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Mortality and herpesvirus infections of the Pacific oyster Crassostrea gigas in Tomales Bay, California, USA

2006; Inter-Research; Volume: 72; Linguagem: Inglês

10.3354/dao072031

1616-1580

CA Burge, FJ Griffin, CS Friedman,

Aquaculture Nutrition and Growth

DAO Diseases of Aquatic Organisms Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout the JournalEditorsSpecials DAO 72:31-43 (2006) - doi:10.3354/dao072031 Mortality and herpesvirus infections of the Pacific oyster Crassostrea gigas in Tomales Bay, California, USA Colleen A. Burge1, Frederick J. Griffin2, Carolyn S. Friedman1,* 1School of Aquatic and Fishery Sciences, University of Washington, Box 355020, Seattle, Washington 98195, USA 2University of California, Davis, Bodega Marine Laboratory, PO Box 247, Bodega Bay, California 94923, USA *Corresponding author. Email: carolynf@u.washington.edu ABSTRACT: Seed losses of Pacific oysters Crassostrea gigas have been associated with an ostreid herpesvirus-1 (OsHV-1) in Europe, and in 2002, a similar OsHV was detected in Tomales Bay, California, USA. In May of 2003, 5 stocks of seed Pacific oysters were planted at 2 sites (Inner Bay and Outer Bay) in Tomales Bay and monitored for mortality, presence/prevalence of OsHV (using polymerase chain reaction [PCR] and histology), and growth. Temperature (°C) and salinity data were collected every half an hour at each site. OsHV was detected at both the Inner and Outer Bay sites on the same sample date and mean temperature predicted OsHV presence (p < 0.0005). High levels of mortality occurred 2 wk (Inner Bay site) and 4 wk (Outer Bay site) after OsHV detection. OsHV presence predicted mortality (p = 0.01). Temperature maximums and overall temperature exposure were greater at the Inner Bay site and may explain why mortality affected these oysters sooner than oysters planted at the Outer Bay site. Differences in cumulative mortality were significant among stocks (p < 0.0001), but not between sites (p > 0.05). OsHV prevalence was similar among stocks (p > 0.05) and between sites (p > 0.05). No evidence of herpesvirus-induced Cowdry type A nuclear inclusions or other pathogens were observed. Changes in tissue and cellular architecture including dilation of the digestive tubules and nuclear chromatin margination and pycnosis were observed in OsHV-infected oysters, consistent with previously observed OsHV infections. Stocks with smaller oysters had higher mortality rates than those with larger oysters; growth rate did not correlate with mortalities (p > 0.05). Taken together, these data suggest that the OsHV may cause or act in synergy with temperature to kill Pacific oyster seed in Tomales Bay, but further investigation of OsHV etiology in seed oysters is needed. KEY WORDS: Pacific oyster · Oyster herpesvirus · Mortality · Tomales Bay · California · Temperature Full text in pdf format PreviousNextExport citation RSS - Facebook - Tweet - linkedIn Cited by Published in DAO Vol. 72, No. 1. Online publication date: September 14, 2006 Print ISSN: 0177-5103; Online ISSN: 1616-1580 Copyright © 2006 Inter-Research.