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Fish Disease
Leaflet 80Ceratomyxa shasta, a Myxosporean Parasite of SalmonidsJ. L. Bartholomew, J. L., J. S. Rohovec and J. L. FryerU.S. Fish and Wildlife Service, National Fisheries Research Center, P. O. Box 700, Kearneysville, West Virginia 25430 UNITED STATES DEPARTMENT OF THE INTERIOR, Fish and Wildlife Service. 1989.
IntroductionCeratomyxosis is a disease of salmonid fishes caused by the myxosporean Ceratomyxa shasta. The parasite has a tropism for the intestinal tissue of the fish and causes high mortalities in susceptible strains of salmonids. The disease was first observed in 1948 in fall spawning rainbow trout (Salmo gairdneri) from Crystal Lake Hatchery, Shasta County, California (Wales and Wolf 1955). The etiological agent was established as a new species by Noble (1950), who described C. shasta as the first species of Ceratomyxa to parasitize freshwater fish and the only member that is histozoic. Other species of Ceratomyxa that occur in marine fishes parasitize the lumen of the gall bladder and urinary bladder. Ceratomyxa shasta is an important parasite in the Pacific Northwest because it not only causes losses in hatcheryreared and wild juvenile salmonids but also contributes significantly to prespawning mortality in adult salmon. Although the parasite has not been detected outside the Pacific Northwest, its distribution in that region has expanded. It is not known whether this increase reflects a true spread of the disease or only improved detection methods. Diagnosis and IdentificationExternal and Internal SignsClinical signs of ceratomyxosis vary among salmonid species. Infected juvenile rainbow trout (and steelhead) become anorexic, lethargic, and darken. Ascites may distend the abdomen, the vent may be swollen and hemorrhaged, and exopthalmia is common (Schafer 1968). Infected juvenile chinook salmon (Oncorhynchus tshawytscha) first become emaciated and later sometimes develop large fluidfilled blebs and kidney pustules (Conrad and Decew 1966). Internally, the intestinal tract of juvenile rainbow trout becomes swollen and hemorrhaged and the intestinal contents mucoid, and caseous material lines the intestine and pyloric caeca (Conrad and Decew 1966). The entire digestive tract, the liver, gall bladder, spleen, gonads, kidney, heart, gills, and skeletal muscle may become diseased, hemorrhaged, and necrotic (Wales and Wolf 1955). Infected adult chinook salmon may have nodular lesions in the intestine that perforate, causing death. These nodules may be accompanied by gross lesions in the liver, kidney, spleen, and muscle. Infected adult coho salmon (O. kisutch) show grossly thickened intestinal walls and pyloric caeca and large abscessed lesions in the body musculature (Wood 1979). HistopathologyIn juvenile rainbow trout the first sign of infection appears in the posterior intestine. The progress of the infection is temperature dependent, the first sign of infection appearing between days 12 and 18 postexposure in fish held at 12°C, and at 7 days in fish held at 18°C (Yamamoto and Sanders 1979). Trophozoites are first seen in the mucosa; their appearance is followed by a strong inflammatory response in the lamina propria. As the infection progresses, the parasite multiplies in all layers of the intestine and causes severe inflammation and desquamation of the mucosal epithelium. Trophozoites penetrate the intestinal tract, spread into the surrounding adipose and pancreatic tissues, and enter the bloodstream, which carries them to other tissues and organs. In late stages of infection, the parasite is in most tissues and organs adjacent to the intestine, including the liver, kidney, pyloric caeca, and spleen. Diagnosis of the disease is sometimes delayed because the spore stage of C. shasta is not evident until the terminal stages of the infection. IdentificationDiagnosis requires that spores be found and identified by their size, shape, and location. The American Fisheries Society Fish Health Blue Book (Amos 1985) recommends the following procedures: (1) examination of wet mounts from the lower intestinal wall, ascites, gall bladder, and lesions by phase contrast or bright light microscopy at x400; (2) examination of airdried smears stained by the ZiehlNeelsen method but without heating; or (3) fixation of smears in Schaudin's fixative and staining with Heidenhain's iron hematoxylin (for permanent preparations). For examination of live fish, an intestinal lavage technique can be used (Coley et al. 1983). Spores of C. shasta are about 14 to 23µm long and 6 to 8µm wide at the suture line (Fig. 1). The ends of the spores are rounded and reflected posteriorly; the suture line is distinct (Noble 1950). In smears stained by the ZiehlNeelsen method, the polar capsules stain red against a bluish sporoplasm and background. Trophozoites, which are rounded but variable in shape, mature to form a sporoblast that usually contains two spores (Fig. 2). Because of the variability in size and shape of the trophozoites and their similarity to this stage in other myxosporeans, observation of trophozoites by light microscopy is not sufficient for diagnosis. Consequently, serological techniques have been developed in which monoclonal antibodies are used. The antibodies produced react specifically with the prespore stages of the parasite and do not crossreact with trophozoite or spore stages of other myxosporeans. Use of the monoclonal antibodies and fluorescein or enzyme conjugated secondary antibodies enables the reliable detection of early infections (J. L. Bartholomew, J. S. Rohovec, and J. L. Fryer, in preparation).
