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Current location: Home > Biological Effects Model > 1° Driver: Susceptibility > 2° Driver: Exposure to Parasites and Pathogens |
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Secondary Driver: Exposure to Parasites Jump down this page to: Steelhead | Chinook Salmon | Delta Smelt | Longfin Smelt | Sacramento Splittail | White Sturgeon | Green Sturgeon | Striped Bass Environmental conditions, including natural and anthropogenic stressors, can heavily influence parasite-host interaction because they regulate the physiological condition of both the host and the parasite (Lenihan et al. 1999). Stressful environmental conditions (such as low DO concentrations) can increase the susceptibility of fish to infectious diseases and parasites. Parasites and pathogens alone are known to cause significant changes in reproduction, survival, and growth of individual fish. This is not surprising considering individual organisms have a limited amount of energy, which must be diverted to fight infection and parasitism. Affected animals often may become debilitated, reproduce less, and become more susceptible to predation and less tolerant to environmental extremes (Krebs 2001). Although it may be difficult to separate the combined effects of multiple stressors acting simultaneously, combining low DO concentrations with parasites and pathogens likely exacerbates negative effects. The following summary of the stress response is based on information presented in Rottman et al. (1992). Reduced DO concentrations trigger a stress reaction beginning with a release of hormones from the adrenal gland. This subsequently causes an increase in blood sugar by triggering the release of liver glycogen. Hormones from the adrenal gland suppress the inflammatory response normally used to fight off infection. As minerals are metabolized differently, water imbalance ensues, causing fish to invest more energy in osmoregulation. Continued stress results in depleted energy reserves, hormone imbalance, and immune system suppression, increasing susceptibility to infections. One of the side effects associated with disease and parasitism may be an increased metabolic rate of fish as they attempt to fight infection. This increased metabolic rate increases DO demands in the fish. The compounding impacts of multiple stressors elicit significant physiological and behavioral responses (Sigismondi and Weber 1988; Mesa and Schreck 1989; Jarvi 1990 in Mesa 1994) that may result in increased rates of mortality (Mesa 1994). For example, Nile tilapia incur higher rates of mortality when exposed to Streptococcus agalactiae under nonlethal low DO concentrations (Evans et al. 2003). In general, the metabolic (e.g., oxygen) demands of fish are increased by parasites and pathogens as the fish’s immune system fights infection. In addition, parasites and pathogens may target systems (e.g., gills, blood) that are essential for acquiring and distributing oxygen to fish tissues. Parasites and diseases may have both lethal and sublethal effects, although in an ecological context sublethal effects are usually of greater importance to animals than lethal effects (direct mortality). Such ecological consequences may include changes in reproduction, survival, and growth that can reduce individual fitness and perhaps even lead to population-level effects. Jump to "General Effects" discussion under other Secondary Drivers: Steelhead (Oncorhynchus mykiss) Hypothesis: Low DO concentrations increase the susceptibility of steelhead to parasites and pathogens. 1. How does this driver operate? Pathogens are present in most waters and can become a problem when fish become stressed by low DO or other stressors. In fish that are already stressed or subject to high rates of parasitism or disease, low DO may impose additional stress and further increase the susceptibility of fish to parasites or pathogens. 2. Are there critical thresholds associated with this driver? Physiological stress associated with low DO concentrations (at or below 5 mg/L) is known to increase the susceptibility of hatchery salmonids to diseases such as furunculosis, aeromonad and pseudomonad hemorrhagic septicemia, and vibriosis (Wedemeyer 1970) and Wedemeyer and Wood (1974 in Karna 2003). 3. How important is this driver? Adult and juvenile steelhead use the DWSC as a migratory route and are not expected to spend much time in the area of low DO. Therefore, any stress associated with exposure to low DO would likely not be of sufficient duration to substantially affect the ability of steelhead to resist disease or parasites. 4. How well is this driver understood? This potential driver is poorly understood because of the lack of baseline information on the health status of steelhead in the DWSC and the incidence and distribution of specific pathogens and parasites in Central Valley salmonids in general. Only a few studies have been conducted to investigate the susceptibility of hatchery salmonids to pathogens under hypoxic conditions. Jump to "Steelhead" discussion under other Secondary Drivers: Chinook Salmon (Oncorhynchus tshawytscha) Hypothesis: Low DO concentrations (less than 6.9 mg/L) increase the susceptibility of Chinook salmon to parasites and pathogens. 