Assorted Viruses Detected in Oysters and of Unknown Significance

Category

Category 4 (Negligible Regulatory Significance in Canada)

Common, generally accepted names of the organism or disease agent

  1. IPN-like virus.
  2. Reo-like virus, 13P2.
  3. Unidentified virus within virus-like inclusions.

Scientific name or taxonomic affiliation

  1. Infectious pancreatic necrosis (IPN)-like virus which did not have any detectable cross-neutralization activity with the fish pathogen IPN but produced specific fluorescence using the indirect fluorescence antibody technique indicating an antigenic relationship with IPN, possibly between internal proteins (e.g., the ribonucleo-protein) (Hill 1976, Hill and Alderman 1977, Farley 1978).
  2. 13P2 an undescribed virus belonging to the family Reoviridae (Meyers 1979).
  3. Unidentified virus-like particles observed in virus-like inclusions within the hypertrophied nuclei of digestive gland epithelial cells (Pass et al. 1988, Perkins 1993).

Geographic distribution

  1. Coast of Britain and east coast of Canada.
  2. Juvenile Crassostrea virginica from a hatchery on Long Island Sound, New York, U.S.A.
  3. Coastal regions of northwestern Australia.

Host species

  1. Isolated from Ostrea edulis on various finfish cell lines but grew best in BF-2 (bluegill fibroblasts). A similar virus isolated from the clam Tellina tenuis was infective to Ostrea edulis and Crassostrea gigas.
  2. Isolated from Crassostrea virginica on the finfish cell line BF-2 (bluegill fibroblasts).
  3. Observed in Pinctada maxima during investigations into mass mortalities (Pass et al. 1988). Similar inclusions have been found in a wide diversity of marine bivalve molluscs (Perkins 1993).

Impact on the host

  1. No reported pathology in naturally infected hosts. Infectivity experiments with O. edulis and C. gigas indicated that some of the isolates caused a mild pathological effect (some haemocyte infiltration and necrosis of connective tissue in the digestive gland) including an increase in the number of inclusion bodies in the cells of the digestive gland but no associated oyster mortalities. However, experimental results have been inconsistent and a firm conclusion on the significance of these viruses for shellfish is not known.
  2. No reported pathology in naturally infected hosts. Infectivity experiments with O. edulis and C. gigas indicated that some of the isolates caused a mild pathological effect (some haemocyte infiltration and necrosis of connective tissue in the digestive gland) including an increase in the number of inclusion bodies in the cells of the digestive gland but no associated oyster mortalities. However, experimental results have been inconsistent and a firm conclusion on the significance of these viruses for shellfish is not known.
  3. Although the inclusions containing virus-like structures were first detected in diseased pearl oysters, similar structures were observed in many apparently normal pearl oysters and no pathological significance was assigned to them. Apart from hypertrophy of the nucleus, there were no other changes seen in affected cells nor were lesions noted in the digestive gland that could be associated with the presence of the inclusion bodies (Pass et al. 1988). Pass et al. (1988) concluded that if the nuclear inclusions were virogenic stroma containing viral particles, infection was common in P. maxima in northwestern Australia but there was no evidence that they were related to disease in this species. The cause of the mortalities in P. maxima was determined to be a bacterial syndrome (mainly Vibrio harveyi) associated with transport stress (Pass et al. 1987, McGladdery 1999).

Diagnostic techniques

Histology:

  1. Mild haemocytic infiltration and connective tissue necrosis observed in the digestive gland of experimentally exposed oysters. Also, the cells of the digestive gland showed a progressive increase in the number of inclusion bodies with time post exposure.
  2. Not described.
  3. Basophilic or amphophilic intranuclear inclusion bodies in the basophilic cells of the digestive gland tubules and less commonly in epithelial cells of the gut. The inclusions tended to be centrally located within nuclei and were surrounded by a clear zone. They stained purple with phloxine tartrazine, faint pink with methyl green pyronin, and slightly basophilic with Feulgen stain. They were acid fast negative and periodic acid-Schiff-negative. The inclusions measured 2.5-5.0 µm in diameter. Affected nuclei were 4.3-7.5 µm in diameter compared to unaffected nuclei which measured 2.5-3.0 µm (Pass et al. 1988).

Culture:

  1. All isolates seem to grow best, with the formation of cytopathic effects consisting of discrete plaques, in the bluegill fry fibroblast (BF-2) cell line.
  2. All isolates seem to grow best, with the formation of cytopathic effects consisting of discrete plaques, in the bluegill fry fibroblast (BF-2) cell line.
  3. None described.

Electron Microscopy:

  1. Icosahedral (by negative staining) nonenveloped virions about 55 nm in diameter.
  2. Icosahedral particles (by negative staining) with a mean diameter of 79 nm. Some particles had definite hexagonal profiles and an inner capsid layer. However, most appeared slightly oval with clear spike-like projections on the outer capsid and a distinct inner core.
  3. The inclusions consisted of an electron dense, finely granular matrix (virogenic-like stroma) containing “doughnut-shaped” subunits surrounded by an electron-lucent halo (presumptive virions). The subunits measured 33-38 nm and the subunit and halo were 53-71 nm in diameter. Occasionally small inclusions or individual particles were seen adjacent to the nuclear membrane (Pass et al. 1988).

Methods of control

No known methods of prevention or control.

References

Farley, C.A. 1978. Viruses and virus-like lesions in marine mollusks. Marine Fisheries Review 40: 18-20.

Hill, B.J. 1976. Properties of a virus isolated from the bivalve mollusc Tellina tenuis (da Costa). In: Page, L.A. (eds), Wildlife Diseases. Plenum Press, New York and London, pp. 445-452.

Hill, B.J. and D.J. Alderman. 1977 (1979). Observations on the experimental infection of Ostrea edulis with two molluscan viruses. Haliotis 8: 297-299.

McGladdery, S.E. 1999. Shellfish diseases (viral, bacterial and fungal). In: Woo, P.T.K., D.W. Bruno (eds.) Fish Diseases and Disorders, Volume 3: Viral, Bacterial and Fungal Infections, Vol. 3. CABI Publishing, Wallingford, UK. pp. 723-842.

Meyers, T.R. 1979. A Reo-like virus isolated from juvenile American oysters (Crassostrea virginica). Journal of General Virology 43: 203-212.

Pass, D.A., R. Dybdahl and M.M. Mannion. 1987. Investigations into the causes of mortality of the pearl oyster, Pinctada maxima (Jamson), in Western Australia. Aquaculture 65: 149-169.

Pass, D.A., F.O. Perkins and R. Dybdahl. 1988. Viruslike particles in the digestive gland of the pearl oyster (Pinctada maxima). Journal of Invertebrate Pathology 51: 166-167.

Perkins, F.O. 1993. Infectious diseases of molluscs. In: Couch, J.A., J.W. Fournie (eds.) Pathobiology of Marine and Estuarine Organisms. CRC Press, Boca Raton. pp. 255-287.

Citation Information

Bower, S.M. (2010): Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish: Assorted Viruses Detected in Oysters and of Unknown Significance

Date last revised: February 2010
Comments to Susan Bower

Date modified: