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**Fish Disease Leaflet 80***Ceratomyxa shasta*, a Myxosporean Parasite of SalmonidsJ. L. Bartholomew, J. L.,  J. S. Rohovec and  J. L. Fryer 
 U.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.
- Introduction  Diagnosis and IdentificationEcology
- Host Range and Susceptibility  Transmission and Life CycleControl
- Acknowledgments   Annotated BibliographyIntroduction
 Ceratomyxosis is a disease of salmonid fishes caused by themyxosporean *Ceratomyxa shasta*. The parasite has a tropism forthe intestinal tissue of the fish and causes high mortalities insusceptible strains of salmonids. The disease was first observed in 1948in fall spawning rainbow trout (*Salmo gairdneri*) from CrystalLake Hatchery, Shasta County, California (Wales and Wolf 1955). Theetiological agent was established as a new species by Noble (1950), whodescribed *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 fishesparasitize the lumen of the gall bladder and urinary bladder. 

*Ceratomyxa shasta* is an important parasite in thePacific Northwest because it not only causes losses in hatcheryrearedand wild juvenile salmonids but also contributes significantly toprespawning mortality in adult salmon. Although the parasite has notbeen detected outside the Pacific Northwest, its distribution in thatregion has expanded. It is not known whether this increase reflects atrue spread of the disease or only improved detection methods. 
Diagnosis and Identification*External and Internal Signs*
 Clinical signs of ceratomyxosis vary among salmonidspecies. Infected juvenile rainbow trout (and steelhead) becomeanorexic, lethargic, and darken. Ascites may distend the abdomen, thevent may be swollen and hemorrhaged, and exopthalmia is common (Schafer1968). Infected juvenile chinook salmon (*Oncorhynchus tshawytscha*)first become emaciated and later sometimes develop large fluidfilledblebs and kidney pustules (Conrad and Decew 1966). 

 Internally, the intestinal tract of juvenile rainbow troutbecomes swollen and hemorrhaged and the intestinal contents mucoid, andcaseous material lines the intestine and pyloric caeca (Conrad and Decew1966). 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 chinooksalmon may have nodular lesions in the intestine that perforate, causingdeath. These nodules may be  accompanied by gross lesions in the liver, kidney, spleen, and  muscle. Infected adult coho salmon (*O. kisutch*) showgrossly thickened intestinal walls and pyloric caeca and large abscessedlesions in the body musculature (Wood 1979). 
*Histopathology*
 In juvenile rainbow trout the first sign of infectionappears in the posterior intestine. The progress of the infection istemperature dependent, the first sign of infection appearing betweendays 12 and 18 postexposure in fish held at 12°C, and at 7 days infish held at 18°C (Yamamoto and Sanders 1979). Trophozoites arefirst seen in the mucosa; their appearance is followed by a stronginflammatory response in the lamina propria. As the infectionprogresses, the parasite multiplies in all layers of the intestine andcauses severe inflammation and desquamation of the mucosal epithelium.Trophozoites penetrate the intestinal tract, spread into the surroundingadipose and pancreatic tissues, and enter the bloodstream, which carriesthem to other tissues and organs. In late stages of infection, theparasite is in most tissues and organs adjacent to the intestine,including the liver, kidney, pyloric caeca, and spleen. Diagnosis of thedisease is sometimes delayed because the spore stage of *C*. *shasta*is not evident until the terminal stages of the infection. 
*Identification*
Diagnosis requires that spores be found and identified by theirsize, shape, and location. The American Fisheries Society *FishHealth 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 microscopyat x400; (2) examination of airdried smears stained by the ZiehlNeelsenmethod but without heating; or (3) fixation of smears in Schaudin'sfixative and staining with Heidenhain's iron hematoxylin (for permanentpreparations). For examination of live fish, an intestinal lavagetechnique 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 theZiehlNeelsen method, the polar capsules stain red against a bluishsporoplasm and background. Trophozoites, which are rounded but variablein shape, mature to form a sporoblast that usually contains two spores(Fig. 2). Because of the variability in size and shape of thetrophozoites and their similarity to this stage in other myxosporeans,observation of trophozoites by light microscopy is not sufficient fordiagnosis. Consequently, serological techniques have been developed inwhich monoclonal antibodies are used. The antibodies produced reactspecifically with the prespore stages of the parasite and do notcrossreact with trophozoite or spore stages of other myxosporeans. Useof the monoclonal antibodies and fluorescein or enzyme conjugatedsecondary antibodies enables the reliable detection of early infections(J. L. Bartholomew, J. S. Rohovec, and J. L. Fryer, in preparation).

