Ceratomyxa shasta is a myxosporidan parasite of salmonids. The distribution of sites in which fish become infected with C. shasta appears to be restricted to several river systems of the Pacific Northwest coast of the United States. The objective of this study was to investigate the biology of C. shasta in hopes that this information would lead to measures of controlling ceratomyxosis. As the result of this study, the range of occurance of C. shasta was extended to include the lower Willamette River, Oregon. Susceptible salmonids were held in liveboxes within the river system to determine the extent of the river where they would become exposed to ceratomyxosis. No infections were obtained in the exposed fish at or upstream from mile 134.
The source of ceratomyxosis for the Willamette appears to be the main river channel and the disease agent does not enter from tributaries. For most years tested, salmonids developed ceratomyxosis when exposed to Willamatte River water from early April through mid-November
. Attempts to transmit the disease using infected tissues, a mud substrate, and flowing Pathogen free water were unsuccessful. Laboratory transmission of C. shasta was accomplished by injection of the trophozoite stage of the parasite. The susceptibility of selected salmonid species to ceratomyxosis by injection was also determined.
Nine salmonid species were tested for their susceptibility to ceratomyxosis by natural exposure.
A high percent mortality and a short mean time to death characterized salmonids with high susceptibility to the disease. These inclued rainbow, cutthroat and brook trout and chum and one strain of fall chinook salmon. Sockeye and spring chinook salmon had low susceptibility to ceratomyxosis as indicated by low percent mortality and an extended mean time to death. Brown trout, Atlantic and coho salmon were moderately susceptible and had intermediate values for percent mortality and mean time to death.
Variation in susceptibility to ceratomyxosis was investigated between four strains of fall chinook salmon. Three strains originated from hatcheries located within the lower Columbia River system, which has been shown to contain C. shasta, while the fourth was from an Oregon coastal river, where the disease does not occur. Fish of these four strains were exposed to ceratomyxosis which was subsequently detected in 95 percent of the coastal fall chinook salmon strain and only 9 percent of the Columbia River basin strains. Fish of the strains originating from the Columbia River basin possessed a high degree of resistance to the disease. That resistance can be passed genetically, is possible, since none of the individuals tested had been previously exposed to the disease.
Two strains of rainbow trout which were cultured for resistance to cetatomyxosis were exposed to the disease. Both strains displayed resistance to ceratomyxosis and illustrated that resistant strains could offer a solution to fisheries agencies which manage waters where ceratomyxosis occurs.
The histopathology of rainbow trout infected with C. shasta was described. A group of rainbow trout were exposed to ceratomyxosis and tissue samples were examined histologically to check the progress of the disease with time. Infection was first detected in the pyloric caeca and descending intestine followed by a massive infection of the digestive tract and its associated organs. Cells of the lamina propria, stratum compactum, and stratum granulosum proliferated to form a fibrous granulomatous layer in places where the intestinal mucosal epithelium was sloughed off. Infection of visceral organs other than the intestines occurred from trophozoites which penetrated into the surface of the organs from the body cavity. Death of the host occurred when trophozoites infected the digestive system for most of its length.
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