Description
Kingdom, Phylum, Synonymy - The phylogenetic affinities of the genus Perkinsus have always been uncertain. It was originally identified as a fungus (now kingdom Fungi), and placed in the same genus as a parasite of fishes (Mackin et al. 1950), but later moved to the 'slime mold' group (Labyrinthomycota or Labyrinthomycetes) and given the name Labyrinthomyxa marina (Mackin and Ray 1966). Perkins found that this genus was not related and that it had little in common with the slime molds, but did have an apical complex (Perkins 1976). Subsequently, Levine (1978) renamed the genus Perkinsus, and transferred it to the phylum Apicomplexa. In recent years, ultrastructural and molecular studies have indicated that Perkinsus belongs to the clade Alveolata, including the phyla Ciliophora, Apicomplexa, and Dinoflagellata, but may not belong in the Apicomplexa (Perkins 1996; Siddall 1996).
Potentially Misidentified Species - Currently 6 species of Perkinsus are known: P. marinus, a parasite of Crassostrea virginica (Eastern Oyster); P. atlanticus, found in Ruditapes decussatus (Portuguese Clam); P. olseni, a parasite of the Australian abalones Haliotis ruber and H. laevigata; P. qugwadi a parasite of the Japanese Scallop Patinopecten yessoensis; P. chesapeaki; P. andrewsi, found in Macoma petalum = (M. balthica) and Crassostrea virginica in Chesapeake Bay (Coss 2002, personal communication; Perkins 1996; Siddall et al. 1996).
Other Taxonomic Groups - Bushek and Allen (1996) have found that P. marinus isolates from estuaries along the Atlantic coast of the United States vary in spore size, virulence, and possibly in environmental tolerance. Further studies will be needed to determine the systematic and ecological significance of this variation.
References - Bushek and Allen 1996; Coss 2002, personal communication; Levine 1978; Mackin et al. 1950; Mackin and Ray 1966; Perkins 1976; Perkins 1996; Siddall 1996
Taxonomy
| Kingdom | Phylum | Class | Order | Family | Genus |
|---|---|---|---|---|---|
| Protista | Apicomplexa | Perkinsea | Perkinsida | Perkinsidae | Perkinsus |
Synonyms
Invasion History
Chesapeake Bay Status
| First Record | Population | Range | Introduction | Residency | Source Region | Native Region | Vectors |
|---|---|---|---|---|---|---|---|
| 1949 | Established | Expanding | Cryptogenic | Regular Resident | Unknown-Marine | Unknown-Marine | Fisheries(Oysters-accidental), Shipping(Ballast Water) |
History of Spread
Perkinsus marinus (Dermo) was described (as Dermocystidum marinum) from Barataria Bay, LA, Gulf of Mexico, as a result of studies of seasonal patterns of Crassostrea virginica (Eastern Oyster) mortality. These studies began in 1946, as a result of lawsuits by oystermen against the oil industry (Mackin et al. 1950). Fisherman attributed the mortality to pollution by oil drilling operations, but field and laboratory investigations established the parasite as a major cause of oyster mortality in the Gulf of Mexico (Ray 1954; Ray 1996). The thioglycollate assay developed by Ray (1954) provided a reliable method of diagnosis. The organism is presumed to be native to the Gulf of Mexico. 'Dr. Owen found Dermo in some preserved Louisiana oysters that had been exhibited at a World's Fair (Chicago?) circa 1920. This finding indicates that Dermo was present in Lousiana oysters for at least several decades prior to its discovery' (Ray 1996). Perkinsus marinus has been reported from Brazil, Venezuela, Cuba, and throughout the Gulf of Mexico (Ford and Tripp 1996; Quick 1977). A massive mortality of C. virginica in Pearl Harbor HI was due to infection with P. marinus or a very similar organism (Kern et al. 1973).
Subsequent to the description of P. marinus in 1950 from the Gulf of Mexico, oyster infections and mortalities due to P. marinus have been observed along the Atlantic seaboard of the United States. In the 1980's and 1990's, an apparent northward spread of the disease has occurred, from Delaware Bay north to the Darmariscotta River ME (Ford 1996). Ford (1996) has argued that P. marinus has been widely introduced along the northeast Atlantic seaboard, but was persisting at undetectable levels, until a trend of increasing water temperature facilitated extensive outbreaks. Differences in cell size and infection intensity among Atlantic coast P. marinus populations suggest that they are genetically diverse (Bushek and Allen 1996a; Bushek and Allen 1996). Analysis of genotypes could clarify the origins of the Chesapeake and northeastern Perkinsus marinus populations.
