INVITRO INTERACTIONS BETWEEN BIVALVE HEMOCYTES AND THE OYSTER PATHOGEN HAPLOSPORIDIUM-NELSONI (MSX)

Resistance to disease caused by the oyster pathogen Haplosporidium nelsoni (MSX) has developed in nature and through selective breeding, however, examination of tissue slides shows no evidence that phagocytic cells are involved. To investigate this phenomenon further, we quantified in vitro phagocytosis of plasmodial stages of H. nelsoni by hemocytes from 2 oyster and 1 mussel species. Our results show that hemocytes from oysters Crassostrea virginica, whether selected or unselected for resistance to MSX disease, did not ingest plasmodia unless the parasites were damaged or killed. Time-lapse photography suggested that granular hemocytes retreated rapidly after initial contact with living plasmodia and that nearby agranular hemocytes showed little movement. Hemocytes from the Pacific oyster, Crassostrea gigas, which is resistant to diseases caused by other oyster pathogens and is proposed for introduction to the east coast of the United States, also failed to phagocytose living plasmodia. In contrast, hemocytes from the ribbed mussel, Geukensia demissa, a species that co-occurs with C. virginica in some habitats but is not known to become infected by H. nelsoni, rapidly phagocytosed plasmodia. Our results suggest that H. nelsoni may produce a substance inhibitory to hemocytes but that disease resistance has developed even though host hemocytes fail to attack the parasite successfully.