Oyster Diseases of the Chesapeake Bay

— Dermo and MSX Fact Sheet —

Virginia Institute of Marine Science

Scientific Name: Perkinsus marinus 1966 and as Perkinsus marinus in 1978. The disease was found in Chesapeake Bay in 1949 Common Name: Dermo, Perkinsus and it has consistently been present in the Bay since that time. The parasite was observed in Taxonomic Affiliation: Delaware Bay in the mid 1950s following the Kingdom = Protista, Phylum = Undetermined importation of seed from the Chesapeake Bay. An embargo of seed resulted in a disappearance Species Affected: of the disease from Delaware Bay for more than Crassostrea virginica (eastern oyster) 3 decades. However, an epizootic recurred in Delaware Bay in 1990 and since 1991 the Geographic Distribution: parasite has been found in Connecticut, New East coast of the US from Maine to Florida and York, Massachusetts, and Maine. This apparent along the Gulf coast to Venezuela. Also docu- range extension is believed to be associated with mented in Mexico, Puerto Rico, Cuba, and abnormally high winter temperatures, drought Brazil. conditions, and the unintentional introduction of infected oysters or shucking wastes. History: Dermo disease was first In the Chesapeake Bay, Dermo disease has documented in the 1940s in increased in importance since the mid 1980s. the Gulf of Mexico where it Several consecutive drought years coupled with was associated with exten- above average winter temperatures resulted in sive oyster mortalities. The expansion of the parasite’s range into upper causative agent was initially tributary areas and the parasite became estab- thought to be a fungus and lished at all public oyster grounds in Virginia. was called Dermocystidium The parasite has persisted in these areas despite marinum. Based on struc- a return to normal salinity conditions. In tural characteristics the addition to its baywide distribution, Dermo is organism was reclassified also present in the embayments along the Labyrinthomyxa marina in Atlantic coast of Virginia. Dermo Dermo Dermo Dermo Dermo Biology and Epizootiology: infections intensify above a threshold of 20°C. The seasonal cycle of P. marinus has been well At temperatures above 25°C, the parasite documented in Chesapeake Bay. Transmission of rapidly multiplies, spreads, and kills oysters. the parasite is direct from oyster to oyster. Infections decline at temperatures below 15- Waterborne infective stages are present through- 20°C. In nature the most dramatic decline is out the warm months, May through October. observed in late winter and early spring. Abnor- Initial infections are typically observed in July mally warm winters may result in a higher and peak prevalences and maximum mortalities proportion of over-wintering parasite cells. are observed in September and October. Preva- lence in surviving oysters declines dramatically Prevalence and infection intensities of P. marinus during the late winter and spring and infections increase with increasing salinity. During may become undetectable by the standard drought years, elevated salinities result in an diagnostic assay. However, low numbers of intensification of the disease. High intensity parasites remain and these parasites proliferate infections and high mortalities often occur in once temperatures increase in late spring. areas with salinities above 12-15 ppt. Infection Infective stages of the parasite are released from intensities remain low in areas with salinity infected and dying oysters, thereby initiating consistently below 9 ppt. Once established in a another infection cycle. The infective stages low salinity area the parasite can persist for become waterborne and are acquired as oysters years. feed. Within the oyster, early infections are observed in digestive gland tissues. The most Control Measures: prominent stage is a single cell stage called the Dermo disease is easily transmitted from oyster trophont. These cells divide forming a multicel- to oyster so it is imperative to avoid moving lular stage called a meront. Meronts enlarge infected oysters into an area containing and rupture releasing many small single cells. uninfected oysters. Holding oysters at salinities Under certain conditions, in artificial media and less than 9 ppt will retard disease development occasionally in moribund oysters, the parasite and restrict disease associated mortalities. If produces a third stage known as a biflagellate possible, let grow out areas remain fallow for one zoospore. to two years before planting seed stocks.

