This comprehensive review examines pathogens affecting adult anadromous Pacific salmon (Oncorhynchus spp.) during their terminal freshwater migration and spawning across populations from California through Alaska, including Oregon, Washington, and British Columbia. We systematically reviewed selected pathogens based on their significance to adult salmon health or role in epizootiology, categorizing them by their impact on prespawn mortality (PSM), disease severity, and maternal or ‘egg-associated’ transmission risks to progeny. Our analysis encompasses macroparasites, microparasites, bacteria, and viruses affecting anadromous Pink (O. gorbuscha), Chum (O. keta), Coho (O. kisutch), Sockeye (O. nerka), and Chinook Salmon (O. tshawytscha) and Steelhead Trout (O. mykiss), integrating extensive literature analysis with direct field observations and case studies from representative geographic regions. Understanding pathogen impacts during the spawning life stage is crucial for salmon population sustainability, as the unique semelparous nature of Pacific salmon makes this terminal phase critical for reproductive success and the continuation of these ecologically, economically, and culturally vital species.

Adult Salmon Enteritis (ASE), characterized by severe ulcerative enteritis, has been linked to pre-spawn mortality (PSM) in spring Chinook Salmon ( Oncorhynchus tshawytscha ) in certain rivers in Oregon, USA. Catastrophic losses of spring Chinook Salmon have resulted from PSM, a significant threat to their population stability. Understanding the causes of ASE is therefore critical for mitigating PSM and supporting conservation. This study investigates the potential infectious etiology of ASE using a juvenile Chinook Salmon model. Fish were immunocompromised with dexamethasone implants, fasted, and exposed to intestinal tissues from ASE-affected adult Chinook. Histopathology of recipient fish revealed mid-intestinal lesions consistent with ASE. The microsporidium Enterocytozoon schreckii , which is observed in ASE-affected adults from rivers, was transmitted for the first time to juvenile Chinook Salmon, making E. schreckii a potential new pathogen of juvenile salmon. Additionally, intranuclear inclusions were identified in enterocytes by histopathology and viral particles were detected by electron microscopy in recipient fish. The study demonstrates that intestinal lesions consistent with ASE can be experimentally induced in juvenile Chinook Salmon through oral exposure to infected tissues, supporting an infectious etiology. Further research is needed to isolate specific pathogens, including viruses and E. schreckii , and to elucidate their roles in ASE development.

Adult salmon enteritis (ASE) is a severe intestinal disease affecting spring Chinook Salmon ( Oncorhynchus tshawytscha ) in the Pacific Northwest. ASE is strongly associated with pre-spawn mortality (PSM), a critical concern for endangered populations and continued Chinook Salmon management. This study characterizes the geographic distribution of ASE across Oregon and Washington watersheds, examines its association with two common parasites ( Ceratonova shasta and Enterocytozoon schreckii ), and provides detailed histopathological characterization of the disease. We examined intestinal tissues from 256 adult spring Chinook Salmon collected from multiple hatcheries across the Columbia River Basin and Puget Sound between 2022 and 2025 using routine histopathology, specific histochemical stains, and immunohistochemistry. ASE was highly prevalent in all Columbia Basin populations, with chronic ulcerative and necrotizing enteritis, but was absent in Puget Sound populations. C. shasta prevalence was high in most Columbia Basin locations (10-100%), while E. schreckii prevalence was more variable (0-67%). Consistent histopathological findings of ASE included ≥ 10% mucosal ulceration, mixed inflammation expanding the lamina propria and extending into surrounding intestinal layers, and dissolution of the stratum granulosum. In chronic ASE lesions, we further characterized granulation tissue formation. Cold water holding of spawning adults appears to slow disease progression and reduce PSM without preventing ASE development. These findings demonstrate that ASE is a geographically restricted disease of the Columbia Basin that may have associations with diverse environmental exposures including water temperature and pathogens.