Atlantic coast records of P. marinus are summarized:
Gulf of Mexico - Perkinsus marinus has been present in LA at least as early as ~1920 (Ray 1954; Ray 1996), and is widely and abundantly distributed in the Gulf (Ford and Tripp 1996; Quick 1977).
FL- Perkinsus marinus was found in oyster samples (Mackin 1951).
GA- Perkinsus marinus was observed 'as early as 1966' in Wassaw Creek and the Duplin and Woodbine Rivers. Heavy mortalities were reported in the state in 1985-1987 (Lewis et al. 1992).
SC - Perkinsus marinus was found in oyster samples (Mackin 1951). Extensive disease monitoring is lacking here, but the current status of the disease does not seem to have changed greatly since the 1980's, in contrast to more northern regions (Burreson and Ragone Calvo 1996).
NC - The first documented oyster mortality attributed to P. marinus was reported in 1988. Drought conditions in late the 1980's were associated with the spread of the disease throughout Pamlico Sound. High mortality continued through 1994 in Pamilco Sound, but may have declined slightly in Bogue Sound (Burreson and Ragone Calvo 1996).
Chesapeake Bay - Perkinsus marinus was first detected in oyster samples from the Rappahannock and James Rivers, which were collected in 1949 (Mackin 1951).
Chincoteague and Hog Island Bays, MD and VA - In early surveys, P. marinus was absent from the MD-VA Atlantic coast (Andrews and Hewatt 1957; Andrews 1988) In 1985-88, high prevalences of infection, and mortality were found in MD and VA waters of Chincoteague Bay in 1985-88 (Ford 1996; Lewis et al. 1992).
Delaware Bay- Perkinsus marinus was detected in planted oysters, imported from Chesapeake Bay, and in nearby native oysters, on the NJ side of the bay, as early as 1955. During 1955-1958, prevalences were usually below 40%, and mortalities were low, probably below 20%. The prevalence of the disease droped sharply after the onset of the Haplosporidium nelson (MSX) epizootic, due to reduction in the host population, and the cessation of oyster transplants. The parasite remained present in Delaware Bay, and some heavy infections were found in 1970's. In 1990, high rates of mortality were observed at Bivalve NJ. Intense infections contined through 1994 on the NJ side, with prevalences reaching 100%. However, infections remained scattered on the DE side (Ford 1996).
NJ Atlantic Bays (Great Bay, Tuckahoe River, Great Egg Harbor Bay) - Perkinsus marinus was first detected on the NJ Atlantic Coast in 1982, at low prevalence. By 1992, prevalence of the parasite reached 100%. In 1991, light infections were detected on the northern NJ coast, Manisquam River, and Raritan Bay (Ford 1996).
Long Island Sound - Perkinsus marinus was mentioned as enzootic (established and stable) by Quick (1977), but the basis for this unknown (Lewis et al. 1992; Kern, 1998). The first verfied report of the parasite was from Oyster Bay NY, where a high prevalence of light infections was seen in 1992. Previous samples at this site in 1991 had been negative (Ford 1996). By 1993-1994, P. marinus was abundant (26-75% prevalence) in western CT oyster beds (Milford, Bridgeport, Westport) (Brousseau 1996). However, extensive mortalities have not yet been reported from this region (Ford 1996).
Cape Cod, Martha's Vineyard MA - Heavily infected oysters were detected in several 'mainland' MA locations in 1991. By 1995, high prevalences were found in Wareham River (Buzzard's Bay), Cotuit Harbor (Nantucket Sound), Edgartown Great Pond (Vineyard Sound) and Wellfleet Harbor (Cape Cod Bay). Extensive mortalities had not been reported, however (Ford 1996).
Gulf of Maine (Damariscotta River)- In 1995, 26% of a sample of 70 oysters was found to be lightly infected with P. marinus (Kleinschuster and Parent 1995).
