HOST-PARASITE INTERACTIONS AMONG BROADLY DISTRIBUTED POPULATIONS OF THE EASTERN OYSTER CRASSOSTREA-VIRGINICA AND THE PROTOZOAN PERKINSUS-MARINAS

The protozoan oyster parasite Perkinsus marinus causes extensive morta lity in eastern oyster (Crassostrea virginica) populations during summ er and fall across much of the oyster's distribution. Despite more tha n 40 yr of research on this particular parasite, no study has unequivo cally demonstrated a genetic basis for host resistance to P. marinus n or has it been determined whether or not there are races of Fl marinus that vary in virulence. Using recently developed techniques to cultur e P. marinus in vitro, we examined the resistance of 4 genetically dis tinct oyster populations that had different natural histories of expos ure to P. marinus and the virulence of 4 geographically distinct isola tes of P. marinus. Offspring were produced from each oyster population and reared in a common environment, then exposed to each isolate of P . marinus. Oysters showed levels of resistance roughly corresponding t o the duration parental populations had been exposed to P. marinus (Te xas > Virginia > New Jersey = Maine), indicating that those population s which have been exposed to P. marinus for more than 40 yr have devel oped some resistance. Parasites isolated from the Atlantic coast (Mobj ack Bay, VA and Delaware Bay, NJ, USA) produced heavier infections tha n those isolated from the Gulf of Mexico coast (Barataria Bay, LA and South Bay Laguna Madre, TX, USA), indicating that Atlantic isolates we re more virulent than Gulf isolates. These data indicate that resistan t races of the eastern oyster exist, and imply the existence of virule nt parasite races. No statistically significant interaction was detect ed between oyster populations and parasite isolates. Relative infectio n intensities among oyster populations remained more or less constant across parasite isolates and vice versa. The lack of a significant int eraction between host populations and parasite isolates indicated that mechanisms of resistance and virulence were general, not race-specifi c.