible because CqBV and CGV are not transmitted vertically and thus, progeny free of these virsus can be produced from infected mothers by removing the eggs, disinfecting their surfaces and hatching them in clean water.


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Citation Information

Bower, S.M. (2006): Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish: Viral Diseases of Crabs.

Date last revised: August 2006
Comments to Susan Bower

Date modified: