The haplosporidian parasite Haplosporidium nelsoni, popularly known as MSX disease, has caused extensive epizootics of the eastern oyster, Crassostrea virginica, along the middle Atlantic coast of the United States, especially in Delaware Bay and Chesapeake Bay (Andrews, 1968; Farley, 1975; Ford and Haskin, 1982, Haskin and Andrews, 1988). The pathogen was first observed in 1957 during unprecedented, large-scale epizootics in oysters in Delaware Bay (Haskin et al., 1966). Similar oyster mortality attributable to H. nelsoni began in the lower Chesapeake Bay in 1959 (Andrews and Wood, 1967). Within two years more than 90% of the oysters growing in high salinity areas in the two Bays were killed (Andrews, 1980). The pathogen is now present along the Atlantic coast from Maine to Florida, although significant oyster mortality attributable to H. nelsoni occurs primarily in high salinity portions of middle Atlantic estuaries. Neither the abundance nor the virulence of H. nelsoni have abated since 1959 in the lower Chesapeake Bay. During the years 1992-95, maximum annual prevalences of H. nelsoni in oysters in this region ranged from 88 to 92% and are the highest values recorded in the 34-year continuous monitoring record (Burreson, 1993; Burreson & Calvo, 1994; Ragone Calvo & Burreson, 1995, 1996). The continuing presence and virulence of the pathogen has prevented recovery of oyster populations in the lower Chesapeake Bay and has limited development of extensive oyster aquaculture.
The reason for the sudden, unprecedented epizootics of H. nelsoni in Delaware Bay and Chesapeake Bay in the late 1950s is unknown. Hypotheses have been advanced that H. nelsoni is endemic in C. virginica in high salinity waters along the mid-Atlantic coast and that a pathogenic race developedby mutation or hybridization (Andrews, 1968) or that the parasite became more pathogenic after transfer to lower salinity in mid-Atlantic estuaries (Ford, 1992). There has also been speculation that H. nelsoni was introduced with exotic oysters (Rosenfield and Kern, 1979, Andrews, 1980).