148 



Fishery Bulletin 98(1) 



Table 5 



Differential densities of hemocytes (xlOi^ hemocytes/ml ) in relation to days after inoculation for crabs in the early infection experi- 

 ment. Sample sizes are given in Table 2. 



Days 



Uninfected control crabs 



Presample 



10 

 Inoculated, infected crabs 



Presample 



3 



5 



7 



Granulocyte density 



Mean ±SE 



3.72 ±0.31 

 7.48 ±1.60 



6.88 ±0.92 

 4.95 ±0.40 

 2.51 ±0.91 

 2.93 ±0.68 



Semigranulocyte density 



Mean ±SE 



7.66 ±0.50 

 11.20 ±1.94 



11.43 ±1.00 

 4.36 ±0.31 

 5.40 ±1.60 

 6.92 ±0.80 



Hyalinocyte density 



Mean ±SE 



4.53 ±0.79 

 5.30 ±1.47 



4.97 ±0.40 

 2.80+0.15 

 1.49 ±0.51 

 1.56 ±0.31 



Delmarva Peninsula (Messick, 1994; Messick and 

 Shields^) and show significantly gi-eater changes 

 than females in certain blood parameters.'' Infected 

 blue crabs apparently die before acquiring the bitter 

 flavor found in infected Tanner and snow crabs. 



Survival analysis indicated that parasite density 

 was not associated with mortality. Similarly, survival 

 time of Norway lobsters did not show a significant 

 relationship with severity of infection, but host mor- 

 tality did increase with the progression of the disease 

 (Field et al., 1992). In blue crabs, absolute declines in 

 ln( total hemocyte density) were associated with host 

 mortality. Hence, the cellular defensive response of 

 the host appeared seriously compromised by infec- 

 tion. Anecdotal evidence from hosts used to maintain 

 the parasite suggests that infections established with 

 Plasmodia are more pathogenic than those estab- 

 lished with trophonts; this may explain the similar 

 mortality curves for the high and low doses of Plas- 

 modia in the mortality-II experiment. Observations 

 on naturally and experimentally infected crabs indi- 

 cate three possible outcomes to the disease: 



1 Crabs with acute infections, such as those 

 reported here, show rapid mortalities, typically 

 dying within 40 d. Acute infections rarely lead 

 to heavy infections (10'^"^ parasites/mL), and may 

 not lead to the development of dinospores. 



•• Messick, G. and J. D. Shields. 1999. The cpizootiology of the 

 parasitic dinoflagellate HcmatiHiiniuin perezi in the blue crab, 

 Callinectes sapidus. Oxford Cooperative Laboratory, 904 S. 

 Morris St., Oxford, MD 21654. Unpubl. data. 



^ Shields, J. D. 1999. Mortality and pathophysiology studies 

 of blue crabs infected with the parasitic dinoflagellate Hcmnlo- 

 dinium perczi. Saltonstall-Kenncdy Program. NOAA/National 

 Marine Fisheries Service. Final Report. 



2 Crabs with chronic infections (observed in very 

 cases, n=4) endure the acute stage, survive for 

 longer periods (up to 90 days), and develop infec- 

 tions that lead to massive numbers of dinospores 

 (Fig. 6). 



3 Some crabs successfully resist the parasite or are 

 refractory to the infection. Preliminary experi- 

 ments (not shown) suggest that resistant crabs 

 (/! = 10) may become refractory to further inocula- 

 tions with H. perezi. 



Blue crab catches fluctuate yearly in Chesapeake 

 Bay but causes for these fluctuations are not well 

 understood. Since salinity appears to limit the dis- 

 tribution of H. perezi (Newman and Johnson, 1975), 

 the dinoflagellate could feasibly infect and cause 

 significant mortalities to juvenile and adult crabs 



