Fish Hatchery Management - fisheries & aquaculture

FISH HEAL'I'H MANAGEMEN'I 327areas in the tissue of the large intestine. As the disease progresses, the entireintestine becomes swollen and hemorrhagic.The disease has been transferred by inoculating ascites (containingschizonts, trophozoites, and spores) from infected rainbow trout into thevisceral cavity of noninfected rainbow trout. Fish-to-fish transmission byother methods has failed. Infection seemingly does not depend on theingestion of food organisms or any of the known stages of the parasite. Themode of transmission remains unknown.There is no known treatment for Ceratomyxa shasta, so the parasite shouldbe avoided at all costs. Water supplies known to be contaminated should not beutilized for hatchery purposes without pretreatment. There should be no transferof'eggs, young fish, or adults liom inf'ected to noninfected areas.MTXOSOMAMltxosoma cerebralis is the causative agent of whirling disease, a serious conditionof salmonid fishes. Because of its importance, special emphasisshould be given to it. The disease was endemic in central Europe, but nowis well-established in France, Italy, Czechoslovakia, Poland, the Soviet Union,Denmark, and the United States. It first appeared in the United Statesat a brook trout hatchery in Pennsylvania and has spread as far west asCalifornia and Nevada. The obvious sign of tail-chasing (whirling) becomesevident about 40 to 60 days after infection and may persist for about Iyeaf.The whirling symptom is caused by erosion of the cranial cartilage, particularlyaround the auditory equilibrium organ behind the eye, by the trophozoitephase of the parasite. Infected fingerling trout can become soexhausted by the convulsive whirling behavior that they fall to the bottomand remain on their sides (Figure 98). In general, only young trout (fry tosmall fingerlings) exhibit whirling disease so it has been referred to as a"childhood disease." However, older fish can become infected even thoughthey 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, andthat the sporoplasm leaves the sPore, penetrates the intestinal mucosa, andmigrates to the cartilage where it resides as the trophozoite. However, thishypothesis has never been verified experimentally and other means of infectionmay be possible. Most recent studies suggest that the sPores are notinfective upon release from the fish, but must be aged in mud for 4-5months.External signs alone are not adequate for positive diagnosis of Myxosomacerebralis infections. Verification requires identification of the spore stage,