Cumulative Effects of Natural and Anthropogenic Stress on Immune Function and Disease Resistance in Juvenile Chinook Salmon

Jacobson, Kym C.; Arkoosh, Mary R.; Kagley, Anna N.; Clemons, Ethan; Collier, Tracy K.; Casillas, Edmundo

doi:10.1577/1548-8667(2003)015<0001:ceonaa>2.0.co;2

Cited by 58 publications

(48 citation statements)

References 38 publications

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“…Gastropods infected with larval digeneans were less resistant to dessication and hypoxia (Jensen et al 1996, Wegeberg & Jensen 1999. Lastly, juvenile Chinook salmon Oncorhynchus tshawystscha infected with metacercariae of the trematode Nanophyetus salmonicola exposed to PCBs suffered higher mortalities when challenged with the pathogenic bacterium Listonella anguillarum (Jacobson et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…exposed to zinc and benzene experienced decreased haematocrit values compared to uninfected fish (Sakanari et al 1984). More recently, Jacobson et al (2003) elegantly demonstrated that juvenile Chinook salmon infected with Nanophyetus salmonicola and exposed to PCBs displayed a decreased immune response measured by a hemolytic plaque-forming cell assay. Thus, these studies along with the results herein provide ample evidence suggesting that fish exposed to sublethal levels of contaminants experience greater stress when infected by parasites, or in other words, parasites and toxicants may act together to increase stress.…”

Section: Discussionmentioning

confidence: 99%

“…For example, in a recent study Jacobson et al (2003) effectively demonstrated that a combination of anthropogenic stressor, the PCB micture Aroclor 1254, and a natural stressor, the digenean parasite Nanophyetes salmonicola, has a greater negative effect than either of these alone, on B cell function and immunosuppression in juvenile Chinook salmon Oncorhynchus tshawustscha.…”

Section: Introductionmentioning

confidence: 99%

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Joint effects of parasitism and pollution on oxidative stress biomarkers in yellow perch Perca flavescens

Marcogliese¹,

Brambilla²,

Gagné³

et al. 2005

Dis. Aquat. Org.

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Yellow perch Perca flavescens were collected from a contaminated site and a reference site in the St. Lawrence River, Quebec, Canada. Fish were assessed for oxidative stress (lipid peroxidation and reduced glutathione levels) and parasitism by the nematode Raphidascaris acus and metacercariae of the digenean Apophallus brevis. Lipid peroxidation is not only considered a measure of oxidative stress, but of stress in general, and thus serves as an indicator of fish health. Fish from the contaminated site exhibited higher levels of lipid peroxidation than those from the reference site, independent of parasitic infections. However, fish infected with R. acus at the contaminated site tended to have higher levels of lipid peroxidation than uninfected fish at the same site, whereas no difference was observed between infected and uninfected fish at the reference site. Yellow perch infected with >10 metacercariae of A. brevis expressed higher levels of lipid peroxidation than those infected with <10 metacercariae at both the contaminated and the reference sites. No differences were found in levels of reduced glutathione in liver or muscle in relation to site or either parasite species. Results support the use of lipid peroxidation as a biomarker of water contamination. They further suggest that lipid peroxidation may be used as a biomarker of pathological effects caused by parasitism. Most importantly, results demonstrate that contaminants and parasites occurring together exacerbate oxidative stress in fish, suggesting that parasitized fish in polluted environments are in a poorer state of health than uninfected fish.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Joint effects of parasitism and pollution on oxidative stress biomarkers in yellow perch Perca flavescens

Marcogliese¹,

Brambilla²,

Gagné³

et al. 2005

Dis. Aquat. Org.

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“…The swimming performance of coho salmon (57 to 60 mm FL) can be impaired as much as 95% following exposure to 1500 metacercariae (Butler & Millemann 1971). Also, laboratory infections of 257 to 543 metacercariae impaired immune function and increased susceptibility to the marine pathogen Listonella anguillarum in subyearling Chinook salmon (100 mm mean FL) (Jacobson et al 2003). It is possible that our measures of early ocean growth are not sensitive enough to capture a population-level effect caused by N. salmincola infection.…”

Section: Discussionmentioning

confidence: 99%

“…Pacific salmon serve as an intermediate host for the freshwater trematode Nanophyetus salmincola, a parasite documented to cause significant losses of Pacific salmon fry (Milleman & Knapp 1970) and to increase disease susceptibility of Chinook salmon smolts (Jacobson et al 2003). The first intermediate host of the parasite is a freshwater snail, Juga plicifera, common in streams and rivers from northern California through western Washington (Simms et al 1931).…”

Section: Introductionmentioning

confidence: 99%

Parasite-associated mortality of juvenile Pacific salmon caused by the trematode Nanophyetus salmincola during early marine residence

Jacobson

Teel²,

Doornik³

et al. 2008

Mar. Ecol. Prog. Ser.

