Early Life Stage Mortality Syndrome in Fishes of the Great Lakes and Baltic Sea

<em>Abstract</em>.—Juvenile and adult lake trout <em>Salvelinus namaycush </em>that were fed semipurified, thiaminedeficient diets or alewives <em>Alosa pseudoharengus </em>containing thiaminase, a thiamine-destroying enzyme, showed no overt symptoms of thiamine deficiency. Growth rates and ovulation rates were similar among all treatments. However, liver thiamine pyrophosphate (TPP), a biochemical indicator of impending thiamine deficiency, in juvenile lake trout fed thiamine-deficient diets was reduced to 35 pmol/ g compared with 59 pmol/g in control groups. Blood TPP in adult female lake trout fed alewives was one-third of that in controls fed a commercial diet. Adult lake trout from Lake Michigan had blood TPP levels similar to those of fish fed the alewife diet in the laboratory. Lake Superior lake trout had TPP levels similar to those of fish fed the control diet in the laboratory. Thiamine synthesis occurred in the intestine of lake trout. At least 81% of thiamine in the posterior intestine was synthesized, presumably by bacteria, when a ¹⁴C-labeled thiamine diet was force-fed to lake trout. Thiamine had a long retention time in the lake trout: at 27 weeks after fish were injected with radioactive thiamine, blood cells retained 11% of the radioactivity that was present at 2 d and liver tissue retained 34% of the 2-d level. Lack of self-sustaining lake trout reproduction by Lake Michigan fish may be related to their lower blood thiamine levels. Thiamine deficiency may cause early mortality syndrome, which is common in Lake Michigan but not Lake Superior fish with higher blood thiamine levels.