Monitoring of toxic cyanobacterial blooms in Lalla Takerkoust reservoir by satellite imagery and microcystin transfer to surrounding farms.

Cyanobacterial harmful algal blooms (CyanoHABs) threaten public health and freshwater ecosystems worldwide. In this study, our main goal was to explore the dynamics of cyanobacterial blooms and how microcystins (MCs) move from the Lalla Takerkoust reservoir to the nearby farms. We used Landsat imagery, molecular analysis, collecting and analyzing physicochemical data, and assessing toxins using HPLC. Our investigation identified two cyanobacterial species responsible for the blooms: Microcystis sp. and Synechococcus sp. Our Microcystis strain produced three MC variants (MC-RR, MC-YR, and MC-LR), with MC-RR exhibiting the highest concentrations in dissolved and intracellular toxins. In contrast, our Synechococcus strain did not produce any detectable toxins. To validate our Normalized Difference Vegetation Index (NDVI) results, we utilized limnological data, including algal cell counts, and quantified MCs in freeze-dried Microcystis bloom samples collected from the reservoir. Our study revealed patterns and trends in cyanobacterial proliferation in the reservoir over 30 years and presented a historical map of the area of cyanobacterial infestation using the NDVI method. The study found that MC-LR accumulates near the water surface due to the buoyancy of Microcystis. The maximum concentration of MC-LR in the reservoir water was 160 µg L-1. In contrast, 4 km downstream of the reservoir, the concentration decreased by a factor of 5.39 to 29.63 µgL-1, indicating a decrease in MC-LR concentration with increasing distance from the bloom source. Similarly, the MC-YR concentration decreased by a factor of 2.98 for the same distance. Interestingly, the MC distribution varied with depth, with MC-LR dominating at the water surface and MC-YR at the reservoir outlet at a water depth of 10 m. Our findings highlight the impact of nutrient concentrations, environmental factors, and transfer processes on bloom dynamics and MC distribution. We emphasize the need for effective management strategies to minimize toxin transfer and ensure public health and safety.

A new look at the potential role of marine plastic debris as a global vector of toxic benthic algae.

Marine plastic debris provides a significant surface area for potential colonization by planktonic and benthic harmful microalgae and for the adsorption of their toxins. Furthermore, floating plastics may substantially expand the substrate area available for benthic algae in the ocean, intensifying the transfer of potent toxins through pelagic food webs. In this study, we quantify the available surface area of micro- and macroplastics in different oceanic regions and assess the potential role of floating plastics as vectors for the transfer of toxins from three widespread benthic dinoflagellates, Gambierdiscus spp., Ostreopsis cf. ovata and Prorocentrum lima. To avoid bias associated to the occurrence of benthic algae in deep waters, we selected only records from 0 to 100 m depths. We estimate that 26.8 × 1010 cm2 of plastic surface area is potentially available in surface waters of the global ocean, mostly in the size range of large microplastics (1.01-4.75 mm). Based on the distribution of floating plastics and the habitat suitability of the selected microalgal species, the plastic relative colonization risks will be greater in the Mediterranean Sea and in the subtropical and temperate western margins of the oceans, such as the North American and Asian eastern coasts and, to a lesser extent, southern Brazil and Australia. In places where the colonization of O. cf. ovata cells on floating plastic debris has been properly quantified, such as the Mediterranean and southern Brazil, we estimate a colonization potential of up to 2 × 106 cells km-2 of ocean surface during the regular occurrence period and up to 1.7 × 108 cells km-2 during massive blooms of this species. As plastic pollution and harmful benthic algal blooms have both increased substantially over the past decades, we suggest that their interactive effects can become a major and novel threat to marine ecosystems and human health.

Ostreopsis cf. ovata Bloom in Currais, Brazil: Phylogeny, Toxin Profile and Contamination of Mussels and Marine Plastic Litter.

Ostreopsis cf. ovata is a toxic marine benthic dinoflagellate responsible for harmful blooms affecting ecosystem and human health, mostly in the Mediterranean Sea. In this study we report the occurrence of a summer O. cf. ovata bloom in Currais, a coastal archipelago located on the subtropical Brazilian coast (~25° S). This bloom was very similar to Mediterranean episodes in many aspects: (a) field-sampled and cultivated O. cf. ovata cells aligned phylogenetically (ITS and LSU regions) along with Mediterranean strains; (b) the bloom occurred at increasing temperature and irradiance, and decreasing wind speed; (c) cell densities reached up to 8.0 × 104 cell cm-2 on fiberglass screen and 5.6 × 105 cell g-1 fresh weight on seaweeds; (d) and toxin profiles were composed mostly of ovatoxin-a (58%) and ovatoxin-b (32%), up to 35.5 pg PLTX-eq. cell-1 in total. Mussels were contaminated during the bloom with unsafe toxin levels (up to 131 µg PLTX-eq. kg-1). Ostreopsis cells attached to different plastic litter, indicating an alternate route for toxin transfer to marine fauna via ingestion of biofilm-coated plastic debris.

Cell-to-cell propagation of the bacterial toxin CNF1 via extracellular vesicles: potential impact on the therapeutic use of the toxin.

Eukaryotic cells secrete extracellular vesicles (EVs), either constitutively or in a regulated manner, which represent an important mode of intercellular communication. EVs serve as vehicles for transfer between cells of membrane and cytosolic proteins, lipids and RNA. Furthermore, certain bacterial protein toxins, or possibly their derived messages, can be transferred cell to cell via EVs. We have herein demonstrated that eukaryotic EVs represent an additional route of cell-to-cell propagation for the Escherichia coli protein toxin cytotoxic necrotizing factor 1 (CNF1). Our results prove that EVs from CNF1 pre-infected epithelial cells can induce cytoskeleton changes, Rac1 and NF-κB activation comparable to that triggered by CNF1. The observation that the toxin is detectable inside EVs derived from CNF1-intoxicated cells strongly supports the hypothesis that extracellular vesicles can offer to the toxin a novel route to travel from cell to cell. Since anthrax and tetanus toxins have also been reported to engage in the same process, we can hypothesize that EVs represent a common mechanism exploited by bacterial toxins to enhance their pathogenicity.