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TWENTY-FOURTH ANNUAL EASTERN FISH HEALTH WORKSHOP


Royal Pavilion Resort, Atlantic Beach, NC
MARCH 9-11, 1999


Effects Of Chronic Low-Level Exposure To Infectious Pancreatic Necrosis Virus (IPNV) On Early Life Stages Of Rainbow Trout, Oncorhynchus mykiss.

Philip E. McAllister1 and Julie Bebak2

1U.S. Geological Survey, Biological Resources Division, National Fish Health Research Laboratory, 1700 Leetown Road, Kearneysville, WV 25430; 2Freshwater Institute, P.O. Box 1889, Shepherdstown, WV 25443.

In a previous study, we documented that infectious pancreatic necrosis virus (IPNV) was detected in stream water for a distance of at least 19.3 kilometers below the point of effluent discharge from a fish hatchery. A low prevalence of IPNV infection was found in stream resident fishes. However, notable IPNV titer (3.0 x 104 plaque forming units (PFU/gram of tissue), but no clinical signs of disease, was detected in a young trout--ostensibly the progeny of in-stream reproduction. In the current study, laboratory trials were conducted to estimate the effects of chronic, low-level IPNV exposure on early life stages of rainbow trout, Oncorhynchus mykiss. fish. Using three concentrations of IPNV (101, 103, and 105 PFU/liter of water) to simulate conditions found in the affected stream, eyed eggs of rainbow trout (O. mykiss) were exposed continuously to IPNV beginning 7 days before hatch, and exposure was continued through alevin, fry, and fingerling life stages until progeny were 44 days old. Cumulative IPNV-related mortality and IPNV-carrier prevalence in survivors were affected by virus concentration and by population density. At low population density (about 35 fish/one liter tank; water flow = 250 milliliters/minute), IPNV-related mortality began as early as 19 days post hatch. As ambient virus concentration increased, average cumulative IPNV-related mortality increasing from 0% to 22%, and average IPNV-carrier prevalence in survivors increasing from 0% to 100%. At high population density (about 140 fish/one liter tank; water flow = 250 milliliters/minute), IPNV infection was detected at 6 days post hatch, and IPNV-related mortality began at 16 days post hatch. As ambient virus concentration increased, average cumulative IPNV-related mortality increased from 1% to 95% and average IPNV-carrier prevalence in survivors increased from 0% to 68%. Ambient virus concentration, population density, and excretion augmentation of ambient virus interact to pressure threshold conditions requisite to initiate and sustain infection and disease in a population.

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