Deconstructing dams and disease: predictions for salmon disease risk following Klamath River dam removals

The health of fish populations and the river systems they inhabit have broad ecological, cultural, recreational, and economic relevance. This is exemplified by the iconic anadromous salmonid fishes native to the West Coast of North America. Salmon populations have been constrained since the mid nineteenth century by dam construction and water reallocation. In the Klamath River (Oregon and California, USA), a series of dams built in the early-mid 20th century cut the basin in two and blocked anadromous fish access to more than 600 river kilometers. This dramatic loss of habitat, coupled with infectious diseases and resulting epizootics, have impacted the wellbeing of these salmonid populations. In 2023-2024, the Klamath River will undergo the largest river restoration project in US history. Removal of the four lowermost dams will cause profound physical changes to the river, including flow, water temperature, and channel geomorphology. The dam removals will reconnect the lower and upper portions of the basin, and provide fish passage after a century of segregation. Reestablishment of upstream and downstream fish movements will also alter the occupancy and abundance of the salmonid hosts and their pathogens. The increased habitat availability and longer migration routes will increase duration of pathogen exposure and potential impacts on juvenile survival and adult pre-spawn mortality. However, restoration of more natural flow and sediment regimes will decrease overall fish disease risk by disrupting complex parasite life cycles. To better understand these multifarious, competing factors, we review the salmonid species in the Klamath River, and provide an overview of their historical pathogen challenges and associated diseases and use this as a framework to predict the effects of dam removals on disease dynamics. Our review and predictions are a synthesis of expertise from tribal biologists, fish health specialists and fish biologists, many of whom have lived and worked on the Klamath River for decades. We conclude with recommendations for expansion of current pathogen monitoring and research efforts to measure changes in host-pathogen dynamics basin-wide

State of Idaho Augmented Anadromous Fish Health Monitoring, 1988 Annual Report.

This report documents the progress in the assigned tasks which have occurred during the second year of the Augmented Anadromous Fish Health Monitoring Project. Fish at seven Idaho Department of Fish and Game facilities were monitored for various pathogens and organosomatic analyses were performed on smolts prior to their release in the Spring of 1989. A disease database has been developed and facility impediments to fish health have been identified

State of Idaho Augmented Anadromous Fish Health Monitoring, 1987 Annual Report.

The anadromous fish health monitoring program began in full operation in January 1988 after the hiring of the lead pathologist. This short operating period limits the amount of information available at the time of this writing. Pre-release sampling of smolts revealed the presence of several sub-clinical pathogens. Organosomatic analysis results demonstrated no major abnormalities in the examined stocks. The results of the 1988 steelhead broodstock sampling are still pending

Infectious Hematopoietic Necrosis Virus Transmission and Disease among Juvenile Chinook Salmon Exposed in Culture Compared to Environmentally Relevant Conditions

The dynamics of IHNV infection and disease were followed in a juvenile Chinook salmon population both during hatchery rearing and for two weeks post-release. Cumulative weekly mortality increased from 0.03%–3.5% as the prevalence of viral infection increased from 2%–22% over the same four-week period. The majority of the infected salmon was asymptomatic. Salmon demonstrating clinical signs of infection shed 1000 pfu mL-1 of virus into the water during a 1 min observation period and had a mean concentration of 106 pfu mL-1 in their mucus. The high virus concentration detected in mucus suggests that it could act as an avenue of transmission in high density situations where dominance behavior results in nipping. Infected smolts that had migrated 295 km down river were collected at least two weeks after their release. The majority of the virus positive smolts was asymptomatic. A series of transmission experiments was conducted using oral application of the virus to simulate nipping, brief low dose waterborne challenges, and cohabitation with different ratios of infected to naïve fish. These studies showed that asymptomatic infections will occur when a salmon is exposed for as little as 1 min to >102 pfu mL-1, yet progression to clinical disease is infrequent unless the challenge dose is >104 pfu mL-1. Asymptomatic infections were detected up to 39 d post-challenge. No virus was detected by tissue culture in natural Chinook juveniles cohabitated with experimentally IHNV-infected hatchery Chinook at ratios of 1:1, 1:10, and 1:20 for either 5 min or 24 h. Horizontal transmission of the Sacramento River strain of IHNV from infected juvenile hatchery fish to wild cohorts would appear to be a low ecological risk. The study results demonstrate key differences between IHNV infections as present in a hatchery and the natural environment. These differences should be considered during risk assessments of the impact of IHNV infections on wild salmon and trout populations

