Akoya Virus Infection of Pearl Oysters

Category

Category 3 (Host Not in Canada)

Common, generally accepted names of the organism or disease agent

Akoya oyster disease caused by "Akoya virus".

Scientific name or taxonomic affiliation

"Akoya virus" (small viral particles). Miyazaki et al. (1998) reported that the size was similar to that of Picornaviridae and resembled the virus from the scallop Pecten novaezelandiae described by Hine and Wesney (1997). However, Wada (2003) was critical of the identification of the causative agent because the putative "Akoya virus" was isolated from diseased pearl oyster using fish cells, only Dr. T. Miyazaki and co-workers have successfully isolated the virus, and they have not provided any genetic data nor antibodies for peer confirmation of the identity of the pathogen. Suzuki et al. (1998) isolated a birnavirus from symptomatic pearl oysters (Pinctada fucata) from the Uwa Sea, Ehime Prefecture, Japan. This marine birnavirus was isolated on finfish cell lines (CHSE-214 and RSBK-2) and detected and identified using a 2 step (nested) PCR (Suzuki et al. 1998, Kitamura et al. 2002). However, the virulence of this isolate against P. fucata was weak suggesting that this marine birnavirus is an opportunistic pathogen (Kitamura et al. 2002). The relationship between the "Akoya virus" and the marine birnavirus is not known.

Geographic distribution

Western regions of Japan. Virus-like particles associated with pathology have also been detected in Pinctada fucata from China (Miyazaki et al. 1999) and Pinctada margaritifera in French Polynesia (Comps et al. 1999, 2001).

Host species

Pinctada fucata, Pinctada fucata martensii (spat and adults) and possibly Pinctada margaritifera. Crassostrea gigas and Chlamys nobilis cultured in close proximity to diseases pearl oysters also showed mass mortalities, muscular damage and the "Akoya virus" was isolated from them (Miyazaki et al. 1998).

Impact on the host

Infection associated mass mortalities (over 50% of the annual production in 1996 and 1997) among Japanese pearl oysters, P. fucata, from 1994 to 1999. The exact nature and the role of virus-like particles observed in Pinctada margaritifera are unknown because a virus has not been purified nor chemically characterized from diseases pearl oysters. Also, it has not been demonstrated that the "Akoya virus" infects P. margaritifera (Comps et al. 2001).

Diagnostic techniques

Gross Observations: Poor growth as indicated by the edge of the shell and sluggish closing of the valves when the oyster was disturbed by touching the lip of the mantle lobe. Atrophy of the adductor muscle, mantle lobes (which were transparent) and the body accompanied by yellowish to brown discolouration (Miyazaki et al. 1998, 1999). Diseased P. margaritifera in French Polynesia had an unusual secretion of mucus and displayed grossly visible abscesses in the adductor muscle (Comps et al. 1999, 2001).

Histology: Necrosis (including karyopyknosis, karyorrhexis and marginal hyperchromatosis) and degeneration (atrophy and vacuolization) of muscle fibres. Heamocyte (many agranulocytes and granulocytes) infiltration into the adductor muscle and musculature of the foot, mantle lobe, heart and gills. In severe cases, the perimysium (a fibrous tissue that encloses the adductor muscle) also contained many haemocytes and necrotic cells. The Periodic Acid Schiff (PAS) reaction indicated decreased levels of glycogen in the severely damages muscle fibres. No Feulgen-positive inclusions were observed suggesting that the putative virus had RNA (Miyazaki et al. 1999). In pearl oysters that survived the infection, necrotized muscle fibres are replaced by dense fibrous tissues that develop between the thinned muscle fibres which remained in the lesion (Miyazaki et al. 2000). Lesions in the adductor muscle of diseased P. margaritifera in French Polynesia were similar to those described in P. fucata. At the periphery of the lesion, the muscle was infiltrated by haemocytes with a progressive increase in haemocyte concentrations and alteration of muscle structure towards the centre. The centre of the lesion was occupied by a granulomatous tissue consisting of granulocytes, macrophages and cellular debris. Internal areas of dense connective tissue including muscle fibre debris in some pearl oysters suggested the occurrence of a healing process (Comps et al. 1999, 2001).

Electron Microscopy: The sarcoplasm of necrotic muscle fibres of the adductor muscle contained membranous inclusion bodies within electron-dense debris. The inclusion bodies contained many round, non-enveloped, viral particles (25 to 33 nm in diameter). In addition, the infected muscle fibres had thinned or fragmented myofibrils, vacuoles in the sarcoplasm, mitochondria with destroyed cristae, expanded reticula and almost no glycogen granules (Miyazaki et al. 1999). In the adductor muscle, healed lesion contained cells that actively produced many microfibrils within the cytoplasm (Miyazaki et al. 2000). The virus-like particle from diseased P. margaritifera in French Polynesia had a diameter of 40 nm with a membrane like envelope coating an electron dense core about 35 nm in diameter (Comps et al. 1999). Within the altered muscle of P. margaritifera, numerous interstitial or glial cells containing electron-dense and membrane bound ovoid bodies appeared associated with muscle fibres and connective tissue which could be related to the process of regeneration of muscle tissue (Comps et al. 2001)

Culture: Miyazaki et al. (1998, 1999) indicated that they could culture the virus in finfish cell lines (EK-1 from eel kidney and EPC from epithelioma papilosum cyprini). Akoya pearl oysters experimentally inoculated into the lip of the mantle lobe with the cultured virus showed pathological signs of the disease, marked mortalities and the virus was isolated from the adductor muscle of the moribund and dead oysters (Miyazaki et al. 1998).

