Epizootiology Of Perkinsus Marinus Disease Of Oysters In Chesapeake Bay, With Emphasis On Data Since 1985

Since 1987 Perkinsus marinus has been the most important pathogen of the eastern oyster, Crassostrea virginica, in Chesapeake Bay because of its widespread distribution and persistence in low salinity areas. The pathogen became established on all oyster beds in the Chesapeake Bay as a result of natural spread during the consecutive drought years from 1985 to 1988 or by movement of infected oysters during the same period. Elevated salinities resulting from drought conditions and concomitant warm winters allowed P. marinus to proliferate in what were historically low salinity areas. Oyster mortality was high on most beds and landings of market oysters declined to record low levels in both Maryland and Virginia during the late 1980s and early 1990s. The seasonal periodicity of P. marinus is primarily controlled by temperature. Both prevalence and intensity of infections begin to increase in June as temperature increases above 20 degrees C and overwintering infections begin to proliferate. Maximum values of prevalence and intensity occur in September immediately following maximal summer temperatures. Infection regression occurs during winter and spring as temperature declines resulting in minimum prevalence and intensity values in April and May. Prevalence and intensity of P. marinus infections in oysters from the James River, VA, over a five year period were significantly correlated with temperature when temperature data were lagged three months. Temperature explained 39% of the variability in prevalence and 46% of the variability in intensity. The relationship between temperature and annual variability in P. marinus abundance is somewhat obscure, in part because of the difficulty separating salinity and temperature effect. Nonetheless, data from 1988 to 1994 from the James River, VA, suggest that abnormally warm winters have a more significant Impact on summer P. marinus abundance than abnormally cold winters. Salinity is the primary environmental factor that controls local distribution and intensity of P. marinus infections. Long-term oyster disease monitoring along a salinity gradient in the James River, VA, revealed a statistically significant relationship between salinity and P. marinus prevalence and intensity. P. marinus infections remain light in intensity and no oyster mortality results if salinity is consistently less than 9 ppt. However, infections may persist for years in low salinity areas. If summer/fall salinities range from 9 to 15 ppt some infections may progress to moderate and heavy intensity, but oyster mortality is relatively low. If summer/fall salinities are consistently greater than 15 ppt, moderate and heavy infections may be numerous and oyster mortality may be high. Field studies in the York River, VA, suggest that new P. marinus infections are acquired from July through early October, but peak infection acquisition occurs during late August and is correlated with oyster mortality. The early infection process in oysters and the role of zoospores in transmission dynamics in nature are poorly understood. No direct link between oyster defense mechanisms and control of P. marinus infections has been established. If oyster defense mechanisms do modulate P. marinus infections, the components have not been identified. There is little evidence to support the common perception that pollution is responsible for the dramatic increase in P. marinus abundance since 1985. Pathogen abundance is clearly correlated with salinity increases resulting from drought conditions in the late 1980s, although there may be subtle effects of toxicants or poor water quality on the host/parasite interaction

QPX Susceptibility in Hard Clams Varies with Geographic Origin of Brood Stock

T he results of recent investigations by VIMS and collaborating scientists in Massachusetts and New Jersey indicate that clam strains produced from brood stocks of South Carolina and Florida origin are more susceptible to QPX (Quahog Parasite Unknown) disease than clam strains originating from Virginia, New Jersey, and Massachusetts brood stocks. During a 3-year study clam strains produced at VIMS from brood stocks originating from Massachusetts, New Jersey, Virginia, South Carolina, and Florida were grown at sites in Massachusetts, New Jersey and Virginia and evaluated for survival, growth, condition and QPX disease susceptibility. The clams originating from South Carolina and Florida brood stocks had significantly higher prevalence of QPX and higher mortality than clams originating from Virginia, New Jersey and Massachusetts brood stocks. At the termination of the experiment cumulative mortality was 79% in FL and 52% in SC, as compared to 36% in VA, 33% in MA, and 20% in NJ clams. Differences between stocks were highly significant with mortality in FL and SC being significantly higher than the northern stocks. QPX prevalence in the FL and SC stocks ranged from 19-21% and 27-29% respectively in the second and third year of the study, while QPX prevalence in the VA, NJ, and MA stocks was 10% or less. Mortality was significantly correlated with QPX prevalence during the second and third years of the investigatio

Characterization Of Overwintering Infections Of Perkinsus-Marinus (Apicomplexa) In Chesapeake Bay Oysters

