**The title, authors, and abstract for this completion report are provided below. For a copy of the completion report, please contact the GLFC via e-mail or via telephone at 734-662-3209**

Food web dynamics and Thiamine Deficiency Complex: Identifying trophic pathways

Allison Evans², Jim Zajicek³, Cathy Richter³, Jacques Rinchard⁴, Scott Heppell²,

Don Tillitt³, and Stephen Riley⁵

² Department of Fisheries and Wildlife

Oregon State University

Nash Hall, Rm 104

Corvallis, OR 97331, USA

³ U. S. Geological Survey

Columbia Environmental Research Center (CERC)

4200 New Haven Rd.

Columbia, MO 65201, USA

⁴ Department of Environmental Science and Biology

State University of New York, the College at Brockport

350 New Campus Drive,

Brockport, NY 14420, USA

⁵ U. S. Geological Survey

Columbia Environmental Research Center (CERC)

4200 New Haven Rd.

Columbia, MO 65201, USA

December 2010

ABSTRACT:

Thiamine Deficiency Complex (TDC) is caused by a lack of thiamine (vitamin B1). In salmonid embryos, lack of thiamine causes an early mortality syndrome (EMS) between the hatching and swim-up stages. Lack of thiamine in embryos is thought to result from the adult female’s dietary intake of excessive amounts of thiaminase-containing prey fish such as alewife. The source of thiaminase activity in prey fish and other food web components, however, remains unknown. One potential source of thiaminase in food web components is the bacterium Paenibacillus thiaminolyticus, a thiaminase-producing organism which has been isolated from the gut of alewife. Another potential source of thiaminase is ingestion of thiaminase-containing zooplankton. The purpose of this study was to evaluate both hypotheses by assessing whether (1) the distribution of thiaminase activity in prey fish and other food web components is explained by the distribution of P. thiaminolyticus and (2) the distribution of thiaminase activity in fishes is explained by trophic structure. Thiaminase activity in fish and zooplankton was not related to the abundance of P. thiaminolyticus (as determined by Q-PCR to quantify the 16S rRNA gene specific to P. thiaminolyticus). Furthermore, thiaminase activity in fish and zooplankton was not related to the quantity of thiaminase I protein produced by P. thiaminolyticus, which was quantified using Western blots. Results clearly showed that P. thiaminolyticus was not responsible for the observed thiaminase activity in fish and zooplankton from the Great Lakes. Thiaminase activity of fish viscera was not strongly related to gut contents. No specific diet item was consistently present in fish species with high thiaminase activity, but absent in species with low thiaminase activity, suggesting that no individual diet item or no combination of several diet items accounted for high thiaminase activity by its presence nor accounted for low thiaminase activity by its absence. Ordinations revealed that gut contents accounted for approximately 7% of the variation in thiaminase activity. Fatty acid profiles were more strongly related to thiaminase activity than gut content, with variation in fatty acid profiles accounting for approximately 21 to 38% of the thiaminase activity. The percentage of most individual fatty acids were negatively related to thiaminase activity, indicating that lower percentages of fatty acids are associated with increased thiaminase activity in sampled fishes. Few fatty acids (C12:0, C14:1, and C20:1) were positively related to thiaminase activity. Overall, our results refute the hypothesis that P. thiaminolyticus is the source of thiaminase in Great Lakes food webs, does not support the hypothesis that specific diet items are responsible for thiaminase activity observed in fishes, and suggests that higher thiaminase activities are associated with lower percentage of a variety of fatty acids.