Potential mechanisms in the early mortality of juvenile Chinook salmon exposed concurrently to infectious hematopoietic Necrosis Virus (IHNV) and esfenvalerate

Replicate groups of juvenile Chinook salmon (Oncorhynchus tshawytscha) were exposed to infectious hematopoietic necrosis virus (IHNV), sub-lethal levels of esfenvalerate, or to both agents concurrently. A lethal synergistic effect of concurrent exposure to IHNV and esfenvalerate resulted in 24.1% mortality by 68 h post-virus exposure with no mortality observed in any other treatment groups at this time. Analyses of spleen samples from fish sampled at 68 h following exposure to both IHNV and esfenvalerate was suggestive of a disruption of transcription, and demonstrated a significant decrease in the production of two early, non-specific anti-viral genes (Mx-1 and Vig-8). Analyses of blood serum suggested that osmolality was not a contributing factor to the observed early mortality event. Examinations of stained sections of the gill and anterior kidney from fish in all treatment groups at 68 h did not reveal pathologic microscopic changes. This study suggests that the lethal synergistic effect of exposure to IHNV and esfenvalerate to juvenile Chinook salmon may be related to inhibited transcription of early, non-specific, anti-viral cytokines.