A RAPID INCREASE IN Perkinsus marinus VIRULENCE CAUSED THE HISTORICALLY SIGNIFICANT 1980S EPIZOOTIC

Ryan B. Carnegie*, Susan E. Ford, Rita K. Crockett and Peter R. Kingsley-Smith
 
 Virginia Institute of Marine Science
 College of William & Mary
 P.O. Box 1346
 Gloucester Point, Virginia 23062, USA
 carnegie@vims.edu

Marine diseases are increasing in significance, yet the factors underlying these disease increases are seldom fully understood. Dermo disease in the eastern oyster Crassostrea virginica is the unusual case of an established disease that was relatively innocuous but which became markedly worse in a short period of time. When Perkinsus marinus was initially characterized in the Chesapeake Bay region following its discovery in the Gulf of Mexico, it generally infected oysters slowly and caused only modest annual mortality, typically up to 30% in oysters that were three or four years old. When its activity intensified in the 1980s, it infected oysters much more rapidly and caused annual mortality that could exceed 70%. Because the intensification occurred during a time of drought in the Chesapeake Bay region, drought was believed to be primarily responsible for the increased parasite activity, more saline conditions along with milder winters favoring P. marinus.

The realization that archival histological material revealed a shift in P. marinus presentation between the early period and more recent times prompted a systematic analysis of P. marinus phenotypic presentation in Chesapeake Bay (1960-present) as well as New Jersey (primarily Delaware Bay, 1960-2013) and South Carolina (1986-1993). The "original" phenotype was characterized by generally larger cells infecting oyster connective tissues and proliferating via polynucleate schizonts > 6 μm in diameter. The "emergent" phenotype was characterized by smaller cells generally infecting host digestive epithelia and proliferating via oligonucleate schizonts of < 4 μm. The emergent phenotype was first observed in Chesapeake Bay in 1983 and became dominant by 1986, completely supplanting the original phenotype by 1989. A similar phenotype shift was associated with increased P. marinus activity in South Carolina in the late 1980s and the devastating epizootic in Delaware Bay in 1990. While climate warming surely promoted the range expansion of P. marinus to more northern waters, the appearance of a hypervirulent phenotype was likely central to the rise of P. marinus as a major pathogen in recent decades.