A mass mortality of the deep sea scallop, Plaeopeeten magellanieus, which occurred in the autumn and winter of 1979-80, in Narragansett Bay, Rhode Island was studied. Grossly the animals possessed greyish, flaccid adductor muscles and histologically they showed myodegeneration. Eighty-eight per cent of the 34 animals examined were infected with intracellular prokaryotes on the gills, plicate membranes and other epithelial surfaces of the body. The morphology of this prokaryotic organism is suggestive of rickettsia. Heavy infection was positively correlated with extensive myodegeneration.

A rickettsia-like organism from the gills and plicate membrane of the sea scallop, Placopecten magellanicus, was prevalent in near-shore Rhode Island scallop populations such as Block Island Sound and Narragansett Bay, but relatively scarce in Georges Bank samples. Fifty-three per cent of scallops transplanted in cages to Narragansett Bay became infected with the rickettsiae in 2-5-3-5 months. Scallops that were transferred to aquaria with Narragansett Bay water were 100% infected with rickettsiae in 5 months or less. There is some evidence that heavy infection of P. magellanicus inhibits swimming response and that rickettsial infection may contribute indirectly to mortalities by reducing scallop mobility and avoidance of predators. The organism was successfully cultured in gill organ culture and by direct injection of infected tissue homogenate, but could not be grown on artificial media or in yolk sac of embryonated hens' eggs. Other bivalve species could not be infected with the rickettsia of P. magellanicus through the water column or by direct injection.

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Histopathological studies on the cirripede crustacean, Balanus eburneus, at light and electron microscopic levels indicated that the chitin-inhibiting insecticide, diflubenzuron, caused similar disruption of the exoskeleton as observed in insects. Under the light microscope, globular particles were present within the chitinous layers of the cuticle, and these particles appeared electron dense and pleomorphic at the ultrastructural level. The cytoplasm of the cuticle-secreting epidermal cells appeared more dense and showed at least a five-fold increase in multivesicular bodies, which possessed electron dense cores. Barnacles exposed to diflubenzuron for 10 days or longer at 750 and 1,000 ppb were delayed in the premolt phase of cuticle secretion.