**Figure 1. Phasecontrast photomicrograph showing morphology of***Ceratomyxa shasta*spores. 

**Figure 2. Phase contrast photomicrograph of trophozoite and disporoblaststages of***Ceratomyxa shasta*. 
Ecology *Effects of Temperature*
 Infection by *C*. *shasta* was once believed tooccur only when water temperatures exceeded 10°C, thus accountingfor the seasonal occurrence of the disease; however, later reportsindicated that fish can become infected in water at temperatures as lowas 4 to 6°C (Ratliff 1983; Ching and Munday 1984a). Although fishare infected at these lower temperatures, the progress of the disease istemperature dependent and most infections are detected later, after thewater warms. Udey et al. (1975) reported that rainbow trout exposed tothe infective stage of *C*. *shasta* and held at watertemperatures of 6.7 to 23.3°C had little or no ability to overcomethe infection, and that the mean time from exposure to death wasdirectly correlated to temperature (e.g., about 155 days at 6.7°Cand 14 days at 23.3°C). In rainbow trout the disease process wassuppressed at 3.9°C; however, when the infected fish held at thistemperature were transferred to water at 17.8°C, many died. Cohosalmon appeared better able to combat the infection at low watertemperatures, but the mean time to death remained temperature dependent.
*Effects of Salinity*
Only limited information is available about the effects of saltwater on the progress of a *C*. *shasta* infection. Johnson(1975) reported that infections were prevented at salt concentrationsgreater than 15 ppt. Although this would protect juvenile salmonids frominfection in estuarine areas, the fate of fish that were infected infresh water and then migrated into salt water was not determined. Acuteceratomyxosis has been reported in juvenile chum salmon captured off thecoast of British Columbia, Canada (Margolis and Evelyn 1975),demonstrating that the disease is not attenuated by salt water. Chingand Munday (1984b), who exposed chinook salmon to the infective stage of*C*. *shasta*, found that the disease caused 100% mortalitywhen the fish were held in either fresh water or salt water. Similarlydesigned experiments with steelhead indicated that migration to saltwater may reduce the progress of the disease, but the extent ofattenuation may be masked in fish overwhelmed by a high number ofinfectious units (Hoffmaster 1985). 
Host Range and Susceptibility
 It is accepted that only salmonids are susceptible to *C*.*shasta* infection (Table 1), but this susceptibility may varywithin a species. Experiments to test resistance of different strains ofthe same species to *C*. *shasta* indicated that juvenilesalmonids originating from waters containing the infective stage of theparasite were more resistant than strains from areas free of theinfective 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 betweenresistant and susceptible coho salmon is intermediate between that ofthe parental stocks (Hemmingsen et al. 1986). The managementimplications of these studies are that relocation of salmonids fromareas where *C*. *shasta* is not endemic into areas endemicfor the parasite is not likely to be successful, and that theseintroductions may adversely affect the survival of resident resistantstrains if interbreeding occurs. 

 Although juvenile salmonids from waters endemic for *C*.*shasta* are resistant to infection, ceratomyxosis has beendetermined to be an important cause of prespawning mortality in theadults. Coley et al. (1983) reported that 94% of adult spring chinooksalmon at Rapid River Hatchery, Idaho, were infected with *C*. *shasta*.Similar incidences of infection in adults have been reported by otherresearchers (Sanders et al. 1970; Yasutake et al. 1986; Chapman 1986). Although infection by C. shasta occurs during the freshwaterphase of the fish's life cycle, it is not known whether these fishwere infected before they entered salt water or after they reenteredfresh water. 

