Relationship Of Salinity Research Articles

Haplosporidium nelsoni (MSX) on delaware bay seed oyster beds: A host-parasite relationship along a salinity gradient

Epizootic mortalities of oysters in Delaware and Chesapeake Bays during the late 1950s and early 1960s diminished in an upbay direction, indicating that the causative agent, the sporozoan parasite, Haplosporidium nelsoni (formerly Minchinia nelsoni), or MSX, was salinity limited. Since 1959, native Delawere Bay oysters have been sampled for presence of MSX and for mortality along a salinity gradient that ranges at mid-tide and mean river flow from 20 to 23 ppt on the lower bay planted grounds, and from 9 to 18 ppt on the upper bay seed beds. This study has clarified the relationship of salinity to the distribution and effect of the parasite in native oysters in the estuary. The sampling period included a drought in the mid-1960s when very low Delaware River flows produced high salinities in the upper bay. It also included a period of very high flows, and low salinities, in the early 1970s. On Arnolds and Cohansey, two of the uppermost seed beds, with mean salinities of 9 and 12 ppt, respectively, MSX activity was significant only during the drought. Farther downbay, at New Beds and Bennies Bed (15–16 ppt), the disease was present in all years, but with clearly elevated activity during the drought. On the planted grounds, however, where the effects of MSX are felt most strongly by the oyster industry, there was no correlation of disease levels with river flow. In fact, MSX prevalence was higher there in the early 1970s when river flows were high, than it was during the drought. When disease and mortality statistics for each location along the salinity gradient were pooled for the entire sampling period, two distinct patterns emerged: (1) Prevalence (proportion of oysters diagnosed as having MSX) showed a regular decrease from high to low salinity that paralleled the salt gradient. (2) However, infection intensity, a better measure of disease stress than prevalence, showed a sharp drop between the planting grounds and the seed beds, then no further change with lower salinity. MSX-related mortality followed a pattern similar to infection intensity: on a long-term average, 30% of all oysters have died with MSX infections during their first year after planting on the leased grounds. On the seed beds, regardless of location, annual disease-related kill was only 4 to 9%. Correlation of mortality rates with infection intensity rather than with prevalence is explained by the fact that infections must reach a certain intensity before they become lethal. The sharp drop in infection intensity and MSX-related mortality occurs between the upbay edge of the leased grounds and the lowermost seed bed, locations that are separated by less than 2 miles and an average of only 2 ppt salinity. This suggests a salinity threshold that has little effect on the distribution of infective stages of MSX or on their ability to infect, but that severely limits the parasite's capacity to develop once it has entered the oyster.

The density and speed of sound of Orca basin waters1

The composition of samples of waters collected in the Orca depression (Gulf of Mexico) above and below the seawater‐brine interface was characterized by measuring chlorinity (Cl) and salinity (S). The ratio of S:Cl = 1.6823 in the brines, compared with 1.6817 calculated from composition data. Densities and sound speeds of the waters were measured at 15°, 25°, and 35°C and the results fit to chlorinity functions. The standard deviations in density are ≈60 × 10−6 g·cm−3, in sound speed ≈1.2 m·s−1. These standard errors are about 6 times larger than the precision of the measurements and are due to errors in determining Cl and to changes in the brine composition across the interface.Conductivity, density, and sound speed were measured in weight‐diluted brine samples and the results used to calculate the relationship of evaporation salinity (Sevap) to salinity calculated from measurements on standard seawater. The differences in Sevap and S determined from properties of standard seawater are caused by hydration changes in the major constituents.The measured brine densities were compared with values calculated by using an additivity method and the known composition of the waters and agree to within ±280 × 10−8 g·cm−3 over the temperature range measured.

INTERACTION OF SALINITY AND TEMPERATURE ON NET PROTEIN SYNTHESIS AND VIABILITY OF VIBRIO MARINUS1,2

The relationship of temperature and salinity to protein synthesis was determined for cells of Vibrio marinus. The critical temperature of the lesion in protein synthesis increased with increasing salinity of the growth medium. Protein synthesis was significantly inhibited at 22C at a salinity of 25‰, but not at a salinity of 35‰ until the cells were incubated for 20 min at 24C. The thermal lesion did not involve precursor accumulation mechanisms rather than protein synthesis at salinities between 25 and 35%. At 40‰, the uptake of extracellular proline by whole cells was inhibited at 24C and preceded the inhibition of precursor into protein.Total RNA synthesis continued for 50 min at 22C in growth media at salinities between 15 and 35‰ but at 40‰ decreased after 20 min of cell incubation. At salinities between 15‰ and 30‰, total RNA synthesis continued at 15 and 22C, but cellular protein synthesis was inhibited by either temperature or salinity effects.Loss of cell viability at 22 and 25C at salinities of 25 and 35‰ showed that the onset of cell death occurs simultaneously with thermal inhibition of protein synthesis.