To determine the nature and abundance of over-wintering P. marinus infections, infected oysters (Crassostrea virginica) collected from the upper James River, VA, were placed in a tray and suspended from a pier in the lower York River, VA in November 1991. Every six weeks through May 1992 oysters (n = 25) were removed from the tray, examined for P. marinus by hemolymph culture in fluid thioglycollate medium (FTM), gradually warmed in individual containers to 25-degrees-C and held for one month. After the incubation period, which permitted the development of very light and/or cryptic parasite stages to detectable levels, the oysters were reanalyzed for P. marinus by both hemolymph and tissue cultures in FTM. A second group of 25 oysters from the tray was sacrificed at the initiation of each incubation, diagnosed using FTM cultures of hemolymph and tissue, and examined for cryptic stages using immunoassays. On the basis of FTM assays, prevalence of P. marinus gradually declined from 100% in November 1991 to 32% in May 1992. Incubation of oysters at 25-degrees-C always resulted in an increase of P. marinus prevalence and intensity, suggesting that the parasite was more abundant than initial FTM cultures indicated. Immunoassay diagnosis revealed infections in many of the oysters diagnosed as negative by FTM cultures. Most infections detected by immunoassay were comprised of individual P. marinus meronts within hemocytes in the midgut epithelial lining. Previously unidentified cryptic stages were not observed. Perkinsus marinus appears to overwinter at very low intensities in a high proportion of oysters. Comparison of P. marinus prevalence and intensity in transplanted oysters maintained in the York River to that in oysters monitored at the original James River collection site suggests that salinity may greatly influence overwintering infections. Infection intensity and prevalence declined earlier and to a greater extent at the James River site (4-12 ppt) than at the York River location (19-23 ppt). It appears that the synergistic effect of low temperature and low salinity may be more important in regulating P. marinus epizootics than either factor acting alone

Status of the Major Oyster Diseases in Virginia 2001 A Summary of the Annual Monitoring Program

Thirty-nine oyster populations were surveyed for disease in fall 2001. Perkinsus marinus was found in all areas sampled and prevalence exceeded 90% at all but 5 sample locations. In the James River P. marinus prevalence ranged from 88-100% at Deepwater Shoal, Horsehead Rock, Point of Shoals, Wreck Shoal, Mulberry Point, Swash, Long Shoal, and Dry Shoal. A lower prevalence was observed down river at Thomas Rock, 72%, and at Nansemond Ridge, 12%. The extremely low prevalence at Nansemond Ridge is likely age and density related; the oyster population was primarily comprised of spat; few small to market oysters were present at the site in October 2001

Status of the Major Oyster Diseases in Virginia 1999 A Summary of the Annual Monitoring Program

As a consequence of the relatively warm temperatures and high salinities severe epizootics of both H. nelsoni and P. marinus occurred in most tributaries in VA. In the upper James River, VA prevalences and intensities of P. marinus were the highest on record. The proportion of advanced infections (moderate and heavy intensity) in October was 60% at Wreck Shoal and 48% at Horsehead Rock suggesting that significant oyster mortalities occurred in these areas. 1 Record high levels of P. marinus were also observed in Virginia\u27s other major tributaries. Of the 39 bay oyster populations surveyed in the fall, P. marinus was present at all bμt one (Bell Rock in the York River) and most sites had prevalences exceeding 90%. Advanced infections bf the parasite were numerous, particulctrly in the Rappahannock River, and oyster mortality was high

Prevalence and distribution of QPX, Quahog Parasite Unknown, in hard clams Mercenaria mercenaria in Virginia, USA

In July 1996, the Virginia Institute of Marine Science initiated a sampling program to examine wild and cultured hard clams Mercenaria mercenaria for QPX, Quahog Parasite Unknown, a protistan parasite associated with severe mortalities of hard clams in localized areas in maritime Canada and Massachusetts, USA. The sampling program set out to seasonally monitor wild clams from one site, James River, Virginia, and cultured clams from 2 sites, Chincoteague Bay and Mattawoman Creek, Virginia. Histological examination of initial samples revealed 8% prevalence of the parasite in 1-2 yr old cultured clams in Chincoteague Bay. This is the first documentation of QPX in Virginia. To ascertain the distribution of the parasite in Virginia, the survey was expanded between August 1996 and July 1997 to include 16 additional sites. A total of 1305 wild and cultured clams was sampled from Chesapeake Bay tributaries and coastal areas where harvest and culture occur. QPX was not found in Chesapeake Bay, but was present in cultured clams from 3 coastal embayments-the original Chincoteague Bay site, Burton Bay and Quinby Inlet. The parasite was found in Chincoteague Bay at each sample period at prevalences ranging from 8 to 48 %. Infections were generally Light to moderate intensity and were most often observed in mantle and gill tissues. The maximum prevalence was observed in May 1997 and coincided with notable clam mortalities. QPX prevalences at the other sites were low, ranging from 4 to 15%. To date QPX has not had a significant impact on Virginia\u27s hard clam fishery and aquaculture industry; however, the presence of the pathogen in 3 of the state\u27s most productive hard clam growout areas warrants continued monitoring and research