Factors Influencing Ostreid Herpesvirus Mortality of Pacific Oysters05 May 2015
Mortalities of oyster Crassostrea gigas seed associated with ostreid herpesvirus have been observed in many oyster-producing countries since 2008. This report, by Bruno Petton and colleagues from the French Research Institute for Exploitation of the Sea, looks into the factors affecting mortality from this disease.
Since 2008, mass mortalities of juvenile Pacific oysters Crassostrea gigas have occurred at rearing sites along the coast of France when seawater temperature exceeds 16°C. Mortality of oyster seed (<1 yr) ranges from 40 to 100%, depending on locations and batches, whereas older animals are generally much less affected.
This represents the most serious crisis the French oyster industry has faced since the mass mortality of Crassostrea angulata in the late 1960s, which lead to the introduction of C. gigas in the early 1970s.
Although Pacific oyster mortalities have mainly been reported in France during this period, there have also been several cases in the UK, Australia and New Zealand, and more recently in Norway. Results of diagnostic tests indicate that recent mortality events are associated with the detection of a particular genotype of the ostreid herpesvirus 1, named µVar (OsHV-1).
Limited knowledge regarding risk factors of disease transmission and subsequent mortality has limited the development of specific protective measures for oyster farming. Additionally, unlike most other animal productions, disease curative treatments or vaccinations are not feasible in oysters.
As a result of the inherent dependence of the productive system on environmental hazards, oyster farmers regularly develop and conduct adaptation and risk integration strategies. Restrictions on the movements of livestock between production basins, spatial planning and density regulation in oyster beds are a few examples of farming practices implemented in response to mass mortality events.
In this context, additional mitigation measures are clearly needed to reduce the risks of disease transmission and mortality in conjunction with selective breeding to improve disease resistance.
The objective of the present study was to examine the effects of specific environmental and life-history parameters of oysters on disease susceptibility, transmission and subsequent mortality, in order to aid in mitigation strategies. To that end, 4 experiments were designed to test the effects of (1) rearing history of oyster seed, (2) timing and duration of exposure to the disease in the field, (3) age and size of oysters and (4) water renewal and biomass of infected animals on disease transmission and related mortalities in C. gigas.
These experiments relied on (1) the production of standardised oyster seed under controlled conditions, (2) the use of this oyster seed for investigating the infection pressure in different environments and (3) the development of a protocol based on seawater temperature elevation in the laboratory to activate OsHV-1 in asymptomatic carriers.
The first question was addressed by investigating the effect of the origin of oysters (i.e. natural spatfall vs. nurseries) on disease transmission and mortality risk. In France, oysters originate either from natural spatfall collected along the Atlantic coast, or alternatively, from hatcheries and nurseries. In the field, oysters are unpredictably exposed to OsHV-1, whereas in hatcheries and nurseries they can be protected by means of prophylactic methods such as ultra-violet light and seawater filtration).
Here, we tested whether the sanitary status of oyster seed is influenced by its rearing history, and explored how this could be taken into account for building disease management scenarios.
The next question we addressed was to assess the effect of timing and duration of exposure to field conditions that would result in infection and mortality in a safe environment. This parameter was evaluated in winter, spring and summer as it could potentially reflect the seasonality of virus−host interactions.
It is likely that during the winter when seawater temperature is far below 16°C, the risk of OsHV-1 µVar transmission to healthy oysters is low, so that oysters could be transferred from one location to another with an acceptable risk of disease transmission. This parameter might be useful for managing the movements of livestock among shellfish culture sites, which is a common practice in France in order to optimize growth.
Thirdly, we tested the effect of age and/or size on disease susceptibility in oysters. Although several studies have reported that disease-induced mortality is lower in adults compared to other age groups, this generally reflects a mechanism whereby oysters that have survived a mortality event are naturally selected for resistance to that disease. However, it has generally not been possible to disentangle the relative importance of age and prior OsHV-1 exposure.
The effect of age and/or size on disease mortality in oysters was recently investigated by exposing healthy oysters at ages varying from 3 to 20 mo to field conditions between July 2009 and September 2011 in the Marennes-Oléron Bay (France), where mortalities were occurring seasonally (Dégremont 2013). In that study, both age and/or size of oysters were negatively correlated with final cumulative mortality.
In contrast, in Thau lagoon (another oyster production area in France), oysters remained highly susceptible to pathogen-related mortality pressure during their first 2 yr (Pernet et al. 2012). The novelty of our work is that oysters of different ages were exposed to the same mortality event, contrary to previous studies where the timing of exposure and age and/or size of oysters were confounded.
Finally, the last question we addressed was to study the effect of water renewal and biomass of infected animals on disease mortality of oysters. Transmission of OsHV-1 within an oyster population occurs when susceptible hosts encounter infectious particles in the environment that have been shed by neighbouring infected individuals.
We hypothesized that disease-induced mortality risk would increase with the biomass of neighbouring infected oysters and decrease with water renewal, reflecting concentration and dilution effects of viral particles in seawater, respectively.
Results of these experiments suggest that wild oyster seed is more likely to carry OsHV-1 than nursery batches, and that OsHV-1 becomes a problem when seawater temperature reaches ~15.3°C during spring warming. Further, we observed that odds of disease mortality decreased with water renewal and increased with the biomass of neighbouring infected oysters under controlled conditions.
Based on these findings, we propose mitigation strategies in terms of the regulation of oyster movements between sites, timing of seeding and spatial planning, taking into account seawater temperature and seed origin.
You can view the full report and author list by clicking here.