Infectious Hematopoietic necrosis Virus Transmission and Disease Among Juvenile Chinook Salmon Exposed in culture Compared to Environmentally Relevant Conditions

The dynamics of IHNV infection and disease were followed in a juvenile Chinook salmon population both during hatchery rearing and for two weeks post-release. Cumulative weekly mortality increased from 0.03%–3.5% as the prevalence of viral infection increased from 2%–22% over the same four-week period. The majority of the infected salmon was asymptomatic. Salmon demonstrating clinical signs of infection shed 1000 pfu mL-1 of virus into the water during a 1 min observation period and had a mean concentration of 106 pfu mL-1 in their mucus. The high virus concentration detected in mucus suggests that it could act as an avenue of transmission in high density situations where dominance behavior results in nipping. Infected smolts that had migrated 295 km down river were collected at least two weeks after their release. The majority of the virus positive smolts was asymptomatic. A series of transmission experiments was conducted using oral application of the virus to simulate nipping, brief low dose waterborne challenges, and cohabitation with different ratios of infected to naïve fish. These studies showed that asymptomatic infections will occur when a salmon is exposed for as little as 1 min to &gt;102 pfu mL-1, yet progression to clinical disease is infrequent unless the challenge dose is &gt;104 pfu mL-1. Asymptomatic infections were detected up to 39 d post-challenge. No virus was detected by tissue culture in natural Chinook juveniles cohabitated with experimentally IHNV-infected hatchery Chinook at ratios of 1:1, 1:10, and 1:20 for either 5 min or 24 h. Horizontal transmission of the Sacramento River strain of IHNV from infected juvenile hatchery fish to wild cohorts would appear to be a low ecological risk. The study results demonstrate key differences between IHNV infections as present in a hatchery and the natural environment. These differences should be considered during risk assessments of the impact of IHNV infections on wild salmon and trout populations.</p

Infectious Hematopoietic Necrosis Virus Transmission and Disease among Juvenile Chinook Salmon Exposed in Culture Compared to Environmentally Relevant Conditions

The dynamics of IHNV infection and disease were followed in a juvenile Chinook salmon population both during hatchery rearing and for two weeks post-release. Cumulative weekly mortality increased from 0.03%–3.5% as the prevalence of viral infection increased from 2%–22% over the same four-week period. The majority of the infected salmon was asymptomatic. Salmon demonstrating clinical signs of infection shed 1000 pfu mL-1 of virus into the water during a 1 min observation period and had a mean concentration of 106 pfu mL-1 in their mucus. The high virus concentration detected in mucus suggests that it could act as an avenue of transmission in high density situations where dominance behavior results in nipping. Infected smolts that had migrated 295 km down river were collected at least two weeks after their release. The majority of the virus positive smolts was asymptomatic. A series of transmission experiments was conducted using oral application of the virus to simulate nipping, brief low dose waterborne challenges, and cohabitation with different ratios of infected to naïve fish. These studies showed that asymptomatic infections will occur when a salmon is exposed for as little as 1 min to &gt;102 pfu mL-1, yet progression to clinical disease is infrequent unless the challenge dose is &gt;104 pfu mL-1. Asymptomatic infections were detected up to 39 d post-challenge. No virus was detected by tissue culture in natural Chinook juveniles cohabitated with experimentally IHNV-infected hatchery Chinook at ratios of 1:1, 1:10, and 1:20 for either 5 min or 24 h. Horizontal transmission of the Sacramento River strain of IHNV from infected juvenile hatchery fish to wild cohorts would appear to be a low ecological risk. The study results demonstrate key differences between IHNV infections as present in a hatchery and the natural environment. These differences should be considered during risk assessments of the impact of IHNV infections on wild salmon and trout populations.</p

The biophysical basis of thermal tolerance in fish eggs.

