Poor population recovery of lake Washington Chinook Salmon (Oncorhynchus tshawytscha) in Pacific Northwestern USA may be associated with disease caused by Ceratonova shasta in an urban-influenced watershed.

Abstract

Understanding the effects of anthropogenic changes on fish disease is vital for supporting mitigative actions for fisheries population recovery. The Lake Washington watershed in the Pacific Northwestern United States is influenced by high urban development and climate change, compromising the sustainability of anadromous salmon. We investigated Ceratonova shasta, a myxozoan parasite, in Chinook Salmon Oncorhynchus tshawytscha to determine the impacts of C. shasta-induced enteronecrosis during salmon freshwater migrations within this watershed. All sampled adult Chinook Salmon returning to an enhancement hatchery to spawn were infected with genotype I C. shasta with a high prevalence of severe enteritis and enteronecrosis. Parasite loads and associated pathology were more severe in adult fish succumbing to prespawn mortality than in fish that spawned. Natural prespawn mortality of Chinook Salmon in the Cedar River was also associated with high C. shasta loads. Sentinel exposure studies with Chinook Salmon juveniles in the spring and fall demonstrated high levels of C. shasta genotype II actinospores in the Lake Washington Ship Canal, a human engineered canal that salmon must traverse in their freshwater migrations from the Puget Sound. The sentinel juvenile Chinook Salmon succumbed to clinical disease and high mortality from genotype II C. shasta, suggesting that these stocks have high susceptibility to this genotype. The results show that both genotypes I and II pose disease risks to adult and juvenile stages of Chinook Salmon in the watershed, and that the Lake Washington Ship Canal could be a C. shasta ‘hot spot’ for genotype II that may increase disease risk for juveniles during smolt emigration.