Investigation of the stress response, summer mortality and disease resistance of oysters, Crassostrea spp

The ability to mount a stress response is often essential for an organism's survival, especially for oysters inhabiting dynamic and stressful environments. We have characterized the response of Pacific oysters, Crassostrea gigas, to heat shock (HS), hypoosmotic acclimation and disease. Pacific oysters synthesized heat shock proteins (HSP) in the 70 kD family and exhibited prolonged induced thermotolerance (ITT, at least 3 wk) after exposure to heat shock. The temperature needed to induce a stress response appears to be related to the upper thermal limit of the oyster (43.5-44 C) not on the magnitude of thermal shock. Despite an increase in thermal tolerance after HS, we observed a significant reduction in chemotaxis and percent phagocytosis in oysters after HS relative to those without a heat treatment. Hypo-osmotic acclimation delayed HSP production and tolerance to lethal temperatures. Oysters challenged with Nocardia synthesized HSPs in a pattern similar to control animals. However, the degree of ITT was reduced in oysters with nocardiosis. Although reproductive stress does not alter the stress response of Pacific oysters, the chemotactic ability of hemocytes from gravid oysters was significantly reduced as compared with nonreproductive animals (p < 0.001). The Eastern oyster, C. virginica, produced HSPs after heat shock a similar manner as the Pacific oyster. However, the magnitude of ITT was reduced relative to that of Pacific oysters held under the same culture and experimental conditions.