Methods of control

No known methods of prevention or control. Because the causative agent is still unknown, and because the pearl oysters are cultured in open sea, there is no efficient control method available (Wada 2003). Miyazaki et al. (1999) proposed that the "Akoya virus" were harboured by juvenile oysters during the winter. These infected oysters then became diseased on the return of optimum water temperatures (above 25°C) and served as a source for horizontal transmission of the infection and resulting mass mortalities. Anecdotal information suggested that short durations (less than 1 month) of high temperatures (above 25°C) during the summer resulted in lower mortality of oysters with "Akoya virus" infections (Miyazaki et al. 2000). Thus, moving the pearl oysters into areas where the water temperature is lower during summer to autumn months may reduce the mortality by this disease. Transplantation of the pearl oysters from areas where the existence of the disease is suspected, should be prohibited (Wada 2003).

Miyazaki et al. (2000) reported that an anti-viral, recombinant feline interferon-ω (rFeIFN-ω) administered by injection was efficacious in preventing mortality of P. fucata with "Akoya virus" infection for at least 30 days following challenge via inoculation with cultured viruses. Miyazaki et al. (2002) determined that this treatment was effective because haemocytes of P. fucata possessed receptors for binding the rFeIFN-ω, a mammalian interferon produced in silkworms by a recombinant baculovirus. However, prophylactic rFeIFN-ω administration was not completely effective in preventing mortality especially when viral invasions occurred several days after rFeIFN-ω administration (Miyazaki et al. 2000).

References

Comps, M., C. Herbaut and A. Fougerouse. 1999. Virus-like particles in pearl oyster Pinctada margaritifera. Bulletin of the European Association of Fish Pathologists 19: 85-88.

Comps, M., C. Herbaut, A. Fougerouse and F. Laporte. 2001. Progress in pathological characterization of Syndrome 85 in the black-lip pearl oyster Pinctada margaritifera. Aquatic Living Resources 14: 195−202.

Hine, P.M. and B. Wesney. 1997. Virus-like particles associated with cytopathology in the digestive gland epithelium of scallops Pecten novaezelandiae and toheroa Paphies ventricosum. Diseases of Aquatic Organisms 29: 197-204.

Kitamura, S.-I., Y. Tomaru, Z. Kawabata and S. Suzuki. 2002. Detection of marine birnavirus in the Japanese pearl oyster Pinctada fucata and seawater from different depths. Diseases of Aquatic Organisms 50: 211–217.

Mortensen, S., I. Arzul, L. Miossec, C. Paillard, S. Feist, G. Stentiford, T. Renault, D. Saulnier and A. Gregory. 2007. Molluscs and crustaceans. In: Raynard, R., T. Wahli, I. Vatsos, S. Mortensen (eds.) Review of disease interactions and pathogen exchange between farmed and wild finfish and shellfish in Europe. VESO on behalf of DIPNET, Oslo. Chapter 5.3.4, pp. 329. For electronic version see www.dipnet.info under "Documents" subgroup "Reports and project deliverables".

Miyazaki, T., K. Goto, T. Kobayashi and M. Miyata. 1998. An emergent virus disease associated with mass mortalities in Japanese pearl oysters Pinctata fukata martensii. Proceedings of the VIIth International Colloquium on Invertebrate Pathology and Microbial Control, Sapporo, Japan, August 23-28, 1998. pp. 154-159

Miyazaki, T., K. Goto, T. Kobayashi, T. Kageyama and M. Miyata. 1999. Mass mortalities associated with a virus disease in Japanese pearl oysters Pinctada fucata martensii. Diseases of Aquatic Organisms 37: 1-12.

Miyazaki, T., N. Nozawa and T. Kobayashi. 2000. Clinical trial results on the use of a recombinant feline interferon-v to protect Japanese pearl oysters Pinctada fucata martensii from akoya-virus infection. Diseases of Aquatic Organisms 43: 15–26.

Miyazaki, T., T. Taniguchi, J. Hirayama and N. Nozawa. 2002. Receptors for recombinant feline interferon-ω in hemocytes of the Japanese pearl oyster Pinctadafucata martensii. Diseases of Aquatic Organisms 51: 135–138.

Renault, T. and B. Novoa. 2004. Viruses infecting bivalve molluscs. Aquatic Living Resources 17: 397-409.

Suzuki, S., M. Kamakura and R. Kusuda. 1998. Isolation of birnavirus from Japanese pearl oyster Pinctada fucata. Fisheries Science (Tokyo) 64: 342-343.

Wada, K.T. 2003. Akoya oyster disease-disease card. Developed to support the NACA/FAO/OIE regional quarterly aquatic animal disease (QAAD) reporting system in the Asia-Pacific. NACA, Bangkok, Thailand. 3 pp. For electronic version see http://library.enaca.org/Health/DiseaseLibrary/AkoyaDisease.pdf.

Citation Information

Bower, S.M. (2010): Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish: Akoya Virus Infection of Pearl Oysters.

Date last revised: February 2010
Comments to Susan Bower

Date modified: