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Figure 1. The Delaware Bay oyster population consists of three overlapping regions roughly defined by salinity regime: upper (UB) = 0 to 15 ppt, middle (MB) = 10 to 20 ppt, lower (LB) = 15 to 30 ppt. Population and disease characteristics generally increase or decrease along this gradient. Disease refugia potentially occur in lower salinity regions where reproductive output is generally low. Most of the oyster population exists in the middle region, but oysters also exist in the lower salinity portions of the tributaries.

In 1957 a new and highly lethal parasite called Haplosporidium nelsoni or MSX began killing oysters (Crassostrea virginica ) in Delaware Bay. Shortly thereafter, we noted that the natural population of oysters in the Bay had become somewhat resistant to MSX disease. The distribution of both oysters and parasites (including a second oyster parasite, Perkinsus marinus or Dermo ) is strongly influenced by salinity (Fig. 1), so many oysters were protected from continuing selective mortality by residing in the upper, low-salinity portion of the Bay.

Figure 2. Prevalence of Haplosporidium nelsoni (MSX) infections in oysters from lower Delaware Bay. Note the sharp decline after 1987.

The motivation for the study stems from a subsequent episode in Delaware Bay that occurred in 1984-86 in which a widespread epizootic of MSX disease. The event was associated with drought that allowed H. nelsoni to move into low-salinity regions of the Bay that had previously been a refuge from disease. About 70% of the oysters in this former refuge were killed. After this episode, the prevalence of MSX infections in native oysters declined dramatically (Fig. 2), implying that the oysters that repopulated Bay after 1984/86 event were dominated by MSX-disease resistant individuals and that the event increased the resistance of the general oyster population in Delaware Bay.

1. Can environmentally modulated selection (i.e., the drought) produce rapid genetic changes such as that seen in Delaware Bay in 1984 -1986 or is it necessary to invoke a sweepstakes event, in which only a small number of highly selected parents were reproductively successful?


2. How much temporal and spatial variability does exist in the number of parents that successfully produce offspring?


3. Do the very low-salinity regions of the upper bay and the tributary rivers refuge areas harbor oysters that are genetically different from oysters in high disease areas and, if so, what mechanism(s) allow how the refugia to persist?


4. Can we use circulation and other models, knowledge of oyster larval behavior, and genetic information to help determine the origin (including potential refugia) of larvae that set in different regions of the Bay?


5. How does the oyster-disease interaction respond to climate change and how does this change the overall genetic structure of the host population?

• Identity and map MSX-disease resistant genes
• Identify possible phenotypic and genotypic differences in oysters from putative refugia and high-disease areas
• Determine mechanisms that allow refugia to exist
• Identify spatial and temporal differences in the number of parents contributing to spat set in different regions of Delaware Bay

• Integrate genetic and population processes
• Delaware Bay circulation model
• Couple larval and circulation models

An integral part of the program is providing Research Experience for Undergraduates (REU).