Infections are usually not acquired in oysters less Diagnostic Method: than a year old but prevalences may be high Fluid thioglycollate media (FTM) culture assay during the oysters second year and mortality is the standard diagnostic technique. This may result. Moderately to heavily infected method involves culturing small pieces of oyster oysters usually exhibit a reduction in growth tissue in FTM for 4-7 days. Following culture rate, poor condition, and reduced reproductive the tissue is stained with Lugol’s iodine and capacity. Oyster death results as a consequence examined using a light microscope. Perkinsus of hundreds of thousands of parasites “taking marinus cells will appear as blue to black stained over” the oyster, lysing tissues, and occluding spheres. Modifications of this assay exist for the hemolymph vessels. examination of oyster hemolymph and total parasite burdens in whole oyster tissues. Poly- Environmental Influences: merase reaction chain (PCR) assays have also Temperature and salinity are the two most been developed; however, PCR is not employed important environmental factors influencing for routine diagnosis. Dermo disease. The parasite proliferates and Scientific Name: Haplosporidium nelsoni occurred in Maine and New York. Description of the spore stage of the parasite led to it being Common Name: MSX (multinucleated named Minchinia nelsoni in 1966. The parasite sphere unknown) was later renamed Haplosporidium nelsoni in 1980. Taxonomic Affiliation: Kingdom = Protista, Phylum = Haplosporidia Biology & Epizootiology: Haplosporidium nelsoni is a spore-forming proto- Species Affected: zoan. The predominant stage of the organism in Crassostrea virginica (eastern oyster), possibly the oyster is a multinucleated plasmodium, Crassostrea gigas (pacific oyster) which ranges in size from 5-100 m. The production of spores (sporulation) is rare in Geographic Distribution: adult oysters but has been observed at In the US, MSX disease ranges from prevalences as high as 40% in spat. Sporulation Damariscotta River, Maine to Biscayne, Florida. occurs in late June through early July and in the It is not present in the Gulf of Mexico. Epi- autumn. The infective stage has never been zootic mortalities have been limited to Chesa- recognized but it is believed to be a uninucleate peake and Delaware Bays and recently Long form that is released by a spore. The complete Island Sound. The parasite has also been found life cycle remains unknown. Controlled trans- in C. gigas from Korea and Japan. mission of the parasite has not been achieved despite many laboratory attempts. The inability History: to transmit the parasite combined with the rarity The disease was first documented in 1957 in of spore stages, the lack of correlation of the Delaware Bay where it caused massive oyster disease with oyster density and its ability to mortalities and two years later it was found in spread rapidly over long distances has led to the the lower Chesapeake Bay. At that time the hypothesis that an alternate or intermediate disease agent was given the acronym MSX- host exists. multinucleated sphere X (unknown). In the 1960s the parasite was found in coastal bays of In the Chesapeake Bay, oysters become infected North Carolina, Virginia, from mid-May through October; however, Maryland, Delaware, New infection pressure during late summer and Jersey, Connecticut and autumn is quite variable from year to year. New York, but associated Infections develop rapidly in susceptible oysters oyster mortalities did not resulting in mortalities from July through Octo- occur south of Virginia or ber. Surviving oysters may maintain a high north of New Jersey. In prevalence of the disease through the winter the 1980s, an apparent and a second period of mortality may occur in range extension occurred spring. Oysters acquiring infections in late as the parasite was re- autumn may harbor low level infections, which ported as far north as intensify the following summer. These infec- MSX MSX MSX

MSX MSX Maine and as far south as tions often proliferate as temperatures warm in Florida. Since 1995, MSX June causing early summer mortalities. associated mortalities have The disease can affect all ages of oysters, spat to Control Measures: adult. Infections are acquired through gill and Use MSX disease resistant oyster strains. Main- mantle tissue, and can rapidly spread through- tain oysters in disease-free areas (low salinity). out the oyster. If oysters must be moved to high salinity areas for growth and conditioning, the move should Environmental Influences: be timed to avoid the early summer infection Temperature and salinity play an important role period. Low-salinity immersion to expulse MSX in regulating MSX. Infections are acquired at infections may be valuable, but critical time- temperatures above about 20°C. Three critical temperature-salinity combinations have not temperatures have been proposed for oyster-H. been thoroughly determined. Avoid importa- nelsoni interactions. Both parasite and oyster are tion of infected oysters into grow-out area. inactive at temperatures <5°C. At 5-20°C, the parasite proliferates more rapidly than the oyster Diagnostic Method: can control it. Above 20°C, resistant oysters Histological examination using light microscopy can overcome the parasite while susceptible of paraffin embedded tissue sections is the oysters are killed. standard diagnostic technique for MSX. Alter- native methods include screening of hemolymph Salinity is important in determining the distribu- and employment of molecular tools including tion of the disease within an estuary. A salinity polymerase chain reaction (PCR) and DNA of 15 ppt is required for infection, 20 ppt is probe assays. required for rapid and high mortality, and 10 ppt or below results expulsion of the parasite at temperatures above 20°C.

WMILLIAM& ARY

VIIRGINIA NSTITUTE OF MS ARINE CIENCE SMSCHOOL OF ARINE CIENCE