Juvenile Chinook Salmon Oncorhynchus tshawytscha moving downstream through tributaries of the upper Willamette River basin can spend months in reservoirs created by dams. While residing in the reservoirs, they often obtain heavy infections of the freshwater parasitic copepod Salmincola californiensis. The physiologic effect these parasites have on salmonids is poorly understood. We developed a method to infect juvenile Chinook Salmon in a laboratory with the copepodid stage of S. californiensis. Infected and uninfected fish were subjected to a swimming challenge to ascertain swimming endurance. Severity of gill damage was assessed using a dissecting microscope. Juvenile Chinook Salmon naturally infected with S. californiensis in Cougar Reservoir, Oregon, were also challenged and compared with their lab-infected counterparts. Copepod infection greatly impaired the swimming ability of laboratory fish, and the naturally infected fish were entirely incapable of swimming at low velocity. Chinook Salmon collected in the wild were more heavily infected than the laboratory fish and had trouble surviving collection and transport to our laboratory. The intensity of infection and severity of gill damage were positively correlated with diminished swimming ability, suggesting that heavy infection with copepods impairs gas exchange and osmotic regulation, which likely results in diminished fitness and decreased survival of infected fish.

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Pacific salmon experience prolonged elevation in corticosteroid hormones during important life history events including migration, reproduction, and senescence. These periods of elevated corticosteroids correspond with changes to immunity and energy metabolism; therefore, fish may be particularly vulnerable to mortality at these times. Recent studies found that stress-induced cortisol release associated with microbial community shifts in salmonids, raising the question of how longer-term corticosteroid dynamics that accompany life history transitions affect salmonid microbiomes. In this work, we experimentally evaluated the relationships between gut microbiome composition, chronically elevated corticosteroids, and mortality in juvenile Chinook salmon (Oncorhynchus tshawytscha). We found that treatment with slow-release implants of the corticosteroids cortisol or dexamethasone resulted in changes to the gut microbiome. Morbidity was also associated with microbiome composition, suggesting that the gut microbiome reflects individual differences in susceptibility to opportunistic pathogens. Additionally, we analyzed a small number of samples from adult fish at various stages of senescence. Results from these samples suggest that microbiome composition associated with gut integrity, and that the microbial communities of corticosteroid treated juveniles shift in composition toward those of senescent adults. Overall, findings from this work indicate that the gut microbiome correlates with mortality risk during periods of chronic corticosteroid elevation.