**Table 1.** Host range of *Ceratomyxa shasta*.

**Common name**-- **Scientific name**--**Reference**

 Rainbow trout*Salmo gairdneri* Noble 1950 

 Chinook salmon*Oncorhynchus tshawytscha* Conrad andDecew 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 Traxler1985 *Geographic Distribution*
*Ceratomyxa shasta* has been identified in salmonidsfrom marine and freshwater environments in northern California, Oregon,Washington, Idaho, and British Columbia. However, waters where infectedfish have been found do not necessarily contain the infective stage ofthe parasite (Johnson et al. 1979). This is exemplified in the ColumbiaRiver Basin, where infected adult coho and chinook salmon and steelheadmigrate and distribute spores throughout the drainage, but the infectivestage of *C*. *shasta* has not been demonstrated in manytributaries to which these fish have access. This suggests that thepresence of spores alone is insufficient to cause transmission anddisease. 

 The presence of the infective stage of *C*. *shasta*is demonstrated by using sentinel populations of susceptible salmonidsand examining them for development of the disease and appearance ofspores. The distribution of the infective stage (Fig. 3) has beendocumented by Johnson et al. (1979), Ching and Munday (1984a), andHoffmaster et al. (1988). 

 The confinement of this parasite to salmonids of the PacificNorthwest is unique. The distribution of many other fish pathogens hasbeen expanded as a result of shipments of eggs or fish. This geographicisolation is compatible with the hypothesis that an as yet unknownfactor is required for the completion of the life cycle of thisparasite. 
Transmission and Life Cycle 
 The life history of *C*. *shasta*, like that ofmost other myxosporeans, is unknown. Natural transmission occurs whensusceptible salmonids are exposed to water or sediments containing theinfective stage (Schafer 1968; Fryer and Sanders 1970; Johnson 1975) andexposure periods as short as 30 min are sufficient for infection tooccur. Neither attempts to transmit ceratomyxosis from fish to fish northe feeding of infected tissues containing spores and trophozoites haveresulted in transmission of the disease (Wales and Wolf 1955; Schafer1968; Wood 1968; Johnson 1975). But infections developed whensusceptible fish were exposed to bottom sediments collected from a siteendemic for the parasite (Fryer and Sanders 1970). 

 Laboratory transmission of ceratomyxosis has been establishedby intraperitoneal injection and anal intubation of ascites frominfected fish (Schafer 1968; Fryer and Sanders 1970; Johnson et al.1979; Bower 1985). The natural route of infection has not beenestablished, but Schafer (1968) suggested that the establishment ofinfection 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 susceptiblefish has led to speculation that an intermediate host may be involved inthe life cycle. As yet there is no conclusive evidence to support thishypothesis. 
Control
 Because *C*. *shasta* infections are nottransmitted directly between fish, outbreaks of the disease in hatcheryfish occur only as a consequence of introducing the infective stagethrough the water supply. Because no chemotherapeutic agent yet testedhas been useful in controlling ceratomyxosis, the most effective meansof disease prevention in a hatchery situation is avoidance of watersupplies containing the infective stage. In hatcheries where alternativewater supplies are unavailable, water treatment methods to eliminate theinfective stage have been developed. Bedell (1971) found thatultraviolet irradiation or chlorination of water supplies reduced thenumber of *C*. *shasta* infections but did not eliminatethem. Sanders et al. (1972) and Bower and Margolis (1985) determinedthat sand filtration, in combination with either ultraviolet irradiationor chlorination, was effective in reducing the incidence of disease.Tipping (1986) reported that ozone was effective in controllingceratomyxosis in hatchery fish. However, the most successful approachfor control of ceratomyxosis in both hatchery and wild populations isthe introduction of resistant salmonids (Buchanan et al. 1983). 
Acknowledgments 
 We thank J. E. Sanders and D. G. Stevens for theirparticipation in studies on the geographic distribution, C. E. Smith forhis help and expertise in histology, and G. L. Hendrickson for providingcurrent information on the distribution of *C*. *shasta* inCalifornia. This research was supported by the Oregon Sea Grant throughNOAA Office of Sea Grant, under Grant No. 8788 (FY88) NA85AAD5G095(Project No. R/FSD10) and by the Bonneville Power Administration undercontract No. DEA17983 BP 11987; G. R. Bouck, Contracting Officer'sTechnical Representative. Oregon Agricultural Experiment StationTechnical Paper No. 8519. 
Annotated Bibliography
 Amos, K. H., editor. 1985. Procedures for the detection andidentification of certain fish pathogens. 3rd edition. Fish HealthSection, American Fisheries Society, Corvallis, Oreg. 

