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Abstracts
Workgroup: Oyster Fisheries Management and Restoration
Field and laboratory study of the process and dynamics of Perkinsus marinus infection in the eastern oyster, Crassostrea virginica
Principal Investigator(s):
Eugene M. Burreson (gene@vims.edu) and Lisa M. Ragone Calvo, Virginia Institute of Marine Science, School of Marine Science
Co-Investigator(s):
CO-INVESTIGATORS and AFFILIATIONS: Christopher F. Dungan, Cooperative Oxford Laboratory, Maryland Department of Natural Resources, Oxford Maryland, Bob S. Roberson, Department of Microbiology, University of Maryland
Funding Period: FUNDING PERIOD 4/1/94-3/31/95
This project represents the second year of a two-year study, which is the first study to systematically examine the seasonality of P. marinus infection acquisition in oysters in relation to water column abundance of P. marinus cells, oyster mortality, and temperature. The timing and magnitude of seasonal peaks in environmental abundances of P. marinus cells and local oyster mortalities at an upper (Tred Avon River, MD) and lower (York River, VA) Chesapeake Bay site were also contrasted. Lastly, a specific and sensitive immunoassay detection technique was employed to examine the process and site(s) of pathogen invasion into host oysters in both field and laboratory P. marinus exposures.
Uninfected sentinel oysters were naturally exposed to the parasite during two-week intervals throughout the course of the study to determine the periodicity and rates of parasite transmission. The timing and magnitude of disease-associated oyster mortalities in a local P. marinus-infected oyster population were estimated by monitoring a captive subset of the local oyster population. Flow cytometric immunodetection methods were employed to estimate the abundance of P. marinus cells in water samples collected three times each week.
In the lower York River, VA, environmental abundance of P. marinus cells, infection acquisition by sentinel oysters, and mortality of P. marinus-infected oysters varied seasonally. Distinct peaks of all three parameters occurred during the month of August, following maximal summer temperatures. Water column parasite cell abundances, infection pressure, and oyster mortalities decreased from summer maximums as temperatures decreased in September and October, and remained at "wintertime" low levels from October through the termination of the study in March. Counts of antibody-labeled cells ranged from 10 to 11,900 cells per liter, Strong and significant positive correlations were found between water column parasite cell abundance and temperature, water column parasite cell abundance and oyster mortality, oyster mortality and temperature, and oyster mortality and P. marinus prevalence in sentinel oysters.
In the Tred Avon River, MD, maximum abundances of P. marinus cells in the water column were also observed during August. Environmental cell abundance was significantly correlated with temperature, but not with local oyster mortality rates. Abundance levels overall were generally higher than at the York River site but were still of the same order of magnitude. Local oyster mortality at the upper Bay site occurred later in the summer and was much lower than at the York River site.
These results support the prevailing model of P. marinus transmission dynamics that maximum transmission rates are observed during periods of maximum P. marinus-associated host mortality. However, results also indicate that transmission can occur when host mortality is low or absent; so alternative mortality-independent dissemination mechanisms are likely. Results also suggest that atypically early summer oyster mortality from Haplosporidium nelsoni infection, at a time when infections of P. marinus are light, has a significant indirect influence on P. marinus transmission dynamics. Elimination of these hosts prior to late summer P. marinus infection intensification effectively reduces the overall number of P. marinus cells disseminated.
Finally, the results of P. marinus initial infection studies suggest that the digestive tract may not be the only, or even the primary, site of infection. The localization of many parasite cells in gill and mantle epithelia may be indicative of alternate pathogen entry routes.
IMPACTS and/or BENEFITS:
The project resulted in improved understanding of P. marinus transmission dynamics. Such understanding was key to the development of predictive models of P. marinus disease dynamics and this information has also been valuable in the development of disease avoidance strategies promoting enhanced management of oyster fisheries and oyster aquaculture.
PROJECT PUBLICATIONS:
Ragone Calvo, LM., C. F. Dungan, B. S. Roberson and E. M. Burreson. 2002. A systematic evaluation of factors controlling Perkinsus marinus transmission dynamics in the lower Chesapeake Bay, Diseases of Aquatic Organisms. Diseases of Aquatic Organisms. In Press.
Ragone Calvo, L.M., R.L. Wetzel, E.M. Burreson. 2001. Development and verification of a model for the population dynamics of the protistan parasite Perkinsus marinus within its host, the eastern oyster, Crassostrea virginica in Chesapeake Bay. Journal of Shellfish Research 20(1): 231-241.
Burreson, E.M. and L. Ragone Calvo. 1996. Epizootiology of Perkinsus marinus disease of oysters in Chesapeake Bay, with emphasis on data since 1985. Journal of Shellfish Research Special Publication. Journal of Shellfish Research. 15(1):17-34.
Calvo, L.M. ; Burreson, E.M. ; Dungan, C.F.; Roberson, B.S. 1996. Perkinsus marinus transmission dynamics in Chesapeake Bay. Journal of Shellfish Research 15 (2):496.
Dungan, C.F., Hamilton, R.M. ; Burreson, E.M.; Ragone-Calvo, L.M. 1996. Identification of Perkinsus marinus portals of entry by histochemical immunoassays of challenged oysters. Journal of Shellfish Research 15 (2):500.
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