gametogenesis and spawning of crassostrea virginica from disease-intense waters of virginia, usa

Ryan B. Carnegie and Eugene M. BurresonDepartment of Environmental and Aquatic Animal Health

Virginia Institute of Marine Science

Gametogenesis and Spawning of Crassostrea virginica from Disease-Intense Waters of Virginia,

USA

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

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

Natural Resistance in a Dual-Disease Environment

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No Simple Increase in Disease with Size/Age

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Perkinsus marinus Haplosporidium nelsoni

DISEASE IN VIRGINIA OYSTER POPULATIONS: A MODEL

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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) < 50 mm, 50-76 mm, 76-100 mm, > 100 mm

Pathology (RFTM) and histology Gonadal staging Condition indices Gonadal area indices (forthcoming)

Reproductive Stages: Sandy Point, GWR, 2007

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Reproductive Stages: Broad Creek, Rapp. River, 2007

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Gametogenesis Largely Precedes the Dermo Peak

Reproductive Stage

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Serious Perkinsus marinus

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“Serious” Perkinsus marinus Infections

Reproductive Stage

Sandy Point, 76-100 mm, 2007

Gametogenesis Largely Precedes the Dermo Peak

Reproductive Stage

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Reproductive Stage

“Serious” Perkinsus marinus Infections

Broad Creek, > 100 mm, 2007

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

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

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 outputSandy Point

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Abolished

Some Impact

Unimpacted

Broad Creek

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Unimpacted

A substantial reproductive contribution should be expected from oysters in natural beds in disease-

enzootic watersNote 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

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?

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)

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

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

gametogenesis and spawning of crassostrea virginica from disease-intense waters of virginia, usa

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