Epidemiology and Control of Infectious Diseases of Salmonids in the Columbia River Basin, 1984 Annual Report [electronic resource].
- Portland, Ore : United States. Bonneville Power Administration, 1985.
Oak Ridge, Tenn. : Distributed by the Office of Scientific and Technical Information, U.S. Dept. of Energy.
- Physical Description:
- 61 pages : digital, PDF file
- Additional Creators:
- Oregon State University
United States. Bonneville Power Administration
United States. Department of Energy. Office of Scientific and Technical Information
- The Department of Microbiology at Oregon State University with funding from the Bonneville Power Administration has conducted a study since 1983 relating to the epidemiology and control of three diseases of salmonids in the Columbia River Basin. These diseases are ceratomyxosis, caused by the protozoan parasite Ceratomyxa Shasta, bacterial kidney disease, the etiological agent of which is Renibacterium salmoninarum and infectious hematopoietic necrosis which is caused by a rhabdovirus. Each of these diseases is difficult or impossible to treat with antimicrobial agents. The presence of the infectious stage of C. shasta was again detected at Little Goose Dam on the Snake River. The prevalence of ceratomyxosis increased from 1.1% in 1984 to 10% in 1985. None of the susceptible rainbow trout exposed in the Yakima and Umatilla Rivers died of this disease. Ceratomyxosis in resistant chinook salmon smolts seined from the Columbia River just above the estuary seems dependent on whether or not they are held after capture in fresh or salt water. In fresh water the disease incidence ranged from 7--19%, whereas in salt water it ranged from 0--3%. These results which suggest that recovery from ceratomyxosis may occur after the smolts enter salt water are different from those obtained with susceptible Alsea steelhead trout where experimental groups in salt water have died at the same rate as those in fresh water. Comparing data from groups of Columbia River chinook smolts held after capture in either fresh or salt water, R. salmoninarum is a much more effective pathogen in the salt water environment. After four years of sampling smolts in the open ocean, numbers of this microorganism sufficient to cause death have been detected in chinook (7%) and, coho salmon (2%) and steelhead trout (1%). Results from three years of sampling have consistently indicated that additional fish infected with R. salmoninarum will be detected if egg washings are included in the procedures for monitoring bacterial kidney disease in adults. Antigenic differences among strains of R. salmoninarum and common antigens present on both R. salmoninarum and other Gram positive bacteria have been demonstrated for the first time using monoclonal antibodies. All of the monoclonal antibodies belong to the murine IgGl, IgG3 or TgG2a class and subclass. Field studies at Round Butte Hatchery with the molecular filtration apparatus detected IHNV in effluent water from the adult holding pond and in water from a tank containing steelhead trout fry infected with IHN disease. The concentrations of IHNV detected in these samples suggested that in the order of 10¹° virions are being released each day into the Deschutes River at the peak of steelhead trout spawning at Round Butte Hatchery. Isolation of IHNV from dead eggs suggested that virus replication during incubation may be a possible cause of egg mortality. Two possible reasons for inconsistencies in the data from the IHNV transmission studies at Round Butte Hatchery are: (1) UV treatment does not completely sterilize the water and (2) vertical transmission occurs but under, as yet, undescribed conditions. Constant IHNV production over a prolonged period has been recorded in unfiltered ovarian fluid samples. Filtration eliminates this virus production. These observations suggest that cellular components in ovarian fluid are responsible for producing the delayed appearance of IHNV after storage at 4 C for 8 to 16 days.
- Published through SciTech Connect.
Fryer, John L.
- Type of Report and Period Covered Note:
- Annual; 01/01/1984 - 12/31/1984
- Funding Information:
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