t'.as been via contaminated adult sockeye viscera 

 fed to the young finger lings. The random occur- 

 rence and the sporadic nature of the outbreaks 

 of the infection in any one hatchery at first 

 threw considerable doubt on this method of en- 

 'ry since it would be expected that almost all 

 of the fish receiving the same diet would become 

 infected simultaneously, but the hematological 

 studies and other experimental work have shown 

 that there are three possible beginnings to the 

 chain of infection: the virus particles can enter 

 the population in a comparatively large quantity 

 at one feeding but the particles may be concen- 

 trated in one portion cf the feed since not all 

 iscera may be infected; the particles can enter 

 the population over an extended period of time 

 and accumulate in the fish until their natural re- 

 sistance to the disease is overcome; or a small 

 percentage of the fingerlings may be hyper- 

 sensitive to the etiologic agent and the infection 

 spread througfi cannibalism of the healthy fish 

 on the dead and moribund, thus ircreasing the 

 number of virus particles in the population by 

 serial transmission. 



affects the fingerlings two ways: by its effect 

 on the size, or physiological age of the fish and 

 by either decreasing the susceptibility of the fish 

 or adversely affecting the virus . The decrease 

 in water temperature in late summer and early 

 fall re-establishes optimum temperature con- 

 ditions thus accounting for the comparatively few 

 outbreaks during the summer and the fall 

 epidemics. 



The total mortality due to the virus dis- 

 ease at the Winthrop hatchery has usually been 

 proportionately lower than that of the Leaven- 

 worth hatchery. At first it was thought that a 

 strain difference in either the sockeye salmon 

 fingerlings or the virus was the cause of this 

 phenomenon, but since fingerlings reared at one 

 station from eggs spawned at another station 

 showed the same mortality pattern of the rearing 

 station, this excluded the possibility of strain 

 differences . The warmer average winter and 

 early spring water temperatures at the Winthrop 

 station caused a more rapid growth rate and was 

 considered the major contributing factor. 



Of the three possibilities, the last meth- 

 od appears to be the most probable since mori- 

 bund, virus infected fingerlings, were found in 

 troughs which never suffered a full-scale epidem- 

 ic . Perhaps only those ponds or troughs with a 

 higher than average proportion of hypersensitive 

 fingerlings first manifest the infection. A com- 

 bination of contaminated cleaning and feeding 

 equipment and hypers^n^Jitive fish can cause the 

 infection to become widespread throughout the 

 hatchery. It cannot be said, however, that the 

 other two methods never operate . During the 

 early part of the year, when the fish are young 

 and small, they have slight resistance to path- 

 ogenic agents. Thus, the exact method of entry 

 of the virus into the population is usually masked 

 by the short incubation period of the disease and 

 the high rate of mortality. 



The effect of water temperature on the 

 virus is not noticeaWe until late summer or 

 early fall of the year. During the spring and 

 early summer any effect of water temperature 

 is over -ridden by the high susceptibility of the 

 fingerlings to the disease coupled with water 

 temperatures within the optimum range of the 

 pathogenic agent, 40-60 degrees F. The rise in 

 water temperatures during the summer months 



Other modes of entry of the virus disease 

 into the hatcheries, in addition to the feeding ol 

 infected viscera may exist, but more sensitive 

 techniques than those presently being used will 

 be required to detect the pathogenic agent. Re- 

 covered fingerlings do not carry virus in sufficient 

 quantity to infect seven-month-old healthy finger- 

 lings when suspensions prepared from these 

 recovered fish are inoculated into the healthy ones 

 intraperitoneally. Nevertheless, when healthy 

 fish are placed in the same water supply as the 

 recovered fish, transmission of the infection does 

 eventually occur even though a full-scale epidemic 

 does not develop in the exposed fish. Perhaps 

 there is some transmission of the virus via the 

 eggs from "carrier" adults -- the fish hatched 

 from these eggs may be the "hypersensitive" fing- 

 erlings. However, the virus was in so small a 

 quantity that the inoculated one-year-old finger- 

 lings used to test the samples of eggs were 

 sufficiently refractile to resist the agent. Ex- 

 clusion of sockeye salmon viscera from the diets 

 of fingerlings may therefore exclude the major 

 mode of entry of the infection in the hatcheries, 

 but the losses in any one hatchery due to a virus 

 epidemic are so great that all possible sources 

 must be eliminated if sockeye salmon fingerlings 

 are to be reared successfully. 