Chesapeake Bay region records are summarized below:
Lower Bay - Perkinsus marinus was first identified in oyster samples from the Rappahannock River, collected in 1949, during a period of extensive oyster mortality (Andrews and Hewatt 1957; Mackin 1951). 'There is no proof that the disease was present in Chesapeake Bay prior to 1949. Until there is evidence of recent introduction, we must assume that it has been present for many years and that oystermen do not have a new source of mortality with which to contend' (Andrews and Hewatt 1957). Extensive sampling in 1954 indicated that P. marinus was found from Hampton Roads into the lower James, York, Rappahannock, and Potomac, and Patuxent Rivers on the western shore, and up to Smith Island on the eastern shore (Andrews and Hewatt 1957).
The onset of the Haplosporidium nelsoni (MSX) epizootic altered the dynamics of the diseases, by drastically reducing oyster density, and by killing oysters at an earlier age than P. marinus did. In 1965, oysters artificially infected with P. marinus were placed in the York River. Most of these died of H. nelsoni infection. Lethal infections of P. marinus take 1-3 years to develop, and are favored by high oyster density and high water temperature (Andrews 1965; Andrews 1967). Through the 1970's into the mid-1980's, P. marinus was of secondary importance relative to H. nelsoni (Andrews 1979; Andrews 1988; Andrews 1996; Burreson and Ragone Calvo 1996). Its distribution in lower Bay rivers did not greatly change between 1954 (Andrews and Hewat in 1957) and 1985 (Burreson and Ragone Calvo 1996).
From 1985 to 1988, droughts greatly extended the distribution of P. marinus in the Chesapeake Bay. In 1986, seed oysters from the upper James River estuary became heavily infected, for the first time since P. marinus was discovered in the Bay. Oysters transplanted from these beds into Potomac tributaries, which had also been disease free, suffered extensive mortality. By 1988, P. marinus had reached Deepwater Shoal, the uppermost oysterbed in the James River, and prevalence continued to increase through 1991. In the Rappahannock, the uppermost oysterbed, Ross Rock, was infected for the first time in 1991. While the upstream spread of the disease was correlated with drought, subsequent wet years and cold winters (1993-1994) had little effect on the distribution of the disease in the James River (Burreson and Ragone Calvo 1996).
Upper Bay - Up to 1985, P. marinus was absent from the upper half of Chesapeake Bay. The pre-1985 distribution, mapped by Burreson and Ragone Calvo, was only slightly more extensive than that charted by Andrews and Hewat in 1954 (Andrews and Hewat 1957; Burreson and Ragone Calvo 1996). The upper Bay limit before 1985 extended from ~ 20 km north of Solomons to Taylors Island, both in MD waters. By 1987, as a result of drought conditions, the disease had spread north to the mouth of the Chester River. By 1992, P. marinus was present on every productive oyster bar in MD waters. Some decline in prevalence occurred due to high rainfall in 1994 (Burreson and Ragone Calvo 1996).
Hog Island - Chincoteague Bays - Andrews and Hewatt (1957) in the 1950's found that P. marinus was absent in the Atlantic coastal bay, even though seed oysters from Chesapeake Bay were often planted there. This was true until the mid 1980's (Andrews 1988). In 1985-1988, heavy infections occurred, with prevalences up to 96% and mortalities up to 84% have been found in MD and VA waters of Chincoteague Bay (Calvo et al. 1996; Lewis et al. 1992).
History References - Andrews 1965; Andrews 1967; Andrews 1979a; Andrews 1988; Andrews 1996; Andrews and Hewat 1957; Burreson and Ragone Calvo 1996; Bushek and Allen 1996a; Bushek and Allen 1996b; Calvo et al. 1996; Ford 1996; Ford and Tripp 1996; Kern et al. 1973; Kleinschuster and Parent 1995; Lewis et al. 1992; Mackin 1951; Mackin et al. 1950; Quick 1977; Ray 1954; Ray 1996
Invasion Comments
Invasions Status - Oyster disease researchers in the mid-Atlantic region disagree about the status of Perkinsus marinus in Chesapeake and Delaware Bays. Andrews (1996) suggested that the disease might have originated in Asia, where Perkinsus-like organisms are known, but evidence for this is lacking. A more likely source is the Gulf of Mexico, where P. marinus occurred at least as early as the 1920's (Ray 1954; Ray 1996). However, Chesapeake Bay did not receive extensive oyster transplants from the south until after the devastation of native stocks by Haplosporidium nelsoni (MSX) in the late 1950's, after the discovery of P. marinus in the Chesapeake. Some seed oysters from Pamlico Sound NC were planted in the Bay in the 1940's, and transplants from the Gulf of Mexico may also have occurred (Andrews 1980), but these are poorly documented (Carlton and Mann 1996). The spread of P. marinus northward from Chesapeake Bay is more clearly linked to movements of oysters. In Delaware Bay, the spread of oysters from imported Chesapeake seed to native oysters is well-documented. In addition to live oysters, shells and waste from shucking are potential vectors for spread of the diseases, as is ballast water (Ford 1992). However, Ford (1992, 1996) argues that transport of the parasite alone was not sufficient to produce outbreaks, and that warming of northeastern waters was a major cause of epizootics north of Chesapeake Bay.
