BackgroundCoral bleaching (i.e., the release of coral symbiotic zooxanthellae) has negative impacts on biodiversity and functioning of reef ecosystems and their production of goods and services. This increasing world-wide phenomenon is associated with temperature anomalies, high irradiance, pollution, and bacterial diseases. Recently, it has been demonstrated that personal care products, including sunscreens, have an impact on aquatic organisms similar to that of other contaminants.ObjectivesOur goal was to evaluate the potential impact of sunscreen ingredients on hard corals and their symbiotic algae.MethodsIn situ and laboratory experiments were conducted in several tropical regions (the Atlantic, Indian, and Pacific Oceans, and the Red Sea) by supplementing coral branches with aliquots of sunscreens and common ultraviolet filters contained in sunscreen formula. Zooxanthellae were checked for viral infection by epifluorescence and transmission electron microscopy analyses.ResultsSunscreens cause the rapid and complete bleaching of hard corals, even at extremely low concentrations. The effect of sunscreens is due to organic ultraviolet filters, which are able to induce the lytic viral cycle in symbiotic zooxanthellae with latent infections.ConclusionsWe conclude that sunscreens, by promoting viral infection, potentially play an important role in coral bleaching in areas prone to high levels of recreational use by humans.

Although the relationships between trophic conditions and viral dynamics have been widely explored in different pelagic environments, there have been few attempts at independent estimates of both viral production and decay. In this study, we investigated factors controlling the balance between viral production and decay along a trophic gradient in the north Adriatic basin, providing independent estimates of these variables and determining the relative importance of nanoflagellate grazing and viral life strategies. Increasing trophic conditions induced an increase of bacterioplankton growth rates and of the burst sizes. As a result, eutrophic waters displayed highest rates of viral production, which considerably exceeded observed rates of viral decay (up to 2.9 ؋ 10 9 VLP liter ؊1 h ؊1 ). Viral decay was also higher in eutrophic waters, where it accounted for ca. 40% of viral production, and dropped significantly to 1.3 to 10.7% in oligotrophic waters. These results suggest that viral production and decay rates may not necessarily be balanced in the short term, resulting in a net increase of viruses in the system. In eutrophic waters nanoflagellate grazing, dissolved-colloidal substances, and lysogenic infection were responsible together for the removal of ca. 66% of viral production versus 17% in oligotrophic waters. Our results suggest that different causative agents are primarily responsible for the removal of viruses from the water column in different trophic conditions. Factors other than those considered in the past might shed light on processes responsible for the removal and/or decay of viral particles from the water column.Viruses have been recognized as responsible for a relevant fraction of bacterial mortality (see references 5, 36, and 41 and references therein). Viral lysis, by causing the release of new viruses and host cell contents, can lead to a significant increase of dissolved organic carbon (DOC) in the environment, which in turn can affect bacterial community structure (30) and have a large impact on bacterial carbon cycling (17, 24).Virus-induced bacterial mortality has been shown to be strongly dependent on local trophic conditions (20,33,34). Several authors have found that eutrophic environments support a higher standing stock of bacteria and consequently of bacteriophages than oligotrophic systems. Trophic conditions can influence the production of new viral particles by changing the metabolism and size of the host cells (3, 9, 23).Since the maintenance of viral assemblages and the hostvirus relationships are controlled by the decay and replenishment (production) of viral particles, estimates of viral turnover times are crucial to evaluate the potential of viruses to change in space and time (20). In order to test the steady-state assumption, often utilized as a basic assumption in viral ecology studies (4), a correct balance of viral production versus viral decay rates has to be evaluated. A correct analysis of viral dynamics should require an independent measurement of both viral produ...

We investigated bacterial assemblages associated with corals displaying symptoms of the 'White Syndrome' (WS), a general term used for indicating the appearance of bands, spots or patches of tissue loss, which is devastating wide areas of tropical ecosystems worldwide. We collected WS-diseased (n = 15) and healthy (n = 15) corals from the natural reef (Indonesia, Indian Ocean) and from four large public aquaria. By using culture-dependent and culture-independent techniques, we found that a large fraction (73%) of the investigated WS events was associated with the presence of a high bacterial abundance and, specifically, of Vibrio spp. Vibrio harveyi, a pathogen of many marine organisms and recently involved in coral Yellow Band disease, was the most represented species, being recovered from five out of 15 diseased corals. In experimental infection assays, two V. harveyi strains, isolated from diseased corals, were inoculated on a total of 62 healthy colonies of Pocillopora damicornis. WS signs appeared in 57 corals, confirming the ability of V. harveyi strains to induce the disease. We conclude that V. harveyi is one of the coral pathogens involved in the appearance of WS. However, not all of the investigated WSs were associated to V. harveyi detection, nor to other Vibrio species (such as V. coralliilyticus), which supports the hypothesis that WS is not caused exclusively by Vibrio spp., but rather can have a multifactorial aetiology, or can represent a group of diseases caused by a variety of agents. Further investigations to identify specific virulence traits will contribute to the understanding of the role of V. harveyi in WS pathogenesis.

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Deep-water coral ecosystems are hot spots of biodiversity and provide habitats and refuges for several deep-sea species. However, their role in shaping the biodiversity of the surrounding open slopes is still poorly known. We investigated how meiofaunal biodiversity varies with and is related to the occurrence of deep-water living scleractinian corals and coral rubble in two deep-sea areas (the Rockall Bank, north-eastern Atlantic) and the Santa Maria di Leuca (central Mediterranean). In both areas, replicated sampling on alive and dead coral areas and from the adjacent slope sediments without corals (at the same and increasing depths) allowed us to demonstrate that sediments surrounding the living corals and coral rubble were characterised by higher meiofaunal biodiversity (as number of higher taxa, and nematode species richness) than the slope sediments. Despite the soft sediments surrounding the living coral having a higher nutritional value than those not associated with corals, with the opposite seen for coral rubble, the presence of both alive and dead corals had a significant effect on nematode assemblages. Our data suggest that, due particularly to the effects on habitat heterogeneity/complexity, both living coral and coral rubble promoted higher biodiversity levels than in surrounding slope sediments. We conclude that the protection of deep-water corals can be crucial to preserve the biodiversity of surrounding open slopes, and that the protection of dead corals, a so-far almost neglected habitat in terms of biological conservation, can further contribute to the maintenance of a high deep-sea biodiversity along continental margin