Molecular investigations into Winter mortality disease of Saccostrea glomerata (Sydney rock oyster)

A project undertaken at the Elizabeth Macarthur Agricultural Institute (Industry and Investment NSW) under the supervision of Dr Cheryl Jenkins

Sydney rock oysters (Saccostrea glomerata) are native to Australian estuaries and also represent an important commercial species. In recent years, microbial diseases of S.glomerata have become more signficant, in some cases causing mass mortality events of both wild and farmed oysters.

Winter mortality (WM) is a poorly studied disease affecting Sydney rock oysters in the colder waters of NSW’s southern estuaries, causing significant losses each year. WM is more severe in oysters located deeper in the water column and appears linked to higher salinities, however significant gaps exist in our understanding of the causes of disease. Current dogma is that WM is caused by the protozoal parasite, Bonamia roughleyi, however evidence linking clinical signs and histopathology of oyster tissues to molecular data is lacking. Indeed, recent molecular data suggested that a different protozoal organism, similar to Haplosporidium costale, a parasite of the Northern hemisphere oyster species (Crassostrea virginica), may be more prevalent in oysters during the WM season. In this study, we conducted a longitudinal study over the winter season, in which clinical disease signs and histopathology were linked to the presence of Bonamia and Haplosporidium and environmental factors.

One of the major findings of this study was that “winter mortality” does not have a single cause, but is a multifactorial phenomenon that may differ in aetiology between, and perhaps within, estuaries. Oysters sampled from the Georges River where winter mortality was first described in 1926, showed pathologic signs of an infectious process during the winter months, which may well have contributed to oyster mortality. The infectious process involved hyperplasia (thickening), ulceration and haemocyte (blood cell) infiltration of the gut and palp epithelium (Fig 1 & 2). Structures resembling microcell parasites were observed in association with these lesions (Fig 3), but molecular testing failed to identify these structures as either Bonamia or Haplosporidium. Indeed, we could find no credible evidence that Bonamia roughleyi causes winter mortality, given the extremely low prevalence of Bonamia sp. with only 8 oysters PCR positive out of 780 tested over the course of the study. In contrast, during the winter months, nearly 90% of Georges River oysters displayed histopathology consistent with an infection. Further work is needed to identify the infectious agent, but it does not appear to be a haplosporidian parasite.

Oysters sampled from the Shoalhaven River did not display pathology that could be linked to a specific disease process and instead appeared to die due to a confluence of environmental factors. Starvation effects due to a reduction in phytoplankton levels during the winter may be a contributing factor to winter kill.

The outcomes of this study suggest that the term “winter mortality” should be redefined. Bonamia roughleyi is on Australia’s National List of Reportable Diseases of Aquatic Animals, therefore the implication that this organism causes winter mortality has a direct impact on oyster growers. Perhaps “winter kill” is a preferable term for general mortalities observed during the winter months, while “winter mortality” should be reserved for the specific disease observed in the GR as initially described by Roughley in 1926.


Spiers, Z B; Gabor, M; Fell, S A; Carnegie, R B; Dove, M; O'Connor, W; Frances, J; Go, J; Marsh, I B and Jenkins, C. (2014). Longitudinal study of winter mortality disease in Sydney rock oysters Saccostrea glomerata. doi: 10.3354/dao02629


Figure 1. Hyperplasia, ulceration and haemocyte infiltration of the gut epithelium of S. glomerata sampled from the Georges River in early September, 2010.

Figure 2.. Microcell-like structures (arrowheads) observed within S. glomerata sampled from the Georges River in early September, 2010.

Figure 3. Depigmentation of areas within the digestive diverticula observed in S. glomerata during early spring. Depigmentation may result from decreased phytoplankton (food) intake.