Two silver‐contaminated diets were prepared by exposing juvenile rainbow trout for 8 d to waterborne silver thiosulfate as Ag at either 0.1 μg/L (low‐Ag diet) or 80 mg/L (high‐Ag diet). The level of total Ag accumulated in whole low‐Ag fish was below the detection limit of analysis. Whole high‐Ag fish accumulated Ag at 21.3 nmol/g. The livers of the low‐ and high‐Ag fish accumulated Ag at 0.43 nmol/g and 1.01 μmol/g, respectively. The Ag‐contaminated fish were then fed whole to adult crayfish in an 80‐d dietary study to determine the effects of long‐term trophic accumulation of Ag. In a second experiment, the livers of the high‐Ag trout were fed to juvenile crayfish for either one or five weeks. Accumulation of Ag was demonstrated in both adult and juvenile crayfish. Silver accumulation in juvenile crayfish peaked at approximately 650 nmol/g at three weeks, after which Ag depuration occurred. In adult crayfish that consumed the high‐Ag diet, the hepatopancreas accumulated more than 90% of assimilated Ag, rising 1,000‐fold over control animals to approximately 740 nmol/g at 80 d. Crayfish that consumed the low‐Ag diet had small, statistically insignificant elevations of Ag in some tissues. Dietary Ag had no effect on juvenile crayfish growth or adult mortality. Disturbances in osmoregulation, which are normally associated with acute waterborne Ag exposure, were not detected. Dietary Ag also had no effect on hemolymph concentrations of Na+, Cl−, Ca2+, Mg2+, or Cu; did not affect the concentration kinetics of Na+ or Cl− influx; and had no effect on the activity of gill Na+/K+‐dependent adenosine triphosphatase. Hemolymph concentrations of glucose and lactate were similarly unaffected, indicating an absence of stress‐related metabolic disturbance. However, a disproportionately low number of ecdysis events occurred among crayfish that consumed the high‐Ag diet.