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Effects of elevated pCO2 on bioenergetics and disease susceptibility in Pacific herring (Clupea pallasii)

C. S. Murray*, J. L. Gregg, A. H. Mackenzie, H. T. Jayasekera, S. Hall, T. Klinger, P. K. Hershberger

*Corresponding author:

ABSTRACT: Ocean acidification can affect the immune responses of fish, but effects on pathogen susceptibility remain uncertain. Pacific herring (Clupea pallasii) were reared from hatch under three pCO2 treatments [ambient (~650 μatm), intermediate (~1,500 μatm), and high (~3,000 μatm)] through metamorphosis (98 days) to evaluate effects of ocean acidification on bioenergetics and susceptibility to an endemic viral disease. Mortality from viral hemorrhagic septicemia (VHS) was comparable between herring reared under ambient and intermediate pCO2. In contrast, fish reared under high pCO2 experienced significantly higher rates of VHS mortality, and the condition factor of survivors was significantly lower compared to the other pCO2 treatments. However, prevalence of infection among the survivors was not influenced by pCO2 treatment. [Note that the VHS trial was conducted under ambient pCO2 due to experimental constraints]. Pre-flexion larval development was not affected by elevated pCO2, as growth rate, energy use, and feeding activity were comparable across treatments. Similarly, long-term growth (14 weeks) was not affected by chronic exposure to elevated pCO2. Maximum swimming speed of juvenile fish was likewise not significantly affected by pCO2 treatment. Herring reared under both elevated pCO2 treatments showed an average reduction in swimming speed; however, wide intra-treatment variability rendered the effect nonsignificant. This study demonstrates that the VHS susceptibility and bioenergetics of larval and post-metamorphic Pacific herring are not affected by near-future ocean acidification predicted for coastal systems of the North Pacific. However, increased susceptibility to VHS in fish reared under 3,000 μatm pCO2 indicates potential health and fitness consequences from extreme acidification.