- Ceratonova shasta is an obligate endoparasite of salmonid fish that is endemic to the Pacific Northwest of North America. The parasite has a complicated lifecycle with two distinct spore stages and two obligate hosts, a salmonid and a freshwater annelid. Myxospores released from infected salmonid hosts, infect Manayunkia occidentalis (freshwater annelid), and actinospores released from infected annelid hosts infect salmonids. C. shasta infects multiple salmonid species, and genetically distinct strains (genotypes I, II and 0) vary in specificity and virulence in their respective fish hosts. In the Deschutes River, OR, high pre-spawn mortality in Spring Chinook salmon has been associated with genotype I. Genotypes 0 and II are also present but have not been associated with disease. Previous studies on the Deschutes River showed that C. shasta exhibits temporal variability with onset (first date of detection of >1 spore/L) typically occurring in late spring and peak densities occurring in summer. However, it was not clear whether there were differences in timing of genotypes’ onsets and peaks. To explore this question, I used water sampling data from 2015-2019, qPCR, and genotyping to describe the temporal distributions of genotypes (Chapter 2). I observed that genotype I had the earliest onset (late spring) and peak (late spring-early summer), while genotype 0 was primarily detected in mid-late summer, and genotype II was primarily detected in late summer-fall. To further study temporal dynamics of each genotype, I back-calculated hypothetical infection dates for the annelid hosts based on thermal development units (Chapter 2). I found evidence that adult Fall Chinook Salmon correlated with genotype I onsets and adult Spring Chinook Salmon run size correlated with genotype I peaks. Genotypes 0 and II correlations were less robust, but data suggested adult Steelhead and Rainbow trout were contributors of genotype 0, and Coho correlated with genotype’s II onset while adult and juvenile Sockeye correlated to its peak. Using linear models, I tested how peak discharge, total number of fish host during a year, and mean temperature during last 200 dd of development within the annelid host were related to the genotypes’ peaks (Chapter 2). I found that the temperature model explained the majority of the variation in peak sizes (R2>0.5 in all models), while fish host run size and peak discharge explained less variation, and not at all sites. In Chapter 3 I explored relationships between spatial distribution of C. shasta and M. occidentalis, including the prevalence of C. shasta infection in M. occidentalis. I used spatial surveys from 2018-2020 and simple correlations. I observed correlations between spatial distribution of C. shasta and its annelid host in spring surveys: Sites having high densities of C. shasta also had high densities of C. shasta-infected M. occidentalis. In addition, densities of M. occidentalis were correlated with prevalence of C. shasta infection in annelid hosts in spring surveys but these relationships were undetectable in late summer surveys suggesting targeted habitats (e.g., spawning sites in spring surveys) may be important.
I concluded that abiotic variables (temperature) were correlated with C shasta dynamics (timing of onset and peak spore release) and both biotic and abiotic variables were associated with the magnitude of C. shasta genotype peaks in the Deschutes River below the dams. I recommend conducting more annelid surveys along with C. shasta surveys that target M. occidentalis habitats stratified throughout the lower basin to better understand how their distribution and densities affect the risk of C. shasta for salmonids. Furthermore, annelid host surveys should be conducted in June or July so they correspond with the periods of peak C. shasta densities.