DISEASE OF SALMON 



41 



ney and muscle cultures from dead fish, but usually 

 these cultures yielded miscellaneous forms, pre- 

 sumably contaminants or secondary invaders. 

 Thirty-four days after inoculation, one intramus- 

 cularly inoculated fish showed a slight reddening 

 in the dorsal-fin area and a tendency toward 

 lordosis. Photographs of this fish demonstrate the 

 progressive nature of the disease (fig. 4). One 



OUTBREAK OF DISEASE AT THE 

 BLUEBACK BROOD OF 1950 



At the time of he outbreak of disease at the 

 Leavenworth station in the spring of 1951, there 

 was a similar occurrence of disease at the Win- 

 throp station. Blueback-salmon eggs taken at 

 Winthrop in (he fall of L950 were hatched both at 

 (he Winthropand the Leavenworth stations. Fin- 

 gerlings from the eggs retained at the Winthrop 

 station were raised without significant loss up to 

 the time of their release on April 20, 1!>.M. A 

 group of 69,000 fingerlings from the same group 

 of eggs, hatched and raised at the Leavenworth 

 station to a size of aboul 1 1 ■_. inches, was trans- 

 ferred to the Winthrop station on .March 8, L951. 

 .Mortality among this group of fish was above nor- 

 mal in April, and most of the lish were lost from 

 disease during May when they were about _'•_. 

 inches long and .~> months old. The disease began 

 in one trough, approximately 7 days later was 

 found in two more troughs, and then became 

 general. 



The disease was characterized by the rapidity 

 with which it spread and by the death of mau\ 

 lish without apparent gross abnormalities. Many 

 fish had hemorrhagic areas on or at the base of 

 the fins and on the isthmus. Some had fungus 

 growing on the peduncle, around the dorsal fin, 

 or at the base of the pectoral tins. The gills were 

 a normal red, but the spleen often appeared pink. 

 Moribund fish showing external lesions had nor- 

 mal-appearing spleens. No solid material was 

 found in the stomach which, in common with the 

 intestine, contained a clear to yellowish fluid. 

 There was no response to sulfadiazine or aureomy- 

 cin therapy. Scoliosis developed in about 5 per- 

 cent of the diseased lish. 



BLUEBACK BROOD OF 1948 



Losses among the blueback-salmon tingerlings 

 and yearlings at the Winthrop station over the 



intraperitoneally inoculated fish showed the first 

 signs of developing scoliosis 42 days after injec- 

 tion. This fish was photographed to show the 

 progressive development of scoliosis (fig. 5). Ob- 

 servations on this experiment were terminated 

 November 30, 1951, 5 weeks after the last mor- 

 tality occurred. 



WINTHROP STATION, 1949-51 



previous several years had on occasion been rather 

 high. Necrosis of the kidneys was common and 

 bacteriologic studies indicated that a short (Tram- 

 positive rod of the kind described by Earp ( r.>.">0) 

 was the etiologic agent. During the winter of 

 L949 50, sulfadiazine therapy was employed in an 

 attempt to reduce the losses among the blueback- 



sal ii Bngerlings (Winthrop brood of 1048). 



Kucker, et al. (1951) working with a group of 

 these lish found that sulfadiazine controlled the 

 kidney infection among the population at the 

 hatchery, but the mortality rate continued high — 

 about 10 percent a month of 40,000 lish — during 

 January, February, and March at which time t lie 

 lish were released. 



It is considered probable that the continuing 



mortality was due to the same agent encountered 

 at the Leavenworth station in L951. Two other 

 fish pathogens were isolated from moribund fish 

 of this lot of lish at the Winthrop station during 

 1949 50 and tent at ively ident ified as Psi ml < una mix 

 hydrophila and Ps. fiuoreseens. Both produced 



fatal infections when injected into healthy finger- 

 lings. While both may occur in nature as fish 

 pathogens, it was believed that they were not a 

 primary cause of the prevalent disease because, 

 after the kidney infection was controlled, they did 

 not occur consistently in infected fish (see 

 Schaperclaus 1941, Layman 1940). 



Material passed through a Seitz filter was used 

 in tests for a filtrable agent in this group of fish. 

 No evidence of a virus infection was demonstrated. 

 A Seitz filter retains some viruses that will pass 

 through Mandler filters. It will be recalled that 

 in one experiment a Seitz filtrate of extracts of 

 diseased fish from the Leavenworth outbreak was 

 also noninfectious; in another, the agent passed 

 through a Mandler filter and was shown to be 

 infectious. 



