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| 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.
Questions/comments regarding the design of this website should be directed to Gregory Mears.
(This page was last updated 12/08/2005 )