Infectious hematopoietic necrosis is generally considered a disease of salmonid alevins, fry, and early juveniles. It has been suggested that this disease kills only young salmonids and that susceptibility decreases with increased size and age of the fish. To determine if decreased susceptibility occurs with increasing size, we exposed four different sizes of rainbow trout Oncorhynchus mykiss (mean weight, 0.2–13.1 g) and kokanee (lacustrine sockeye salmon) Oncorhynchus nerka (0.2–7.2 g) to two waterborne strains of infectious hematopoietic necrosis virus. Both species were exposed to four concentrations of a type‐1 virus strain, which was isolated from fish in Oregon, and a type‐2 virus strain obtained from fish in Idaho. Neither strain of virus was consistently more virulent over all exposure concentrations for kokanee at the 0.2‐g fish size, At all other sizes, kokanee were consistently more susceptible to the Oregon strain than to the Idaho strain (sign test, P < 0.002). Conversely, all sizes of rainbow trout were consistently more susceptible to the Idaho strain than to the Oregon strain (sign test, P < 0.001). The results showed that there are differences in virulence for type‐1 and ‐2 strains of virus and that these strains have the ability to produce disease in kokanee and rainbow trout as large as 7.2 g and 13.1 g, respectively.
Juvenile steelhead trout (Salmo gairdneri), coho salmon (Oncorhynchus kisutch), and spring chinook salmon (O. tshawytscha) were infected by intraperitoneal or intramuscular injection with Aeromonas salmonicida or A. hydrophila at seven temperatures from 3.9 to 20.5 °C. At 3.9 and 6.7 °C, mortality in fish infected with A. salmonicida varied from 2 to 26% among the three salmonid species. At 20.5 °C 93–100% of these animals died within 2 or 3 days; at 6.7 °C or lower the fish survived for 12–23 days. Growth of A. salmonicida in vitro was influenced by temperature in a manner very similar to its influence on the in vivo infection. Comparable experiments with A. hydrophila gave results much like those with A. salmonicida, though some differences were noted. At a temperature of 20.5 °C percent mortality ranged from 64 to 100%. At 9.4 °C or below no deaths attributed to A. hydrophila occurred. Fatally infected fish died more rapidly at the higher temperatures. Key words: Aeromonas salmonicida, A. hydrophila, water temperature, furunculosis, motile aeromonas septicemia, coho salmon, chinook salmon, steelhead trout
Effects of environmental temperature on juvenile coho salmon (Oncorhynchus kisutch) experimentally infected with Vibrio anguillarum were examined at 7 water temperatures from 3 to 21°C. The mean day to death and total mortality were each related to temperature. The shorter mean day to death and higher mortality were observed at the elevated water temperatures. Growth curves of V. anguillarum cultured in Brain Heart Infusion broth were determined at 6, 12 and 18°C. Growth rates were directly related to temperature. The effect of temperature on the production of V. anguillarum agglutinating antibodies following parenteral injection was determined in juvenile coho salmon held at 6, 12 and 18°C. Titers were first observed on days 10, 15, and 25 in fish held at 18, 12 and 6°C, respectively.
Five fish cell lines (CHSE-214, STE-I37, RTG-2, EPC and FHM) were compared for sensitivity to infeetious haematopoietic necrosis virus (IHNV) from samples obtained from naturally-infected fish. Infeetious ovarian fluids were obtained from steelhead trout, Salmo gairdneri Riehardson, at the Round Butte Hatchery in central Oregon and tissue homogenates were prepared from chinook salmon, Oncorhynchus tshawytscha (Walbaum), alevins during an IHN virus epizootic at the Elk River Hatchery in coastal Oregon. The only lines to show characteristic viral cytopathology by plaque or end-point dilution assay for the steelhead trout virus isolate were the EPC and FHM cell lines. The chinook salmon isolates produced CPE in CHSE-214, STE-137, FHM and EPC cells. The titre of the salmon virus isolate was 10-50-fold higher on FHM and EPC cells by both assay methods. Neither by end-point nor plaque assay did the Round Butte or Elk River isolates produce CPE on RTG-2 cells. With both virus isolants both cell lines showed that greater sensitivity was obtained with plaque assay than with end-point titration. Pre-treatment of the cells with the polyeation. polybrene, did not increase the virus titre in either assay. However, a transient enhancement in virus titre was observed in polybrene-treated STE-137 and CHSE-214 cells.
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