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FISHERY BULLETIN: VOL. 84, NO. 4 





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Figure 1.— Cytology of clam sarcoma, 1 unit =10 ^m. (A) Histologic section: Note large, hyperchromatic nuclei, abundant mitotic 

 figures and metaphase with laggard chromosomes. (B-G) Histocytologic preparations: (B) Stage 5 (all cells neoplastic); rounded cells 

 show mitosis and large, reniform, hyperchromatic nuclei. (C) Stage 3 sarcoma; about 10% of the cells are neoplastic. Compare sizes 

 of normal (small) and neoplastic (large) nuclei. (D) Mitotic figure in anaphase. (E) Binucleate neoplastic cell with prominent, multiple 

 nucleoli (normal hemocyte, arrow). (F) Neoplastic cell with intranuclear inclusion (arrow). (G) Very large neoplastic cell with nucleus 

 and prominent Golgi zone. 



ber progressed to advanced and terminal stages by 

 April in laboratory -held animals. This situation was 

 reflected in the field by an increase in the prevalence 

 of advanced cases as the season progressed. The 

 higher histologic prevalence in the YAGH sample 

 was due to four positive cases from sections of dead 

 animals which were not diagnosable by histocyto- 

 logy. This information provides additional evidence 

 of mortality in feral populations. Cooper et al. 

 (1982a) demonstrated in laboratory experiments the 

 lethal nature of this disease in animals with ad- 

 vanced cases and noted similar implications in field 

 monitored populations. A chronic phase with remis- 

 sion was reported by Cooper, but these features 

 were not evident in the Chesapeake Bay epizootic. 

 It is conceivable that some resistance has developed 



in the long-term occurrence of this disease over 

 generations of clams in New England. Selection has 

 not, as yet, had a chance to develop resistant animals 

 in Chesapeake Bay. The mortality which began in 

 laboratory -held animals in April was 100% by the 

 end of June (Table 2). Field prevalences also dropped 

 to zero in June. Sarcomas reappeared in the popula- 

 tion in October. 



Neoplastic clam cells from OXC 1 and EBC 6 

 (Table 2) were incubated with the murine mono- 

 clonal antibody IE 7 which is specifically reactive 

 with Massachusetts Mya neoplastic cells (Reinisch 

 et al. 1983). Upon fluorescence activated cell 

 sorter analyses, neoplastic cells from OXC 1 

 (Fig. 2) and EBC 6 were positive when stained with 

 IE7. 



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