Biodegradation of multiple microcystins and cylindrospermopsin in clarifier sludge and a drinking water source: Effects of particulate attached bacteria and phycocyanin

Maghsoudi, Ehsan; Fortin, Nathalie; Greer, Charles W.; Duy, Sung Vo; Fayad, Paul B.; Sauvé, Sébastien; Prévost, Michèle; Dorner, Sarah

doi:10.1016/j.ecoenv.2015.06.001

Cited by 24 publications

(22 citation statements)

References 31 publications

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“…The degradation in these waters was attributed to biological activity and the rates were translated to half-lives for comparison with past work. The extracellular MC-LR half-life ranged from 3.12-4.48 days in the USA bloom and 1.97-2.81 days in the CA bloom; these half-lives were similar to those observed in surface waters (1.22-7.66 days for MC-LR) [39] and lake waters (5.4 days for both MC-LR and MC-YR) [40]. A lag phase was observed, but there was not a discernible relationship between the lag phase and the oxidant applied.…”

Section: Impact Of Stagnation (Time Max = 96 or 168 H) On Microcystinsupporting

confidence: 66%

Delayed Release of Intracellular Microcystin Following Partial Oxidation of Cultured and Naturally Occurring Cyanobacteria

Greenstein

Zamyadi

Glover

et al. 2020

Toxins

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Oxidation processes can provide an effective barrier to eliminate cyanotoxins by damaging cyanobacteria cell membranes, releasing intracellular cyanotoxins, and subsequently oxidizing these toxins (now in extracellular form) based on published reaction kinetics. In this work, cyanobacteria cells from two natural blooms (from the United States and Canada) and a laboratory-cultured Microcystis aeruginosa strain were treated with chlorine, monochloramine, chlorine dioxide, ozone, and potassium permanganate. The release of microcystin was measured immediately after oxidation (t ≤ 20 min), and following oxidant residual quenching (stagnation times = 96 or 168 h). Oxidant exposures (CT) were determined resulting in complete release of intracellular microcystin following chlorine (21 mg-min/L), chloramine (72 mg-min/L), chlorine dioxide (58 mg-min/L), ozone (4.1 mg-min/L), and permanganate (391 mg-min/L). Required oxidant exposures using indigenous cells were greater than lab-cultured Microcystis. Following partial oxidation of cells (oxidant exposures ≤ CT values cited above), additional intracellular microcystin and dissolved organic carbon (DOC) were released while the samples remained stagnant in the absence of an oxidant (>96 h after quenching). The delayed release of microcystin from partially oxidized cells has implications for drinking water treatment as these cells may be retained on a filter surface or in solids and continue to slowly release cyanotoxins and other metabolites into the finished water.

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Section: Impact Of Stagnation (Time Max = 96 or 168 H) On Microcystinsupporting

confidence: 66%

Delayed Release of Intracellular Microcystin Following Partial Oxidation of Cultured and Naturally Occurring Cyanobacteria

Greenstein

Zamyadi

Glover

et al. 2020

Toxins

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“…Cyanobacterial blooms can negatively affect human and animal health [ 5 , 6 , 7 , 8 , 9 , 10 , 11 ], the health of the environment [ 3 ] including the contamination of potable water supplies [ 12 , 13 , 14 ] and complications in water treatment processes [ 12 , 15 , 16 ]. Indirectly, it can also impact the economy, since the resulting deterioration in water quality contributes to declines in fisheries productivity and hampers recreational activities as well as tourism [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Toxic Cyanobacterial Bloom Triggers in Missisquoi Bay, Lake Champlain, as Determined by Next-Generation Sequencing and Quantitative PCR