Regular seasonal oyster mortalities in Chesapeake Bay, and occasional more massive events are known to have occurred long before the discovery of P. marinus (Andrews and Hewatt 1954), leading some workers to conclude that the disease may have been native to the Bay and exacerbated by stress and disturbance associated with the fishery (Burreson 1998; Kennedy 1996; Shields personal communication 1998). An ongoing examination of of a large collection of histological slides made by Victor Loosanoff in the 1930's has failed to find P. marinus in oysters from Delaware and Chesapeake Bay so far, but many more slides remain to be examined (Kern 1998).
Ecology
Environmental Tolerances
| For Survival | For Reproduction | |||
|---|---|---|---|---|
| Minimum | Maximum | Minimum | Maximum | |
| Temperature (ºC) | 1.0 | 35.0 | 15.0 | 30.0 |
| Salinity (‰) | 6.0 | 68.0 | 13.0 | 40.0 |
| Oxygen | ||||
| pH | 8.6000000000 | 7.4000000000 | ||
| Salinity Range | meso-eu |
Age and Growth
| Male | Female | |
|---|---|---|
| Minimum Adult Size (mm) | 0.0 | 0.0 |
| Typical Adult Size (mm) | 0.1 | 0.1 |
| Maximum Adult Size (mm) | 0.1 | 0.1 |
| Maximum Longevity (yrs) | ||
| Typical Longevity (yrs |
Reproduction
| Start | Peak | End | |
|---|---|---|---|
| Reproductive Season | |||
| Typical Number of Young Per Reproductive Event |
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| Sexuality Mode(s) | |||
| Mode(s) of Asexual Reproduction |
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| Fertilization Type(s) | |||
| More than One Reproduction Event per Year |
|||
| Reproductive Startegy | |||
| Egg/Seed Form |
Impacts
Economic Impacts in Chesapeake Bay
Perkinsus marinus (Dermo) has had severe economic effects on Chesapeake Bay and the surrounding region. While it is difficult to separate out effects of Haplosporidium nelsoni (MSX) and overharvesting, the intensification and spread of P. marinus infections since 1985 has played a large part in the decline of the Chesapeake Bay fishery for Crassostrea virginica (Eastern Oyster), by producing high oyster mortalities in Bay regions previously unaffected by disease (Burreson and Ragone Calvo 1996; MacKenzie 1996). The parasite affected fisheries directly by drastic reducing oyster biomass and harvests, as well as indirectly, through elimination of oysterbeds as habitats, and possibly also through altering Bay foodwebs, through elimination of a major filter-feeder (Kennedy 1996).
Fisheries - Patterns of mortality consistent with P. marinus infection have been known from VA waters of Chesapeake Bay since the 1940's (Andrews and Hewatt 1957). While P. marinus was studied as a major source of oyster mortality, the period when it was known as the primary oyster disease in Chesapeake Bay (1949-1959) was a period of relatively high oyster harvests (3-4 million bushels per year) (Andrews 1988; Burreson and Ragone Calvo 1996; Ford and Tripp 1996). Its mortality was considered tolerable, and management practices were altered to minimize losses. Recommendations made as a result of studies in the 1950's included not holding oysters after they reached market size, not transplanting oysters from disease-free into P. marinus endemic waters, harvesting in late spring (just before the onset of infection), continual disease monitoring, and development of disease-resistant oyster stocks (Andrews and Ray 1988; Andrews and Hewatt 1957). The last goal has proved elusive (Ford and Tripp 1996; Krantz and Jordan 1996). Natural populations of C. virginica do vary in resistance, but even in areas where P. marinus and C. virginica are known to have long coexisted, epizootic outbreaks are common (Bushek and Allen 1996a; Mackin 1951; Ford and Tripp 1996).
