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Archived - Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish

Mikrocytos mackini (Denman Island Disease) of Oysters

Category | Common Name | Scientific Name | Distribution | Host Species
Impact on Host | Diagnostic Technique | Methods of Control | References | Citation


Category

Category 2 (In Canada and of Regional Concern)

Common, generally accepted names of the organism or disease agent

Mikrocytosis, Denman Island disease, Denman disease, Microcell disease of Pacific oyster.

Scientific name or taxonomic affiliation

Mikrocytos mackini. Maximum parasimony and evolutionary distance phylogenetic analysis based on a 1457 base pair segment of the small-subunit ribosomal DNA (SSU rDNA or 18S) gene suggested that M. mackini may be a basal eukaryote that is not closely related to other known protistan taxa (Carnegie et al. 2003). Mikrocytos mackini is the only described species in the genus. However, genetically divergent Mikrocytos-like protists has been reported from the Atlantic Ocean in Ostrea edulis from Atlantic Canada that had been imported into France for research purposes (Gagn et al. 2008), in Crassostrea gigas from the northern coast of the Yellow Sea, China (Wang et al. 2010), and in C. gigas from a single location (Lemmen's Inlet) on the west coast of Vancouver Island, British Columbia, Canada (Abbott et al. 2011). Although these three Mikrocytos-like isolates were identical to one another at a short fragment of the small-subunit ribosomal DNA (SSU rDNA or 18S) gene, molecular evidence suggests that these protists are not the same species as M. mackini (89% identical over the same short fragment). Additional research into the Mikrocytos-like protists is required to understand the taxonomic relationships between species of Mikrocytos and further genetic analysis is required to determine the phylogenetic position of these unique organisms (Abbott et al. 2012). However, Mikrocytos mackini is not related to other microcells in the genus Bonamia (e.g., B. ostreae, B. exitiosa, B. roughleyi and other Bonamia spp.) which are now known to be within the Haplosporidia (Carnegie and Cochennec-Laureau 2004, Abbott et al. 2012).

Geographic distribution

Protists positively identified as Mikrocytos mackini are known to occur on the Canadian west coast, probably ubiquitous throughout the Strait of Georgia and confined to other specific localities around Vancouver Island, and adjacent areas of the State of Washington, USA. Recently, M. mackini was detected in Humboldt Bay, California, USA and the DNA sequence of the complete internal transcribed spacer (ITS) region of the ribosomal DNA (i.e., ITS1-5.8S-ITS2 array) was 100% homologous with the published M. mackini sequence (Elston et al. 2012). Abbott et al. (2011) hypothesized that the total lack of genetic variation within M. mackini across the complete ITS1-5.8S-ITS2 region in over 70 samples collected throughout its known range on the south coast of British Columbia and Puget Sound, Washington, could be a result of a founder effect if the parasite had been introduced into the west coast of North America alongside Crassostrea gigas, which was imported from the east coast of Asia beginning around 1914 to about 1961. In the original description of M. mackini, Farley et al. (1988) indicated that a closely related candidate for inclusion within this species was found in Crassostrea gigas from Hawaii, USA in September 1972. Friedman et al. (2005) also reported a Mikrocytos-like protist from Ostrea lurida (=conchaphila) in San Francisco Bay, California, USA.

Host species

Crassostrea gigas, Ostrea lurida (=conchaphila) and Crassostrea sikamea; experimentally in Crassostrea virginica and Ostrea edulis. Laboratory bath exposure experiments clearly indicated that juvenile C. gigas were susceptible to infection while juvenile Panope abrupta (geoduck clams) (Bower et al. 2005) and mature Venerupis philippinarum (Manila clams about 28 mm in shell length) (Meyer et al. 2008) were resistant. A Mikrocytos-like protozoa was associated with mortality events of the clam Donax trunculus in France. However, this isolate was different from those in oysters with a DNA sequence of only 79 to 80% homology to M. mackini and 79% homology to the Mikrocytos-like parasite in C. gigas from China and in O. edulis from the Atlantic Ocean (Garcia et al. 2012).

Impact on the host

Focal intracellular infection of vesicular connective tissue cells which results in haemocyte infiltration and tissue necrosis. Severe infections appear to be restricted to older oysters (over 2 years) and mortalities (often about 30% of older oysters at low tide levels) occur predominantly in April and May after a 3-4 month period when temperatures are less than 10 C. Approximately 10% of infected C. gigas appear to recover. Crassostrea gigas seems to be more resistant to the disease than the other species of oysters challenged experimentally under laboratory and field conditions (Bower et al. 1997). In the State of Washington, USA, mortalities attributed to M. mackini have not been encountered.

