Net-pen rearing of salmon is well established in Norway and Scotland, but large-scale production by this method is relatively new in North America, Coho salmon (Oncorhynchus kisutch) and Atlantic salmon (Salmo salar) are the species most commonly reared commercially in seawater net pens in Washington State. The Battelle Marine Research Laboratory provides diagnostic services to fish farmers in the state. We have observed new pathological conditions in pen-reared salmon in Washington in addition to diseases which have previously occurred in European pen culture. Reported here is a summary of diseases observed in pen reared salmon from 1985-1987.

Metazoan Parasites.

Although helminths were frequently observed in the guts of moribund fish at necropsy, we have observed only external copepods (Lepiophtheirus salmonis) in sufficient intensities to consider them significant pathogens. Lepiophtheirus salmonis, commonly called sea louse, is a cosmopolitan parasite that has been reported to cause epizootics in pen-reared salmon in Scotland (Wootten et al. 1977). Moderate infestations were associated with dermal ulcerations on both coho and Atlantic salmon reared in Washington, but severe epizootic episodes such as those seen with heavy infestations as reported in Europe have not occurred.

Protozoans

Epizootic diseases due to protozoan parasites are common in aquaculture, and several are significant pathogens in pen-reared salmon. We have detected Parvicapsula sp. (Myxosporea: Myxozoa) in the kidneys of coho salmon. The parasite sporulates in the epithelium, and lumen of the kidney tubules, causing tubular degeneration and kidney hypertrophy (Hoffman 1984; Johnstone 1984).

We have also detected a microsporidan similar to Loma salmonis (Microspora) in the gills of coho salmon. This parasite is a recognized pathogen of chinook salmon, 0. tshawytscha (Hauck 1984), but this is the first time it has been reported to cause disease in coho. In contrast to chinook salmon infections, the parasite caused severe interstitial hyperplasia in the gills of coho after they were transferred to seawater.

Paramoeba sp. (Sarcodina) was also observed on the gills of coho salmon after seawater transfer. Intense infections have occurred in the fall and winter months, particularly in 1985, and affected fish showed severe epithelia] hyperplasia of the gill, which resulted in fusion of the secondary lamellae. A similar amoeba has been associated with gill disease in seawater-reared salmonids in Tasmania (Munday et al. 1987). External parasites such as these gill amoebae are easily eradicated when fish are maintained in confined ponds or raceways by applying chemotherapeutics to the water, but this is difficult when fish are reared in net pens, which have a constant water exchange.

Bacteria

Renibacterium salmoninarum, the causative agent of bacterial kidney disease of salmonids, was detected in both coho and Atlantic salmon. The bacterium causes a chronic inflammation of the kidney interstitium, spleen, heart and other organs (Fryer and Sanders 1981). It can be transmitted either horizontally or vertically within eggs (Evelyn et al. 1984), and the disease is often exacerbated after infected fish are transferred to seawater. Bacterial kidney disease has occurred in seawater net pens in Europe, and we have detected it in both Atlantic and coho salmon in Washington net pens. Coho are apparently more severely affected, and the disease is prevalent through the spring and summer in this species.

Vibriosis, caused by Vibrio anquillarum and V. ordalii, is a cosmopolitan disease which infects salmonids and other species cultured in seawater (Novotny 1978). The bacteria cause septicemia, and the disease is exacerbated at higher temperatures. We have isolated V. anquillarum from coho during the summer, but it may have been a secondary invader, because most of these fish were also infected with Renibacterium salmoninarum. We have also isolated Vibrio spp. from Atlantic salmon that exhibited visceral hemorrhages. These isolates were serologically distinct from V. anguillarum and V. ordalii, and their role in the disease is unknown.

Furunculosis, caused by Aeromonas salmonicida, often causes severe disease in freshwater fishes. As the culture of fish in seawater has increased, this bacterium has been recognized as a pathogen in seawater as well (Novotny 1978), and we have observed epizootic episodes due to this pathogen in net pens in Washington. As with Renibacterium, epizootic disease in salmon with latent infections occurs after transfer to seawater (Cox et al. 1986; Smith et al. 1982). Although the bacterium often originates in freshwater, it can apparently survive and spread in seawater (Scott 1968), and infections have been reported (Morrison et al. 1984) that are restricted to marine waters.

