FISH HEALTH MANAGEMENT 327 



areas in the tissue of the large intestine. As the disease progresses, the en- 

 tire intestine becomes swollen and hemorrhagic. 



The disease has been transferred by inoculating ascites (containing 

 schizonts, trophozoites, and spores) from infected rainbow trout into the 

 visceral cavity of noninfected rainbow trout. Fish-to-fish transmission by 

 other methods has failed. Infection seemingly does not depend on the 

 ingestion of food organisms or any of the known stages of the parasite. The 

 mode of transmission remains unknown. 



There is no known treatment for Ceratomyxa shasta, so the parasite should 

 be avoided at all costs. Water supplies known to be contaminated should not be 

 utilized for hatchery purposes without pretreatment. There should be no transfer 

 of eggs, young fish, or adults from infected to noninfected areas. 



MYXOSOMA 



Myxosoma cerebralis is the causative agent of whirling disease, a serious con- 

 dition of salmonid fishes. Because of its importance, special emphasis 

 should be given to it. The disease was endemic in central Europe, but now 

 is well-established in France, Italy, Czechoslovakia, Poland, the Soviet Un- 

 ion, Denmark, and the United States. It first appeared in the United States 

 at a brook trout hatchery in Pennsylvania and has spread as far west as 

 California and Nevada. The obvious sign of tail-chasing (whirling) becomes 

 evident about 40 to 60 days after infection and may persist for about 1 

 year. 



The whirling symptom is caused by erosion of the cranial cartilage, par- 

 ticularly around the auditory equilibrium organ behind the eye, by the tro- 

 phozoite phase of the parasite. Infected fingerling trout can become so 

 exhausted by the convulsive whirling behavior that they fall to the bottom 

 and remain on their sides (Figure 98). In general, only young trout (fry to 

 small fingerlings) exhibit whirling disease so it has been referred to as a 

 "childhood disease." However, older fish can become infected even though 

 they show no clinical signs. Mortality has varied greatly among epizootics, 

 sometimes minor, sometimes devastating. 



The complete life cycle of Myxosoma cerebralis has never been established. 

 In the past, it has been thought that the spores are ingested by fish, and 

 that the sporoplasm leaves the spore, penetrates the intestinal mucosa, and 

 migrates to the cartilage where it resides as the trophozoite. However, this 

 hypothesis has never been verified experimentally and other means of in- 

 fection may be possible. Most recent studies suggest that the spores are not 

 infective upon release from the fish, but must be aged in mud for 4-5 

 months. 



External signs alone are not adequate for positive diagnosis of Myxosoma 

 cerebralis infections. Verification requires identification of the spore stage, 