Risk assessment and  risk management strategies in regard to the hazard presented by M. mackini were formulated during a workshop coordinated by R. E. Elston and conducted by the Pacific Shellfish Institute, Tacoma, Washington, USA in 2004. The workshop found that there was negligible risk of exporting M. mackini with live shellfish products in the states of Washington, Oregon and California.  However, the apparent increased pathogenicity of M. mackini and/or increased susceptibility to disease of oysters at a cool temperatures suggest that M. mackini poses a risk to oysters cultured in waters with extended periods (several months) at temperatures less than 10 C. The recent report of M. mackini in C. sikamea from Humboldt Bay, California revealed a higher prevalence of infection in oysters with a longer residence time in the bay and from locations with somewhat colder than typical winter seawater temperatures (Elston et al. 2012).

Diagnostic techniques

Gross Observations: Focal lesions (ulcerations, abscesses, pustules usually green in colour but can be yellow-brown or colourless) up to 5 mm in diameter, within the body wall, adductor muscle or on the surfaces of the labial palps or mantle. Often with a brown scar on the shell, adjacent to abscess on the mantle surface.

Figures 1 and 1a. Crassostrea gigas removed from shell and illustrating lesions (arrows) characteristic of Mikrocytos mackini when the microcell is most abundant in the vesicular connective tissue cells immediately surrounding the lesions. Crassostrea gigas

Figures 1 and 1a. Crassostrea gigas removed from shell and illustrating lesions (arrows) characteristic of Mikrocytos mackini when the microcell is most abundant in the vesicular connective tissue cells immediately surrounding the lesions.

Figure 1b. Three lesions (arrows) characteristic of M. mackini on the labial palps of C. gigas.

Figure 1b. Three lesions (arrows) characteristic of M. mackini on the labial palps of C. gigas.

Crassostrea gigas

Figure 2. Crassostrea gigas removed from shell and illustrating lesions (arrows) observed during later stages of Denman Island disease. Typically, Mikrocytos mackini can no longer be found in oysters at this advanced stage of the disease.

Figures 3. Ostrea edulis, with top valve removed, illustrating numerous lesions in the adductor muscle (arrow) caused by Mikrocytos mackini.

Figures 3. Ostrea edulis, with top valve removed, illustrating numerous lesions in the adductor muscle (arrow) caused by Mikrocytos mackini.

Figure 3a. Crassostrea gigas removed from shell and illustrating lesions in the adductor muscle (arrows) caused by M. mackini.

Figure 3a. Crassostrea gigas removed from shell and illustrating lesions in the adductor muscle (arrows) caused by M. mackini.

 

Figures 3b and 3c. Adductor muscles of C. gigas with cryptic lesions (3b, arrows) and very pronounced lesions (3c, arrows) caused by M. mackini.

Click any image for more details.

Figures 3b and 3c. Adductor muscles of C. gigas with cryptic lesions (3b, arrows) and very pronounced lesions (3c, arrows) caused by M. mackini.

Histology: High power (1000 oil immersion magnification) microscopic examination of vesicular connective tissue cells immediately adjacent to foci of intense haemocyte infiltration (lesions) for the presence of intracellular protozoa 2-3 m in diameter. This parasite has also been observed in muscle cells and occasionally in haemocytes within the lesions. The only other species initially included in the same genus but now known to be unrelated, Bonamia (=Microcytos) roughleyi which causes Australian winter disease in Saccostrea commercialis, differs from M. mackini by having a cytoplasmic vacuole. No such vacuole is found in either M. mackini or other Bonamia spp.

Figure 4. Histological section through a lesion caused by Mikrocytos mackini on the mantle of Crassostrea gigas. This intracellular protozoan (not visible at this magnification) usually occurs in the intact vesicular connective tissue cells immediately surrounding the periphery of the lesion (arrows). Haematoxylin and eosin stain.

Figure 4. Histological section through a lesion caused by Mikrocytos mackini on the mantle of Crassostrea gigas. This intracellular protozoan (not visible at this magnification) usually occurs in the intact vesicular connective tissue cells immediately surrounding the periphery of the lesion (arrows). Haematoxylin and eosin stain.

