No abstract

We describe a disease syndrome that afflicts larval, landlocked Atlantic salmon Salmo salar from Cayuga Lake, one of central New York's Finger Lakes . Mortality associated with the "Cayuga syndrome" is 98-100% . Death usually occurs between 650 and 850 centigrade degreedays after fertilization, approximately 2-4 weeks before yolk resorption is complete . Although there is minor temporal variation in the onset of the Cayuga syndrome in progeny from individual females, all sac fry eventually succumb . Incubation of embryos and sac fry under constant, ambient, or reduced temperature regimens slightly alters the degree-day timing of syndrome onset, but does not improve survival . Based on mortality rate, manifestation of the Cayuga syndrome has not changed in the past 10 years, even though incubation waters of varying chemistry and temperature have been used . Mortality of the negative control stocks used for these studies never exceeded 10% from hatching to first feeding . Findings from reciprocal crossbreeding experiments indicate the problem is associated with ova only . A noninfectious etiology is indicated by the lack of consistently identifiable fish pathogens from syndrome-afflicted sac fry and by the failure to

The "Cayuga syndrome" is a maternally transmitted, naturally occurring thiamine deficiency that causes 100% mortality of larval landlocked Atlantic salmon Salmo salar in several of New York's Finger Lakes . Results of multiyear studies to qualify and quantify the neurobehavioral and gross pathological signs of this condition are described . Affected sac fry became weak and ataxic and responded atypically to stimuli 1-2 weeks before death . Quantitative assays of stimulus-provoked swimming revealed a significant neuropathy whereby the sac fry exhibited abnormal thigmotactic and phototactic behaviors . Gross lesions observed in Cayuga sac fry included yolk-sac opacities, subcutaneous edema, vitelline hemorrhage or congestion, pericardial edema, retrobulbar edema, branchial congestion, foreshortened maxillae, hydrocephalus, and occasional caudal fin deformities. Lesion frequency in progeny differed significantly between dam source . Yolk conversion efficiency was decreased at least 1 week before death, suggesting that the bioenergetics of the fish was compromised and thereby supporting the thiamine residue and treatment data reported elsewhere . Comparisons with coagulated-yolk, blue-sac and swim-up syndromes are presented . The pathological signs of the Cayuga syndrome represent a unique departure from the lesions induced by toxicants or pathogens in other piscine models, and for the first time profile the profound effects of thiamine deficiency on cardiovascular and neurological systems of larval fish .Nielson 1959) . Coagulated-yolk has been attributed to bacterial infection (Von Betegh 1912 ; Guberlet et al . 1931), rough handling (Dietrich 1939 ; I Address reprint requests to