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Ryan B. Carnegie and Eugene M. Burreson Department of Environmental and Aquatic Animal Health Virginia Institute of Marine Science Gametogenesis and Spawning.

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Presentation on theme: "Ryan B. Carnegie and Eugene M. Burreson Department of Environmental and Aquatic Animal Health Virginia Institute of Marine Science Gametogenesis and Spawning."— Presentation transcript:

1 Ryan B. Carnegie and Eugene M. Burreson Department of Environmental and Aquatic Animal Health Virginia Institute of Marine Science Gametogenesis and Spawning of Crassostrea virginica from Disease-Intense Waters of Virginia, USA

2 Hasn’t Someone Looked At This Already?  Major effects of MSX disease on fecundity, condition (e.g., Barber et al. 1988)  Gonadal development, condition reduced by only heavier Perkinsus marinus infections (Dittman et al. 2001)  Oyster with lighter P. marinus infections may “protect” gametogenesis by shunting energy from growth (Kennedy et al. 1995) Perkinsus marinus infection Haplosporidium nelsoni infection

3 Disease Considered a Primary Obstacle to Restoration “...unless these diseases can be substantially controlled -- and no evidence suggests they can -- the outlook for C. virginica is bleak.” C. Ronald Franks, former MD Secretary of Natural Resources “Until we get an organism that beats the disease, we’re not going to have any success, no matter how much money we throw at it.” Robert Johnson, VA seafood executive, November 2008

4 Natural Resistance in a Dual-Disease Environment Bars = 1 SEM

5 No Simple Increase in Disease with Size/Age Perkinsus marinus Haplosporidium nelsoni

6 DISEASE IN VIRGINIA OYSTER POPULATIONS: A MODEL PARASITE IMPACT, OYSTER MORTALITY OYSTER SIZE/AGE MSX DERMO

7 Are Oysters Too Diseased to Reproduce?  Monthly sampling:  Sandy Point, Great Wicomico River: Apr-Nov 2007, Feb & Apr 2008  Broad Creek, Rappahannock River: May-Nov 2007, Mar-Oct 2008  Lynnhaven River: Apr-Oct 2008  Mockhorn Channel: Apr-Oct 2008  Wild oysters, four size bins (each n = 25)  100 mm  Pathology (RFTM) and histology  Gonadal staging  Condition indices  Gonadal area indices (forthcoming)

8 Reproductive Stages: Sandy Point, GWR, 2007 < 50 mm mm mm

9 Reproductive Stages: Broad Creek, Rapp. River, 2007 < 50 mm mm mm > 100 mm

10 Gametogenesis Largely Precedes the Dermo Peak “Serious” Perkinsus marinus Infections Reproductive Stage Sandy Point, mm, 2007

11 Gametogenesis Largely Precedes the Dermo Peak Reproductive Stage “Serious” Perkinsus marinus Infections Broad Creek, > 100 mm, 2007

12 Few Infections are Intense Enough to Arrest Gametogenesis  Gametogenesis and spawning abolished by disease in a maximum of 8.3% of Broad Creek oysters  Not observed at Sandy Point  Even “seriously” infected oysters usually produced gametes and spawned Heavy dual infection, Broad Creek, August Moderate-Heavy Perkinsus marinus, Broad Creek, July

13 Is Reproductive Output Diminished, if Not Abolished, by Disease?  Gonadal area indices yet to be analyzed  Condition indices support earlier observations that only heavier infections depress condition (Dittman et al. 2001)  CI in rare to light infections not significantly different from CIs in oysters appearing to be parasite-free  In more intense Perkinsus marinus infections, CI depression increases with intensity:  Light-moderate: Sandy Point 27%, Broad Creek 37%  Moderate: Sandy Point 33%, Broad Creek 47%  Moderate-Heavy: Sandy Point 41%, Broad Creek 66%  Heavy: Sandy Point 67%, Broad Creek 57%  Very Heavy: Sandy Point 100% Even rare infections H. nelsoni frequently depress condition, but H. nelsoni is not very prevalent

14 What Proportion of Oysters Were Impacted by Disease in 2007?  Consider that some infections do abolish reproduction  Assume P. marinus infections of moderate or greater intensity (Dittman et al. 2001), and any H. nelsoni infections, significantly affect reproductive physiology, reducing reproductive output A substantial reproductive contribution should be expected from oysters in natural beds in disease-enzootic waters Note too that larval supply appears not to be limiting (Hare et al. 2006; Southworth et al. 2008) -- so we should be skeptical that broodstock is

15 Perspective  Abundance of oysters in waters of very high disease underscores the point: disease is not the primary agent limiting oyster restoration Mockhorn Channel, VA Lynnhaven River, VA What are most important among the other factors?

16 Consider: Habitat and Substrate Availability are Keys  Exponential decay of settlement at newly constructed reefs a typical pattern (Southworth et al. 2008); best explained by substrate reduction/deterioration  Oysters are limited by high rates of sediment deposition  Smothering, settlement substrate unavailability  An excessively depositional environment is a fundamental problem, and destruction of the three dimensional reef structure may be its primary cause  Planing of reefs associated with harvesting (DeAlteris 1988; Rothschild et al. 1994; Hargis 1999; Hargis and Haven 1999)  Reduction in flow rates associated with smaller, flatter, deeper subtidal reefs may decrease growth rates (as well as oyster condition), and increase deposition (Lenihan 1999)

17 Moving Forward  Restore focus to habitat and substrate, away from broodstock (abundance, genetics, etc.)  Design new reefs to maximize flows (  deposition,  growth) -- recognizing the positive benefits for recruitment and shell budgets  Keep thinking about sanctuaries  End the physical destruction of reefs  “Landing strips” (E. North presentations)  Increase reproductive contributions from large, resistant survivors  Positive contributions of larger oysters to shell budgets  Reduce impacts of fishery selection?  Focus efforts in areas of peak historical abundance despite disease

18 Acknowledgments  Rita Crockett, Susan Denny, Nancy Stokes, and other VIMS Shellfish Pathology Laboratory staff  VIMS Eastern Shore Laboratory staff and students  Missy Southworth (VIMS) and Jim Wesson (VMRC)  VIMS Vessel Operations


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