Immunosuppression in progeny of chinook salmon infected with Renibacterium salmoninarum: re-analysis of a brood stock segregation experiment

Abstract

Female spawner infection level and temperature variation through rearing are sufficient to explain in-hatchery mortality rates and infection levels and smolt to adult return ratios (SARs) of progeny of Renibacterium salmoninarum infected spring chinook salmon. Data from published reports and manuscripts regarding a 1988 brood stock segregation experiment that held progeny of highly infected female spring chinook salmon spawners separate from progeny of other spawners during 16 mo of hatchery rearing are analyzed to test the hypothesis that immunosuppression could account for differences in survival and infection levels between the 2 segregates. Immunosuppression, caused by the presence of the p57 antigen of R. salmoninarum in sufficient concentration within the salmon egg before spawning, can account for differences in infection levels, mortality rates, and SARs for each hatchery raceway in that study. This immunosuppression may be characterized by immunotolerance, or might only affect cell mediated immunity, which appears the most effective defense mechanism against R. salmoninarum infection, as antibody production can result in tissue damaging antibody-antigen complexes. Low-temperature mediated immunosuppression can account for the nearly identical trajectories of infection and mortality between the 2 segregates during the first 8 mo of hatchery rearing. There is no evidence of widespread vertical infection from spawner to progeny, nor is there evidence that brood stock segregation reduces overall mortality. Rather, the suppression of cell-mediated immune mechanisms may condemn progeny of highly infected female spawners to an almost certain eventual premature demise.