In the late 1980's juvenile oysters, Crassostrea virginica, spawned and cultured in New England and New York, began experiencing up to nearly 100% mortalities in some batches of juveniles. The cause of these mortalities was not ascertained immediately, but examination of dead and dying oysters did not reveal a previously recognized disease syndrome. Early studies showed that it was not an environmental or genetic problem, thus we hypothesized that a new, transmissible disease agent caused the observed mortality. This was verified under laboratory conditions where the disease was readily transmissible. Transmission was enhanced by warm water temperatures, 22–26 °C, and salinities of 18–30 ppt. Also, the infectious agent was filterable and sensitive to erythromycin, supporting the hypothesis that the causative agent may be a protistan parasite in the 2–6 μm size range. No evidence to support a viral or bacterial etiology was found.

A description is provided of the anomalous conchiolin deposits which are formed by Pinctada maxima and which are associated with unusual mortalities. Comparisons are made with brown ring disease found in Ruditapes philippinarum and juvenile Crassostrea virginica. In P. maxima, the deposits are not organized into a ring but rather are broad-based and result in retraction of the mantle with the deposits lying outside the edge of the mantle. Vibrio sp. have been implicated in causing the diseases of P. maximaand R. philippinarum whereas the etiological agent of the disease in C. virginica is unknown. It is suggested that the coccoid bodies formed in the mantle of C. virginica, but not in affected P. maxima and R. philippinarum, are sequestered portions of cytoplasm formed as a result autophagocytosis. Stimuli which could be responsible for inducing sequestration are discussed. The ultrastructure of the presumptive autophagosomes is described and compared to similar bodies found in C. gigas infected with a herpes-like virus.