Disease prevention strategies for QX disease (Marteilia sydneyi) of Sydney rock oysters (Saccostrea glomerata)

The Sydney rock oyster (Saccostrea glomerata) forms the basis of an important aquaculture industry on the east coast of Australia. During the 1970s, production of S. glomerata began to decline, in part as a result of mortalities arising from Queensland unknown (QX) disease. Histological studies implicated the paramyxean parasite Marteilia sydneyi in the disease outbreaks. Disease zoning was implemented to prevent the spread of M. sydneyi-infected oysters. This control measure hindered rock oyster farming, which historically has relied on transferring wild-caught spat between estuaries for on-growing to market size and has not prevented the subsequent occurrence of QX disease in the Georges and Hawkesbury rivers in central New South Wales. Management of QX disease has been hampered by the complicated life cycle of M. sydneyi, with outbreaks of QX disease likely to be regulated by a combination of the abundance of intermediate host of M. sydneyi, environmental stressors, and the immunocompetence of S. glomerata. The future of the Sydney rock oyster industry relies on understanding these factors and progressing the industry from relying on farming wild-caught seed to the successful commercialization of hatchery-produced QX-resistant S. glomerata

Iron and copper limitations differently affect growth rates and photosynthetic and physiological parameters of the marine diatom Pseudo-nitzschia delicatissima

In similar to 50% of the ocean, iron (Fe) limits phytoplankton growth, including that of the diatom Pseudo-nitzschia. Fe-limited Pseudo-nitzschia spp. may produce the potent neurotoxin domoic acid (DA) to access Cu, needed at the core of a high-affinity Fe transport system. To test this hypothesis, we investigated the growth, physiology, and DA production of P. delicatissima under Fe limitations, Cu starvation, and Fe and Cu co-limitations. Compared with the control, Fe limitation decreased chlorophyll content by up to 86% and quantum yield (QY) by 3.6-fold. Severe Fe limitation decreased esterase activity by 60% and maintained lipid content, while mild Fe limitation increased both esterase activity and lipid content by 23% and 100%, respectively. Cu starvation increased chlorophyll content, lipid content, and esterase activity by 76%, 303%, and 47%, respectively, with QY being identical to replete cells. Co-limitations induced modifications close to, but significantly different from, Fe limitations. P. delicatissima produced no DA during these experiments. In this species, the Cu demand for Fe acquisition may be low relative to other cellular Cu pools or this species may not use Cu to uptake Fe

Effects of marine harmful algal blooms on bivalve cellular immunity and infectious diseases: A review

Bivalves were long thought to be “symptomless carriers” of marine microalgal toxins to human seafood consumers. In the past three decades, science has come to recognize that harmful algae and their toxins can be harmful to grazers, including bivalves. Indeed, studies have shown conclusively that some microalgal toxins function as active grazing deterrents. When responding to marine Harmful Algal Bloom (HAB) events, bivalves can reject toxic cells to minimize toxin and bioactive extracellular compound (BEC) exposure, or ingest and digest cells, incorporating nutritional components and toxins. Several studies have reported modulation of bivalve hemocyte variables in response to HAB exposure. Hemocytes are specialized cells involved in many functions in bivalves, particularly in immunological defense mechanisms. Hemocytes protect tissues by engulfing or encapsulating living pathogens and repair tissue damage caused by injury, poisoning, and infections through inflammatory processes. The effects of HAB exposure observed on bivalve cellular immune variables have raised the question of possible effects on susceptibility to infectious disease. As science has described a previously unrecognized diversity in microalgal bioactive substances, and also found a growing list of infectious diseases in bivalves, episodic reports of interactions between harmful algae and disease in bivalves have been published. Only recently, studies directed to understand the metabolic basis of these interactions have been undertaken. This review compiles evidence from studies of harmful algal effects upon bivalve shellfish that establishes a framework for recent efforts to understand how harmful algae can alter infectious disease, and particularly the fundamental role of cellular immunity, in modulating these interactions. Experimental studies reviewed here indicate that HABs can modulate bivalve-pathogen interactions in various ways, either by increasing bivalve susceptibility to disease or conversely by lessening infection proliferation or transmission. Alteration of immune defense and global physiological distress caused by HAB exposure have been the most frequent reasons identified for these effects on disease. Only few studies, however, have addressed these effects so far and a general pattern cannot be established. Other mechanisms are likely involved but are under-studied thus far and will need more attention in the future. In particular, the inhibition of bivalve filtration by HABs and direct interaction between HABs and infectious agents in the seawater likely interfere with pathogen transmission. The study of these interactions in the field and at the population level also are needed to establish the ecological and economical significance of the effects of HABs upon bivalve diseases. A more thorough understanding of these interactions will assist in development of more effective management of bivalve shellfisheries and aquaculture in oceans subjected to increasing HAB and disease pressures