1. How does this driver operate? Wedemeyer and Wood (1974 in Chapman 1986) concluded that pathogens are present in most waters and only become a problem for fish when fish are stressed by other environmental factors. For example, exposure to low DO concentrations can suppress the immune system of fish and increase the incidence of disease and parasitism. 2. Are there critical thresholds associated with this driver? Hatchery salmonids are more susceptible to diseases such as furunculosis, aeromonad and pseudomonad hemorrhagic septicemia, and vibriosis when low DO concentrations (below 6.9 mg/L) exist (Wedemeyer 1970 and Wedemeyer and Wood 1974 in Karna 2003). 3. How important is this driver? The importance of this driver is unknown because of the lack of baseline information on the health status of Chinook salmon in the DWSC and the incidence and distribution of specific pathogens and parasites in Central Valley Chinook salmon. 4. How well is this driver understood? Only a few studies have been conducted to investigate the susceptibility of hatchery salmonids to pathogens and the relationship to low DO concentrations. Jump to "Chinook Salmon" discussion under other Secondary Drivers: Delta Smelt (Hypomesus transpacificus) Hypothesis: The incipient limiting threshold for DO is raised for delta smelt with high pathogen and parasite loads compared to the threshold for healthy delta smelt. 1. How does this driver operate? Almost by definition, parasites and pathogens would have negative effects on delta smelt. One of these effects may be an increase in the DO concentrations required to maintain basic life functions. In general, the metabolic (e.g., oxygen) demands of fish are increased by parasite and pathogen infections as their immune systems fight the infection. In addition, parasites and pathogens may target systems (e.g., gills, blood) that are essential for acquiring and distributing oxygen to fish tissues. 2. Are there critical thresholds associated with this driver? Presumably, there are critical thresholds for parasite and pathogen loads, beyond which the ability of delta smelt to extract oxygen from water is compromised. No studies of the effects of different pathogens or parasites on delta smelt DO tolerances have been published. 3. How important is this driver? The importance of this driver is not known because no studies have assessed how pathogen and parasite loads typically found in delta smelt affect their need for DO. 4. How well is this driver understood? This driver is not well understood because no studies on the synergistic effects of pathogens and low DO concentrations on delta smelt performance have been published. Jump to "Delta Smelt" discussion under other Secondary Drivers: Longfin Smelt (Spirinchus thaleichthys) Hypothesis: The incipient limiting threshold for DO is raised for longfin smelt with high pathogen and parasite loads compared to the threshold for healthy longfin smelt. 1. How does this driver operate? Almost by definition, parasites and pathogens have negative impacts on longfin smelt. One of these impacts may be an increase in the DO concentrations required to maintain basic life functions. In general, the metabolic (e.g., oxygen) demands of fish are increased by parasites and pathogens as the fish immune systems fight infection. In addition, parasites and pathogens may target systems (e.g., gills, blood) that are essential for acquiring and distributing oxygen to fish tissues. No information specific to longfin smelt is available on this topic. 2. Are there critical thresholds associated with this driver? Presumably, there are critical thresholds for exposure to parasite and pathogen loads beyond which the ability of longfin smelt to extract oxygen from water is compromised. At this time, no studies of the effects of different pathogens or parasites on longfin smelt DO tolerances have been published. 3. How important is this driver? No studies have assessed how pathogen and parasite loads typically found in longfin smelt affect their need for DO. 4. How well is this driver understood? No studies on the synergistic effects of parasites and pathogens and low DO on longfin smelt performance have been published. Jump to "Longfin Smelt" discussion under other Secondary Drivers: Sacramento Splittail (Pogonichthys macrolepidotus) Hypothesis: The incipient limiting threshold for DO is raised for Sacramento splittail with high pathogen and parasite loads compared to the threshold for healthy Sacramento splittail. 1. How does this driver operate? Almost by definition, parasites and pathogens have negative effects on Sacramento splittail. One of these effects may be an increase in the DO concentrations required to maintain basic life functions. In general, the metabolic (e.g., oxygen) demands of fish are increased by parasites and pathogens as the fish immune systems fight infection. In addition, parasites and pathogens may target systems (e.g., gills, blood) that are essential for acquiring and distributing oxygen to fish tissues. 