SSO disease is caused by the protistan Haplosporidium costale (= Minchinia costalis)( 13 ) of the phylum Haplosporidia. Haplosporidium costale, commonly known as SSO ( seaside organism ) , infects the oyster Crassostrea virginica( 3 ).
The geographical distribution of H. costale is in high salinity bays ( 25 part per thousand ) along the east coast North America from Virginia, USA , to Nova Scotia, Canada ( 2, 7 ) . Significant oyster mortalities attributable to SSO disease have historically been restricted to coastal Virginia, Maryland and Delaware, USA ( 2, 3 ) , but significant mortality attributable to SSO recently occurred in Massachusetts, USA.
The plasmodial stage of H. costale occurs intercellularly in connective tissue of the digestive gland, mantle and gonad ( 3, 11 ); spores occur throughout connective tissue in the same organs ( 2, 3, 10 ). Haplosporidium costale has a limited seasonality. Oysters become infected in May and June at the time when spores are released from previously infected moribund oysters ( 3, 6 ) . Infections remain subclinical through the autumn and winter, then plasmodia develop the following March/April, followed by synchronous sporulation and oyster mortalities in May/June ( 2, 3, 6 ). This seasonal epizootiology may be more complicated than historically noted; H. costale sporulation recently has been detected, and verified using molecular tools, in oysters collected in October ( 11, 12 ) .
The distribution of H. costale and H. nelsoni( the causative agent of MSX disease ) overlaps in high salinity areas from Virginia, USA, to Nova Scotia, Canada, and co-infections with both pathogens have been reported ( 5, 6, 11 ) . The pathogens can be readily differentiated during sporulation. Haplosporidium costale sporulates throughout the connective tissue of most organs, whereas H. nelsoni sporulates only in the epithelium of the digestive tubules ( 1, 3, 5 ) . The plasmodial stages of these two pathogens, however, cannot be reliably differentiated based on morphology ( 5 ) , and definitive diagnosis in the absence of spores requires molecular tools ( 11, 12 ) .
Sporulation disrupts connective tissue and the high prevalence of spores in dead oysters suggests that sporulation results in the death of the oyster. Sporulation is believed to be the end result of all H. costale infections ( 1 ) and thus infections are invariably fatal ( 7 ) .
It has not been possible to transmit H. costale experimentally in the laboratory. No life cycle has been elucidated for any member of the phylum Haplosporidia, but an intermediate host is suspected ( 7 ) .
For diagnosis, the recommended guidelines for sampling are those stated in Chapter 1.1.4 and Chapter I.2. of this Aquatic Manual .