Epizootiology of Perkinsus marinus disease of oysters in Chesapeake Bay, with emphasis on data since 1985

Eugene M. Burreson, Lisa Calvo

Research output: Contribution to journalArticle

272 Citations (Scopus)

Abstract

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°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 effects. 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.

Original languageEnglish (US)
Pages (from-to)17-34
Number of pages18
JournalJournal of Shellfish Research
Volume15
Issue number1
StatePublished - Apr 1 1996

Fingerprint

Perkinsus marinus
Chesapeake Bay
oysters
epidemiology
salinity
infection
James River (Virginia)
temperature
mortality
defense mechanism
pathogen
winter
Crassostrea virginica
summer
drought
defense mechanisms
river
pathogens
host-parasite interaction
disease surveillance

All Science Journal Classification (ASJC) codes

  • Aquatic Science

Keywords

  • Annual cycle
  • Epizootiology
  • Oyster disease
  • Perkinsus
  • Salinity effects
  • Temperature effects
  • Transmission

Cite this

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title = "Epizootiology of Perkinsus marinus disease of oysters in Chesapeake Bay, with emphasis on data since 1985",
abstract = "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°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 effects. 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.",
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Epizootiology of Perkinsus marinus disease of oysters in Chesapeake Bay, with emphasis on data since 1985. / Burreson, Eugene M.; Calvo, Lisa.

In: Journal of Shellfish Research, Vol. 15, No. 1, 01.04.1996, p. 17-34.

Research output: Contribution to journalArticle

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N2 - 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°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 effects. 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.

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