Figure 5. Many Mikrocytos mackini (arrows) within vesicular connective tissue cells adjacent to a lesion characterized by an accumulation of haemocytes and necrotic cells. Haematoxylin and eosin stain.

Figure 5. Many Mikrocytos mackini (arrows) within vesicular connective tissue cells adjacent to a lesion characterized by an accumulation of haemocytes and necrotic cells. Haematoxylin and eosin stain.

Figure 6. Oil immersion magnification (1000 magnification) of Mikrocytos mackini (arrows) within the cytoplasm of vesicular connective tissue cells of Crassostrea gigas. Haematoxylin and eosin stain.

Figure 6. Oil immersion magnification (1000 magnification) of Mikrocytos mackini (arrows) within the cytoplasm of vesicular connective tissue cells of Crassostrea gigas. Haematoxylin and eosin stain.

Figure 7. As for Fig. 6 but from a different specimen. Because of the small size of this parasite it is very difficult to visualise and photograph in histological preparations. Haematoxylin and eosin stain.

Figure 7. As for Fig. 6 but from a different Crassostrea gigas. Because of the small size of M. mackini, it is very difficult to visualise and photograph in histological preparations. Haematoxylin and eosin stain.

Figure 8. Mikrocytos mackini (A) within fibres of the adductor muscle of Crassostrea gigas. One M. mackini is located close to the nucleus (B) of a muscle cell. Haematoxylin and eosin stain.

Figure 8. Mikrocytos mackini (A) within fibres of the adductor muscle of Crassostrea gigas. One M. mackini is located close to the nucleus (B) of a muscle cell. Haematoxylin and eosin stain.

Tissue Imprints: Imprints of lesions are air dried, fixed and stained as for Bonamia ostreae in oyster tissue smears and examined using 1000 magnification (oil immersion) for the small microcells that are often observed free of the host cells. In such preparations, it is not possible to differentiate between M. mackini and Bonamia spp.

Figure 9. Mikrocytos mackini (arrows) among host cell debris in a tissue imprint from a lesion in the adductor muscle of a laboratory infected Crassostrea gigas. Hemacolor stain.

Figure 9. Mikrocytos mackini (arrows) among host cell debris in a tissue imprint from a lesion in the adductor muscle of a laboratory infected Crassostrea gigas. Hemacolor stain.

Electron Miscroscopy: Ultrastructural morphology differentiates M. mackini from Bonamia spp.; the nucleolus of M. mackini is located towards the centre of the nucleus while that of B. ostreae has an eccentric location and there are no mitochondria in M. mackini.

Figure 10. Electron micrograph of a Crassostrea gigas vesicular connective tissue cell containing Mikrocytos mackini (arrows). Uranyl acetate and lead citrate stain.

Figure 10. Electron micrograph of a Crassostrea gigas vesicular connective tissue cell containing Mikrocytos mackini (arrows). Uranyl acetate and lead citrate stain.

Figure 11. Mikrocytos mackini (arrows) each containing a nucleus with a pronounced nucleolus and lacking mitochondria. Uranyl acetate and lead citrate stain.

Figure 11. Mikrocytos mackini (arrows) each containing a nucleus with a pronounced nucleolus and lacking mitochondria. Uranyl acetate and lead citrate stain.

Detailed studies on the ultrastructure of M. mackini identified three morphological forms (Hine et al. 2001). The quiescent cells (QC) had a central round to ovoid nucleus, less than seven cisternae of inactive nuclear membrane-bound Golgi, few vesicles and lysosome-like bodies. They occurred in the vesicular connective tissue cells, haemocytes (hyalinocytes), adductor and heart myocytes and extracellularly. The vesicular cells (VC) contained many small coated and uncoated vesicles, lacked nuclear membrane-bound Golgi-like arrays and the nuclear membrane was sometimes dilated to form a cisternal chamber. They were rarely extracellular and usually occurred in adductor and heart myocytes, in close association with host cell mitochondria. The endosomal cells (EC) had a dilated nuclear membrane, a well developed anastomosing endoplasmic reticulum connected the nuclear and plasma membranes and endosomes were present in the cytoplasm. They occurred in the vesicular connective tissue cells, haemocytes (hyalinocytes), and extracellularly. Few organelles occurred in all forms of M. mackini and may be due to obligate parasitism and the utilization of host cell organelles, thus reducing the need for parasite organelles.

Figure 12. Proposed developmental cycle of Mikrocytos mackini indicating host cell type and host organelle affiliation for the three recognized morphological forms consisting of quiescent cell (QC), vesicular cell (VC) and edosomal cell (EC).

