Thiamine deficiency complex (TDC) is caused by a lack of thiamine (vitamin B1) in eggs of a particular species and leads to early-life-stage mortality. This disease is also known as early mortality syndrome (EMS) in salmonines (e.g., coho salmon, Chinook salmon, steelhead trout, brown trout, and lake trout) in the Great Lakes (Marcquenski and Brown 1997), M74 in Atlantic salmon in the Baltic Sea (Norrgren et al. 1998), and Cayuga Syndrome in Atlantic salmon in the Finger Lakes (Fisher et al. 1995). Recently, thiamine deficiency has also been reported in Florida alligators (Sepulveda et al. 2004). Clinical signs of these syndromes include loss of equilibrium, hyperexcitability, anorexia and death in affected swim-up fry.

Studies have implicated the presence of a thiaminolytic enzyme, thiaminase I, in salmonid diets as the principal factor responsible for TDC (Fisher et al. 1995, Fitzsimons et al. 1998, Honeyfield et al. 1998a, Ji and Adelman 1998). Although thiaminase activity occurs in a variety of Great Lakes Fishes (Greig and Gnaedinger 1971), the relatively high thiaminase activity in alewife Alosa pseudoharengus and rainbow smelt Osmerus mordax, which are important prey of Great Lakes salmonines, have implicated these species as causative factors of TDC (Tillitt et al. 2005).

TDC was first observed in fish in the late 1960’s and early 1970’s, but it may have been present prior to this time. Anecdotal information from Lake Michigan commercial lake trout fishermen referred to lethargic and dying fish in their gill nets as having “smelt toxicity.” Although TDC probably existed shortly after the arrival of alewife and smelt, recognition of the syndrome was obscured by toxicity of chlorinated organic compounds (dioxin, PCB, DDT, etc.) present in the 1950’s and 1960’s. Sediment levels of these contaminants were sufficient to have caused the death of nearly all salmonid fry during this period based on the toxicity of these compounds described in contemporary research (Phil Cook, EPA, in press).

The complexity, scope, and seriousness of TDC demand that natural resource agencies work together to move forward on an integrated research and monitoring program to better understand TDC and to propose and evaluate possible solutions. Research has not yet identified a specific causal agent for TDC. However, this may be due to the fact that most studies have been short-term or have not considered interactions among the many variables within Great Lakes ecosystems. A long-term research and monitoring program is needed to identify the potential links between anthropogenetic factors (photosynthetic inhibitors, human pharmaceuticals, flame-retardants), climatic factors, and the increasing number of invasive species entering the Great Lakes. Monitoring is critical in order to identify the key causes of early mortality diseases.