 Establishes standard methodology for the inspection of fish forcertain fish pathogens. 

 Bedell, G. W. 1971. Eradicating *Ceratomyxa shasta* frominfected 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 viralerythrocytic 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 fromnaturally infected fish. 

 Bower, S. M., and L. Margolis. 1985. Microfiltration andultraviolet irradiation to eliminate *Ceratomyxa shasta* (Myxozoa:Myxosporea), a salmonid pathogen, from Fraser River water, BritishColumbia. 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 ultravioletirradiation. 

 Buchanan, D. V., J. E. Sanders, J. L. Zinn, and J. L. Fryer.1983. Relative susceptibility of four strains of summer steelhead toinfection by *Ceratomyxa shasta*. Trans. Am. Fish. Soc.112:541543. 

 Reports the susceptibility of four strains of summer steelheadto infection by *C*. *shasta*. 

 Chapman, P. F. 1986. Occurrence of the noninfective stage of*Ceratomyxa shasta* in mature summer chinook salmon in the SouthFork Salmon River, Idaho. Prog. FishCult. 48:304306. 

 Documents the occurrence of *C*. *shasta* and notesthe parasite's contribution to prespawning mortalities in summer chinooksalmon. 

 Ching, H. L., and D. R. Munday. 1984a. Geographic and seasonaldistribution 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 theinfective stage of *C*. *shasta* in the Fraser River system.

 Ching, H. L., and D. R. Munday. 1984b. Susceptibility of sixFraser chinook salmon stocks to *Ceratomyxa shasta* and theeffects of salinity on ceratomyxosis. Can. J. Zool. 62:10811083. 

 Reports the susceptibility to ceratomyxosis of seven chinooksalmon stocks and documents the effects of seawater on infected chinooksalmon. 

 Coley, T. C., A. J. Chaacko, and G. W. Klontz. 1983.Development of a lavage technique for sampling *Ceratomyxa* inadult salmonids. J. Fish Dis. 6:317319. 

 Describes a method of sampling the intestinal tract ofnonfeeding 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 chinooksalmon and steelhead in the Columbia River and Deschutes Riverhatcheries. 

 Fryer, J. L., and J. E. Sanders. 1970. Investigation of *Ceratomyxashasta*, 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 cohosalmon to infection by *Ceratomyxa shasta*. Trans. Am. Fish. Soc.115:492495. 

 Demonstrates that the susceptibility of crossbred progeny wasintermediate between the susceptibilities of fish from the parentalstocks. 

 Hoffmaster, J. L. 1985. Geographic distribution of *Ceratomyxashasta* in the Columbia River basin and susceptibility of salmonidstocks. 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 myxosporeanparasite, *Ceratomyxa shasta* Noble, 1950, in the Columbia Riverbasin, USA. J. Fish Dis. 11:97100. 

 Reports known distribution of the infectious stage of *C*.*shasta*. 

 Johnson, K. A. 1975. Host susceptibility, histopathologic, andtransmission studies on *Ceratomyxa shasta*, a myxosporidanparasite of salmonid fish. Ph. D. thesis, Oregon State University,Corvallis. 134 pp. 

 Comprehensive studies on the aspects of ceratomyxosis mentionedin the title. 