Figure 12. Proposed developmental cycle of Mikrocytos mackini indicating host cell type and host organelle affiliation for the three recognized morphological forms consisting of quiescent cell (QC), vesicular cell (VC) and edosomal cell (EC).

Immunological Assay: Hybridomas that produce monoclonal antibodies specific for M. mackini have been produced (S. M. Bower) and can be made available for the development of diagnostic tool(s) similar to that developed for Bonamia ostreae (ELISA, IFA).

DNA Probes: Polymerase chain reaction (PCR) and fluorescent in situ hybridization (FISH) assays were developed based on a 1457 base pair segment of the small-subunit ribosomal DNA (SSU rDNA or 18S) gene (GenBank accession number AF477623). The primers that were initially used to identify M. mackini DNA were shown to preferentially amplify various parasitic protistan SSU rDNA from metazoan tissues via PCR (Bower et al. 2004). A more specifically designed M. mackini PCR detected 3 to 4 times more M. mackini infections than standard histopathology (Carnegie et al. 2003). However, the PCR assay cross-reacted with the Mikrocytos-like protist from the Atlantic Ocean, Yellow Sea, and west coast of Vancouver Island (Gagn et al. 2008, Wang et al. 2010, and Abbott et al. 2011, respectively). Although the segment of  the Mikrocytos-like protist that was amplified represented a short portion (about 500 base pairs) of the 18S gene, it was surprisingly exactly the same (100%) in samples from O. edulis in the Atlantic Ocean and C. gigas from the Yellow Sea and west coast of Vancouver Island  (Gagn et al. 2008, Wang et al. 2010, Abbott et al. 2011). Sequencing a longer portion of rDNA including both the 18S gene and the more quickly evolving ITS regions would be more informative and recommended for future characterization of Mikrocytos sp. organisms (Abbott et al. 2011). Nevertheless, analysis of the short DNA sequence from the Mikrocytos-like protist was used to demonstrate differences with M. mackini. Subsequently, the entire length of the internal transcribed spacer regions (ITS1 and ITS2) and the intervening 5.8S gene of rDNA of M. mackini was sequenced (GenBank accession number HM563060) and found to contained regions of high divergence from the Mikrocytos-like protist from British Columbia (in ITS1 and ITS2) that could be exploited for differential molecular diagnostics (Abbott et al. 2011). This same gene region (i.e., the complete ITS1-5.8S-ITS2) was surprisingly homologous (100% identical) among numerous M. mackini isolates from throughout its known range (Abbott et al. 2011, Elston et al. 2012). A TaqMan qPCR assay targeting the ITS2-28S that is specific to M. mackini was developed and statistical analysis showed that a mid-body slice of oyster tissue was optimal for detecting the parasite (Lowe et al. 2012).

A digoxigenin-labelled DNA probe employed in an in situ hybridization assay (DIG-ISH), was used to reveal M. mackini in digestive gland tissues, an organ not previously known to be inhabited by this parasite (Meyer et al. 2005).

Figure 13. Consecutive sections of the same area of the digestive gland of an adult Crassostrea gigas infected with Mikrocytos mackini (dark spots on left). The section on the left was stained with a digoxigenin-labelled DNA probe (DIG-ISH) and revealed the parasite within the tubule at relatively low magnifications. Parasites were not discernable in similar tissues stained with haematoxylin and eosin stain (section on right) even when examined at high magnification (1000x - oil emersion objective).

Figure 13. Consecutive sections of the same area of the digestive gland of an adult Crassostrea gigas infected with Mikrocytos mackini (dark spots on left). The section on the left was stained with a digoxigenin-labelled DNA probe (DIG-ISH) and revealed the parasite within the tubule at relatively low magnifications. Parasites were not discernable in similar tissues stained with haematoxylin and eosin stain (section on right) even when examined at high magnification (1000x - oil emersion objective).

The in situ hybridization (ISH) probe for M. mackini cross-reacted with the Mikrocytos-like protist from the Atlantic Ocean and Yellow Sea (Gagn et al. 2008, Wang et al. 2010, respectively) but not with the Mikrocytos-like protist from San Francisco Bay (Friedman et al. 2005). Also, the ISH assay developed for the Mikrocytos-like protist was not specific such that the Mikrocytos-like probe hybridized to both M. mackini and the Mikrocytos-like protist (Gagn et al. 2008).

