|Modeling studies of the effect of climate variability on MSX disease in eastern oyster (Crassostrea virginica) populations|
|Hofmann, E.; Ford, S.; Powell, E.; Klinck, J. (2001). Modeling studies of the effect of climate variability on MSX disease in eastern oyster (Crassostrea virginica) populations, in: Porter, J.W. (Ed.) (2001). The ecology and ethiology of newly emerging marine diseases. Developments in Hydrobiology, 159: pp. 195-212. dx.doi.org/10.1023/A:1013159329598|
|In: Porter, J.W. (Ed.) (2001). The ecology and ethiology of newly emerging marine diseases. Reprinted from Hydrobiologia 460 (2001). Developments in Hydrobiology, 159. Kluwer Academic Publishers: Dordrecht. ISBN 1-4020-0240-8. xvi, 228 pp., more|
|In: Dumont, H.J. (Ed.) Developments in Hydrobiology. Kluwer Academic/Springer: Den Haag. ISSN 0167-8418, more|
Eastern oysters (Crassostrea virginica) often undergo epizootics of MSX (Multinucleated Spore Unknown) disease, which is caused by the protozoan pathogen, Haplosporidium nelsoni. The disease has been present in oyster populations in the mid-Atlantic United States since the 1950s. During the 1980s and 1990s, it became established further north along the east coast of the United States. To investigate the factors underlying the northward progression of MSX disease, a model that simulates the host–parasite–environmental interactions was used. The model is physiologically-based and is structured around the transmission, proliferation and death rates of the parasite. Environmental conditions of temperature, salinity and oyster food supply provide the external forcing that results in variations in the biological rates. For this study, environmental data sets, both average and extreme, were obtained at a site in upper Chesapeake Bay for 1986 through 1995. This site is in the middle of one of the most productive oyster growing regions on the east coast of the United States; thus, both short- and long-term changes in the environment measured here realistically reflect conditions experienced by important oyster populations. The effect of short-term high-salinity (drought) or low-salinity (wet) conditions on MSX disease prevalence and intensity was relatively small because the average salinity regime already favors maximum parasite activity at this site. Even the extreme low salinity events were not low enough to significantly inhibit the parasite. Similarly, simulations using short-term high-temperature extremes for the same site showed only minor deviations from the average pattern because average temperatures were already high enough to support parasite development. In contrast, the measured low temperature conditions, applied for a single year, caused a dramatic reduction in parasite activity, which extended over a 2-year period. Additional simulations show that overall food supply to the host is of little consequence in determining the basic disease pattern; however, the timing of maximum food supply provided to the host, relative to specific times in the parasite life cycle, is important in determining whether or not the parasite attempts sporulation or undergoes density-independent growth. Simulations that test a sequence of changing environmental conditions show that when a year with cold winter temperatures (less than 3 °C) is followed by a year of low salinity (less than 15 ppt), prevalences and intensities of MSX disease are greatly reduced, with the disease becoming almost absent in the oyster populations; however, the disease returns when average environmental conditions return. Simulations using progressive cooling or warming conditions indicate that winter temperatures consistently lower than 3 °C limit the long-term development of MSX disease. These simulations support the suggestion that climate warming is a contributing factor to the northward spread of MSX disease.