 Johnson, K. A., J. E. Sanders, and J. L. Fryer. 1979. *Ceratomyxashasta* in salmonids. U.S. Fish Wildl. Serv., Fish Dis. Leafl. 58. 11pp. 

 Reviews the current knowledge of *C*. *shasta*. 

 Margolis, L., and T. P. T. Evelyn. 1975. *Ceratomyxa shasta*(Myxosporea) disease in chum salmon (*Oncorhynchus keta*) inBritish Columbia. J. Fish. Res. Board Can. 32:16401643. 

 Reports four chum salmon infected with ceratomyxosis caught offthe coast of Vancouver Island. 

 Noble, E. R. 1950. On a myxosporidian (protozoan) parasite ofCalifornia trout. J. Parasitol. 36:457460. 

 First report on spores and trophozoites of the parasite, and ofthe tissues of rainbow trout found to be infected. 

 Ratliff, D. E. 1983. *Ceratomyxa shasta*: longevity,distribution, timing, and abundance of the infective stage in centralOregon. Can. J. Fish. Aquat. Sci. 40:16221632. 

 A study of the characteristics of the infective stage of *Ceratomyxashasta* in the Deschutes River. 

 Sanders, J. E., J. L. Fryer, and R. W. Gould. 1970. Occurrenceof the myxosporidian parasite *Ceratomyxa shasta*, in salmonidfish from the Columbia River basin and Oregon coastal streams. Pages133144 *in* S. F. Snieszko, ed. A symposium on diseases of fishesand 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* bytreating hatchery water supplies. Prog. FishCult. 34:1317. 

 A report of the successful elimination of the infectious stageof *C*. *shasta* from hatchery water supplies by acombination of MicroFloc filtration and chlorination, or by sandfiltration and ultraviolet irradiation. 

 Schafer, W. E. 1968. Studies on the epizootiology of themyxosporidan *Ceratomyxa shasta* Noble. Calif. Fish Game 54:9099. 

 Various aspects of ceratomyxosis are discussed, including thedistribution of the infectious stage in waters in the vicinity ofCrystal Lake Hatchery in Shasta County, California; seasonal occurrenceand signs of the disease; requirements for transmission; and comparativeresistance and susceptibility of different species of salmon. 

 Tipping, J. M. 1986. Control of ceratomyxosis with ozone at theCowlitz Trout Hatchery. Wash. State Game Dep., Fish. Manage. Div. Prog.Rep. 20 pp. 

 Results of a pilot study to determine the minimum effectiveozone dose for control of the infective stage of *C*. *shasta*.

 Udey, L. R., J. L. Fryer, and K. S. Pilcher. 1975. Relation ofwater 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 ofrainbow trout and coho salmon from ceratomyxosis and on the mean timefrom exposure of the fish until death. 

 Wales, J. H., and H. Wolf. 1955. Three protozoan diseases oftrout in California. Calif. Fish Game 41:183187. 

 Description of the first recognized outbreak of the disease atCrystal Lake Hatchery in Shasta County California. 1948. 

 Wood, J. W. 1979. Diseases of Pacific salmon, their preventionand treatment. Washington Department of Fisheries, Olympia. 82 pp. 

 General guide to diseases of Pacific salmon. 

 Yamamoto, T., and J. E. Sanders. 1979. Light and electronmicroscopic observations of sporogenesis in the myxosporidan, *Ceratomyxashasta* (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 currentcertification procedures. 

 Zinn, J. L., K. A. Johnson, J. E. Sanders, and J. L. Fryer.1977. Susceptibility of salmonid species and hatchery strains of chinooksalmon (*Oncorhynchus tshawytscha*) to infections by *Ceratomyxashasta*. 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.*U.S. Department of the Interior**|| U.S. Geological Survey  11649 Leetown Road, Kearneysville, WV  25430, USA  URL: http://www.lsc.usgs.gov  Maintainer: lsc_webmaster@usgs.gov  Last Modified: February 26, 2004 dwnPrivacy Policy and Disclaimers || FOIA || Accessibility*