EcologyEffects of TemperatureInfection by C. shasta was once believed to occur only when water temperatures exceeded 10°C, thus accounting for the seasonal occurrence of the disease; however, later reports indicated that fish can become infected in water at temperatures as low as 4 to 6°C (Ratliff 1983; Ching and Munday 1984a). Although fish are infected at these lower temperatures, the progress of the disease is temperature dependent and most infections are detected later, after the water warms. Udey et al. (1975) reported that rainbow trout exposed to the infective stage of C. shasta and held at water temperatures of 6.7 to 23.3°C had little or no ability to overcome the infection, and that the mean time from exposure to death was directly correlated to temperature (e.g., about 155 days at 6.7°C and 14 days at 23.3°C). In rainbow trout the disease process was suppressed at 3.9°C; however, when the infected fish held at this temperature were transferred to water at 17.8°C, many died. Coho salmon appeared better able to combat the infection at low water temperatures, but the mean time to death remained temperature dependent. Effects of SalinityOnly limited information is available about the effects of salt water on the progress of a C. shasta infection. Johnson (1975) reported that infections were prevented at salt concentrations greater than 15 ppt. Although this would protect juvenile salmonids from infection in estuarine areas, the fate of fish that were infected in fresh water and then migrated into salt water was not determined. Acute ceratomyxosis has been reported in juvenile chum salmon captured off the coast of British Columbia, Canada (Margolis and Evelyn 1975), demonstrating that the disease is not attenuated by salt water. Ching and Munday (1984b), who exposed chinook salmon to the infective stage of C. shasta, found that the disease caused 100% mortality when the fish were held in either fresh water or salt water. Similarly designed experiments with steelhead indicated that migration to salt water may reduce the progress of the disease, but the extent of attenuation may be masked in fish overwhelmed by a high number of infectious units (Hoffmaster 1985). Host Range and SusceptibilityIt is accepted that only salmonids are susceptible to C. shasta infection (Table 1), but this susceptibility may vary within a species. Experiments to test resistance of different strains of the same species to C. shasta indicated that juvenile salmonids originating from waters containing the infective stage of the parasite were more resistant than strains from areas free of the infective stage (Johnson 1975; Zinn et al. 1977; Buchanan et al. 1983; Hoffmaster 1985). The susceptibility to infection by C. shasta in progeny produced from crosses between resistant and susceptible coho salmon is intermediate between that of the parental stocks (Hemmingsen et al. 1986). The management implications of these studies are that relocation of salmonids from areas where C. shasta is not endemic into areas endemic for the parasite is not likely to be successful, and that these introductions may adversely affect the survival of resident resistant strains if interbreeding occurs. Although juvenile salmonids from waters endemic for C. shasta are resistant to infection, ceratomyxosis has been determined to be an important cause of prespawning mortality in the adults. Coley et al. (1983) reported that 94% of adult spring chinook salmon at Rapid River Hatchery, Idaho, were infected with C. shasta. Similar incidences of infection in adults have been reported by other researchers (Sanders et al. 1970; Yasutake et al. 1986; Chapman 1986). Although infection by C. shasta occurs during the freshwater phase of the fish's life cycle, it is not known whether these fish were infected before they entered salt water or after they reentered fresh water. Table 1. Host range of Ceratomyxa shasta. Common name -- Scientific name --Reference Rainbow trout Salmo gairdneri Noble 1950 Chinook salmon Oncorhynchus tshawytscha Conrad and Decew 1966 Coho salmon Oncorhynchus kisutch Conrad and Decew 1966 Steelhead Salmo gairdneri Conrad and Decew 1966 Brook trout Salvelinus fontinalis Schafer 1968 Brown trout Salmo trutta Schafer 1968 Atlantic salmon Salmo salar Sanders et al. 1970 Cutthroat trout Salmo clarki Sanders et al. 1970 Sockeye salmon Oncorhynchus nerka Sanders et al. 1970 Chum salmon Oncorhynchus keta Margolis and Evelyn 1975 Pink salmon Oncorhynchus gorbuscha Bell and Traxler 1985 