FISHERY BULLETIN: VOL. 86, NO. 3 



to be identical to the Denman Island microcell 

 organisms. 



VCT while B. ostreae is primarily a disease of 

 hemocytes. 



Microcell Infections in Ostrea edulis 



Microcell infections were first seen in 0. edulis 

 in moribund oysters which had been transferred 

 from Milford, CT to Chincoteague Bay, VA in 1962. 

 Two animals from the FK sample had developed 

 clinical manifestations of the disease. Other cases 

 appeared in animals transferred from Milford to 

 California, and Milford to Oxford. Morphology of the 

 infectious organisms was identical in all of these 

 episodes and the histopathology always consisted of 

 acute inflammatory infiltration and systemic in- 

 volvement. All episodes were associated with move- 

 ment of oyster stocks originating in Milford, and all 

 experienced severe mortality. No differences were 

 noted between any of the 0. edulis epizootics in 

 regard to morphology of the organisms. Compari- 

 son of the American 0. edulis infections vdth tissues 

 of French oysters experiencing B. ostreae infections 

 (Pichot et al. 1979; Balouet et al. 1983) revealed no 

 morphologic or histologic differences at the light or 

 electron microscope level. Indeed, ultrastructural 

 comparisons demonstrate close similarities. Size 

 comparisons of organisms are identical and the 

 nucleus contains a peripheral nucleolus, and iden- 

 tical haplosporosome-like organelles are present in 

 the cytoplasm. The major difference is in epizootic 

 occurrences. The French epizootic occurred in 

 natural or feral populations of European flat 

 oysters. Since introduction of oysters to French sites 

 from locations outside of France was a common 

 event in the past, the source of the index case may 

 have originated from an introduction of oysters from 

 Elkhorn Slough, CA in the late 1970s (Elston et al. 

 1986). Contagious spread (Tige et al. 1981) is well 

 documented in many locations in France and also 

 the Netherlands. With the exception of the estab- 

 lished breeding populations of flat oysters in the cen- 

 tral Maine coast region, no natural or feral popu- 

 lations of 0. edulis exist in the United States. The 

 State of Maine carefully controls imports into the 

 state; the disease has not been established in this 

 population. The discovery of microcell infections in 

 0. lurida in Oregon suggests that this may be a 

 naturally occurring disease in that species. Infec- 

 tion intensity and prevalences suggest that some 

 animals may die from the disease. The disease ap- 

 pears to be enzootic in the Oregon location. The lack 

 of ultrastructiiral studies prevents close comparison 

 of the 0. lurida disease with the 0. edulis disease. 

 However, the disease in 0. lurida tended to infect 



CONCLUSIONS 



There is a complex of oyster diseases caused by 

 a group of protistan parasites of several species. 

 These small intracellular and extracellular organ- 

 isms designated originally as microcells have been 

 found in association with serious disease in two 

 species of Crassostrea and two species of Ostrea. 

 It appears that the disease in C. gigas and S. com- 

 mercialis, whOe exhibiting some similarities in types 

 of lesions, are probably caused by different species 

 of microcell type parasites. 



A new genus, Mikrocytos g. n., and two new 

 species have been described for the organisms caus- 

 ing disease in oysters: Mikrocytos mackini sp. n. in 

 C. gigas from British Columbia, Canada, and Mikro- 

 cytos roughleyi sp. n. in S. commercialis from 

 Australia. 



Disease that has struck 0. edulis in France is iden- 

 tical to the microcell disease seen in 0. edulis in 

 three episodes in the United States. The organism 

 causing the disease in 0. edulis is Bonamia ostrea£ 

 and is clearly different from the microcell organism 

 found in C. gigas in British Columbia and Hawaii. 

 Finally, additional ultrastructural studies are needed 

 for more complete characterization of the organisms 

 from 0. lurida and S. commercialis. 



ACKNOWLEDGMENTS 



We thank Cecelia Smith, Dorothy Howard, and 

 Gretchen Roe for preparation of histologic ma- 

 terials; Jane Wade for preparation of the ultra- 

 structural material; and Muriel McNeils, Karen 

 Hayman, and Jane Swann for manuscript prepara- 

 tion. The senior author would like to acknowledge 

 the help of the late John Mackin for his expert ad- 

 vice through the years; Daniel B. Quayle and Neil 

 Bourne for assistance with samples of oysters from 

 British Columbia; Fred Kern for allowing us to use 

 his Hawaiian material; and Albert K. Sparks and 

 Inke Sunila for critical review of the manuscript 

 without implying agreement with interpretations 

 herein. Partial support from the Department of 

 Energy under Contract DE-AC06-76RLO 1830 to 

 Battelle Memorial Institute is acknowledged. 



LITERATURE CITED 



Balouet, G., M. Poder, and A. Cahour. 



1983. Haemocytic parasitosis: morphology and pathology of 



592 



