|Abstract or Summary
- This is the first report on the susceptibility of salmonid fish to infection with the glochidia of the freshwater mussel Margaritifera. margaritifera using known numbers of parasites under controlled conditions. The relative susceptibility of six species of salmonid fish, 2O to 80 mm in total length, to glochidiosis was determined by exposing fish individually to different numbers of the parasites and plotting mortalities against these exposure levels 70 days post-exposure and also against the numbers (dosages) of parasites at 48 hrs post-infection. The 70-day exposure curves represented salmonid susceptibility more than the dosage curves. The 70-day interpolated LE₅₀ values (exposure concentrations of glochidia that killed 50% of the fish) for kokanee salmon (Oncorhynchus rierka kennerlyi), cutthroat trout (Salmo clarki). Atlantic salmon (S. salar), steelhead trout (S. gairdneri), and coho salmon (O. kisutch) were 17,500, 29,000, 35,000, 57,000, and 105,000 respectively. Chinook salmon (O. tschawytscha) were the most susceptible species because mortalities were so high at the lowest exposure levels that LE₅₀'s could not be estimated. As shown by the high LE₅₀ value, coho salmon were the most resistant to infection. Additional evidence supporting the difference in susceptibility between coho and chinook salmon came from in vitro tests. Glochidial attachment on excised gills and their survival in hanging drops of fish mucus and plasma were less for coho salmon than chinook salmon. These results suggest the presence of some inhibiting factor in the mucus and blood of coho salmon. Histological sections of infected gill tissue from sublethally infected coho salmon showed that cellular migration of host tissue, which forms the cyst around the parasites, either did not occur or progressed inadequately such that many glochidia were forced to drop off the gills within 16 hrs post-infection. Of the few glochidia that were encysted, most of them were sloughed intact within their cysts by 2 days post-infection. The sloughing was due to a hyperplastic response of the gill epithelia and stroma to the attached parasites. Host epithelial and stromal cells migrated normally in chinook salmon forming well-structured, discrete cysts that were not sloughed. Hematological examinations were made on blood samples taken from control and sublethally-infectedcoho and chinook salmon at periodic intervals during the parasitic period. In comparison with control fish, the leukocyte numbers and the amount of hemoglobin from infected coho salmon increased significantly. The hematocrits from infected fish of both species were significantly higher than those from respective control fish, however the increase was much greater for chinook salmon. Increased erythrocyte numbers from infected chinook salmon were statistically significant when compared to those of control chinook salmon. The results from a limited number of acrylamide gel electrophoresis trials on blood plasma from infected and control fish indicated that the total plasma protein increased in coho salmon and decreased in chinook salmon after infection. The higher hemoglobin values, leukocyte numbers, and total plasma protein concentrations that occurred after infection suggest that coho salmon may have a greater compensatory or inflammatory response than chinook salmon to glochidial infection. These responses may also aid in resistance to secondary infection.