D. Schulte and coworkers' Report ("Unprecedented restoration of a native oyster metapopulation," 28 August 2009, p. 1124, published online 30 July 2009) and E. Stokstad's News of the Week story "Oysters booming on new reefs, but can they survive disease?" (31 July, p. 525), both downplay the impact of disease on Crassostrea virginica in Chesapeake Bay. The impression they convey is inaccurate. Far from being a "red herring," disease continues to profoundly influence oyster population dynamics in the region.
Protistan parasites Haplosporidium nelsoni, which causes MSX disease, and Perkinsus marinus, which causes dermo, thrive today in Chesapeake Bay. The maximum annual prevalence of H. nelsoni in sentinel oysters monitored by the VIMS Shellfish Pathology Laboratory increased from an average of 54% from the 1960s through 1980s to 66% in the 1990s, and 85% over the past 9 years. Annual P. marinus levels in wild oyster beds in Virginia from 2006 through 2008 were the 5th-, 7th-, and 4th-highest recorded in 20 years, exceeded only during the drought of 1999 to 2002. Annual disease-related mortality is substantial, reducing both the longevity of oysters in populations and densities on reefs (1). Contrary to comments by Romuald Lipcius in Stokstad's article, there is no evidence that, genetic differences aside, healthy adult oysters in good habitats resist these pathogens more successfully than oysters in other populations. In the late 1950s H. nelsoni killed millions of oysters from healthy populations in both Delaware Bay and lower Chesapeake Bay, and this mortality continued unabated for decades (2). During the prolonged drought of the late 1980s, P. marinus increased dramatically in abundance and expanded its range into upper Chesapeake Bay where it caused high mortality in healthy oyster populations (3).
The silver lining is that intensified disease may increase selection for disease resistance, the nature of which is at least partly genetic (4, 5). Susceptible oysters have a limited opportunity to reproduce, theoretically putting more-resistant oysters, capable of surviving several years of disease before succumbing, at a selective advantage. Accumulation of older but only lightly parasitized oysters in disease-intense waters (6) indicates that this dynamic may be at work, and maximizing the potential for these older survivors to reproduce underlies the rationale for sanctuaries from harvest. Unfortunately, susceptible oysters persist in waters of salinity unfavorable to the parasites (<15 parts per thousand), with their reproductive contributions likely slowing the advance of resistance (1). Amelioration of oyster disease in Chesapeake Bay, and restoration of oysters in the face of disease, will take time.
Eugene M. Burreson and Ryan B. Carnegie
Virginia Institute of Marine Science, Gloucester Point, VA 23062, USA.
References
1. R. Mann, M. Southworth, J. M. Harding, J. A. Wesson, J. Shellfish Res. 28, 193 (2009).
2. H. H. Haskin, J. D. Andrews, Am. Fish. Soc. Spec. Pub. 18, 5 (1988).
3. E. M. Burreson, L. M. Ragone Calvo, J. Shellfish Res. 15, 17 (1996).
4. H. H. Haskin, S. E. Ford, Mar. Fish. Rev. 41, 54 (1979).
5. L. M. Ragone Calvo, G. W. Calvo, E. M. Burreson, Aquaculture 220, 69 (2003).
6. V. G. Encomio, S. M. Stickler, S. K. Allen Jr., F.-L. Chu, J. Shellfish Res. 24, 143 (2005).
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