ETIOLOGY OF SOCKEYE SALMON "VIRUS" DISEASE 



A virus-like disease has been recognized 

 as the cause of heavy losses among hatchery 

 populations of sockeye salmon fingerlings in the 

 State of Washington. The following is a brief 

 review of observations of this disease for the 

 last few years and an account of the extensive 

 experimental work conducted at two hatcheries 

 and in the laboratory during 1954 . 



HISTORY 



The disease was first recognized in 1950 

 at Winthrop, Washington, and during the ensn - 

 ing years an increasing number of hatcheries 

 were affected by the epizootic (Rucker et al 1953; 

 Watson et al 1954). By 1953 the epizootic had 

 appeared in sockeye salmon fingerlings at four 

 Federal hatcheries in Washington, all located 

 on Columbia River tributaries, and at the Wash- 

 ington State hatchery at Issaquah. The outbreak 

 at Issaquah marked the first appearance of the 

 infection at a hatchery not on a Columbia River 

 tributary . 



The disease is characterized by an ex- 

 plosive increase in mortality which may reach 

 32 percent of the original population per day 

 with a total mortality of over 95 percent of the 

 original population. In 1952, 85 percent of all 

 sockeye fingerlings reared in the State of Wash- 

 ington succumbed to the disease and in 1953 the 

 State-wide toll was 65 percent. Higher hatchery 

 mortalities were prevented in 1953 by the early 

 planting of a considerable number of fish. 



ETIOLOGY 



The disease is highly species specific, 

 affecting only the fresh- and salt-water strains 

 of Oncorhynchus nerka. Other species of sal- 

 mon fingerUngs reared at the same hatcheries 

 are not affected, and it has not been possible to 

 transmit the infection to other species of salmon 

 or various species of trout even by intraperiton- 

 eal injection of highly infectious material 

 obtained from diseased sockeye fingerUngs . 



None of many and varied chemotherapeu - 

 tic treatments has stayed the course of the 

 infection nor has a prophylactic treatment been 



found. Once the epizootic appears, it has been 

 impossible to reduce the high rate of mortality 

 in the diseased population. Not only is the dis- 

 ease impossible to control but it is also highly 

 infectious, particularly in the spring of the year 

 when the fish are very young. The disease is 

 easily transmissible to healthy populations by 

 the feeding of diseased material, placing the fish 

 in a bacteria -free filtrate prepared from infected, 

 moribund, fingerlings for a few moments, intra- 

 peritoneal or intramuscular inoculation, or by 

 placing a dead or moribund fish in the water 

 supply above the healthy population. In some in- 

 stances infectious material obtained from dis- 

 eased fish was diluted as high as 1 part in 10 

 billion without loss of infectivity. 



SOURCE OF THE INFECTION 



Until the fall of 1953 the method of entry 

 of the infection into hatchery populations remained 

 unexplained. As the disease spread to additional 

 hatcheries after it was first detected in 1950 

 certain possibilities became remote, if not en- 

 tirely eliminated. A common air -borne or aquatic 

 vector was unlikely to be the method of entry be- 

 cause of the varied locations and climates of the 

 infected hatcheries, the random distribution of 

 infected troughs, and the occurrence of the in- 

 fection in sockeye salmon being reared in well 

 water . 



Experimental work conducted late in 1953 

 finally produced the first step toward discovery 

 of the source of the infection. During the spawn- 

 ing season of that year the livers of all returning 

 sockeye from which eggs were taken near the 

 Federal hatchery at Leavenworth were tested and 

 a filterable, pathogenic agent, which caused mor- 

 talities in sockeye fingerlings, was found in a 

 number of the adults . Since salmon viscera of 

 mixed and unidentified species, obtained in frozen 

 blocks from commercial canneries, were routine- 

 ly added to the diets of all fish populations affected 

 by the epizootic, it was quite possible that the 

 agent was gaining entry to the hatcheries in the 

 feed. It has been shown that the etiologic agent 

 can withstand freezing for a limited time . This 

 hypothesis could neither be proven nor disproven 

 on the basis of past experience, however, since 



