From January to June 2013 and November to January 2014, mass mortalities were reported in Pacific oysters Crassostrea gigas cultivated in Port Stephens estuary, New South Wales, Australia. In some cases, 100% mortality was reported in both triploid and diploid C. gigas, although native species of oyster cultivated in the same areas remained unaffected. Histological examination of oysters sampled from the time of mortality events revealed consistent but non-specific pathology, involving a diffuse haemocytic infiltrate in the connective tissue surrounding the digestive gland, extending into the mantle in some instances, but no other signs of any infectious aetiological agent. We conducted a structured survey in early January 2014 to compare samples of C. gigas from affected and unaffected areas by bacteriology and histopathology. Quantitative PCR excluded involvement of ostreid herpesvirus-1 (OsHV-1) in these mortality events. To determine whether a directly transmissible aetiological agent was responsible for the mortalities, naïve C. gigas sourced from an estuary where no evidence of mortality was reported were challenged with material derived from affected oysters. Significant mortality was only observed in naïve C. gigas directly inoculated with purified cultures of Vibrio spp. isolated from affected oysters, but this could not be replicated by cohabitation with naïve C. gigas. Analysis of environmental data indicated that mortality events generally coincided with periods of low salinity and high temperature. The results from this study suggest that the cause of the mortality events was multifactorial in nature and not due to any single directly transmissible aetiological agent.
We report on a dense bloom (~1.80 × 105 cells mL−1) of the marine dinoflagellate species Amphidinium carterae (Genotype 2) in a shallow, small intermittently open coastal lagoon in south eastern Australia. This bloom co-occurred with the deaths of >300 individuals of three different species of fish. The opening of the lagoon to the ocean, as well as localized high nutrient levels, preceded the observations of very high cell numbers. A. carterae is usually benthic and sediment-dwelling, but temporarily became abundant throughout the water column in this shallow (<2 m) sandy habitat. Histopathological results showed that the Anguilla reinhardtii individuals examined had damage to epithelial and gill epithelial cells. An analysis of the bloom water indicated the presence of a compound with a retention time and UV spectra similar to Luteophanol A, a compound known from a strain of Amphidinium. Assays with a fish gill cell line were conducted using a purified compound from cells concentrated from the bloom, and was found to cause a loss of 87% in cell viability in 6 h. The fish deaths were likely due to the low dissolved oxygen levels in the water and/or the presence of Luteophanol A-like compounds released during the bloom.
Phone 61 08 9360 24792 ABSTRACT A Minchinia sp. (Haplosporidia: Haplosporidiidae) parasite was identified infecting rock oysters and morphologically described by Hine and Thorne (2002) using light microscopy and transmission electron microscopy (TEM).The parasite was associated with up to 80% mortality in the host species and it is suspected the parasite would be a major impediment to the development of a tropical rock oyster aquaculture industry in northern Western Australia.However, attempts to identify the parasite following the development of a specific probe for Haplosporidium nelsoni were unsuccessful. The SSU region of the parasite's rRNA gene was later characterised in our laboratory and an in situ hybridisation assay for the parasite was developed. This paper names the parasite as Minchinia occulta n sp. and morphologically describes the parasite using histology, scanning electron microscopy and transmission electron microscopy. The non-spore stages were unusual in that they consisted primarily of intracellular, uninucleate stages reminiscent of Bonamia spp. The parasite's spores were ovoid to circular shaped and measured 4.5 μm -5.0 μm x 3.5 -4.1 μm in size. The nucleus of the sporoplasm measured 1.5 -2.3 μm and was centrally located. The spores were covered in a branching network of microtubule-like structures that may degrade as the spore matures.
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