The onset of the MSX epizootic overshadowed P. marinus in the 1960's and 1970's as harvests fell to 0.5-1 million bushels per year, but after 1985, P. marinus greatly expanded its range and apparently intensified its virulence. A major problem resulting from the expansion was the spread of P. marinus into James River areas that had been the primary source of seed oysters in the Bay (McKenzie 1996). Transplants from these seed areas in 1985 greatly aided the spread of the parasite (Burreson and Ragone Calvo 1996).
Currently, fewer than 5% of VA's traditional public oyster grounds are productive (Burreson and Calvo 1996). The state's total market oyster harvest, centered on the James River, but also including many other estuaries, dropped from ~4 million bushels/year in 1958 to 0.4-.6 million bushels/year in 1984-86 (Lipton et al. 1992). 'As a consequence of the small oyster stocks in Virginia, few tongers and planters remain active. The planters spread only test quatities of seed to determine whether they will live. Most oyster boats have decayed, lie in disuse around the Virginia oystering ports, or are used in other ventures' (MacKenzie 1996).
In MD, the economic impact of P. marinus was delayed by the parasite's intolerance of low salinities. However, in 1985-1987, oyster landings in MD waters had been about 2-2.7 million bushels per year in the 1960's to 1981, but following the increased incidence of both P. marinus and H. nelsoni, they fell to 400,000 bushels in 1987, and 125,000 bushels in 1992-93. The oystering fleet fell from 1,200 hand-tonging boats, 700 patent-tonging boats, and 45 skipjacks, in the 1960's to 400 hand-tonging boats, 30 suba divers, and 7 skipjacks in 1992-93. A slight recovery occurred with lower salinities in 1992-94 (MacKenzie 1996). H. nelsoni and P. marinus have also shifted the geography of oyster production up the bay. In 1973-74, 2.1% of the oyster harvest came from the Chester River; in 1993-94, 66% was from the Chester River (Burreson and Calvo 1996). A slight recovery in the harvest occurred in 1993-94 due to lower salinities (Burreson and Ragone Calvo 1996), but this has not altered the overall picture. The last oyster/shucking houses along the Bay have closed, so that the oysters which are harvested must be sent to southern states for packing (Kern 1998). 'Some Maryland ports still have oyster boats in them, but most are in disuse and various states of decay' (MacKenzie 1996).
Intensification and spread of the disease, as well as improved knowledge of the biology of P. marinus, has led to a need for development of new management practices. Disease-free seed areas in the Bay no longer exist (Krantz and Jordan 1996), and infective P. marinus cells are now known to be widespread throughout Chesapeake Bay (Calvo and Burreson 1996). In MD in recent years, fossil shell has been planted in areas several miles from existing beds, for production of seed oysters which were then transplanted to low salinity waters for growth to harvestable size. Six Oyster Recovery Areas were designated in MD tributaries, where no diseased seed oysters (0% prevalence of P. marinus and H. nelsoni) could be planted. Here, only hatchery-reared stock is planted. Comprehensve disease monitoring has been instituted in order to try to prevent the planting of infected seed oysters in MD waters. Additional steps, such as hatchery-rearing of seed and selective rearing of disease-resistant oysters are being investigated (Krantz and Jordan 1996).
Habitat Change - Reduction in the area of oyster beds has the potential to affect feeding and cover for some commercial fish species, including juvenile Morone saxatilis (Striped Bass) (Kennedy 1995).
Aesthetics - It has been suggested that the decrease in the filtering biomass of oysters is linked to an increase in phytoplankton concentrations, which has resulted in decreased visibility. A possible (but poorly documented) consequence of the intensification of the planktonic foodweb is an increased abundance of Chrysaora quinquecirrha (Sea Nettle) (Kennedy 1995).
References- Andrews and Hewatt 1957; Andrews and Ray 1988; Burreson and Ragone Calvo 1996; Bushek and Allen 1996a; Calvo and Burreson 1996; Ford and Tripp 1996; Kennedy 1995; Kern 1998; Krantz and Jordan 1996; Lipton et al. 1992; Mackin 1951; MacKenzie 1996
Economic Impacts Outside of Chesapeake Bay
Perkinsus marinus (Dermo) has long been endemic in the Gulf of Mexico, and for at least 50 years in Chesapeake Bay, but it has only become a major factor in oyster fisheries north of Chesapeake Bay since 1985 (Ford 1996). Management of oyster stocks in the Gulf of Mexico and the Atlantic coast south of Chesapeake Bay is complicated by the extended growth season of the parasite, its widespread occurrence, and high levels of prevalence. In LA, until approximately 1975, oystermen coped with the parasite by harvesting oysters at very small sizes and selling them to the canned oyster trade, until their crop was no longer competitive with imported oysters. Early harvesting is still the primary strategy in dealing with P. marinus in the Gulf of Mexico (Andrews and Ray 1988; Lewis et al. 1992).
