Dermo Fact Sheet
Scientific Name: Perkinsus marinus
Common Name: Dermo, Perkinsus
Taxonomic Affiliation: Phylum = Alveolata,
Family = Perkinsidae
Species
Affected: Crassostrea
virginica (eastern oyster); experimental infections in Crassostrea
gigas (Pacific oyster) and Crassostrea ariakensis (Suminoe oyster)
| Geographic Distribution | Environmental Influences |
| History | Control Measures |
| Biology and Epizootiology | Diagnostic Method |
Geographic Distribution:
East coast of the US from Maine to Florida and along
the Gulf coast to the Yucatan Peninsula. Reports of P. marinus from other
areas need to be confirmed as P. marinus with molecular assays.
History:
Dermo
disease was first documented in the 1940s in the Gulf of Mexico where it was
associated with extensive oyster mortalities. The causative agent was initially
thought to be a fungus and was called Dermocystidium marinum. Based on
structural characteristics the organism was reclassified Labyrinthomyxa
marina in 1966 and as Perkinsus marinus in 1978. The disease was
found in Chesapeake Bay in 1949 and it has consistently been present in the Bay
since that time. The parasite was observed in Delaware Bay in the mid 1950s
following the importation of seed from the Chesapeake Bay. An embargo of seed
resulted in the disappearance of the disease from Delaware Bay for more than 3
decades. However, an epizootic recurred in Delaware Bay in 1990 and since 1991
the parasite has been found in Connecticut, New York, Massachusetts, and Maine.
This apparent range extension is believed to be associated with abnormally high
winter temperatures, drought conditions, and the unintentional introduction of
infected oysters or shucking wastes.
In the Chesapeake Bay, Dermo disease has increased in importance since the mid 1980s. Several consecutive drought years coupled with above average winter temperatures resulted in expansion of the parasite's range into upper tributary areas and the parasite became established at all public oyster grounds in Virginia. The parasite has persisted in these areas despite a periodic return to normal salinity conditions. In addition to its baywide distribution, P. marinus is also present in the embayments along the Atlantic coast of Virginia.
Biology and Epizootiology:
The
seasonal cycle of P. marinus has been well documented in Chesapeake Bay.
Transmission of the parasite is direct from oyster to oyster. Waterborne
infective stages are present throughout the warm months, May through October.
Initial infections are typically observed in July and peak prevalences and
intensities, and maximum mortalities, are observed in September and October.
Prevalence in surviving oysters declines dramatically during the late winter and
spring and infections may become undetectable by the standard diagnostic assay.
However, low numbers of parasites remain and these parasites proliferate once
temperatures increase in late spring. Infective stages of the parasite are
released from infected and dying oysters, thereby initiating another infection
cycle. The infective stages become waterborne and are acquired as oysters feed.
Within the oyster, early infections are observed in digestive gland tissues. The
most prominent stage is a single cell stage called the trophont. These cells
divide forming a multicellular stage called a meront. Meronts enlarge and
rupture releasing many small trophonts. Under certain conditions, in artificial
media and occasionally in moribund oysters, the parasite produces a third stage
known as a biflagellate zoospore.
Infections are usually not acquired in oysters less than a year old but prevalences may be high during the oysters second year and mortality may result. Moderately to heavily infected oysters usually exhibit a reduction in growth rate, poor condition, and reduced reproductive capacity. Oyster death results as a consequence of hundreds of thousands of parasites "taking over" the oyster, lysing tissues, and occluding hemolymph vessels.
Environmental Influences:
Temperature and salinity are the two most
important environmental factors influencing Dermo disease. The parasite
proliferates and infections intensify above a threshold of 20°C. At temperatures
above 25°C, the parasite rapidly multiplies, spreads, and kills oysters.
Infections decline at temperatures below 15-20°C. In nature the most dramatic
decline is observed in late winter and early spring. Abnormally warm winters may
result in a higher proportion of over-wintering parasite cells.
Prevalence and infection intensities of P. marinus increase with increasing salinity. During drought years, elevated salinities result in an intensification of the disease. High intensity infections and high mortalities often occur in areas with salinities above 12-15 ppt. Infection intensities remain low in areas with salinity consistently below 9 ppt. Once established in a low salinity area the parasite can persist for years.
Control Measures:
Dermo disease is easily transmitted from oyster to
oyster so it is imperative to avoid moving infected oysters into an area
containing uninfected oysters. Holding oysters at salinities less than 9 ppt
will retard disease development and restrict disease associated mortalities. If
possible, let grow out areas remain fallow for one to two years before planting
seed stocks.
Diagnostic Method:
Ray's Fluid thioglycollate media (RFTM) culture assay
is the standard diagnostic technique. This method involves culturing small
pieces of oyster tissue in FTM for 4-7 days. Following culture the tissue is
stained with Lugol's iodine and examined using a light microscope. Perkinsus
marinus cells will appear as blue to black stained spheres. Modifications of
this assay exist for the examination of oyster hemolymph and total parasite
burdens in whole oyster tissues. The RFTM assay is not species specific and will
diagnose any Perkinsus sp. Species specific polymerase chain reaction
(PCR) assays have been developed; however, PCR is not employed for routine
diagnosis.