2. Are there critical thresholds associated with this driver? Presumably, there are critical thresholds for parasite and pathogen loads, beyond which the ability of Sacramento splittail to extract oxygen from water is compromised. No studies of the effects of different pathogens or parasites on Sacramento splittail DO tolerances have been published. 3. How important is this driver? No studies have assessed how pathogen and parasite loads typically found in Sacramento splittail affect their need for DO. 4. How well is this driver understood? No information specific to Sacramento splittail is available on this topic. Jump to "Sacramento Splittail" discussion under other Secondary Drivers: White Sturgeon (Acipenser transmontanus) Hypothesis: As white sturgeon pathogen or parasite loads increase, the concentration of DO required to avoid adverse effects also increases. 1. How does this driver operate? Almost by definition, parasites and pathogens have negative impacts on white sturgeon. One of these impacts may be an increase in the DO concentrations required to maintain basic life functions. In general, the metabolic (e.g., oxygen) demands of fish are increased by parasites and pathogens as their immune systems fight infection. In addition, parasites and pathogens may target systems (e.g., gills, blood) that are essential for acquiring and distributing oxygen to fish tissues. No information specific to white sturgeon is available on this topic. 2. Are there critical thresholds associated with this driver? Presumably, there are critical thresholds for exposure to parasite and pathogen loads, beyond which the ability of white sturgeon to extract oxygen from water is compromised. No studies of the effects of different pathogens or parasites on white sturgeon DO tolerances have been published. 3. How important is this driver? No studies have assessed how pathogen and parasite loads typically found in white sturgeon affect their need for DO. 4. How well is this driver understood? No studies on the synergistic effects of pathogens and low DO on white sturgeon performance have been published. Jump to "White Sturgeon" discussion under other Secondary Drivers: Green Sturgeon (Acipenser medirostris) Hypothesis: Although little species-specific information is available for green sturgeon, it is likely that information for white sturgeon is generally applicable to green sturgeon. Jump to "Green Sturgeon" discussion under other Secondary Drivers: Striped Bass (Morone saxatilis) Hypothesis: Striped bass are more vulnerable to impacts from parasites and pathogens when exposed to low DO concentrations. The incipient limiting threshold for DO is higher for striped bass with high pathogen and parasite loads compared to the threshold for healthy striped bass. 1. How does this driver operate? By definition, parasites and pathogens will negatively affect striped bass. One of the side effects associated with increased parasite loads may be an increased metabolic rate (and associated oxygen demand) of fish as they attempt to fight the infection. However, when striped bass are already stressed from low DO concentrations, other stressors can be expected to intensify the effect (Coutant 1985). The compounding effects of multiple stressors elicit significant physiological and behavioral responses (Sigismondi and Weber 1988; Mesa and Schreck 1989; Jarvi 1990 in Mesa 1994) that may result in increased rates of mortality (Mesa 1994). For example, Nile tilapia incur higher rates of mortality when exposed to Streptococcus agalactiae under nonlethal low DO concentrations (Evans et al. 2003). In this respect, it is reasonable to expect striped bass to be increasingly susceptible to parasites and pathogens while under other physiological stresses. However, striped bass can be carriers of IPN (infectious pancreatic necrosis) but not show symptoms of the disease even under stressful pH and temperature conditions (Wechsler et al. 1986b in Richards and Rago 1999). Therefore, the effects of disease or parasites under low DO concentrations may be specific to the pathogen. 2. Are there critical thresholds associated with this driver? Presumably, there are thresholds for parasite and pathogen loads that exacerbate the effects of low DO concentrations on striped bass and vice versa. 3. How important is this driver? The specific effects of parasites and pathogens on striped bass during or following exposure to low DO concentrations are unknown. 4. How well is this driver understood? Few studies are available on the effects of parasites and pathogens on the responses of fish to low DO concentrations. Based on the available studies, it is not possible to conclude how striped bass may be affected by parasites or pathogens during or following exposure to low DO concentrations in the DWSC (see How does this driver operate above). Jump to "Striped Bass" discussion under other Secondary Drivers: |