A survey for Manayunkia speciosa, the freshwater polychaete host for the myxozoan parasite Ceratomyxa shasta, was conducted from 2003 to 2005 as part of an integrated study of the epizootiology of ceratomyxosis in Klamath River salmonids. Substrata samples (n = 257) were collected in a variety of habitats from Klamath Lake to the mouth of the Klamath River to document occurrence and relative abundance of the polychaete by habitat type and to estimate the prevalence of C. shasta within selected polychaete populations. Populations of M. specios a were identified throughout the Klamath River within pools (51.6%), eddy-pools (47.0%), and runs (40.0%). Large populations of M. speciosa were consistently found at the inflow to the main-stem reservoirs where densities were correlated with distance from the inflow into the reservoir. Using polymerase chain reaction assay and composite samples, 12 of 71 populations identified were tested for C. shasta, revealing a mean infection prevalence of 0.27%. An area of elevated infection prevalence (4.9 and 8.3%) was identified with 2 populations below a barrier to salmonid migration, which explains the high infectious spore densities demonstrated in concurrent studies and observations of C. shasta-induced mortality in Klamath River fall Chinook salmon (Oncorhynchus tshawytscha).

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.

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We evaluated a stock for restoring runs of fall Chinook salmon Oncorhynchus tshawytscha in the Upper Klamath River basin by monitoring its development in Iron Gate Hatchery and in net‐pens in the Williamson River and Upper Klamath Lake in Oregon. We transferred age‐1 hatchery fall Chinook salmon to net‐pens in October 2005 and age‐0 fall Chinook salmon in May 2006. Indices of smolt development were assessed in the hatchery and after 3 and 14 d in net‐pens. Based on gill Na+, K+‐ATPase activity and plasma thyroxine (T4) concentration, age‐1 Chinook salmon were not developing smolt characteristics in the hatchery during October. Fish transferred to the river or lake had increased plasma cortisol in response to stress and increased T4 accompanying the change in water, but they did not have altered development. Variables in the age‐0 Chinook salmon indicated that the fish in the hatchery were smolting. The fish in the river net‐pens lost mass and had gill ATPase activity similar to that of the fish in the hatchery, whereas the fish transferred to the lake gained mass and length, had reduced condition factor, and had higher gill ATPase than the fish in the river. These results, along with environmental variables, suggest that the conditions in the lake were more conducive to smoltification than those in the river and thus accelerated the development of Chinook salmon. No Chinook salmon in the hatchery or either net‐pen became infected with the myxosporean parasite Ceratomyxa shasta (the presence of which in the river and lake was confirmed) during either trial or when held for 90 d after a 10‐d exposure in net‐pens (2006 group). We concluded that that there is little evidence of physiological impairment or significant upriver vulnerability to C. shasta among this stock of fall Chinook salmon that would preclude them from being reintroduced into the Upper Klamath River basin.

Discovery of fish exhibiting clinical signs of ceratomyxosis in Washington State prompted concern over the potential impact of the myxozoan parasite Ceratomyxa shasta on native stocks of steelhead Oncorhynchus mykiss (anadromous rainbow trout). To investigate these concerns, a survey of 16 freshwater systems within the Puget Sound watershed, including Lake Washington, was conducted by sentinel exposure of susceptible fish (cutthroat trout O. clarkii and rainbow trout). Fish were exposed for 7 d during September 2003 and May 2004 and then were returned to a holding facility for monitoring of disease signs. Mortality caused by the parasite occurred only in the exposure group held at the University of Washington Hatchery, which receives its water from Portage Bay of Lake Washington. Fish from all other sites were negative for C. shasta, both visually and by polymerase chain reaction (PCR) assay, except for a single fish held at the Tumwater Falls Hatchery in September 2003. A single deformed spore was detected in that fish, but infection could not be confirmed by PCR and the parasite was not detected from any other fish held at that site during either the September or the May exposure. From these results, we conclude that C. shasta is not likely to have contributed significantly to the decline of steelhead populations throughout Puget Sound.