The harmful dinoflagellate Prorocentrum minimum has different effects upon various species of grazing bivalves, and these effects also vary with life-history stage.Possible effects of this dinoflagellate upon mussels have not been reported; therefore, experiments exposing adult blue mussels, Mytilus edulis, to P. minimum were conducted. Mussels were exposed to cultures of toxic P. minimum or benign Rhodomonas sp. in glass aquaria. After a short period of acclimation, samples were collected on day 0 (before the exposure) and after 3, 6, and 9 days of continuousexposure experiment. Hemolymph was extracted for flow-cytometric analyses of hemocyte, immune-response functions, and soft tissues were excised for histopathology.Mussels responded to P. minimum exposure with diapedesis of hemocytes into the intestine, presumably to isolate P. minimum cells within the gut, thereby minimizing damage to other tissues. This immune response appeared to have been sustained throughout the 9-day exposure period, as circulating hemocytes retained hematological and functional properties. Bacteria proliferated in the intestines of the P. minimumexposed mussels. Hemocytes within the intestine appeared to be either overwhelmed by the large number of bacteria or fully occupied in the encapsulating response to P. minimum cells; when hemocytes reached the intestine lumina, they underwent apoptosis and bacterial degradation. This experiment demonstrated that M. edulis is affected by ingestion of toxic P. minimum; however, the specific responses observed in the blue mussel differed from those reported for other bivalve species. This finding highlights the need to study effects of HABs on different bivalve species, rather than inferring that results from one species reflect the exposure responses of all bivalves.

No abstract

The harmful dinoflagellate Prorocentrum minimum has different effects upon various species of grazing bivalves, and these effects also vary with life-history stage.Possible effects of this dinoflagellate upon mussels have not been reported; therefore, experiments exposing adult blue mussels, Mytilus edulis, to P. minimum were conducted. Mussels were exposed to cultures of toxic P. minimum or benign Rhodomonas sp. in glass aquaria. After a short period of acclimation, samples were collected on day 0 (before the exposure) and after 3, 6, and 9 days of continuousexposure experiment. Hemolymph was extracted for flow-cytometric analyses of hemocyte, immune-response functions, and soft tissues were excised for histopathology.Mussels responded to P. minimum exposure with diapedesis of hemocytes into the intestine, presumably to isolate P. minimum cells within the gut, thereby minimizing damage to other tissues. This immune response appeared to have been sustained throughout the 9-day exposure period, as circulating hemocytes retained hematological and functional properties. Bacteria proliferated in the intestines of the P. minimumexposed mussels. Hemocytes within the intestine appeared to be either overwhelmed by the large number of bacteria or fully occupied in the encapsulating response to P. minimum cells; when hemocytes reached the intestine lumina, they underwent apoptosis and bacterial degradation. This experiment demonstrated that M. edulis is affected by ingestion of toxic P. minimum; however, the specific responses observed in the blue mussel differed from those reported for other bivalve species. This finding highlights the need to study effects of HABs on different bivalve species, rather than inferring that results from one species reflect the exposure responses of all bivalves.

No abstract

Apoptosis, or programmed cell death, has been reported as being pivotal in infectious diseases of different organisms. The effects of apoptosis on the progression and transmission of the protistan parasites Perkinsus marinus and Haplosporidium nelsoni in the eastern oyster Crassostrea virginica were studied. Oysters were diagnosed for their respective infections by standard methods, and apoptosis was detected using in situ hybridization to detect DNA fragments by end labeling on paraffin sections. A digoxigenin nucleotide probe was used to label the 200 bp fragment produced by apoptosis and detected immunohistochemically using an antidigoxigenin peroxidase conjugate. The probe/DNA fragment complex was stained with a peroxidase substrate and tissues were counterstained with methyl green. Uninfected oysters had large numbers of apoptotic hemocytes present in the connective tissue underlying the stomach, gill, and mantle epithelia, whereas oysters infected with P. marinus had a reduced number of apoptotic hemocytes. The parasite may prevent hemocyte apoptosis in order to yield a greater number of hemocytes in which to house itself. Large numbers of P. marinus cells in some infected oysters were eliminated via apoptosis in the stomach epithelia, disabling the spread of infectious particles through seawater. The oysters infected with H. nelsoni also had reduced numbers of apoptotic hemocytes, while part of the vesicular connective tissue cells were apoptotic. H. nelsoni plasmodia were eliminated via apoptosis in some oysters. Apoptosis may enhance progression and prevent transmission of infectious oyster diseases. KEY WORDS: Apoptosis · Haplosporidium nelsoni · Perkinsus marinus · In situ hybridizationResale or republication not permitted without written consent of the publisher