Factors affecting the Ceratomyxa shasta infectious cycle and transmission between polychaete and salmonid hosts.

摘要

Ceratomyxa shasta is a myxozoan parasite that infects salmonid fishes causing the disease ceratomyxosis that is characterized by severe hemorrhage and necrosis of the intestine and death of the fish host. Ceratomyxa shasta is endemic to the Pacific Northwestern United States and Canada, where epizootics are reported for both wild and hatchery reared fish. Identification of factors affecting the infectious cycle of C. shasta is complicated by its obligate two host lifecycle. The parasite infects the fish as an actinospore and develops into a myxospore in the fish host. The myxospore infects the freshwater polychaete, Manayunkia speciosa where the actinospore develops. A system for maintaining and infecting M. speciosa in the laboratory was developed and a series of laboratory studies tested the effects of temperature on polychaete survival, actinospore release and longevity. Temperature did not affect polychaete survival, but actinospore release occurred earlier and in greater abundance at the higher temperature, whereas actinospore longevity and temperature had an inverse relationship. A laboratory flow experiment tested the effects of two flow rates on M. speciosa survival, infection prevalence and fish infection. Polychaetes had higher survival at the fast flow with low infection prevalences compared to polychaetes held in the slow flow treatment. Susceptible rainbow trout became infected when exposed to just 1 actinospore per fish. Fatal infections in these fish were documented at 5 actinospores per fish. Infection prevalence and mean day to death increased with increasing actinospore dose. Fish size did not affect the infective dose; however, parasite dilution did have an effect. Actinospores were labeled with a fluorescent stain and C. shasta attachment to the gills was identified. In situ hybridization of histological sections was used to locate the parasite as it migrated from the gill epithelium, to proliferation in the blood vessel, and migration to the intestine. Quantitative PCR was used to quantify the abundance of the parasite in the blood. When the infection of susceptible and Resistant Chinook salmon were compared, there were no differences in actinospore penetration into the gills but resistant Chinook salmon did eliminate parasites in the blood after 2 weeks and isolate parasites in foci of inflammation in the intestine. Resistant Chinook salmon more effectively regulated an immune response to infection, effectively cleared the parasite and showed evidence of recovery after infection. The research presented here has been fundamental in performing C. shasta infection studies in the laboratory in the fish and polychaete hosts. It has greatly affected our understanding of host parasite interactions including the infective dose for rainbow trout and the recognition of the gills and blood as early sites of C. shasta infection. It has also revealed differences in fish host response to infection including the characterization of a recovery from C. shasta infection.