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Outbreak of ‘POMS’ in Tasmanian hatchery offers new insight into ostreid herpesvirus


May 25, 2016
By Bob Milne

Early this year, Tasmanian Pacific oysters (Crassostrea gigas) tested positive for the first time for the presence of an ostreid herpesvirus (OsHV) micro variant. Within two weeks the disease, commonly referred to as Pacific Oyster Mortality Syndrome (POMS), had struck oysters in six marine growing regions. Some growers reported 100% mortalities of their stock within days of seeing the first symptoms of the disease. As a result, Biosecurity Tasmania called for a stop to inter-state transfer of all oysters for on-growing, yet still allowed sales for human consumption as there is no risk to humans.

South Australia’s $40 million Pacific oyster industry relies almost entirely on spat and larvae from Tasmanian hatcheries, and although POMS has not directly affected Australian hatchery production at this time, the ban on inter-state shipping of seed oysters has South Australia’s farmers scrambling to find seed for planting this fall. Hatcheries in SA are ramping up production to meet the demand.

ABC News Australia reported that POMS had been detected at the Shellfish Culture Hatchery in Pipeclay Lagoon, Tasmania. It is unclear from reports available whether disease was observed or if abnormal numbers of mortalities were experienced within the confines of the hatchery. Other reports suggest the positive test results were from the nursery area some distance away.

At one time POMS (a name coined in Australia) was referred to as ”summer mortality” and not known to cause significant losses to the industry. This well known yet little understood minor disease of pacific oysters has been well documented in the scientific literature since the 1960s and possibly earlier before significant losses had occurred.

The year 2008 brought a new paradigm to global oyster culture when France experienced devastating mortalities in their pacific oyster industry. The cause was later discovered to be OsHV-1 over, differing from the reference OsHV-1 in some molecular markers. This newly discovered variant of the ostreid herpesvirus was not only associated with the significant events in France but also with every extreme mortality event since then, including those in New Zealand and New South Wales in 2010, and now for the first time in Tasmania, at the peak of the southern summer.

The Tasmanians are placing great hope in breeding a resistant strain of oyster with some saying a viable product could be as little as one year away, but more likely two. Trials are well underway. Other researchers are convinced the disease is related to aquaculture- and biosecurity practices throughout the culture process. Recent Australian studies have found little difference in resistance to the disease, or mortality, between regular diploid- and induced triploid animals.

 “Summer Mortality,” a term hitherto used to describe Vibrio splendidus outbreaks, is believed to result from a complex interaction between oysters, their environment and pathogens. Others describe it as resulting from a combination of high temperatures, insufficient food, reproduction, and stress. The life cycle and epidemiology of the virus is only now beginning to be understood.

European field studies have shown that other Vibrio species, including, V. aestuarianus and V. harveyi, in association with OsHV-, are correlated with increased mortality. Government scientists in NSW, Australia were able to significantly limit the lethal effects of POMS on farmed Pacific oysters in an estuary by raising the intertidal trays by 30 cm.

A 1995 study in France led by ostreid herpesvirus specialist Tristan Renault found that larval oysters exposed to OsHV-1 virus in a laboratory setting at 20-22°C experienced no abnormal mortalities, while those held at 25-26°C had 100% mortality within nine days of infection. Interestingly, both groups tested positive under PCR to presence of the OsHV-1 virus. This study (and others) supports the idea that the virus is commonly latent in healthy populations and outbreaks are triggered by increased temperature and other factors.

Further insight can be drawn from the lack of mortality events in Japan where native Pacific oysters have been cultured for centuries, and have likely co-evolved with the ostreid herpesvirus variants. Genetic variance in native Japanese Pacific oysters measures slightly higher than in their transplanted, and genetically isolated cousins, feral or cultivated elsewhere in the world.

The first recorded events of abnormal mortalities experienced in larval C. gigas at a shellfish hatchery in France were documented in 1991, and another at a New Zealand hatchery in1992. It was assumed 24 years ago that the virus was vertically transferred from parent oysters through gametogenesis, and there is no solid evidence to support any other mechanism of virus transfer in a hatchery setting.

It is unclear from reports available whether disease was observed or if abnormally high mortalities were experienced within the confines of the shellfish hatchery in Tasmania earlier this year. Nonetheless it is a fact that seed sold to Tasmanian farmers over the last year comprises part of the recent mortalities. It is also likely that the juvenile and yearling oysters that have succumbed to this disease harboured OsHV-1 uvar, possibly below detectable limits, as is likely the case wherever oysters are grown.

Whether the ostreid herpesvirus micro-variant arrived recently in Tasmania as suggested by the media, or has always been present in the environment, or travels naturally along with the pacific oyster, is still not known.

Bob Milne


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