SPECIAL REPORT 



OYSTER GROWTH EXPERIMENT IN 

 EAST LAGOON 



An investigation was initiated in June 1963 to 

 determine if the environment within our lagoon 

 laboratory and the lagoon itself was suitable 

 for oyster culture. For 21 nno., we checked 

 the growth (based on weight increases) and 

 mortality of young oysters placed in the lagoon 

 and also in the circulating water of the 

 laboratory. 



The procedures and results of the first 

 year of the experiment were described in last 

 fiscal year's report. -^^ We mentioned that the 

 initial nnortality (August 1963) shown in figure 

 45 was probably caused by Gonyaulax monilata, 

 and that exannination of the dead oysters showed 

 no evidence of the common oyster disease, 

 Dermocystidium marinum. Mortality was nil 

 during the subsequent 6 nno., but one lagoon 

 oyster was lost. Then in March 1964, a lagoon 

 oyster died. Two more died in May and two in 

 June. All of these oysters were infected with 

 D. marinum . No laboratory oysters died during 

 this period. We hypothesized that the infection 

 was picked up during the period of heavy feed- 

 ing and rapid growth (Septennber through 

 Novennber 1963). The laboratory oysters did 

 not have a period of heavy feeding and rapid 

 growth and, therefore, probably picked up less 

 infection. 



Laboratory oysters began dying fronn Der- 

 nnocystidium infection in late sumnner of 1964. 

 Three died in August, four in September, 

 three in October, and one in December. The 

 lagoon oysters continued to die throughout the 

 summer of 1964: two died in July, two in 

 August, three inSeptember, and one in October, 

 All were infected with Dermocystidium . 



Fronn July 1, 1964, to the end of the experi- 

 ment on February 15, 1965, the lagoon and 

 laboratory oysters grew at about the same 

 rate. Growth was slow through the summer 

 when the laboratory oysters gained about 0.3 g. 

 (0.010 oz.) and those in the lagoon about 

 0.2 g. (0.007 oz.) per week. The growth of 

 both groups increased as the hot weather 

 ended. Through October, November, and De- 

 cember, the laboratory oysters gained 1.2 g. 

 (0.042 oz.) per week connpared to 1.1 g, 

 (0.039 oz.) for those in the lagoon. Both 

 groups had an average weight gain of 0.7 g, 

 (0.025 oz.) per week from January 1, 1965, 

 until the end of the experiment. On the basis 

 of those living at the end of the experinnent, 

 the average nnonthly weight increases of lagoon 



^° Circular No. 230, page 88, paragraph 1, line 3, 

 should read: ". . . gaining 8.3 g. (.291 oz.) in September 

 and 12.7 g. (0.445 oz.) in (October.," and lines 6 and 7 

 should read: "Four oysters of this group died in May and 

 June 1964." 



and laboratory oysters were 5.1 g. (0.179 oz.) 

 and 3.5 g. (0,123 oz.), respectively. 



At the end of the experiment, the remaining 

 oysters were examined for Dermocystidium. 

 Among the four remaining laboratory oysters, 

 infection ranged from light to heavy. Two of 

 the lagoon oysters were uninfected, and in- 

 fection levels in the other seven ranged from 

 light to heavy. 



Growth declined earlier among the labora- 

 tory oysters than among those in the lagoon. 

 In their natural environment, small oysters 

 are known to have a relatively high growth 

 rate, which decreases as their size increases. 

 We found that small oysters placed in the 

 lagoon had a period of relatively rapid growth 

 which began to taper off when they attained 

 an underwater weight of about 70 g. (2.5 oz.). 

 The growth rate of the laboratory oysters, 

 however, decreased when they had reached 

 about 29 g. (1 oz.). As a result, the laboratory 

 oysters rennained smaller than those in the 

 lagoon. 



Oysters that were uninfected with D, marinum 

 becanne infected after being put into lagoon 

 water, thereby showing that the disease existed 

 in the lagoon. Mortality caused by D. m arinum 

 followed previously established patterns that 

 show that oysters usually become infected 

 during periods of heavy feeding and rapid 

 growth in warm weather. If they are able to 

 survive until the arrival of cooler weather, 

 they will continue to survive at a reduced 

 growth rate throughout the winter, then begin 

 to die as warm weather approaches. Since 

 the lagoon oysters took in more food, they also 

 probably took in more D, marinum than those 

 in the laboratory. This greater exposure 

 apparently caused mortality to begin about 

 4 mo. earlier annong lagoon oysters. 



Oyster mortality in the lagoon is also 

 caused by regularly occurring blooms of 

 G. m onilata . We suspected that deaths in 

 August and September 1963 were caused by 

 this organism. Its toxicity to oysters has 

 since been demonstrated by another inves- 

 tigator. Undoubtedly, it contributes to the 

 low population of naturally occurring oysters 

 in the lagoon and would, therefore, make 

 these waters unfit for long-term experiments. 

 We thought that within the laboratory, the 

 effects of G, monilata could be circunnvented 

 by placing experimental oysters in the labora- 

 tory's recirculating water tanks. This action, 

 however, was not successful during the August 

 1963 bloom, possibly because the G. monilata 

 were not detected in time. (See last year's 

 report.) 



This experinnent has indicated that three 

 factors affect the suitability of the lagoon 

 water and the water within our laboratory 

 for oyster experimentation. We have shown 



48 