In Delaware Bay, P. marinus was detected in planted oysters, imported from Chesapeake Bay, and in nearby native oysters, on the NJ side of the bay, as early as 1955 but prevalences and mortalities were low, and became negligable after the onset of the Haplosporidium nelsoni (MSX) epizootic, due to reduction in the host population, and the cessation of oyster transplants. In 1990, high rates of mortality due to P. marinus were observed at Bivalve NJ. Intense infections contined through 1994 on the NJ side, with prevalences reaching 100%. However, infections remained scattered on the DE side (Ford 1996). In 1993-1994, due to P. marinus mortalities, no oysters were produced on the NJ side of the bay, and only 7,000 bushels on the DE side (MacKenzie 1996). The two oyster packing houses, and one shucking house left on the Bay process mainly out of state oysters, and seafood products other than oysters, and many of the remaining oystering boats are in poor condition (MacKenzie 1996). Extensive mortalities due to P. marinus have not yet been seen further north, thought the parasite has been detected north to ME, but are expected, based on the disease's intensification in Delaware and Chesapeake Bays (Ford 1996).
References - Andrews and Ray 1988; Ford 1996; Lewis et al. 1992; MacKenzie 1996
Ecological Impacts on Chesapeake Native Species
Perkinsus marinus (Dermo) has had significant effects on the native biota of the Chesapeake Bay, as a major cause of mortality of the Crassostrea virginica (Eastern Oyster). In combination with human harvesting and Haplosporidium nelsoni (MSX) has played a major role in the decline of oyster populations in Chesapeake Bay. While P. marinus is responsible for widespread oyster mortality, large biomasses of oysters occur in its presumed native regions in the Gulf of Mexico and on the Atlantic coast south of Chesapeake Bay (Andrews 1988; Lewis et al. 1992). A major difference between P. marinus and H. nelsoni is that Dermo typically kills older oysters (1 to 3 years older) and usually permits substantial amounts of reproduction, while MSX can nearly eliminate pre-reproductive oysters (Mackin 1951; Andrews 1967). Perkinsus marinus has long been present in Chesapeake Bay but its recent intensification, and spread to previously unaffected regions, together with H. nelsoni, has devasted Chesapeake oyster populations (Burreson and Ragone Calvo 1996; McKenzie 1996).
Parasitism - Perkinsus marinus (Dermo) is believed to enter oysters though the digestive epithelium, where the earliest lesions are produced. Infection is accompanied by sloughing of digestive epithelia and hemocytes into the stomach and intestine, with atrophy of the digestive tubules and occlusion of hemolymph vessels. Infected oysters are marked by a proliferation of brown cells containing lipofuschin, a residue of lysosomal activity (Mackin 1951; Ford and Tripp 1996). Extensive attack of connective tissue occurs, resulting in many small abcesses or 'conversion of the entire visceral mass into one large abcess' (Mackin 1951). Causes of death include occlusion of hemolymph vessels, lytic factors (proteases) secreted by the parasite and overall energy and nutrient depletion (Ford and Tripp 1996).
Infected oysters may have reduced shell growth, decreased condition index (dry tissue weight/shell volume X 1000) and decreased adductor muscle strength (Ford and Tripp 1996; Paynter 1996). Additional indications of physiological impairment include decreased concentrations of amino acids involved in osmoregulation (Paynter et al. 1995), acidosis of hemolymph, and reduced tolerance of hypoxia. However, filtering rate and reproductive capacity are not greatly affected by low levels of infection (Kennedy et al. 1995; Paynter 1996). Severe infections can interfere with the earlier stages of gametogenesis (Mackin 1961; Ford and Tripp 1996).
