MODELLING DISEASED OYSTER POPULATIONS .2. TRIGGERING MECHANISMS FOR PERKINSUS-MARINUS EPIZOOTICS

Citation
En. Powell et al., MODELLING DISEASED OYSTER POPULATIONS .2. TRIGGERING MECHANISMS FOR PERKINSUS-MARINUS EPIZOOTICS, Journal of shellfish research, 15(1), 1996, pp. 141-165
Citations number
108
Categorie Soggetti
Fisheries,"Marine & Freshwater Biology
ISSN journal
07308000
Volume
15
Issue
1
Year of publication
1996
Pages
141 - 165
Database
ISI
SICI code
0730-8000(1996)15:1<141:MDOP.T>2.0.ZU;2-Q
Abstract
Densities of Crassostrea virginica remain high enough to support subst antial fisheries throughout the Gulf of Mexico despite high mortality rates produced by the endoparasite Perkinsus marinus. The infrequency of epizootics in these populations suggests that controls exist on the disease intensification process. The progression of epizootics in oys ter populations, the factors that trigger epizootics, and the factors that terminate epizootics once started were investigated with a couple d oyster population-P. marinus model. The time development of a simula ted epizootic was triggered by environmental conditions that occurred and disappeared as much as 18 months prior to the onset of mortality i n the oyster population. Initiation of epizootic conditions was detect ed as an increase in infection intensity in the submarket-size adult a nd juvenile portions of the oyster population. Infection intensity of the marker-size adults is maintained at a relatively stable level by t he death of heavily infected individuals and the slow rate of P. marin us division at high infection intensities. Once started, most of the s imulated epizootics resulted in population extinction in 2 to 4 years. Stopping an epizootic required reducing the infection intensity in th e submarket-size adults and juveniles. The infection intensity of mark et-size adults does not need to be reduced to stop an epizootic nor mu st it be raised to start one. The simulated oyster populations show th at a reduction in ingestion rate (by reduced food supply or increased turbidity) can trigger an epizootic, especially if the reduction occur s during the summer. Increasing food supply or decreasing turbidity in the following year does not necessarily prevent the occurrence of an epizootic. Rather, the onset of the event is simply delayed. Additiona l simulations show that the relative combination of variations in sali nity and temperature is important in determining the occurrence of an epizootic. A dry (high-salinity) summer followed by a warm winter prod uces conditions that favor the development of an epizootic. Conversely , a warm dry pear followed by a cool wet year fails to produce an epiz ootic. Simulations that consider variations in the biological characte ristics of oyster populations, such as changes in recruitment rate or disease resistance, show that these are important in regulating the oc currence of an epizootic as well as in terminating the event. In parti cular, increased recruitment rate dilutes the infected population suff iciently to terminate an epizootic. One primary conclusion that can be obtained from these simulations is that epizootics of P. marinus in o yster populations are difficult to generate simply with changes in eit her temperature or salinity. Rather, the epizootics are triggered by s ome other factor, such as reduced food supply or reduced recruitment r ate, that occurs prior to or coincident with high salinity or temperat ure conditions.