Geographic DistributionCeratomyxa shasta has been identified in salmonids from marine and freshwater environments in northern California, Oregon, Washington, Idaho, and British Columbia. However, waters where infected fish have been found do not necessarily contain the infective stage of the parasite (Johnson et al. 1979). This is exemplified in the Columbia River Basin, where infected adult coho and chinook salmon and steelhead migrate and distribute spores throughout the drainage, but the infective stage of C. shasta has not been demonstrated in many tributaries to which these fish have access. This suggests that the presence of spores alone is insufficient to cause transmission and disease. The presence of the infective stage of C. shasta is demonstrated by using sentinel populations of susceptible salmonids and examining them for development of the disease and appearance of spores. The distribution of the infective stage (Fig. 3) has been documented by Johnson et al. (1979), Ching and Munday (1984a), and Hoffmaster et al. (1988). The confinement of this parasite to salmonids of the Pacific Northwest is unique. The distribution of many other fish pathogens has been expanded as a result of shipments of eggs or fish. This geographic isolation is compatible with the hypothesis that an as yet unknown factor is required for the completion of the life cycle of this parasite. Transmission and Life CycleThe life history of C. shasta, like that of most other myxosporeans, is unknown. Natural transmission occurs when susceptible salmonids are exposed to water or sediments containing the infective stage (Schafer 1968; Fryer and Sanders 1970; Johnson 1975) and exposure periods as short as 30 min are sufficient for infection to occur. Neither attempts to transmit ceratomyxosis from fish to fish nor the feeding of infected tissues containing spores and trophozoites have resulted in transmission of the disease (Wales and Wolf 1955; Schafer 1968; Wood 1968; Johnson 1975). But infections developed when susceptible fish were exposed to bottom sediments collected from a site endemic for the parasite (Fryer and Sanders 1970). Laboratory transmission of ceratomyxosis has been established by intraperitoneal injection and anal intubation of ascites from infected fish (Schafer 1968; Fryer and Sanders 1970; Johnson et al. 1979; Bower 1985). The natural route of infection has not been established, but Schafer (1968) suggested that the establishment of infection in rainbow trout was not dependent on ingestion of the spore. Differential filtration of waters endemic for C. shasta shows that the infective stage is larger than 14µm. The inability to transmit ceratomyxosis between susceptible fish has led to speculation that an intermediate host may be involved in the life cycle. As yet there is no conclusive evidence to support this hypothesis. ControlBecause C. shasta infections are not transmitted directly between fish, outbreaks of the disease in hatchery fish occur only as a consequence of introducing the infective stage through the water supply. Because no chemotherapeutic agent yet tested has been useful in controlling ceratomyxosis, the most effective means of disease prevention in a hatchery situation is avoidance of water supplies containing the infective stage. In hatcheries where alternative water supplies are unavailable, water treatment methods to eliminate the infective stage have been developed. Bedell (1971) found that ultraviolet irradiation or chlorination of water supplies reduced the number of C. shasta infections but did not eliminate them. Sanders et al. (1972) and Bower and Margolis (1985) determined that sand filtration, in combination with either ultraviolet irradiation or chlorination, was effective in reducing the incidence of disease. Tipping (1986) reported that ozone was effective in controlling ceratomyxosis in hatchery fish. However, the most successful approach for control of ceratomyxosis in both hatchery and wild populations is the introduction of resistant salmonids (Buchanan et al. 1983). AcknowledgmentsWe thank J. E. Sanders and D. G. Stevens for their participation in studies on the geographic distribution, C. E. Smith for his help and expertise in histology, and G. L. Hendrickson for providing current information on the distribution of C. shasta in California. This research was supported by the Oregon Sea Grant through NOAA Office of Sea Grant, under Grant No. 8788 (FY88) NA85AAD5G095 (Project No. R/FSD10) and by the Bonneville Power Administration under contract No. DEA17983 BP 11987; G. R. Bouck, Contracting Officer's Technical Representative. Oregon Agricultural Experiment Station Technical Paper No. 8519. Annotated BibliographyAmos, K. H., editor. 