FARLEY ET AL.: EPIZOOTIC SARCOMA IN SOFT SHELL CLAMS 



FLUORESCENCE INTENSITY 



Figure 2.— OXC 1 cells were fixed in 0.1% neutral formaldehyde. Following three washes in sterile seawater, the cells were then in- 

 cubated with: (A) a 1:50 dilution of fluoresceinated (FITC) goat and antimouse IgG antibody (---), (B) a 1:100 dilution of heat-inactivated 



normal mouse serum, and subsequently with a 1:50 dilution of FITC-goat antimouse IgG antibody ( ), or (C) monoclonal antibody 



IE7, and subsequently with a 1:50 dilution of FITC-goat antimouse IgG antibody ( ). All the antisera were diluted in sterile sea- 

 water immediately prior to use. The samples were then evaluated by a Becton-Dickinson Fluorescence Activated Cell Sorter IV (Reference 

 to trade names does not imply endorsement by the National Marine Fisheries Service, NOAA). 



DISCUSSION 



Epizootiology 



Laboratory and field observations complement 

 each other and confirm the suspicion that affected 

 animals die from the disease. Individual diseased 

 clams monitored in aquaria from early December 

 1983 to May 1984 had progressed from early stages 

 1 and 2 to advanced stages 4 and 5 with 100% mor- 

 tality. The high prevalences and advancing stages 

 seen in natural populations may signal significant, 

 impending mortalities. Samples collected from Swan 

 Point (YSWP) in July and August 1984 (Table 1) 

 showed 1/15 and 0/25 sarcomas, respectively. Sam- 

 ples from Poplar Island in July and August were 



0/25 and 0/25. High sarcoma prevalences reappeared 

 in the fall in smaller clams at Swan Point (25%) and 

 Poplar Island (32%) in October. The decrease in 

 prevalence to zero corresponds with observations 

 of laboratory-held animals, suggesting that the 

 disease was also 100% fatal in field populations. The 

 experiments of Brown (1980) and others (Oprandy 

 et al. 1981) indicate an infectious etiology for the 

 disease. The nature of the new situation in Chesa- 

 peake Bay suggests that an infectious agent may 

 have been established in clams by introduction from 

 New England, since previous information indicated 

 that the disease was confined to sites north of New 

 Jersey (Barry and Yevich 1975; Yevich and Barszcz 

 1977; Brown etal. 1977, 1979; Brown 1980; Koepp 

 1984). Introductions of clams from New England to 



855 