We have isolated a marine Cytophaga sp. from skin lesions in Atlantic salmon. Cytophaga psychrophila and a related bacterium, Flexibacter columnaris, are well-recognized surface pathogens of freshwater fishes (Anderson and Conroy 1969), but the taxonomy of members of these genera which are associated with disease in seawater-reared fishes is poorly understood. Only C. maritimus, which causes disease in cultured sea bream in Japan, is well-described (Wakabayashi et al. 1986). Shortly after seawater introduction, the Cytophaga sp. which we have observed in Atlantic salmon caused skin lesions that ultimately developed into large ulcers extending into the Muscle. The ulcers were focalized in the posterior region of the fish and were particularly prevalent in fish introduced in March 1985 and 1986. To avoid this infection, 1987 smolts were not introduced at this facility until April. Although some fish became infected, the prevalence of the disease was greatly diminished this year. Wet mounts and histological sections of the lesions revealed massive numbers of Cytophaga-like bacteria. In 1986 and 1987, we isolated a similar Cytophaga sp. from infected fish that is serologically and biochemically distinct from the other known Cytophaga or Flexibacter pathogens of fish.

Idiopathic Diseases

We have also observed a condition similar to pancreas disease in Atlantic salmon reared in Washington (Kent and Elston 1987). Pancreas disease is a syndrome which affects Atlantic salmon reared in Europe during their first year in seawater. Fish become emaciated, and histological examination reveals diffuse necrosis and atrophy of the exocrine pancreas. The cause is unknown. Researchers in Scotland have proposed various etiologies; Ferguson et al. (1986) suggested that the condition may be related to vitamin E and selenium deficiencies, whereas Munro et al. (1984) reported epizootiological evidence consistent with an infectious etiology.

In the fall of 1986, we observed severe necrosis of the liver in moribund Atlantic salmon maintained in net pens near a pulp mill in Washington. Examination of surviving fish throughout the winter revealed basophilic foci of regenerating hepatocytes, intermixed with cells undergoing hydropic degeneration, and parenchymal cells with nuclear inclusion and enlarged nuclei. The latter is similar to megalocytic hepatosis of flatfish from polluted waters in Puget Sound (Myers et al. 1986). Ultrastructural examination of the nuclear inclusions revealed that they originated from cytoplasmic invaginations, and no viruses were detected. Myers et al. proposed that megalocytic hepatosis is a percussor to liver neoplasia; we are maintaining the surviving salmon in our laboratory to determine whether they develop liver tumors.

Acknowledgments

This work was supported by Battelle Memorial Institute (BMI), Columbus Ohio.

References

1.  Anderson, J.I.W., and Conroy, D.A. 1969. J. Appl. Bact. 32:30-39.

2.  Cox, D.I., Morrison, D.J. and Rae, G.H. 1986. Bull. Eur. Assoc. Fish. Pathol. 6(4): 100-102.

3.  Evelyn, T.P.T., and Ketcheson, J.E., Prosperi-Porta, L. 1984. J. Fish Dis. 7: 173-182.

4.  Ferguson, H.W., Rice, D.A. and Lynas, J.K. 1986. Vet. Rec. 119: 297-299.

5.  Fryer, J.L., and Sanders, J.E. 1981. Ann. Rev. Microbiol. 35:273-298.

6.  Hauck, A.K. 1984. J. Fish Dis. 7:217-229.

7.  Hoffman, G.L. 1984. Symp. Biol. Hung. 23: 127-135 Johnstone, A. K. 1984. Ph.D. Dissertation, University of Washington. Kent, M.L., and Elston, R.A. Bull. Eur. Assoc. Fish Pathol. (in press).

8.  Morrison, C.M., Cornick, J.W., Shum, G. and Zwicker, B. 1984. J. Fish Dis. 7: 477-494.

9.  Munday, B.L., Lange, K., Forster, C., Lester, R. and Handlinger, J. 11987, Tasmanian Fish. Res. (submitted).

10. Munro, A.L.S., Ellis, A.E., McVicar, A.H., McLay, H.A. and Needham, E.A. 1984. Hegl. Meeres. 37: 571-586.

11. Myers, M.S, Rhodes, C.D. and McCain, B.B. 1987. J. Natl. Cancer Inst. 78:333-363.

12. Novotny, A.J. 1978. Mar. Fish. Rev. 40: 52-55. Smith, P.R., Brazil, G.M., Drinan, E.M., O'Kelly, J., Palmer, R. and Scallan, A. 1982. Bull. Eur. Ass. Fish Pathol. 3: 41-42.

13. Wootten, R., Smith, J.W. and Needham, T. 1977. Bull. Off. Int. Epiz. 87: 521-522. Scott, M. 1968. J. Gen. Microbiol. 50: 321-327. Wakabayashi, H., Hikida, M. and Masumura, K. 1986. Int. J. Syst. Bacteriol, 36: 396-398.