tible oysters from other peojifraphic areas intro- 

 duced into Prince Edward Island waters. Re- 

 sistant stocks were drawn upon to repopulate 

 other oyster jifrowin^ areas of the Gulf of Saint 

 Lawrence that had been subsequently deci- 

 mated by the same disease. 



Evidence is accumulating th;it increased re- 

 sistance to the haplosporidan pathogen Mi)iclii- 

 nia nelsoni is developing among oysters that 

 have survived the disease in the Middle Atlan- 

 tic States. The disease has been at epizootic 

 levels in some Chesapeake Bay populations for 

 several years. Perhaps resistant strains can be 

 developed with presently available hatchery 

 techniques. Aggregation of survivors on natu- 

 ral beds to which adequate cultch has been 

 added could also do much to improve reproduc- 

 tion, spatfall, and return to full production. 



3. Basic informatiov about the life histotji 

 aud ecolofiy of the disexwie agent must be 

 acciiundatfd, to define viihierable stages or re- 

 strictive e)n'iro)ime)ital )equi)eme)its. As an 

 example, several oyster pathogens, such as M. 

 uelsoiii, are limited to salinities in excess of 

 15 o 00. Plantings during epizootics can be 

 restricted to low-salinity areas, and temporary 

 transfer of infected stocks to low salinities may 

 retard or eliminate infections. Mechanical and 

 chemical treatments can also reduce disease 

 prevalence. Effects of gaffkaemia on impounded 

 lobster populations have been reduced by treat- 

 ing bottom muds of pounds with calcium hypo- 

 chlorite. Damages of dermocystidium disease to 

 oysters have been lessened by planting oysters 

 thinly on the beds, by harvesting within 2 

 years, and by planting and harvesting at pre- 

 scribed seasons to take advantage of the de- 

 crease in pathogen activity during the colder 

 months. 



Korringa (1959) outlined an extensive pro- 

 gram to control the spread of the parasitic co- 

 pepod Mytilicola in cultivated mussel stocks of 

 the Netherlands. Included were extensive 

 dredging of adjacent natural beds, transfer of 

 lightly infested stocks, and destruction of heav- 

 ily infested beds. 



Korringa (1951a) found "shell disease" of 

 oysters to be caused by a fungus that perfo- 

 rated the shell — a fungus that thrived on old 

 shells. He attributed the outbreak of shell dis- 

 ease in 1930 in the Netherlands to the practice 



of spreading enormous (juantities of cockle 

 shells on the beds. The di.sease declined when 

 the spat collectors were placed in areas free of 

 the disease, when old shells were cleared from 

 beds, and when infected young oysters were 

 dipped in mercuric disinfectant (Korringa. 

 1948, 1949, 19r)lc). 



liiological control of othi>i' hosts in the life 

 cycle of parasites, or biological control of the 

 parasite itself, are also possible approach(>s. 



4. Production could be uiaiutaiued in artificial 

 ciivirounicuts where disease cau be controlled. 

 Some i)rogress has been made in this dii'ection 

 with the de\el()i)ment of hatchery methods of 

 producing seed oysters and t-lanis ( LoosanolV 

 and Davis, 1963). Bacterial and fungal epizoo- 

 tics in lar\'al culture tanks can be prevented, or 

 their effects reduced, by ultraviolet treatment 

 of filtered sea water, antibiotic tre.itment of sea 

 water in standing water cultures, maintenance 

 of general cleanliness of all utensils used in 

 handling larvae, and ultraviolet treatment of 

 phytoplankton food derived from impure mass 

 cultures. 



Shellfish i)roduction in artificial ponds 

 (Shaw, 1965) offers distinct possibilities of 

 di.sease and predator control, beginning with 

 disease-free and disease-resistant Iji'ood stock 

 and progressing to filtration and ultraviolet 

 treatment of recirculated water; important also 

 are careful control of contaminants in mass 

 phytoplankton cultures and elimination of shell- 

 fish associates that act as alternate or interme- 

 diate hosts of disease agents. 



CONCLUSIONS 



Many of the great fisheries of the world have 

 undergone large fluctuations in supi)ly. The 

 causes of these fluctuations, although subjects 

 of much discussion, have rarely been precisely 

 determined. Reduction in abund.ince of com- 

 mercially valuable marine species has been at- 

 tributed to overfishing, failure of spawning, 

 sudden and drastic changes in temperature and 

 salinity, and many other factors. One biological 

 factor that has received too little attention is 

 disease. The fact that marine animals become 

 ill and die, often in vast numbers, has been 

 largely ignored. Events in commercial shellfish 



366 



U.S. FISH AND WILDLIFIi SliRVlCE 



