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A link was previously established between the Cayuga syndrome, a condition causing 100% mortality in larval landlocked Atlantic salmon, Salmo salar, in several of New York's Finger Lakes, and a maternal diet of alewife, Alosa pseudoharengus, a non-native thiaminase-rich Clupeid fish. We evaluated salmon larvae viability relative to maternal thiamin status, and investigated the putative link of the Cayuga syndrome to an alewife diet in fish from the geographic regions outside the Finger Lakes/lower Great Lakes watersheds. We identified Cayuga syndrome in Atlantic salmon from Otsego Lake in the Susquehanna River watershed and from Green Pond in New York's Adirondack Mountains. In both systems alewife represent the major component of the diet for the salmon. Thiamin levels in the maternal blood of Otsego salmon with syndrome-negative progeny were three- to four-fold greater than those Otsego females whose progeny exhibited 100% mortality. Thiamin levels in eggs and larvae were directly related to thiamin levels in maternal blood in both syndrome-positive and syndrome-negative stocks. Thiamin bath treatments of syndrome-afflicted larvae eliminated mortality regardless of their lake stock of origin. Maternal blood levels of approximately 0.31 nmol thiamin pyrophosphate/g or 0.44 nmol total thiamin/g appear necessary to achieve egg threshold levels of approximately 0.8 and 1.1 nmol/g unphosphorylated and total thiamin, respectively; these egg thiamin levels should prevent significant syndrome-related mortality in landlocked Atlantic salmon larvae. These results confirm the role of thiamin in the etiology of the Cayuga syndrome and support the dietary link of this naturally occurring thiamin deficiency to the thiaminase-rich alewife. KEY WORDS: * Atlantic salmon * vitamin deficiency * early mortality syndrome * Cayuga syndrome * thiaminase

Two experiments were performed to determine the persistence of viral hemorrhagic septicemia virus (VHSV) genotype IVb on WalleyeSander vitreuseggs. Fertilized Walleye eggs were exposed for 30 min to 105plaque-forming units/mL VHSV genotype IVb, and control eggs were exposed to phosphate-buffered saline. In the first experiment, the eggs were treated with 0 and 50 mg/L iodophor and incubated at 12±1°C until the first fry emerged. In the second experiment, a treatment of 100 mg/L iodophor was also tested. Periodic samples were taken during embryo development and tested for VHSV by viral isolation and quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The effect of tannic acid, an inhibitor of qRT-PCR testing, was evaluated in the second experiment. In both experiments no virus was detected in any control eggs by either test. In the first experiment, virus was isolated in 0-mg/L iodophor-treated eggs up to 3 d postinfection (DPI). Virus was also isolated in the 50-mg/L iodophor-treated group at 1 DPI. Testing by qRT-PCR detected viral RNA at all time points throughout the first experiment. In the second experiment, no VHSV was isolated after the initial 0-DPI sample. Viral RNA was again detected at all time points, including samples collected at the end of the experiment. Inhibition was found in 34 of 36 samples at 0 DPI and 21 of 36 samples at 1 DPI. The number of inhibited samples decreased over time, but virus was still detected in three samples at 24 DPI. These experiments show that VHSV persists on Walleye eggs for longer than was previously known. At early time points VHSV was still detected despite disinfection, and viral RNA was detected at all time points; however, it is unknown whether the virus detected by this qRT-PCR is viable. These experiments reinforce the need for careful disinfection of eggs. Received November 28, 2011; accepted February 26, 2012 [ABSTRACT FROM PUBLISHER]

Because the number of fish being used in research is increasing rapidly, evaluating the analgesic and pathologic effects of NSAID in fish is essential. To determine the biochemical, histopathologic, physiologic and behavioral effects of 3 NSAID, 48 rainbow trout underwent anesthesia with tricaine methanesulfonate and exploratory celiotomy and were randomly assigned to receive flunixin (0.5 mg/kg IM), ketorolac (0.5 mg/kg IM), ketoprofen (2 mg/kg IM), or saline. Clinical pathologic variables were assessed 1 wk before surgery and 48 h after surgery. Histopathology was performed to evaluate the healing of the incision, tissue reaction at the injection site, and potential organ toxicity. Physiologic and behavioral parameters, including weight, feeding, opercular rate, and vertical position in the water, were measured to establish parameters for identifying pain in fish. The difference between the pre- and postoperative phosphorus concentrations was greater in the flunixin group than the saline group and was the only pathologic difference between treatment groups. Histopathology of incision site, injection site, and internal organs appeared normal, and healing did not appear to be inhibited by the drugs used. The physiologic parameters of opercular rate and weight were consistent and may be helpful in identifying pain in fish in future studies, whereas feeding and vertical position in the water were unhelpful as indicators of pain in this rainbow trout surgical model. Overall, according to clinical pathology and histopathology, the use of ketoprofen, ketorolac, and flunixin at the dosages used in this study lack negative effects in rainbow trout undergoing surgery.