Pesticide and pathogen: heat shock protein expression and acetylcholinesterase inhibition in juvenile Chinook salmon in response to multiple stressors.

Rapid expression of heat shock protein (hsp) families in response to a variety of stressors has been demonstrated in many organisms, including fish. The present 60-d challenge study was designed to compare hsp induction in juvenile Chinook salmon following exposure to individual pesticides, virus, and both stressors combined. Heat shock protein expression patterns over time were monitored and related to the extent of virus infection and mortality. Acetylcholinesterase (AChE) inhibition and recovery in response to applied stressors were measured in brain. High enzyme inhibition levels have been correlated with imminent mortality, and other sublethal physiological effects have been observed in fish concurrent with depressed AChE activity. Mortality was elevated considerably in fish exposed to 0.08 microg/L of the pyrethroid esfenvalerate (EV). Mortality due to infectious hematopoietic necrosis virus (IHNV) was lower in groups previously treated with pesticides; however, these fish died sooner than individuals exposed to virus only. Both pesticides, EV and the organophosphate (OP) chlorpyrifos (CP), as well as virus exposure, induced hsp expression, but highest hsp levels were observed after the combined treatments, suggesting an additive effect between virus and pesticides. Highest virus titers were accompanied by strongest hsp induction, indicating a connection between virus concentration and hsp expression. In conclusion, the measurement of hsp expression appears to be a very sensitive, integrative indicator of stress. Esfenvalerate and IHNV did not affect AChE activity, and exposure to 3.7 microg/L CP led to significantly inhibited AChE for at least 20 d. The time required for complete recovery of AChE activity raises concern about deleterious behavioral effects.