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The potential effect of the freshwater trematode Nanophyetus salmincola on early marine survival of Pacific salmon was assessed by monitoring the prevalence and intensity of metacercarial infection in yearling coho salmon Oncorhynchus kisutch, and yearling and subyearling Chinook salmon O. tshawytscha caught off Oregon and Washington during May, June, and September of 1999 to 2002. Annual prevalences of N. salmincola infection in yearling coho salmon were 62 to 78% and were significantly greater each year than in both yearling and subyearling Chinook salmon (19.3 to 53.8% and 40.5 to 53.5%, respectively). Yearling coho salmon also had significantly higher intensities of infection (from approximately 2-fold to 12-fold) than yearling and subyearling Chinook salmon. Prevalences and intensities in coho salmon caught in September were significantly lower (by approximately 21%) than in coho salmon caught in May or June in 3 of the 4 years. Variance to mean ratios of parasite abundance in coho salmon were also lowest in September, suggesting parasiteassociated host mortality during early ocean residence. There was no evidence for a seasonal decline in infection in yearling or subyearling Chinook salmon. Infection intensities, but not prevalences, were significantly greater in naturally produced (wild) coho salmon than in hatchery produced coho salmon and could be due to differences in exposure to the trematode. Highly infected naturally produced coho salmon were not caught in September. This study suggests that coho salmon with high intensities of N. salmincola may not survive early marine residence, and that disease processes need to be considered as a factor affecting marine survival of juvenile salmon.

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Risk Factors Associated with Mortality of Age‐0 Smallmouth Bass in the Susquehanna River Basin, Pennsylvania

et al. 2018

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Evidence of disease and mortalities of young of the year (age‐0) Smallmouth Bass Micropterus dolomieu has occurred during the late spring and summer in many parts of the Susquehanna River watershed since 2005. To better understand contributing factors, fish collected from multiple areas throughout the watershed as well as out‐of‐basin reference populations (Allegheny and Delaware River basins; experimental ponds, Kearneysville, West Virginia) were examined grossly and histologically for abnormalities. Tissue contaminant concentrations were determined from whole‐body homogenates, and water contaminant concentrations were estimated using time‐integrated passive samplers at selected sites. Observed or isolated pathogens included bacteria, predominantly motile Aeromonas spp. and Flavobacterium columnare; largemouth bass virus, and parasites, including trematode metacercariae, cestodes, and the myxozoan Myxobolus inornatus. Although these pathogens were found in age‐0 Smallmouth Bass from multiple sites, no one pathogen was consistently associated with mortality. Chemicals detected in tissue included polychlorinated biphenyl (PCB) congeners, organochlorine, and current‐use pesticides. Pyraclostrobin, PCB congeners 170 and 187, cis‐chlordane and trans‐nonachlor were detected in all Susquehanna watershed samples but rarely in samples from the reference site. The findings support the idea that there is no single cause for disease of age‐0 Smallmouth Bass; rather the cumulative effects of co‐infections and potential immunomodulation by environmental stressors during a sensitive developmental life stage may lead to mortality. Identifying the most important risk factors will be necessary for more in‐depth analyses of individual stressors and better management of the habitat and fish populations.

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Cumulative Effects of Natural and Anthropogenic Stress on Immune Function and Disease Resistance in Juvenile Chinook Salmon

Cited by 58 publications

References 38 publications

Joint effects of parasitism and pollution on oxidative stress biomarkers in yellow perch Perca flavescens

Joint effects of parasitism and pollution on oxidative stress biomarkers in yellow perch Perca flavescens

Parasite-associated mortality of juvenile Pacific salmon caused by the trematode Nanophyetus salmincola during early marine residence

Risk Factors Associated with Mortality of Age‐0 Smallmouth Bass in the Susquehanna River Basin, Pennsylvania

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