Effects of field and laboratory exposure to the toxic dinoflagellate Karenia brevis on the reproduction of the eastern oyster, Crassostrea virginica, and subsequent development of offspring

00000International audienceBlooms of the brevetoxin-producing dinoflagellate, Karenia brevis, are a recurrent and sometimes devastating phenomenon in the Gulf of Mexico. The eastern oyster, Crassostrea virginica, is exposed regularly to these blooms, yet little is known about the impacts of K. brevis upon this important species. The present study considered the effects of exposure to both a natural bloom and cultured K. brevis on the reproductive development of C. virginica. Oysters had been exposed to a bloom of K. brevis that occurred in Lee County, Florida, from September 2012 through May 2013, during a period of gametogenesis and gamete ripening. Ripe adult oysters were collected from this bloom-exposed site and from a site 200 miles north which was not exposed to any bloom. In addition, responses to two 10-day laboratory exposures of either unripe or ripe adult oysters to whole cells of K. brevis at high bloom concentrations (1000 and 5000 cells mL−1) were determined. Both field- and laboratory-exposed adult oysters accumulated PbTx (attaining ∼22 × 103 ng g−1 and 922 ng g−1 PbTx-3 equivalents in the laboratory and the field, respectively), and significant mucal, edematous, and inflammatory features, indicative of a defense response, were recorded in adult tissues in direct contact with K. brevis cells. Laboratory-exposed oysters also showed an increase in the total number of circulating hemocytes suggesting that: (1) new hemocytes may be moving to sites of tissue inflammation, or, (2) hemocytes are released into the circulatory system from inflamed tissues where they may be produced. The area of oyster tissue occupied by gonad (representative of reproductive effort) and reactive oxygen species production in the spermatozoa of oysters exposed to the natural bloom of K. brevis were significantly lower compared to oysters that were not exposed to K. brevis. Additionally, following 10-day exposure of ripe oysters, a significant, 46% reduction in the prevalence of individuals with ripe gametes was obtained in the 5000 cells mL−1 K. brevis treatment.ăăBrevetoxin (PbTx) was recorded within the spermatozoa and oocytes of naturally exposed oysters and was estimated to be 18 and 26% of the adult PbTx load, respectively. Larvae derived from gametes containing PbTx showed significantly higher mortalities and attained a smaller larval size for the first 6 days post-fertilization. These negative effects on larval development may be due to the presence of PbTx in the lipid droplets of the oocytes, which is mobilized by the larvae during embryonic and lecithotrophic larval development. Provision of a non-contaminated food source to larvae however, appeared to mitigate the early negative effects of this neonatal PbTx exposure.ăăResults herein show that adult eastern oysters and their offspring are susceptible to exposure to K. brevis. Caution should therefore be exercised when identifying oyster reef restoration areas and in efforts to establish aquaculture in areas prone to red tides

Fish-Killing Marine Algal Blooms: Causative Organisms, Ichthyotoxic Mechanisms, Impacts and Mitigation.