Methods of control

Oysters from infected areas (currently or historically) should not be moved to areas where Denman Island disease has not been recorded especially if the areas have a cooler water temperature profile. Within the southern half of British Columbia where the disease is known to occur, the effect of the disease on infected populations can be reduced to a manageable level by harvesting or moving large oysters to locations high in the intertidal zone prior to March and not planting oysters at lower tide levels before June (Quayle 1982, 1988). Oysters retained over a two-year oyster production cycle, within areas where the disease is active, can experience in the following spring increased mortalities and the development of obvious lesions (Fig. 2 above) that reduces marketability.

References

Abbott, C.L., S.R. Gilmore, G. Lowe, G. Meyer and S. Bower. 2011. Sequence homogeneity of internal transcribed spacer rDNA in Mikrocytos mackini and detection of Mikrocytos sp. in a new location. Diseases of Aquatic Organisms 93: 243–250.

Abbott, C.L., N. Corradi, G. Meyer, F. Burki, S.C. Johnson and P. Keeling. 2012. Multiple gene segments isolated by next-generation sequencing indicate extreme divergence of Mikrocytos mackini. Journal of Shellfish Research 31: 257. (Abstract).

Bower, S.M. 1988. Circumvention of mortalities caused by Denman Island Oyster Disease during mariculture of Pacific Oysters. American Fisheries Society Special Publication 18: 246-248.

Bower, S.M. 2003. Mikrocytosis (Mikrocytos mackini). Annual Reports of OIE Reference Laboratories and Collaborating Centres 2002: 403-405.

Bower, S.M. 2001. Hazards and risk management of Mikrocytos mackini in oysters. In: Rodgers, C.J. (eds), Proceedings of the OIE International Conference on Risk anaysis in aquatic animal health. World Organisation for Animal Health, Paris, pp. 164-166.

Bower, S.M. 2005. Mikrocytos mackini (microcell). In: Rohde, K. (ed.), Marine Parasitology. CSIRO Publishing, Collingwood, pp. 34-37.

Bower, S. M. and G. R. Meyer. 1999. Effects of cold water on limiting or exacerbating some oyster diseases. Journal of Shellfish Research 18: 296. (Abstract).

Bower, S. M., D. Hervio and G. R. Meyer. 1997. Infectivity of Mikrocytos mackini, the causative agent of Denman Island disease in Pacific oysters Crassostrea gigas, to various species of oysters. Diseases of Aquatic Organisms 29: 111-116.

Bower, S.M., R.B. Carnegie, B. Goh, S.R.M. Jones, G.J. Lowe and M.W.S. Mak. 2004. Preferential PCR amplification of parasitic protistan small subunit rDNA from metazoan tissues. The Journal of Eukaryotic Microbiology 51: 325-332.

Bower, S.M., K. Bate and G.R. Meyer. 2005. Susceptibility of juvenile Crassostrea gigas and resistance of Panope abrupta to Mikrocytos mackini. Journal of Invertebrate Pathology 88: 95-99.

Carnegie, R.B. and N. Cochennec-Laureau. 2004. Microcell parasites of oysters: recent insights and future trends. Aquatic Living Resources 17: 519-528.

Carnegie, R.B., G.R. Meyer, J. Blackbourn, N. Cochennec-Laureau, F.C.J. Berthe and S.M. Bower. 2003. Molecular detection of the oyster parasite Mikrocytos mackini and a preliminary phylogenetic analysis. Diseases of Aquatic Organisms 54: 219-227.

Elston, R.A. 1993. Infectious diseases of the Pacific oyster, Crassostrea gigas. Annual Review of Fish Diseases 3: 259-276.

Elston, R.A., J. Moore and C.L. Abbott. 2012. Denman Island disease (causative agent Mikrocytos mackini) in a new host, Kumamoto oysters Crassostrea sikamea. Diseases of Aquatic Organisms 102: 65-71.

Farley, C.A., P.H. Wolf and R.A. Elston. 1988. A long-term study of "microcell" disease in oysters with a description of a new genus, Mikrocytos (g.n.) and two new species Mikrocytos mackini (sp.n.) and Mikrocytos roughleyi (sp.n.). U.S. National Marine Fish Service Bulletin 86: 581-593.

Friedman, C.S., H.M. Brown, T.W. Ewing, F.J. Griffin and G.N. Cherr. 2005. Pilot study of the Olympia oyster Ostrea conchaphila in the San Francisco Bay estuary: description and distribution of diseases. Diseases of Aquatic Organisms 65: 1-8.