1985. Procedures for the detection and identification of certain fish pathogens. 3rd edition. Fish Health Section, American Fisheries Society, Corvallis, Oreg. Establishes standard methodology for the inspection of fish for certain fish pathogens. Bedell, G. W. 1971. Eradicating Ceratomyxa shasta from infected water by chlorination and ultraviolet irradiation. Prog. FishCult. 33:5154. A report of successful methods of water treatment to eliminate C. shasta. Bell, G. R., and G. S. Traxler. 1985. First record of viral erythrocytic necrosis and Ceratomyxa shasta Noble,1950 (Myxozoa: Myxosporea) in feral pink salmon (Oncorhynchus gorbuscha Walbaum). J. Wildl. Dis. 21:169171. First report of ceratomyxosis in pink salmon. Bower, S. M. 1985. Ceratomyxa shasta (Myxozoa: Myxosporea) in juvenile chinook salmon (Oncorhynchus tshawytscha): experimental transmission and natural infections in the Fraser River, British Columbia. Can. J. Zool. 63:17371740. Describes a method for experimentally transmitting C. shasta by intraperitoneal inoculation of trophozoites from naturally infected fish. Bower, S. M., and L. Margolis. 1985. Microfiltration and ultraviolet irradiation to eliminate Ceratomyxa shasta (Myxozoa: Myxosporea), a salmonid pathogen, from Fraser River water, British Columbia. Can. Tech. Rep. Fish. Aquat. Sci. 1364. 11 pp. Reports elimination of the infective stage of C. shasta from Fraser River water by sand filtration, followed by ultraviolet irradiation. Buchanan, D. V., J. E. Sanders, J. L. Zinn, and J. L. Fryer. 1983. Relative susceptibility of four strains of summer steelhead to infection by Ceratomyxa shasta. Trans. Am. Fish. Soc. 112:541543. Reports the susceptibility of four strains of summer steelhead to infection by C. shasta. Chapman, P. F. 1986. Occurrence of the noninfective stage of Ceratomyxa shasta in mature summer chinook salmon in the South Fork Salmon River, Idaho. Prog. FishCult. 48:304306. Documents the occurrence of C. shasta and notes the parasite's contribution to prespawning mortalities in summer chinook salmon. Ching, H. L., and D. R. Munday. 1984a. Geographic and seasonal distribution of the infectious stage of Ceratomyxa shasta Noble, 1950, a myxozoan salmonid pathogen in the Fraser River system. Can. J. Zool. 62:10751080. Demonstrates the geographical and seasonal distribution of the infective stage of C. shasta in the Fraser River system. Ching, H. L., and D. R. Munday. 1984b. Susceptibility of six Fraser chinook salmon stocks to Ceratomyxa shasta and the effects of salinity on ceratomyxosis. Can. J. Zool. 62:10811083. Reports the susceptibility to ceratomyxosis of seven chinook salmon stocks and documents the effects of seawater on infected chinook salmon. Coley, T. C., A. J. Chaacko, and G. W. Klontz. 1983. Development of a lavage technique for sampling Ceratomyxa in adult salmonids. J. Fish Dis. 6:317319. Describes a method of sampling the intestinal tract of nonfeeding adult salmonids for C. shasta. Conrad, J. F., and M. Decew. 1966. First report of Ceratomyxa in juvenile salmonids in Oregon. Prog. FishCult. 28:238. Reports ceratomyxosis in juvenile coho and spring chinook salmon and steelhead in the Columbia River and Deschutes River hatcheries. Fryer, J. L., and J. E. Sanders. 1970. Investigation of Ceratomyxa shasta, a protozoan parasite of salmonid fish. J. Parasitol. 56:759 A summary of existing knowledge of the parasite C. shasta and difficulties in transmission of the infection. Hemmingsen, A. R., R. A. Holt, R. D. Ewing, and J. D. McIntyre. 1986. Susceptibility of progeny from crosses among three stocks of coho salmon to infection by Ceratomyxa shasta. Trans. Am. Fish. Soc. 115:492495. Demonstrates that the susceptibility of crossbred progeny was intermediate between the susceptibilities of fish from the parental stocks. Hoffmaster, J. L. 1985. Geographic distribution of Ceratomyxa shasta in the Columbia River basin and susceptibility of salmonid stocks. M.S. thesis, Oregon State University, Corvallis. 57 pp. Hoffmaster, J. L., J. E. Sanders, J. S. Rohovec, J. L. Fryer, and D. G. Stevens. 1988. Geographic distribution of the myxosporean parasite, Ceratomyxa shasta Noble, 1950, in the Columbia River basin, USA. J. Fish Dis. 11:97100. Reports known distribution of the infectious stage of C. shasta. Johnson, K. A. 1975. Host susceptibility, histopathologic, and transmission studies on Ceratomyxa shasta, a myxosporidan parasite of salmonid fish. Ph. D. thesis, Oregon State University, Corvallis. 