The myxozoan parasite Ceratonova shasta threatens both juvenile and adult salmonid populations in the Pacific Northwest region of the United States, causing intestine necrosis and hemorrhaging, along with high mortality in some fish strains. It induces an inflammatory tissue response in susceptible strains of fish; understanding the interactions between C. shasta and the fish immune system may thus provide new avenues for treatments. Fish have both innate and adaptive immunity to combat pathogens, which often enter through mucosal tissues; therefore, how mucosal tissues respond to pathogens is of paramount importance in the study of intestine pathogens. The mucosal immunoglobulin IgT may play a role in protecting against C. shasta and other parasites. It is upregulated in response to C. shasta in Chinook salmon (Oncorhynchus tshawytscha Walbaum, 1792) and rainbow trout (O. mykiss Walbaum, 1792) and has been shown to produce a parasite-specific response in rainbow trout. This project sought to understand the interplay between C. shasta and specific components of the innate and adaptive immune responses. Both IgT and the systemic immunoglobulin IgM were shown to be upregulated in response to both acute and chronic C. shasta infections, but IgT was not sufficient to provide protection against disease. Interestingly, depletion of IgT led to lower pathogen loads, suggesting a more complicated role in C. shasta infections than previously hypothesized. Expression of the pro-inflammatory cytokines IL6 and IL8 was decreased in chronic, low mortality C. shasta infections, suggesting that inflammation may contribute to pathology and mortality in acute infections. The results of this study indicate that targeting inflammatory components of the immune system may decrease pathology and mortality in acute C. shasta infections.