A warming climate poses a fundamental problem for embryos that develop within eggs because their demand for oxygen (O2) increases much more rapidly with temperature than their capacity for supply, which is constrained by diffusion across the egg surface. Thus, as temperatures rise, eggs may experience O2 limitation due to an imbalance between O2 supply and demand. Here, we formulate a mathematical model of O2 limitation and experimentally test whether this mechanism underlies the upper thermal tolerance in large aquatic eggs. Using Chinook salmon (Oncorhynchus tshawytscha) as a model system, we show that the thermal tolerance of eggs varies systematically with features of the organism and environment. Importantly, this variation can be precisely predicted by the degree to which these features shift the balance between O2 supply and demand. Equipped with this mechanistic understanding, we predict and experimentally confirm that the thermal tolerance of these embryos in their natural habitat is substantially lower than expected from laboratory experiments performed under normoxia. More broadly, our biophysical model of O2 limitation provides a mechanistic explanation for the elevated thermal sensitivity of fish embryos relative to other life stages, global patterns in egg size and the extreme fecundity of large teleosts

The biophysical basis of thermal tolerance in fish eggs

A warming climate poses a fundamental problem for embryos that develop within eggs because their demand for oxygen (O2) increases much more rapidly with temperature than their capacity for supply, which is constrained by diffusion across the egg surface. Thus, as temperatures rise, eggs may experience O2 limitation due to an imbalance between O2 supply and demand. Here, we formulate a mathematical model of O2 limitation and experimentally test whether this mechanism underlies the upper thermal tolerance in large aquatic eggs. Using Chinook salmon (Oncorhynchus tshawytscha) as a model system, we show that the thermal tolerance of eggs varies systematically with features of the organism and environment. Importantly, this variation can be precisely predicted by the degree to which these features shift the balance between O2 supply and demand. Equipped with this mechanistic understanding, we predict and experimentally confirm that the thermal tolerance of these embryos in their natural habitat is substantially lower than expected from laboratory experiments performed under normoxia. More broadly, our biophysical model of O2 limitation provides a mechanistic explanation for the elevated thermal sensitivity of fish embryos relative to other life stages, global patterns in egg size and the extreme fecundity of large teleosts

Disease in Central Valley Salmon: Status and Lessons from Other Systems

Chinook Salmon (Oncorhynchus tshawytscha) are increasingly vulnerable to anthropogenic activities and climate change, especially at their most southern species range in California’s Central Valley. There is considerable interest in understanding stressors that contribute to population decline and in identifying management actions that reduce the impacts of those stressors. Along the west coast of North America, disease has been linked to declining numbers of salmonids and identified as a key stressor resulting in mortality. In the Central Valley, targeted studies have revealed extremely high prevalence of infectious agents and disease. However, there has been insufficient monitoring to understand the effect that disease may have on salmon populations. In order to inform future research, monitoring, and management efforts, a two-day workshop on salmon disease was held at UC Davis on March 14-15, 2018. This paper summarizes the science presented at this workshop, including the current state of knowledge of salmonid disease in the Central Valley and current and emerging tools to better understand its impacts on salmon. We highlight case studies from other systems where successful monitoring programs have been implemented. First, in the Klamath River where the integration of several data collection and modeling approaches led to the development of successful management actions, and second in British Columbia where investment in researching novel technologies led to breakthroughs in the understanding of salmon disease dynamics. Finally, we identify key information and knowledge gaps necessary to guide research and management of disease in Central Valley salmon populations