Previous studies have shown that juvenile chinook salmon Oncorhynchus tshawytscha from a contaminated estuary of Puget Sound, Washington, are immunosuppressed. Immunosuppressed fish may be more susceptible to disease and ultimately experience an increase in mortality. To evaluate this possibility, differences in susceptibility to a marine pathogen in outmigrating juvenile chinook salmon from an urban estuary and a nonurban estuary in Puget Sound were assessed. Juvenile chinook salmon were sampled from hatcheries before their release and subsequently from their respective estuaries as the population outmigrated from freshwater to the saltwater environment during the springs of 1993 and 1994. The study was repeated during a 3-month period to assess the duration of the effect after the fish were removed from the source of contaminants and was replicated during a 2-year period to examine interannual variation. Bile, liver, and stomach contents were collected from fish after capture to determine exposure to organic chemical pollutants. Examination of these tissues demonstrated that juvenile salmon from the urban estuary were exposed to higher concentrations of polycyclic aromatic hydrocarbons and polychlorinated biphenyls than juveniles from the nonurban estuary or hatcheries. Juvenile salmon were challenged with serial doses of a marine pathogen, Vibrio anguillarum (serotype 1575), and mortality was measured daily for 7 d. In both years, salmon from the urban estuary challenged with V. anguillarum exhibited a higher cumulative mortality after exposure to the pathogen than salmon from the hatcheries or the nonurban estuary. Our results together with our previous findings support the hypothesis that contaminant-associated immunodysfunction in juvenile chinook salmon may lead to increased susceptibility to infection by a virulent marine bacterium.

Anthropogenic factors have contributed to the precipitous decline of wild Pacific salmon stocks, although the mechanisms and processes at work are largely unknown. Pollution may be one of these factors. Sediments in estuaries are known to act as repositories for contaminants , and estuaries are important habitats for ocean-and river-migrating salmon. We have shown that juvenile salmon Oncorhynchus spp. and their prey bioaccumulate chlorinated hydrocarbons and aromatic hydrocarbons-important classes of toxic xenobiotics. Furthermore, we have shown that exposure to these pollutants can lead to immunosuppression and increased disease susceptibility in juvenile salmon. Whether pollution influences natural disease outbreaks in host populations, including salmon, is currently unknown. It is postulated that the occurrence of disease depends on the interaction of the host, the environment, and the pathogen. Absence of pathogens would reduce the potential for adverse environments to influence disease outbreaks. However, a recent reconnaissance survey of juvenile chinook salmon Oncorhynchus tshawytscha from Oregon coastal rivers revealed that pathogens were an integral component in all systems studied, although the prevalence of the pathogens varied. Furthermore, recent studies of natural fish populations have demonstrated that infectious-disease-induced mortality can significantly reduce the size of the host population. By creating adverse environments (e.g., polluted estuaries) which alter the susceptibility of the host to pathogens that are integral and ubiquitous components of the habitat, pollution increases the probability of disease-related impacts on fish populations.

Juvenile chinook salmon (Oncorhynchus tshawytscha) were injected intraperitoneally with either the polycyclic aromatic hydrocarbon, 7,12-dimethylbenz[a]anthracene (DMBA)1 or with the commercial polychlorinated biphenyl (PCB) mixture, Aroclor 1254, to assess effects on the B-cell mediated immune response. B-cell mediated immunity was assessed by examination of the primary and secondary plaque-forming cell (PFC) responses of anterior kidney and splenic leukocytes to a T-independent antigen, TNP-keyhole limpet hemocyanin (TNP-KLH). Salmon exposed to DMBA at dosages of 20% or 1% of the 96 hr LD50 (12.7 mg and 0.6 mg/kg of salmon, respectively) or to PCBs at a dosage of 20% of the 96 hr LD50 (54.0 mg/kg of salmon) exhibited a suppressed PFC response. The secondary PFC response of anterior kidney and splenic leukocytes to both antigens and the primary splenic PFC response to TNP-LPS were suppressed in salmon exposed to either DMBA or PCBs. However, only the primary PFC response of anterior kidney leukocytes to TNP-LPS was suppressed in salmon exposed to PCBs and no suppression of this response was observed in salmon exposed to DMBA. Neither anterior kidney or splenic leukocytes from salmon exposed to DMBA or PCBs showed an altered primary PFC response to the T-dependent antigen, TNP-KLH. These results suggest that B-cell mediated immunity in salmon is suppressed by known mammalian immunosuppressants and that suppression of the PFC response observed previously in salmon from an urban estuary may be due to contaminant exposure.