MSX disease in C. virginica is caused by the protistan parasite Haplosporidium nelsoni. MSX refers to Multinucleate Sphere Unknown, as this pathogen was known before its description in 1966.
Haplosporidium nelsoni was introduced from Asia and is notorious as the cause of catastrophic (more than 90 percent) oyster mortality in Delaware Bay beginning in 1957 and in Chesapeake Bay beginning in 1959.
These were the first catastrophic oyster disease outbreaks in the region. In Chesapeake Bay, because of continued overharvesting, the spread of dermo disease to lower salinity waters in the 1980s, and the general deterioration of the Bay environment, oyster populations have never completely recovered.
Haplosporidium nelsoni has been documented along the Atlantic coast from Nova Scotia to Florida, with epizootic disease and significant mortality occurring from Maine to Virginia. It is apparently not a serious cause of mortality south of Virginia, for reasons that are not known.
A recent molecular survey hinted at the presence of H. nelsoni in the Gulf of Mexico, but its presence there has never been visually confirmed. Seed produced from Gulf oysters are highly susceptible to MSX disease when cultured in Mid-Atlantic waters, which suggests that Gulf populations have never been exposed to MSX.
Unlike P. marinus, H. nelsoni is not directly transmissible among oysters. The intermediate host or hosts that are thus presumed to be involved in H. nelsoni transmission have never been identified.
Susceptible oysters become infected from some unknown environmental source and die from May through October in the Chesapeake region. Initial infections occur in the epithelia of the gills
and palps. From these epithelia, H. nelsoni colonizes connective tissues and large, multinucleate H. nelsoni plasmodia (to 50 µm; Fig. 2) spread throughout the host.
Spores, presumably a cell form essential to transmission of the parasite, form in the digestive tubules, primarily of younger oysters. Salinity plays a key role in determining the distribution of H. nelsoni.
The parasite cannot withstand salinities below 10 ppt for more than 2 weeks when temperatures are above 20 °C, so periods of low salinity, particularly in the warmer months, effectively purge MSX from oyster beds.
Following Tropical Storm Agnes in June 1972, for example, H. nelsoni disappeared from most Chesapeake Bay oyster populations. The effects of temperature are more subtle and complicated. Studies in Delaware Bay indicated that although H. nelsoni can proliferate rapidly at temperatures from 5 to 20 °C, resistant oysters can manage H. nelsoni at higher temperatures while susceptible oysters cannot.
The apparent insignificance of H. nelsoni south of Virginia—and its absence from the Gulf—may relate partly to temperature, in that warm southern water may favor the oyster’s defenses over the parasite. The distribution of MSX disease may also be influenced by the distribution and abundance of H. nelsoni’s unknown intermediate host(s).
The management of MSX in disease-enzootic waters begins with the use of disease-resistant oyster stocks, which have been in development since the 1960s. These oysters either resist infection entirely or are able to restrict parasites to gill and palp epithelia.
Few resistant oysters are killed by MSX. Even wild oysters from the Mid-Atlantic have developed some MSX resistance; very little MSX disease is observed in adult oysters in the Mid-Atlantic, while naïve oysters transplanted from low salinity waters are greatly affected. Aquaculturists in the Gulf of Mexico should avoid introducing H. nelsoni from Atlantic waters.
SSO disease in eastern oysters:
SSO disease in C. virginica is caused by the protistan parasite Haplosporidium costale, a relative of the MSX disease agent H. nelsoni that generally occurs in higher salinity (? 20 ppt) coastal waters. SSO refers to Sea Side Organism, as this protist was first known.
It was discovered in Virginia’s coastal sounds during the initial investigations on MSX, and is now known to range north from Virginia to the Atlantic provinces of Canada.
In Virginia waters, H. costale parasitism and the associated SSO disease and mortality display a distinct seasonality, peaking sharply in April-June of each year. New infections at this time coincide with the deaths of previously infected oysters, though transmission is still thought to occur through some intermediate host(s).
Infection probably occurs through digestive tubules, with multinucleate parasite plasmodia (like those of H. nelsoni, but smaller, to 10 µm) then proliferating in connective tissues. Spores form in the connective tissues (Fig. 3).
While SSO disease has been reported to cause more than 50 percent mortality, it is unlikely that it does so today, at least in Virginia waters. While a maximum of 56 percent of adult oysters were infected by H. costale at one Virginia site in April 2008, the percentage of advanced infections was just 4 percent and the parasite could barely be detected (4 percent prevalence) 1 month later.
Compared with P. marinus, H. costale is a minor pathogen in the region today. Where it does occur, planting fast growing oyster seed after the peak infection period (April- June) should ensure minimal problems the subsequent spring, and allow oysters to grow to market size before serious problems develop the following year.
Author:
Ryan B. Carnegie1