Garcia, C., I. Arzul, J.P. Joly, B. Guichard, B. Chollet, E. Omnes, C. Haond, M. Robert, C. Lupo and C. Francois. 2012. Mikrocytos like protozoans and the shellfish Donax trunculus mortality events in France. Journal of Shellfish Research 31: 273. (Abstract).

Gagn, N., N. Cochennec, M. Stephenson, S. S. McGladdery, G.R. Meyer and S.M. Bower. 2008. First report of a Mikrocytos-like parasite in European oysters Ostrea edulis from Canada after transport and quarantine in France. Diseases of Aquatic Organisms 80: 27-35.

Hervio, D., S. M. Bower and G. R. Meyer. 1995a. Life cycle, distribution and lack of host specificity of Mikrocytos mackini, the cause of Denman Island disease in Pacific oysters, Crassostrea gigas. Journal of Shellfish Research 14: 228. (Abstract)

Hervio, D., G. R. Meyer, S. M. Bower and R. D. Adlard. 1995b. Development of specific molecular probes for serological and PCR assays for the identification and diagnosis of Mikrocytos mackini, the cause of Denman Island disease in the Pacific oyster Crassostrea gigas. Journal of Shellfish Research 14: 268. (Abstract).

Hervio, D., S.M. Bower and G.R. Meyer. 1996. Detection, isolation and experimental transmission of Mikrocytos mackini, a microcell parasite of Pacific oysters Crassostrea gigas (Thunberg). Journal of Invertebrate Pathology 67: 72-79.

Hine, P.M., S.M. Bower, G.R. Meyer, N. Cochennec-Laureau and F.C.J. Berthe. 2001. Ultrastructure of Mikrocytos mackini, the cause of Denman Island disease in oysters Crassostrea spp. and Ostrea spp. in British Columbia, Canada. Diseases of Aquatic Organisms 45: 215-227.

Joly, J.-P., S.M. Bower and G.R. Meyer. 2001. A simple technique to concentrate the protozoan Mikrocytos mackini, causative agent of Denman Island disease in oysters. The Journal of Parasitology 87: 432-434.

Lowe, G., G. Meyer, M.G. Abbott, S.C. Johnson and C.L. Abbott. 2012. Development of a q-PCR assay to detect Mikrocytos mackini and assessment of optimum tissue for diagnostic testing. Journal of Shellfish Research 31: 315. (Abstract).

Meyer, G.R., S.M. Bower and R.B. Carnegie. 2005. Sensitivity of a digoxigenin-labelled DNA probe in detecting Mikrocytos mackini, causative agent of Denman Island disease (mikrocytosis) in oysters. Journal of Invertebrate Pathology 88: 89-94.

Meyer, G.R., S.M. Bower, G. Lowe and S. Davies. 2008. Resistance of the Manila clam (Venerupis philippinarum) to infection with Mikrocytos mackini. Journal of Invertebrate Pathology 98: 54-57.

Quayle, D.B. 1961. Denman Island disease and mortality, 1960. Fisheries Research Board of Canada Manuscript Report 713. Ottawa.

Quayle, D.B. 1969. Pacific oyster culture in British Columbia. Fisheries Research Board of Canada Bulletin 169: 192 p. (For information on Denman disease see pages 166-168).

Quayle, D.B. 1982. Denman Island oyster disease 1960-1980. British Columbia Shellfish Mariculture Newsletter 2(2): 1-5. (Victoria, Canada).

Quayle, D.B. 1988. Pacific oyster culture in British Columbia. Canadian Bulletin of Fisheries and Aquatic Sciences 218: 241 p. (For information on Denman disease see pages 115-117).

Wang, Z., Y. Liang and X. Lu. 2010. Use of histopathology, PCR and in situ hybridization methods to detect the parasite Mikrocytos sp. in Pacific oyster Crassostrea gigas from the northern coast of the Yellow Sea, China. Aquatic Living Resources 23: 125-130.

Citation Information

Bower, S.M. (2013): Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish: Mikrocytos mackini (Denman Island Disease) of Oysters.


URL: ftp://ftpdeviosiis.ent.dfo-mpo.gc.ca/science/species-especes/shellfish-coquillages/diseases-maladies/pages/mikmacoy-eng.htm

Date last revised: March 2013.
Comments to Susan Bower