Geographic and Seasonal Distribution of Ceratomyxa shasta (Myxozoa) in Northern California
IAAAM 1988
Gary L. Hendrickson, BS, MS, PhD; Annelise Carleton, BS


Ceratomyxa shasta is a myxozoan parasite of salmonid fishes. It was first observed in hatchery rainbow trout (Salmo gairdneri) in Shasta County, California in 1948 (Wales and Wolf 1955). Noble (1950) described C. shasta as a new species noting that it was the only freshwater species and the only histozoic parasite in the genus. The life history of C. shasta is poorly understood. Noble (1950) and others described trophozoite and spore stages. Yamamoto and Sanders (1979) examined development in the fish host ultrastructurally. Little is known about stages off of the fish host. Natural transmission of C. shasta occurs when salmonids come in contact with water containing the infective stage. Exposure for a period of 30 minutes is sufficient for transmission (Johnson 1975) and one infectious unit is capable of causing death of one susceptible fish (Ratliff 1983). Direct fish to fish transmission has never been observed.

Ceratomyxa shasta produces devastating disease in susceptible salmonids. Ceratomyxosis has caused significant losses among hatchery salmonids both before and after release (Rucker et al. 1954, Wales and Wolf 1955, Conrad and DeCew 1966, Schafer 1968, Sanders et al. 1972, Zinn et al. 1977, Buchanan et al. 1983) and among wild salmonids (Sanders et al. 1.970, Ratliff 1981). In anadromous salmonids, ceratomyxosis is thought to contribute to prespawning mortalities in infected adults (Sanders et al. 1970, Johnson et al. 1979, Horsch, C. 1986, U.S. Fish and Wildlife Service, Coleman National Fish Hatchery, Anderson, California, personal communication). Ceratomvxa shasta is also thought to inhibit the ability of juveniles to osmoregulate in seawater after outmigration (Ching and Munday 1984b). Fryer (1986) suggested that as many as 12% of salmonids entering the Columbia River estuary were lethally infected with C. shasta. The devastating nature of ceratomyxosis is sufficiently documented that 14 states (of 20 specifying particular diseases), the Canadian government, Great Lakes Fishery Commission, and Colorado River Fish Disease Control Program have classified it as a certifiable disease (Busch 1980).

Development of the parasites takes place primarily in the gastrointestinal tract. Pathology is severe but variable 0 according to the species involved. In juvenile rainbow trout at 17 C, the infection is initiated in the pyloric caeca. Trophozoites first appear between mucosal cells at about three days postexposure (PE) (Johnson 1975). About 13 days PE, parasites spread into the mucosa of the posterior intestine and subsequently to all intestinal layers. The posterior intestine becomes swollen and hemorrhagic.

There is a generalized inflammation of the lamina propria, muscle necrosis and edema (Johnson 1975). Trophozoites and spores can be found in mucosa and lumen of the pyloric caeca and posterior intestine. Intestinal contents are mucoid and caseous material lines the abdomen and area around the pyloric caeca (Conrad and DeCew 1966). Liver, gall bladder, spleen, gonads, kidney, heart, gills, and skin may also be affected (Wales and Wolf 1955, Conrad and DeCew 1966). Adult chinook salmon frequently exhibit nodules on the gut which may perforate resulting in death. Gross lesions may occur in the liver, kidney, spleen, and musculature (Wood 1974). Adult coho usually show grossly thickened intestinal and pyloric caecal walls. Large abscessed lesions may occur in the musculature (Wood 1974).

Three features concerning C. shasta are of prime concern to management of anadromous salmonids. First, only certain waters contain the infective stage of the parasite (Johnson 1975, Sanders et al. 1970, Johnson et al. 1979, Hoffmaster 1985). Infectivity is demonstrated by exposure of susceptible fish and later examination for the parasite. Other waters contain infected salmonids but lack the infective stage. Fish in such waters are assumed to have contacted the parasite while migrating through "infective waters." The reason for the limited distribution of the infective stage is unknown. Second, salmonid species and strains vary widely in their susceptibility to C. shasta (Schafer 1968F Johnson 1975, Zinn et al. 1977, Ratliff 1981, Buchanan et al. 1983, Ching 1984, Ching and Munday 1984b, Hoffmaster 1985). Within a species (e.g., rainbow trout) susceptibility may vary from highly susceptible to completely resistant. When susceptible fish are stocked in waters containing the infective stage, most die. Hemmingsen et al. (1986) and Wade (1986) found that when susceptible and resistant strains of coho salmon and steelhead, respectively, were crossed, progeny were intermediate in susceptibility. Third, the infection process is apparently seasonal in that infective waters are not necessarily infective throughout the year (Schafer 1968 Johnson 1975, Ratliff 1981, Ching and Munday 1984a).

There is no known treatment for ceratomyxosis hence prevention and management are paramount. Management involves stocking resistant species or strains wherever waters are known to harbor the infective stage and releasing fish during periods of low or no infectivity. The objectives of this study are to determine the geographic distribution and seasonal occurrence of the infective stage of Cexatomyxa shasta in California. Further studies are being carried out to examine the relative susceptibilities of anadromous salmonid strains. Such information is essential to management of resident and anadromous salmonids.

Geographic Distribution

The geographic distribution of the infective stage of C. shasta was determined using sentinel fish. Caged sentinels were stocked into test rivers and were left for ten to fourteen days to allow for infection to take place. Sentinels were then returned to the Humboldt State University, Telonicher Marine Laboratory or the California Department of Fish and Game, Fish Disease Laboratory for rearing. Sentinels were reared for 70 days or until ceratomyxosis was diagnosed. This rearing period allowed for development of the characteristic spores of Ceratomyxa shasta.

The infective stage of C. shasta is limited to the mainstem of the Klamath River, mainstem of the Sacramento River, and some major tributaries of the Sacramento River including the Mokelumne River, Feather River, and Butte Creek. Coastal rivers (Smith, Prairie Creek, Redwood Creek, Mad, Eel, Mattole, Ten-Mile, Noyo, Big, Gualala, Navarro, Russian) lack the infective stage.

The geographic distribution of the infective stage of C. shasta in California is limited. The reasons for this limited distribution are unknown. The "patchy" distribution of the infective stage might reflect the distribution of an intermediate host as has been suggested for the related Myxosoma cerebralis (Markiw and Wolf 1983).

Seasonal Distribution

Field exposures to determine the seasonal occurrence of the infective stage of Ceratomvxa shasta were carried out in the Klamath River at Klamath Glen during the winter of 1986-1987. Caged sentinels were placed in the river for ten days at ten day intervals. Following exposure, sentinels were brought to the Humboldt State University, Telonicher Marine Laboratory for rearing. Sentinels were reared for 70 days or until certomyxosis was diagnosed.

During winter 1986, the Klamath River was infective up to and including the exposure interval from December 5-15. At this time, water temperature was 7 C. The river was not infective until spring 1987. Sentinels were first infected during the exposure interval from April 9-20 at a water temperature of 15 C.

Schafer (1968), Johnson (1975), Ratliff (1981) and Ching and Munday (1984a) also found lack of infectivity during winter. However, it seems likely that in "warm water" years, fish could be infected at any time.


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Speaker Information
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Annelise Carleton, BS

Gary L. Hendrickson, BS, MS, PhD

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