The use of thiamine and thiamine antagonists to investigate the etiology of early mortality syndrome in lake trout (Salvelinus namaycush)

Early mortality syndrome (EMS) is a non-infectious disease affecting lake t rout and other salmonids in the Great Lakes and in inland lakes. It is char acterised by loss of equilibrium, hyperexcitability, anorexia, and eventual ly death. EMS is associated with low thiamine and treatment of eggs or fry with thiamine-HCl eliminates symptoms and mortality. To verify the role of the active form of the vitamin as the prophylactic agent, we used thiamine pyrophosphate (TPP) to reverse EMS symptoms. We also investigated the abili ty of specific thiamine antagonists that either block TPP production or int erfere with its function to induce EMS. When graded doses of TPP were admin istered to EMS-susceptible sac-fry, there was a dose-dependent reduction in EMS. The egg concentration of TPP that was associated with reduced EMS was similar to the threshold thiamine concentration found in feral lake trout stocks where EMS occurs. A thiamine deficient stock from Lake Ontario was v ery sensitive to the thiamine antagonist oxythiamine (OXY) with total morta lity associated with developmental arrest occurring at an antagonist to thi amine molar ratio (ATR) above 7:1. The threshold ATR with OXY for developme nt of EMS-like neurological signs in this stock was 1.6:1. In addition to E MS-like neurological signs, OXY caused dose-dependent increases in hydrocep halus, developmental arrest, and vitelline congestion in the Lake Ontario s tock. These signs are consistent with those observed in feral fish exhibiti ng EMS. Much higher doses of antagonists were required (both pyrithiamine ( PT) and OXY) to induce EMS-like clinical signs in the thiamine replete Lake Manitou stock. PT was a more potent inducer in this stock as the ATR assoc iated with development of clinical signs was 111:1 for PT compared with 892 :1 for OXY. These data provide experimental evidence supporting the hypothe sis that a thiamine deficiency in the natural environment is the cause of E MS. (C) 2001 Elsevier Science B.V. All rights reserved.