Harold H. Haskin

History and epizootiology of Haplosporidium nelsoni (MSX), an oyster pathogen in Delaware Bay, 1957–1980

Abstract Between 1957 and 1959, a previously unknown sporozoan parasite, now designated as Haplosporidium nelsoni (formerly Minchinia nelsoni ), or MSX, killed 90–95% of the oysters in lower Delaware Bay. Native oysters have been studied for more than 20 years since then to determine long-term disease and mortality patterns resulting from this host-parasite association. Development of resistance to MSX-kill in native oysters has reduced disease mortality to about half the original level, even though the pathogen continues to be very active in the bay. Since the initial epizootic, MSX levels have fluctuated in a cyclic pattern with peaks every 6 to 8 years. Periods of low disease pressure follow very cold winters, while average or above average winter temperatures correlate with high MSX activity. During peak years, every oyster in the lower bay may become infected. Although the parasite is salinity limited, salinities in the lower bay, the area from which oysters are marketed, are nearly always favorable for MSX, and fluctuations in river flow have almost no effect on MSX in this region. Infection periods recur each summer. Some oysters die soon after becoming infected; others survive through winter, but die in spring as the pathogen compounds normal overwinter stresses. Many survivors are able to suppress or rid themselves of infections when temperatures approach 20°C in late spring. Resistance to MSX-kill in native oysters is not correlated with an ability to prevent infection, but with restriction of parasites to localized, nonlethal lesions. The persistence of “hot spots” for infection in areas where oysters are sparse, the lack of spores in infected oysters, and failure to transmit the disease experimentally lead to the hypothesis that an alternate or reservoir host produces infective stages of MSX.

INFECTION AND MORTALITY PATTERNS IN STRAINS OF OYSTERS CRASSOSTREA VIRGINICA SELECTED FOR RESISTANCE TO THE PARASITE HAPLOSPORIDIUM NELSONI (MSX)

Strains of oysters Crassostrea virginica resistant to mortality caused by the parasite Haplosporidium nelsoni (MSX) were developed and tested through 6 generations. In addition, strains in each generation were followed for up to 6 yr of continuous exposure to the parasite in nature. Selected strains responded to challenge by the parasite with gradually improved survival in successive generations. They were slower to develop patent infections than were unselected groups and were able to delay mortality after infections did develop, but under repeated exposure most oysters eventually died with H. nelsoni parasitism. Many selected strains, however, reached market size before significant mortalities occurred. The data suggest that resistance to H. nelsoni mortality is under the influence of many genes. No clear defense mechanism has been described and we hypothesize that resistance to H. nelsoni may, in part, involve a physiological state in which selected oysters temporarily fail to provide a suitable habitat for the parasite. Temporary insusceptibility would, in this view, be followed by an increased ability to tolerate the parasite when conditions for its development are present. Selection would then favor individuals that are able to prolong periods of insusceptibility and/or to carry out basic life processes while parasitized.

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

Abstract 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 parasites capacity to develop once it has entered the oyster.

Swimming speeds of oyster larvaeCrassostrea virginica in different salinities and temperatures

Swimming speeds of oyster larvaeCrassostrea virginica were determined in constant and increasing salinities to learn more about the oyster larval “salinity response”. “Normal” non-directed swimming speeds ranged from less than 1 cm/min for early veligers to 5 cm/min for “eyed” veligers with temperature an important variable. When subjected to hourly salinity increases of 0.5‰, most larvae swam upward or downward at approximately 3 times the above speeds. Larvae with values closed in response to traces of formalin sank at speeds of 5 to 50 cm/min depending on larval stage. The results may explain the differential vertical position of larval stages in estuaries and suggest the presence of a taxic component to the salinity response.

Effects of the parasite MSX (Haplosporidium nelsoni) on oyster (Crassostrea virginica) energy metabolism—II. Tissue biochemical composition

1. 1. Tissue biochemical composition of oysters (Crassostrea virginica) from Delaware Bay (USA) was examined from May to November 1985 as a function of infection intensity by the endoparasite, Haplosporidium nelsoni (MSX). 2. 2. The lipid, glycogen, protein and ash content (mgDW) of a standard 100mm (shell height) oyster was determined for uninfected, epithelial and systemic infection categories. 3. 3. All biochemical components generally decreased in content with increasing MSX infection intensity (and duration). Overall reductions were significant in glycogen [epithelial (P < 0.05) and systemic (P = < 0.001)], protein [systemic (P < 0.05)] and ash [systemic (P < 0.02)] categories. 4. 4. Glycogen was the substrate most readily catabolized to meet the energetic burden posed by MSX. The reduction by MSX of nutrient reserves affects other metabolic functions such that the ecological fitness of surviving oysters is reduced.

The effects of petroleum hydrocarbons on the growth of phytoplankton recognised as food forms for the eastern oyster, Crassostrea virginica gmelin

Abstract The effects of water-soluble extracts of a Nigerian crude oil and two No. 2 fuel oils on the growth of five species of phytoplankton recognised as food sources for the eastern oyster, Crassostrea virginica Gmelin, have been examined. Unialgal cultures of Monochrysis lutheri, Isochrysis galbana, Dunaliella euchlora, Nannochloris oculata and Skeletonema costatum were exposed to water-soluble extracts in a closed culture system. The relative sensitivity of the five species was found to vary among oils. Inhibitory effects, when present, were often transitory. In general, concentrations at which toxic effects were noted were far in excess of levels previously demonstrated to be lethal to adult and larval oysters. Three clones of the diatom Skeletonema costatum were utilised and distinct interclonal differences in responses were noted. This variation among clones indicates that the response of an algal culture composed of only one genotype may not necessarily be representative of a species response.

Oyster-MSX interactions: Alterations in hemolymph enzyme activities in Crassostrea virginica during the course of Minchinia nelsoni disease development☆

Abstract Hemolymph enzyme activities were investigated during the course of Minchinia nelsoni (MSX) disease development in Crassostrea virginica. Aspartate aminotransferase, alanine aminotransferase, and phosphohexose isomerase activities increase significantly during the gill lesion stage of MSX disease. Enzyme activities are not significantly elevated during the general infection stage of MSX disease. The alteration of hemolymph enzyme activity is discussed with respect to host metabolism and possible humoral defense mechanisms.

Delaware Bay Oyster Populations: Effects of Seed Movement, Harvesting, and Diseases

Oysters are not directly harvested for market from Delaware Bay natural beds. They have been moved from upper Delaware Bay seed beds to planting grounds, located in lower Delaware Bay, since the mid 1800’s. The States of Delaware and New Jersey have retained control of the seed beds, but lease bottom to private individuals in the planting grounds. Oysters placed on leased areas become the property of the lease holder and may be harvested at any time. Depending on the size of the oyster moved to the planting grounds (oysters from the uppermost seed beds are smaller on average than those from lower bay seed beds), one to three or more years are required for the oysters to reach market size. This mixture of direct harvest from the seed beds and subsequent grow-out on the planting grounds prior to final harvest has, in the presence of. oyster disease and predation, changed the patterns of oyster abundance in Delaware Bay.