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

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 < 0.005). 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 OsHVinfected 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 Resale or republication not permitted without written consent of the publisherDis Aquat Org 72: [31][32][33][34][35][36][37][38][39][40][41][42][43] 2006 tion (between 4 d and 2 wk), cause high levels of losses (up to 100%), and are associated with temperatures in excess of 25°C (for example: Le Deuff et al. 1996or Arzul et al. 2001b. Interestingly, OsHV infects multiple hosts, which is unique among members of the family Herpesviridae (Davison 2002). Larval Pacific oysters Crassostrea gigas (Hine et al. 1992, Nicolas et al. 1992, Manila clams Venerupis (=Ruditapes) phillippinarum , European clams Ruditapes decussates (Arzul et al. 2001c, flat oysters Tiostrea chilensis (Hine et al. 1998), European oysters C. angulata (Arzul et al. 2001b), and French scallops Pecten maximus (Arzul et al. 2001a) are all susceptible to OsHV infection-induced mortalities. Mortality of juvenile Pacific oysters and European flat oysters Ostrea edulis has been associated with OsHV (Comps & Cochennec 1993, Renault et al. 1994, 2000a, Friedman et al. 2005, but the ability of the virus to...

Complementary approaches to diagnosing marine diseases: a union of the modern and the classic

“…parasite identity in conjunction with differential staining used to elucidate subcellular components linked to a specific taxon. Although viral morphology cannot be observed using light microscopy, microscopic observations of cellular changes may suggest a specific aetiology such as a specific viral infection [80,81] or suggest viral type [75]. Pathogen presence can then be confirmed using additional special stains or molecular methods (described below) and morphology can be confirmed using electron microscopy [82].…”

Antiviral immunity in marine molluscs

“…Furthermore, microarray-based gene expression studies have observed elevated expression of genes associated with autophagy in Crassostrea gigas undergoing a mass mortality event in California, USA (Moreau et al, 2015). Chaney & Gracey (2011) did not investigate the cause of mortality, but OsHV-1 is often associated with oyster mortality in California (Burge et al, 2006). Future research should identify which OsHV-1 ligand induces autophagy and whether autophagy targets the OsHV-1 virion or an essential OsHV-1 protein.…”

“…The first description of herpes-like virus associated with mollusc mortality was reported in 1972 in the Eastern oyster (Crassostrea virginica) from the east coast of the USA (Farley et al, 1972). Since this time, herpes-like viruses have been described in other species of oyster (Burge et al, 2006;Hine et al, 1992;Renault et al, 1994), scallops (Arzul et al, 2001a;Ren et al, 2013) and clams (Renault et al, 2001). The virus has been purified from naturally infected Crassostrea gigas larvae (Le Deuff & Renault, 1999) and its genome entirely sequenced (Davison et al, 2005).…”

Ostreid herpesvirus: A pathogen of oysters

“…Moreover, the observation by electron microscopy of capsids or nucleocapsids in the nucleus and virus particles in the cytoplasm or in cytoplasmic vesicles could only confirm the presence of a herpesviruslike and/or a viral disease [10,[18][19][20][22][23][24].…”

“…Regarding the histopathological examination, what can be observed are the typical signs of a viral infection: connective tissue cells with pycnosis, nuclear changes (moon shaped), including nuclei hypertrophy with marginated chromatin, and large intranuclear acidophilic inclusion bodies (Cowdry type A inclusions) [10,[18][19][20][21]. Moreover, the observation by electron microscopy of capsids or nucleocapsids in the nucleus and virus particles in the cytoplasm or in cytoplasmic vesicles could only confirm the presence of a herpesviruslike and/or a viral disease [10,[18][19][20][22][23][24].…”