Oyster populations show varying degrees of resistance, depending on frequency and duration of previous exposure. Early observations indicated that oysters from areas where the disease was absent were much more vulnerable to P. marinus than those from areas where the disease was enzootic (Andrews and Hewatt 1957). However, early breeding experiments failed to show evidence of heritable resistance (Ford and Tripp 1996, possibly because of interference from Haplosporidium nelsoni (MSX) (Andrews 1967; Ford and Tripp 1996). Bushek and Allen (1996a) found evidence of heritable geographic variation in resistance to P. marinus, related to the apparent length of exposure of populations to the parasite, but also evidence for variation in the virulence of the parasite. However, oysters resistant to another pathogen, H. nelsoni did not show increased resistance to P. marinus, indicating that resistance to the two diseases involves separate mechanisms, and that loss of genetic diversity through inbreeding for H. nelsoni resistance may decreased the possibility of evolution of P. marinus resistance (Burreson 1991; Ford and Tripp 1996).
The occurrence of geographical variation in resistance of C. virginica and and of virulence of P. marinus suggests that some co-evolution of host and parasite has occurred. However, even in the Gulf region, where the disease is long-established, epizootic outbreaks occur every few years (Mackin 1961; Ford and Tripp 1996). Possible reasons for expansion and intensification of the disease include transfers of new strains of the parasite with oyster transplants, or changes in environmental conditions such as drought or pollution, which favor the parasite or decrease host resistance (Bushek and Allen 1996b; Ford and Tripp 1996).
Population effects of P. marinus epizootics may be greater in the Chesapeake Bay region than in the Gulf of Mexico, because the slower growth rate of oysters means that fewer animals are likely to reproduce before the infection becomes lethal (Bushek and Allen 1996a). Chesapeake isolates of P. marinus produced heavier infections than Gulf isolates at 27 C, suggesting that northern strains have been selected for more rapid proliferation during a shorter growing season (Bushek and Allen 1996a).
Since its discovery in lower Chesapeake Bay in 1949, P. marinus was responsible for significant oyster mortality, but because of heavy sets and good supplies of disease-free seed oysters, oyster biomass and harvests were not greatly affected until the onset of the Haplospridium nelsoni (MSX) epizootic in 1959 (Andrews and Hewatt 1957; Burreson and Ragone Calvo 1996). Annual mortalities, primarily due to Dermo, of test seed oysters in trays at Gloucester Point in 1959 ranged from 24-59% . With the arrival of Haplospridium nelsoni, mortalities increased to above 90%, and the significance of Dermo declined, since Haplospridium nelsoni killed most oysters before they could be infected with P. marinus (Andrews 1988).
Beginning in 1985, a period of prolonged droughts was marked by the rapid expansion of P. marinus into previously uninfected lower-salinity areas, including seed oyster beds in VA tributaries, and the uppermost oysterbeds in MD waters (Andrews 1988; Burreson and Ragone Calvo 1996; Calvo et al. 1996). At the same time, the virulence of the disease appears to have increased compared to the 1950's pattern, so that oysters now have up to 90% mortality in their second year, greatly reducing reproductive stocks (Burreson and Ragone Calvo 1996). As result of intensified Dermo epizootics, combined with widespread Haplosporidium nelsoni epizootics, 5% of traditional oyster grounds in VA are still productive, and areas in the James River, formerly used as seed areas, are now the primary harvesting sites, and the bulk of the MD harvest now occurs north of the Bay Bridge. In 1972-74, 2% of the MD harvest came from the Chester River; in 1993-1994, 66% came from there (Burreson and Ragone Calvo 1996; MacKenzie 1996).
Competition - A haplosporidian oyster parasite, Haplosporidium costale (SSO; Seaside Disease), believed to be native to the Chesapeake region (Burreson 1998; Kern 1998) now co-occurs with Perkinsus marinus in Atlantic coastal embayments of VA-MD, north to NJ and possibly ME in high-salinity waters (above 25 ppt) (Andrews 1976; Ford and Tripp 1996; Wood and Andrews 1962). Perkinsus marinus was formerly absent from Chincoteague and other coastal Atlantic Bays, but after 1985 it was detected in these waters (Burreson and Ragone Calvo 1996; Lewis et al. 1992). Interactions between these two diseases have not been studied.