Fish-killing microalgal blooms are responsible for much greater global socio-economic impacts than the well-studied HAB species causing seafood biotoxin contamination. Examples are the 1972 Chattonella marina bloom in the Seto Inland Sea, Japan (estimated USD 71M loss to yellowtail aquaculture), the 1988 Prymnesium polylepis bloom in the European Kattegat with broad marine ecosystem impacts, and the 2015/16 Pseudochattonella verruculosa bloom in Chile (USD 800M loss to salmon aquaculture).Highly potent fish-killers include the globally distributed, taxonomically unrelated dinoflagellate genera Alexandrium, Karenia, Karlodinium and Margalefidinium, raphidophytes Chattonella and Heterosigma, dictyochophytes Pseudochattonella and Vicicitus, and haptophytes Chrysochromulina and Prymnesium. All these species have in common their propensity to produce lytic compounds that irreparably damage the sensitive gill tissues of fish which ultimately die from suffocation. Except for recent advances with Karlodinium (karlotoxins), Prymnesium (prymnesins), and Karenia brevisulcata (brevisulcenals), the precise mechanisms of how such microalgae kill finfish remain poorly understood. Reactive Oxygen Species can be a co-factor in ichthyotoxicity, notably with raphidophytes such as Chattonella. While some species are always ichthyotoxic, others such as Heterosigma, Pseudochattonella and Alexandrium catenella kill fish only under certain conditions or life stages. Broad scale ecosystem impacts from fish killing algae are less common with raphidophytes and dictyochophytes that require intimate cellular contact for harmful effects, compared to Karenia and Prymnesium where intracellular or excreted toxins are responsible.Critical hurdles that limit progress in our understanding of ichthyotoxins and their control and mitigation include: HABs at fish farms are not usually a research priority until a major bloom occurs; data sharing between industry and scientists is very limited; and there is a lack of standardized methods to detect ichthyotoxins in low concentrations dissolved in seawater. Currently, the RT fish-gill W1 (rainbow trout epithelial gill cell line) and Chaetoceros Quantum Yield bioassays are the most promising candidates for international standardization and intercalibration for some HABs.The abundance of HABs that will adversely impact or kill fish is of considerable interest to fish farmers, open-water fishers, and natural resource management authorities. However, this varies with HAB strains and species, type and age of fish, but also local conditions of water temperature, salinity, turbulence and tidal flushing. Climate change also contributes to the unpredictability of fast fish killing blooms. Prevention, prediction and monitoring are no longer sufficient, but we actively need to pursue broad-scale tools to stop the blooms, for example by means of clay flocculation of algal biomass and/or targeted mopping up of ichthyotoxins.We review existing knowledge and provide a roadmap for scientists, aquaculturists and insurance companies to improve management of fish-killing algal blooms that put pressure on seafood security for an ever-increasing human population

FISH-KILLING MARINE ALGAL BLOOMS: Causative Organisms, Ichthyotoxic Mechanisms, Impacts and Mitigation: GlobalHAB (2023)

5Fish-Killing Marine Algal Blooms - Executive SummaryFish-killing microalgal blooms are responsible for much greater global socio-economic impactsthan the well-studied HAB species causing seafood biotoxin contamination. Examples are the 1972Chattonella marina bloom in the Seto Inland Sea, Japan (estimated USD 71M loss to yellowtailaquaculture), the 1988 Prymnesium polylepis bloom in the European Kattegat with broad marineecosystem impacts, and the 2015/16 Pseudochattonella verruculosa bloom in Chile (USD 800M loss tosalmon aquaculture).Highly potent fish-killers include the globally distributed, taxonomically unrelated dinoflagellategenera Alexandrium, Karenia, Karlodinium and Margalefidinium, raphidophytes Chattonella andHeterosigma, dictyochophytes Pseudochattonella and Vicicitus, and haptophytes Chrysochromulinaand Prymnesium. All these species have in common their propensity to produce lytic compounds thatirreparably damage the sensitive gill tissues of fish which ultimately die from suffocation. Except forrecent advances with Karlodinium (karlotoxins), Prymnesium (prymnesins), and Karenia brevisulcata(brevisulcenals), the precise mechanisms of how such microalgae kill finfish remain poorly under-stood. Reactive Oxygen Species can be a co-factor in ichthyotoxicity, notably with raphidophytes suchas Chattonella. While some species are always ichthyotoxic, others such as Heterosigma, Pseudochat-tonella and Alexandrium catenella kill fish only under certain conditions or life stages. Broad scaleecosystem impacts from fish killing algae are less common with raphidophytes and dictyochophytesthat require intimate cellular contact for harmful effects, compared to Karenia and Prymnesium whereintracellular or excreted toxins are responsible.Critical hurdles that limit progress in our understanding of ichthyotoxins and their control and miti-gation include: HABs at fish farms are not usually a research priority until a major bloom occurs; datasharing between industry and scientists is very limited; and there is a lack of standardized methods todetect ichthyotoxins in low concentrations dissolved in seawater. Currently, the RT fish-gill W1 (rain-bow trout epithelial gill cell line) and Chaetoceros Quantum Yield bioassays are the most promisingcandidates for international standardization and intercalibration for some HABs.The abundance of HABs that will adversely impact or kill fish is of considerable interest to fish farm-ers, open-water fishers, and natural resource management authorities. However, this varies withHAB strains and species, type and age of fish, but also local conditions of water temperature, salinity,turbulence and tidal flushing. Climate change also contributes to the unpredictability of fast fish killingblooms. Prevention, prediction and monitoring are no longer sufficient, but we actively need to pursuebroad-scale tools to stop the blooms, for example by means of clay flocculation of algal biomass and/or targeted mopping up of ichthyotoxins.We review existing knowledge and provide a roadmap for scientists, aquaculturists and insurancecompanies to improve management of fish-killing algal blooms that put pressure on seafood securityfor an ever-increasing human population