Abstract:Infection levels of eastern oysters by the unicellular pathogen Perkinsus marinus have been associated with anthropogenic influences in laboratory studies. However, these relationships have been difficult to investigate in the field because anthropogenic inputs are often associated with natural influences such as freshwater inflow, which can also affect infection levels. We addressed P. marinus-land use associations using field-collected data from Murrells Inlet, South Carolina, USA, a developed, coastal estua… Show more
“…Multiple generations per year may further insulate the population from a reduction in abundance that should accompany an increment in mortality; but here, too, the rate of development of disease resistance is little changed if not slowed. The mortality rate drives selection and, thus, the rate of increase in disease resistance and the mortality rate are independent of abundance and other abetting processes maintaining abundance (discounting the possible contribution of density to transmission (Andrews 1988, White et al 1998, Ford 1992, Gray et al 2009).…”
Section: The Case Of the Gulf Of Mexicomentioning
confidence: 99%
“…The potential for the development of disease resistance would appear to exist, however. Oyster strains are observed to vary in their response to Dermo disease (Ray & Chandler 1955, Andrews & Hewatt 1957, Bushek & Allen 1996, Gaffney & Bushek 1996, Brown et al 2005a, Brown et al 2005b), suggesting a potential for disease resistance, although associations with environmental variables that might degrade the immune response (Craig et al 1989, Chu & Hale 1994, Lenihan et al 1999, Bushek et al 2007, Gray et al 2009, also well documented, limit the inference based on currently available data. Of more significance, perhaps, alleles associated with resistance or tolerance are known, so that an inherent capability would seem present.…”
Today, populations of eastern oysters, Crassostrea virginica, are commonly limited by disease mortality. Resistance to MSX disease has developed in a number of cases, but the development of resistance to Dermo disease would appear to be limited, despite the high mortality rates and frequency of epizootics. Can aspects of the host's genetics or population dynamics limit the response to the disease despite the apparent opportunity afforded by alleles conferring disease resistance or tolerance? To answer this question, we use a gene-based population dynamics model, configured for C. virginica, to simulate the development of disease resistance using mortality as the agent of selection. Simulated populations were exposed to 4 levels of mortality covering the range in mortality observed in Delaware Bay in the 1990s. In each case, disease resistance increased in the simulated population over time, normally proportional to the increase in mortality rate imposed by the disease. However, simulations show that the population responds even at its most rapid rate on multidecadal to half-century timescales. As the mortality rate declines with increasing disease resistance, the rate of further improvement in disease resistance likewise declines. Thus, disease resistance develops over decadal timescales at a 40%-per-year mortality rate, but, as mortality rate falls to 25% per year, the rate of further development of disease resistance extends to half-century timescales. The discouraging profundity is that a mortality rate of 25% per year, yielding a rate of selection profoundly slow, is still very high. In northern climes, significant decrements in oyster abundance will occur. Evidence from fisheries retrospectives suggests that oysters cannot withstand a constant removal at this scale without compromising population integrity noticeably. So, a mortality rate that grievously limits the development of disease resistance still sorely strains the speciesÕ ability to maintain a vibrant population necessary to its long-term survival.
“…Multiple generations per year may further insulate the population from a reduction in abundance that should accompany an increment in mortality; but here, too, the rate of development of disease resistance is little changed if not slowed. The mortality rate drives selection and, thus, the rate of increase in disease resistance and the mortality rate are independent of abundance and other abetting processes maintaining abundance (discounting the possible contribution of density to transmission (Andrews 1988, White et al 1998, Ford 1992, Gray et al 2009).…”
Section: The Case Of the Gulf Of Mexicomentioning
confidence: 99%
“…The potential for the development of disease resistance would appear to exist, however. Oyster strains are observed to vary in their response to Dermo disease (Ray & Chandler 1955, Andrews & Hewatt 1957, Bushek & Allen 1996, Gaffney & Bushek 1996, Brown et al 2005a, Brown et al 2005b), suggesting a potential for disease resistance, although associations with environmental variables that might degrade the immune response (Craig et al 1989, Chu & Hale 1994, Lenihan et al 1999, Bushek et al 2007, Gray et al 2009, also well documented, limit the inference based on currently available data. Of more significance, perhaps, alleles associated with resistance or tolerance are known, so that an inherent capability would seem present.…”
Today, populations of eastern oysters, Crassostrea virginica, are commonly limited by disease mortality. Resistance to MSX disease has developed in a number of cases, but the development of resistance to Dermo disease would appear to be limited, despite the high mortality rates and frequency of epizootics. Can aspects of the host's genetics or population dynamics limit the response to the disease despite the apparent opportunity afforded by alleles conferring disease resistance or tolerance? To answer this question, we use a gene-based population dynamics model, configured for C. virginica, to simulate the development of disease resistance using mortality as the agent of selection. Simulated populations were exposed to 4 levels of mortality covering the range in mortality observed in Delaware Bay in the 1990s. In each case, disease resistance increased in the simulated population over time, normally proportional to the increase in mortality rate imposed by the disease. However, simulations show that the population responds even at its most rapid rate on multidecadal to half-century timescales. As the mortality rate declines with increasing disease resistance, the rate of further improvement in disease resistance likewise declines. Thus, disease resistance develops over decadal timescales at a 40%-per-year mortality rate, but, as mortality rate falls to 25% per year, the rate of further development of disease resistance extends to half-century timescales. The discouraging profundity is that a mortality rate of 25% per year, yielding a rate of selection profoundly slow, is still very high. In northern climes, significant decrements in oyster abundance will occur. Evidence from fisheries retrospectives suggests that oysters cannot withstand a constant removal at this scale without compromising population integrity noticeably. So, a mortality rate that grievously limits the development of disease resistance still sorely strains the speciesÕ ability to maintain a vibrant population necessary to its long-term survival.
“…Disease mortality is expected to show strong spatial and temporal dependence due to the epidemic process of local transmission. Although terrestrial studies on the spatial aspects of diseases have a long history, driven by a necessity to understand diseases of humans, crops, farm animals and wildlife [25], spatial studies of aquatic diseases are much less frequent and generally focused on distribution of macro-parasites [26]–[33].…”
Although spatial studies of diseases on land have a long history, far fewer have been made on aquatic diseases. Here, we present the first large-scale, high-resolution spatial and temporal representation of a mass mortality phenomenon cause by the Ostreid herpesvirus (OsHV-1) that has affected oysters (Crassostrea gigas) every year since 2008, in relation to their energetic reserves and the quality of their food. Disease mortality was investigated in healthy oysters deployed at 106 locations in the Thau Mediterranean lagoon before the start of the epizootic in spring 2011. We found that disease mortality of oysters showed strong spatial dependence clearly reflecting the epizootic process of local transmission. Disease initiated inside oyster farms spread rapidly beyond these areas. Local differences in energetic condition of oysters, partly driven by variation in food quality, played a significant role in the spatial and temporal dynamics of disease mortality. In particular, the relative contribution of diatoms to the diet of oysters was positively correlated with their energetic reserves, which in turn decreased the risk of disease mortality.
“…Reporting prevalences of higher-intensity infections provides an alternative statistic for projecting mortalities (Gray et al, 2009), in which it is critical to understand what infection intensity threshold increases the probability of mortality. In Fig.…”
Section: Development Of An Infection Intensity Ranking Systemmentioning
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