Habitat Change- Perkinsus marinus has had significant effects on Chesapeake Bay habitats through its effects on Crassostrea virginica (Eastern Oyster). Oysters are a major source of structure, providing substrate and cover for a wide range of mobile and sessile fauna (Kennedy 1996; Lippson and Lippson 1984), as well as filter feeders removing phytoplankton from a large fraction of the water column (Newell 1988). Before 1985, P. marinus appears not to have seriously affected the extent of oyster bed habitat or prevented the occurrence of a substantial filtering biomass. However, the expansion and intensification in the 1980's of Dermo disease has played a major role, together with MSX and human harvesting, in reducing the ecological role of oysters in Chesapeake Bay (Burreson and Ragone Calvo 1996; Kennedy 1996).
References - Andrews 1967; Andrews 1976; Andrews 1988; Andrews and Hewatt 1957; Burreson 1998; Burreson and Ragone Calvo 1996; Bushek and Allen 1996a; Bushek and Allen 1996b; Calvo et al. 1996; Ford and Tripp 1996; Kennedy 1996; Kennedy et al. 1995; Kern 1998; Lewis et al. 1992; Mackin 195; Mackin 1961; MacKenzie 1996; Newell 1988; Paynter 1996; Paynter et al. 1995; Wood and Andrews 1962
Ecological Impacts on Other Chesapeake Non-Native Species
Parasitism - Perkinsus marinus (Dermo) is not known to infect any established introduced species in Chesapeake Bay, but the parasite does grow in Crassostrea gigas (Pacific Oyster) and C. ariakensis, which have been proposed as introductions to Chesapeake Bay, because of its disease resistance. Small, poorly documented illegal introductions of C. gigas have occured, but no established populations are known on the Atlantic coast (Andrews 1980; Mann and Burreson 1991). In trials in closed systems and quarantined flumes, C. gigas had lower P. marinus prevalences (80 vs 100%) and lighter infections than C. virginica (Eastern Oyster) under the same conditions. P. marinus thus would appear to have less impact on introduced C. gigas populations than on the native C. virginica. However, C. gigas suffered from high non-disease mortality (Barber and Mann 1994; Barber 1996), rasing doubts about its suitability for Chesapeake Bay (Gottlieb and Schweighofer 1996). Researchers turned to another Asian oyster, C. ariakensis (Suminoe Oyster), which showed both rapid growth under Chesapeake Bay conditions, and considerable disease resistance. In field trials, sterile triploid C. ariakensis had 0 to 75% prevalence of P. marinus, but suffered only light infections, which did not interfere with rapid growth and good survival (Calvo et al. 2001).
Competition - We consider H. nelsoni (MSX) to be a probable introduction to Chesapeake Bay. Perkinsus marinus can be considered a competitor with H. nelsoni, since both parasites can kill oysters, depriving the other of hosts. H. nelsoni is now found from FL north to ME, and occurs at salinities above 10 ppt (Ford and Tripp 1996). During the onset of the H. nelsoni epizootic in the lower York River, 'Dermo' infections were rare because oyster populations had become too sparse to support the epidemic. (Andrews and Wood 1967). 'Dermo' requires dense populations and high temperatures to produce epizootics (Andrews 1967). Intensifications of P. marinus infections in the 1980's and 1990's are likely to have affected the extent of mortality due to H. nelsoni (Haskin and Andrews 1988). Oysters have evolved some resistance to each parasite, but the existence of two major parasites (H. nelsoni, P. marinus) in Chesapeake Bay, and the probable evolution of the parasites themselves means that complex interactions are likely.
Habitat Change - Since reduction of oyster biomass is likely to have far-reaching effects on habitat and foodwebs (Kennedy 1996), introduced and cryptogenic species are likely to be affected as well. Infaunal filtering species such as Rangia cuneata could benefit by increased phytoplankton biomass, while fouling species, such as the cryptogenic Ischadium recurvum (Hooked Mussel), and introduced Garveia franciscana (Rope Grass hydroid), Cordylophora caspia (Freshwater Hydroid), Diadumene lineata (Striped Sea Anemone), and others, could suffer from the loss of hard substrate, even while benefitting from increased phyto- and zoo- plankton abundance. In the absence of long-term monitoring of these organisms, population effects due to H. nelsoni or other oyster diseases remain speculative.
References - Andrews 1980; Andrews and Wood 1967; Barber and Mann 1994; Barber 1996; Ford and Tripp 1996; Gottlieb and Schweighofer 1996; Haskin and Andrews 1988; Kennedy 1996; Mann and Burreson 1991
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