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Gametogenesis and Spawning of Crassostrea virginica from Disease-Intense Waters of Virginia, USA. Ryan B. Carnegie and Eugene M. Burreson Department of Environmental and Aquatic Animal Health Virginia Institute of Marine Science. Hasn’t Someone Looked At This Already?. - PowerPoint PPT Presentation
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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
0
10
20
30
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50
60
70
80
90
100
1 2 3 4 5 6
Month
Cumulative Mortality (%)
WS
AB
DB
RR
J NOSAJ
RR > WS > AB,DB
RR > WS,AB,DB
WS > RR,AB,DB
Bars = 1 SEM
No Simple Increase in Disease with Size/Age
0
10
20
30
40
50
60
70
80
90
100
May Jun Jul Aug Sep Oct Nov
Prevalence (%)
< 50
50-76
76-100
> 100
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
May Jun Jul Aug Sep Oct Nov
Average Intensity
< 50
50-76
76-100
> 100
0
10
20
30
40
50
60
70
80
90
100
May Jun Jul Aug Sep Oct Nov
Prevalence (%)
< 50
50-76
76-100
> 100
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
May Jun Jul Aug Sep Oct Nov
Average Intensity
< 50
50-76
76-100
> 100
Perkinsus marinus Haplosporidium nelsoni
DISEASE IN VIRGINIA OYSTER POPULATIONS: A MODEL
PA
RA
SIT
E I
MP
AC
T,
OY
ST
ER
MO
RT
AL
ITY
OYSTER SIZE/AGE
MSX
DERMO
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
0%10%20%30%40%50%60%70%80%90%
100%
May Jun Jul Aug Sep Oct Nov
C
P
S
M
LD
ED
I
0%10%20%30%40%50%60%70%80%90%
100%
May Jun Jul Aug Sep Oct Nov
C
P
S
M
LD
ED
I
0%10%20%30%40%50%60%70%80%90%
100%
May Jun Jul Aug Sep Oct Nov
C
P
S
M
LD
ED
I
< 50 mm
76-100 mm
50-76 mm
Reproductive Stages: Broad Creek, Rapp. River, 2007
< 50 mm
76-100 mm
50-76 mm
> 100 mm
0%10%20%30%40%50%60%70%80%90%
100%
May Jun Jul Aug Sep Oct Nov
C
P
S
M
LD
ED
I
0%10%20%30%40%50%60%70%80%90%
100%
May Jun Jul Aug Sep Oct Nov
C
P
S
M
LD
ED
I
0%10%20%30%40%50%60%70%80%90%
100%
May Jun Jul Aug Sep Oct Nov
C
P
S
M
LD
ED
I
0%10%20%30%40%50%60%70%80%90%
100%
May Jun Jul Aug Sep Oct Nov
C
P
S
M
LD
ED
I
Gametogenesis Largely Precedes the Dermo Peak
Reproductive Stage
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
May Jun Jul Aug Sep Oct Nov
C
P
S
M
LD
ED
I
Serious Perkinsus marinus
0.00
0.10
0.20
0.30
0.40
0.50
0.60
0.70
0.80
0.90
1.00
May Jun Jul Aug Sep Oct Nov
“Serious” Perkinsus marinus Infections
Reproductive Stage
Sandy Point, 76-100 mm, 2007
Gametogenesis Largely Precedes the Dermo Peak
Reproductive Stage
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
May Jun Jul Aug Sep Oct Nov
C
P
S
M
LD
ED
I
Serious Perkinsus
0.00
0.10
0.20
0.30
0.40
0.50
0.60
0.70
0.80
0.90
1.00
May Jun Jul Aug Sep Oct Nov
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
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
< 50 mm 50-76 mm > 76 mm
Abolished
Some Impact
Unimpacted
Broad Creek
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
< 50 mm 50-76 mm 76-100 mm > 100 mm
Abolished
Some Impact
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
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