Document Type



Virginia Institute of Marine Science

Publication Date



Proceedings of the National Shellfisheries Association



First Page


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Intensive epizootics in Crassostrea virginica caused by Minchinia nelsoni (MSX) show no signs of abating in lower Chesapeake Bay. Prevalences of the pathogen have commonly exceeded 50% in susceptible stocks during the first year of exposure; mortalities of 50 to 70% occurred during the first year and slightly lower losses in succeeding years. Disease activity increased in isolated lots of oysters from 1963 to 1966 during a drought period with high salinities. Native and planted oysters were extremely scarce in the lower Chesapeake Bay hence density of populations appears not to be important for disease activity. Seasonal patterns of death rates have remained stable through eight years of observations but morbidity has occurred earlier in drought years. These patterns are influenced by time of import of unexposed susceptible oysters to areas of disease prevalence.

Laboratory-bred progeny from susceptible (unexposed) and selected (by MSX) parents were held to marketable size in areas where MSX is intensively active without serious losses (10 to 20% annually). Early exposure appears to be important for subsequent survival of large oysters; hence, acquired resistance is postulated.

M. nelsoni has not produced epizootics of oysters in the high-salinity environment of the Seaside of the Eastern Shore of Virginia; M. costalis (SSO) regularly causes a sharp mortality there in May-June each year. Since these congeneric sympatric pathogens are very similar morphologically, it is postulated that their annual life cycles are similar, with June the period of sporulation. MSX appears to be highly virulent since death of the host usually occurs before sporulation which is rare. A hypothesis on the origin of a virulent strain which arose in Delaware Bay in 1957 and appeared to spread to Chesapeake Bay in 1959 is based on seed oyster transplantations between the areas.