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Spatial and Temporal Occurrence of the Salmonid Parasite Ceratomyxa shasta in the Oregon–California Klamath River Basin
Author(s) -
Stocking Richard W.,
Holt Richard A.,
Foott J. Scott,
Bartholomew Jerri L.
Publication year - 2006
Publication title -
journal of aquatic animal health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.507
H-Index - 52
eISSN - 1548-8667
pISSN - 0899-7659
DOI - 10.1577/h05-036.1
Subject(s) - chinook wind , tributary , rainbow trout , drainage basin , oncorhynchus , fishery , juvenile , structural basin , biology , geology , ecology , geography , fish <actinopterygii> , geomorphology , cartography
The parasite Ceratomyxa shasta has been implicated as a significant source of salmonid mortality in the lower Klamath River, California (i.e., below Iron Gate dam). A study of the prevalence of C. shasta and its geographic and temporal distribution throughout the Klamath River basin was conducted to determine when and where juvenile salmonids encounter lethal parasite doses. Susceptible rainbow trout Oncorhynchus mykiss were exposed to C. shasta 3–4 d at seven locations in the Klamath River between Beaver Creek and Keno Reservoir in April, June, July, September, and November 2003. Individuals from a Klamath River strain of fall Chinook salmon O. tshawytscha were held in three locations in the upper Klamath River in April, June, and July. In June 2004, rainbow trout were exposed to the parasite for 4 d at 18 locations from Klamath Lake to the mouth of the Klamath River, including several major spawning tributaries; one exposure occurred in the lower Klamath River. Rainbow trout mortality due to infection for groups exposed in the upper Klamath River was lower (<8.0%) and delayed (mean time to death, 40–110 d) in comparison with that in groups exposed in the lower Klamath River (>98%; mean time to death, 33–36 d). Experimental fall Chinook salmon did not become infected in the upper Klamath River, but infection was detected in Chinook salmon exposed in the lower Klamath River, nearly 50% of these succumbing to infection. These dramatic differences in mortality between the upper and lower Klamath River could not be explained by differences in water temperatures during exposure and are probably a result of differences in infectious dose. Lack of infection in groups exposed in tributaries supports the hypothesis that the parasite life cycle and the invertebrate host are largely confined to the main‐stem Klamath River.