FISHERY BULLETIN: VOL. 86, NO. 3 



til fed upon by at least 25 average-sized (1.75 mm 

 maximum width) snails. Seven snails, a typical value 

 in our experiments, would reduce net productivity 

 by only 5 to 30%, on a daily basis. In addition, con- 

 dition index and mantle glycogen levels increased 

 during the treatment period in both control and 

 parasitized oysters and the effect of snail parasitism 

 on all biochemical components was small (oysters 

 can regulate some biochemical components even 

 during starvation, Swift and Ahmed 1983; but see 

 Riley 1976). 



Consequently, both reduced growth and impaired 

 reproductive capacity can be attributed to a reduc- 

 tion in assimilated carbon available to the host, as 

 a result of either a reduction in filtration rate result- 

 ing in less energy being assimilated (Ward and 

 Langdon 1986) or the direct removal of assimilated 

 carbon by the snail. Neither effect was permanent. 

 Growth rate resumed and reproductive state re- 

 turned to control levels during recovery. In both 

 cases compensatory adjustments occurred during 

 the recovery period so that previously parasitized 

 oysters gained weight and increased egg number 

 faster than the controls. Loosanoff and Nomejko 

 (1955) and Eagle and Chapman (1953) also noted 

 compensatory shell growth in oysters. 



Perkinses marirms infection is an important cause 

 of mortality in oysters (Mackin and Sparks 1962; 

 Mackin 1962; Hofstetter 1977). Boonea impressa can 

 transmit P. marinus from one oyster to another and 

 can also increase the intensity of infection (White 

 et al. 1987). Continued deterioration after a stress 

 is removed occurs frequently in "recovery" experi- 

 ments (Kendall et al. 1984; Powell et al. 1984) 

 demonstrating the necessity of examining recovery 

 capacity in acute (vs. chronic) stresses. Growth rate 

 typically recovers more rapidly than most biochem- 

 ical parameters. In snail-parasitized oysters, both 

 prevalence and intensity of P. marinus infection in- 

 creased during the recovery period. Hence, in con- 

 trast to growth rate, no recovery from P. marinus 

 actually occurred. By the end of the 8-wk period, 

 infection intensity had increased by about 1 unit on 

 Mackin's (1962) 5 point scale. Growth still occurred 

 and reproductive capacity returned to control levels, 

 however, during this period. These results contra- 

 dict those of Menzel and Hopkins (1955) who showed 

 that P. marinus retarded growth in proportion to 

 the intensity of infection and Mackin (1953) who 

 observed decreased fecundity in heavily infected 

 oysters. Haven (1962) obtained results analogous to 

 ours. Possibly, the oysters in our study were not 

 infected heavily enough to retard growth and 

 reproduction. Mean infection intensity in previous- 



ly parasitized oysters after the recovery period was 

 only 2.2, a light to moderate infection. 



Changes observed at the biochemical level among 

 the previously parasitized oysters after the recovery 

 period, particularly in fatty acid and lipid phosphate 

 content, were related to increased infection inten- 

 sity of P. marinus (Table 9). Stein and Mackin 

 (1955), Mackin (1962), and White et al. (in press) 

 also noted changing lipid levels related to infection 

 intensity. Lipid phosphate is predominantly a struc- 

 tural component whereas fatty acids, usually as tri- 

 glycerides, are storage materials in many marine 

 invertebrates (Gabbott 1976; Trider and Castell 

 1980; Gehron and White 1982). The increased lipid 

 phosphate content in mantle tissue, however, prob- 

 ably indicates an increase in structural material, 

 noted histologically by Stein and Mackin (1955, 

 1957) to occur in conjunction with P. marinus 

 infections. 



Glycogen is the primary storage material in most 

 bivalves (Beninger and Lucas 1984). Parasitism fre- 

 quently affects carbohydrate metabolism (Cheng 

 1963; Mohamed and Ishak 1981; Thompson and 

 Binder 1984; Thompson 1986). White et al. (in press) 

 suggested that P. marinus alters oyster metabolism 

 favoring gluconeogenesis. Our results support this 

 hypothesis. Glycogen levels dropped only in recovery 

 control oysters in which P. marinus infection inten- 

 sity also declined. Changing fatty acid content might 

 be similarly explained. In contrast. Stein and Mackin 

 (1957) noted decreased glycogen levels in heavily in- 

 fected oysters (3 to 5 on Mackin's scale). Few of our 

 oysters were this heavily infected, however. An 

 alternative explanation, that slower reproductive 

 development in parasitized oysters was responsible 

 for variation in glycogen and fatty acid content, can- 

 not be completely excluded because P. marinus in- 

 fection intensity did not correlate with glycogen 

 levels in recovery oysters. Parasitized oysters had 

 fewer eggs than control oysters, however. Addi- 

 tionally, neither the number of eggs present nor the 

 number of oysters spawning differed significantly 

 between control and previously parasitized oysters 

 during the recovery period. 



Results of previous workers suggest that signif- 

 icant decreases in storage compounds, whether 

 caused by B. impressa or P. marinus, only occur 

 in heavily infected animals (e.g.. Stein and Mackin 

 1957; White et al. in press). This, too, is true for the 

 amino acid pool where significantly decreased levels 

 are usually associated with more severely stressed 

 animals (e.g., Powell et al. 1982, 1984). The few 

 significant effects on amino acids in this study, like 

 all the other biochemical components measured. 



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