134 pp. Comprehensive studies on the aspects of ceratomyxosis mentioned in the title. Johnson, K. A., J. E. Sanders, and J. L. Fryer. 1979. Ceratomyxa shasta in salmonids. U.S. Fish Wildl. Serv., Fish Dis. Leafl. 58. 11 pp. Reviews the current knowledge of C. shasta. Margolis, L., and T. P. T. Evelyn. 1975. Ceratomyxa shasta (Myxosporea) disease in chum salmon (Oncorhynchus keta) in British Columbia. J. Fish. Res. Board Can. 32:16401643. Reports four chum salmon infected with ceratomyxosis caught off the coast of Vancouver Island. Noble, E. R. 1950. On a myxosporidian (protozoan) parasite of California trout. J. Parasitol. 36:457460. First report on spores and trophozoites of the parasite, and of the tissues of rainbow trout found to be infected. Ratliff, D. E. 1983. Ceratomyxa shasta: longevity, distribution, timing, and abundance of the infective stage in central Oregon. Can. J. Fish. Aquat. Sci. 40:16221632. A study of the characteristics of the infective stage of Ceratomyxa shasta in the Deschutes River. Sanders, J. E., J. L. Fryer, and R. W. Gould. 1970. Occurrence of the myxosporidian parasite Ceratomyxa shasta, in salmonid fish from the Columbia River basin and Oregon coastal streams. Pages 133144 in S. F. Snieszko, ed. A symposium on diseases of fishes and shellfishes. Am. Fish. Soc. Spec. Publ. 5. Reports the occurrence and distribution of C. shasta in juvenile and adult salmonids in the Columbia River basin. Sanders, J. E., J. L. Fryer, D. A. Leith, and K D. Moore. 1972. Control of the infectious protozoan Ceratomyxa shasta by treating hatchery water supplies. Prog. FishCult. 34:1317. A report of the successful elimination of the infectious stage of C. shasta from hatchery water supplies by a combination of MicroFloc filtration and chlorination, or by sand filtration and ultraviolet irradiation. Schafer, W. E. 1968. Studies on the epizootiology of the myxosporidan Ceratomyxa shasta Noble. Calif. Fish Game 54:9099. Various aspects of ceratomyxosis are discussed, including the distribution of the infectious stage in waters in the vicinity of Crystal Lake Hatchery in Shasta County, California; seasonal occurrence and signs of the disease; requirements for transmission; and comparative resistance and susceptibility of different species of salmon. Tipping, J. M. 1986. Control of ceratomyxosis with ozone at the Cowlitz Trout Hatchery. Wash. State Game Dep., Fish. Manage. Div. Prog. Rep. 20 pp. Results of a pilot study to determine the minimum effective ozone dose for control of the infective stage of C. shasta. Udey, L. R., J. L. Fryer, and K. S. Pilcher. 1975. Relation of water temperature to ceratomyxosis in rainbow trout (Salmo gairdneri) and coho salmon (Oncorhynchus kisutch). J. Fish. Res. Board Can. 32:15451551. Reports the effect of seven water temperatures on mortality of rainbow trout and coho salmon from ceratomyxosis and on the mean time from exposure of the fish until death. Wales, J. H., and H. Wolf. 1955. Three protozoan diseases of trout in California. Calif. Fish Game 41:183187. Description of the first recognized outbreak of the disease at Crystal Lake Hatchery in Shasta County California. 1948. Wood, J. W. 1979. Diseases of Pacific salmon, their prevention and treatment. Washington Department of Fisheries, Olympia. 82 pp. General guide to diseases of Pacific salmon. Yamamoto, T., and J. E. Sanders. 1979. Light and electron microscopic observations of sporogenesis in the myxosporidan, Ceratomyxa shasta (Noble, 1950). J. Fish Dis. 2:411428. Describes investigation of developmental stages of C. shasta by light and electron microscopy. Yasutake, W. T., J. D. McIntyre, and A. R. Hemmingsen. 1986. Parasite burdens in experimental families of coho salmon. Trans. Am. Fish. Soc. 115:636-640. Reports infection and tissue reaction to C. shasta in returning coho salmon and suggests reassessment of current certification procedures. Zinn, J. L., K. A. Johnson, J. E. Sanders, and J. L. Fryer. 1977. Susceptibility of salmonid species and hatchery strains of chinook salmon (Oncorhynchus tshawytscha) to infections by Ceratomyxa shasta. J. Fish. Res. Board Can. 34:933936. Reports the susceptibility to infection by C. shasta of
nine salmonid species and nine hatchery strains of chinook salmon.
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