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Presentation Abstract
This study examined how chronic exposure to ocean acidification affects the bioenergetics and immune functionality of juvenile Pacific herring (Clupea pallasii). Wild herring offspring were reared from hatch under three contrasting pCO2 treatments [low (~650 µatm), intermediate (~1,500 µatm), and high (~3,000 µatm)] to assess impacts on long-term growth, critical swim speed (Ucrit), and susceptibility to the viral hemorrhagic septicemia virus (VHSV). During the first two months of larval development, growth trajectories were largely unaffected by pCO2 level. However, between 60 - 105 days post-hatch (dph), treatment mean growth rates (±SD) were significantly reduced under high (0.59±0.09 mm·d-1) and intermediate (0.67±0.02 mm·d-1) compared to low pCO2 conditions (0.75±.0.02 mm·d-1). Juvenile Ucrit (standardized to body lengths (BL) per second) were evaluated between 90-105 dph. Median Ucrit was fastest under low pCO2 (8.05±2.63 BL·s-1) relative to intermediate (6.36±2.16 BL·s-1) and high pCO2 (5.59±2.73 BL·s-1), but high variability within treatment groups precluded a significant CO2 effect. Exposure to VHSV increased rates of juvenile mortality compared to a control population, resulting in a significantly elevated hazard ratio (HR) of 27.98. Within the VHSV treated population, long-term exposure to high pCO2 slightly increased the risk of death (HR = 1.31), particularly in the days immediately following viral exposure. However, this effect was minimized when the model accounted for size differences between pCO2 treatments, suggesting that body size rather than pCO2 history increased susceptibility to the pathogen. Together, these results suggest that chronic exposure to high levels of pCO2 have can have an accruing deleterious effect on herring growth. But with small and inconsistent consequences for aerobic performance and vulnerability to pathogenic disease.
Session Title
Poster Session 1: Applied Research & Climate Change
Conference Track
SSE14: Posters
Conference Name
Salish Sea Ecosystem Conference (2022 : Online)
Document Type
Event
SSEC Identifier
SSE-posters-451
Start Date
26-4-2022 4:00 PM
End Date
26-4-2022 4:30 PM
Type of Presentation
Poster
Genre/Form
conference proceedings; presentations (communicative events); posters
Subjects – Topical (LCSH)
Pacific herring--Effect of water acidification on--Salish Sea (B.C. and Wash.)
Geographic Coverage
Salish Sea (B.C. and Wash.)
Rights
Copying of this document in whole or in part is allowable only for scholarly purposes. It is understood, however, that any copying or publication of this document for commercial purposes, or for financial gain, shall not be allowed without the author's written permission.
Type
Text
Language
English
Format
application/pdf
Included in
Fresh Water Studies Commons, Marine Biology Commons, Natural Resources and Conservation Commons
Does ocean acidification affect the bioenergetics and susceptibility to pathogenic disease in juvenile Pacific herring (Clupea pallasii)?
This study examined how chronic exposure to ocean acidification affects the bioenergetics and immune functionality of juvenile Pacific herring (Clupea pallasii). Wild herring offspring were reared from hatch under three contrasting pCO2 treatments [low (~650 µatm), intermediate (~1,500 µatm), and high (~3,000 µatm)] to assess impacts on long-term growth, critical swim speed (Ucrit), and susceptibility to the viral hemorrhagic septicemia virus (VHSV). During the first two months of larval development, growth trajectories were largely unaffected by pCO2 level. However, between 60 - 105 days post-hatch (dph), treatment mean growth rates (±SD) were significantly reduced under high (0.59±0.09 mm·d-1) and intermediate (0.67±0.02 mm·d-1) compared to low pCO2 conditions (0.75±.0.02 mm·d-1). Juvenile Ucrit (standardized to body lengths (BL) per second) were evaluated between 90-105 dph. Median Ucrit was fastest under low pCO2 (8.05±2.63 BL·s-1) relative to intermediate (6.36±2.16 BL·s-1) and high pCO2 (5.59±2.73 BL·s-1), but high variability within treatment groups precluded a significant CO2 effect. Exposure to VHSV increased rates of juvenile mortality compared to a control population, resulting in a significantly elevated hazard ratio (HR) of 27.98. Within the VHSV treated population, long-term exposure to high pCO2 slightly increased the risk of death (HR = 1.31), particularly in the days immediately following viral exposure. However, this effect was minimized when the model accounted for size differences between pCO2 treatments, suggesting that body size rather than pCO2 history increased susceptibility to the pathogen. Together, these results suggest that chronic exposure to high levels of pCO2 have can have an accruing deleterious effect on herring growth. But with small and inconsistent consequences for aerobic performance and vulnerability to pathogenic disease.