Fortin

Muñoz-Ramos

Bird

et al. 2015

Life

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Missisquoi Bay (MB) is a temperate eutrophic freshwater lake that frequently experiences toxic Microcystis-dominated cyanobacterial blooms. Non-point sources are responsible for the high concentrations of phosphorus and nitrogen in the bay. This study combined data from environmental parameters, E. coli counts, high-throughput sequencing of 16S rRNA gene amplicons, quantitative PCR (16S rRNA and mcyD genes) and toxin analyses to identify the main bloom-promoting factors. In 2009, nutrient concentrations correlated with E. coli counts, abundance of total cyanobacterial cells, Microcystis 16S rRNA and mcyD genes and intracellular microcystin. Total and dissolved phosphorus also correlated significantly with rainfall. The major cyanobacterial taxa were members of the orders Chroococcales and Nostocales. The genus Microcystis was the main mcyD-carrier and main microcystin producer. Our results suggested that increasing nutrient concentrations and total nitrogen:total phosphorus (TN:TP) ratios approaching 11:1, coupled with an increase in temperature, promoted Microcystis-dominated toxic blooms. Although the importance of nutrient ratios and absolute concentrations on cyanobacterial and Microcystis dynamics have been documented in other laboratories, an optimum TN:TP ratio for Microcystis dominance has not been previously observed in situ. This observation provides further support that nutrient ratios are an important determinant of species composition in natural phytoplankton assemblages.

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“…A similar trend was observed in the CA bloom, though at a lower magnitude. These losses were attributed to biological degradation by aerobic bacteria following cyanobacterial cell die off with increasing concentrations of copper sulfate [37][38][39][40][41][42][43]. Previous work has shown that biodegradation of extracellular toxin depends on the congeners present as well as the background water matrix.…”

Section: Impact Of 24 H Exposure To Hydrogen Peroxide and Copper Sulfmentioning

confidence: 99%

“…Previous work has shown that biodegradation of extracellular toxin depends on the congeners present as well as the background water matrix. For example, Maghsoudi et al [42] found that the presence of phycocyanin acts as a supplementary carbon source and results in enhanced biodegradation of MCs. Although this process should be evaluated further (using additional microbial characterization techniques), the range of degradation observed here is within the maximum values found in lake waters-20 µg/day [41,42].…”

Section: Impact Of 24 H Exposure To Hydrogen Peroxide and Copper Sulfmentioning

confidence: 99%

“…For example, Maghsoudi et al [42] found that the presence of phycocyanin acts as a supplementary carbon source and results in enhanced biodegradation of MCs. Although this process should be evaluated further (using additional microbial characterization techniques), the range of degradation observed here is within the maximum values found in lake waters-20 µg/day [41,42]. As expected, the two bloom waters were more resistant to hydrogen peroxide as compared against the monoculture of MA.…”

Section: Impact Of 24 H Exposure To Hydrogen Peroxide and Copper Sulfmentioning

confidence: 99%

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Impact of Hydrogen Peroxide and Copper Sulfate on the Delayed Release of Microcystin

Zamyadi

Greenstein

Glover

et al. 2020

Water

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Algicides, like hydrogen peroxide and copper sulfate, are commonly applied to recreational waters and drinking water sources to mitigate cyanobacterial blooms. In this work, the effects of hydrogen peroxide and copper sulfate were evaluated in two natural bloom samples (collected from Canadian and American waterbodies) and one lab-cultured Microcystis aeruginosa suspended in Colorado River water. Five algicide to dissolved organic carbon (DOC) dose ratios were evaluated during an initial exposure period of 24 h. One dose ratio (0.4 H2O2:DOC or 0.25 CuSO4:DOC) was then evaluated during stagnation after quenching (hydrogen peroxide) or extended exposure (copper sulfate) for up to 96 or 168 h. During the initial hydrogen peroxide exposure, the CA bloom had no release of intracellular microcystins (MCs) and the USA bloom only released MC at 4 H2O2:DOC. The reverse occurred with copper sulfate, where the CA bloom released MCs at 0.6 CuSO4:DOC but the USA bloom had no detectable extracellular MCs. Extracellular MC was released from the lab-cultured Microcystis at the lowest hydrogen peroxide and copper sulfate doses. In the hydrogen peroxide stagnation experiment, intracellular MC decreased in the USA bloom after 168 h despite the low dose applied. Similarly, the extended copper sulfate exposure led to intracellular MC decreases in both bloom samples after 168 h, despite showing no impact during the initial 24 h monitoring period. The lab-cultured Microcystis was again less resistant to both algicides, with releases observed after less than 2 h of stagnation or exposure. The damage to cells as measured by pigments during these experiments did not match the MC data, indicating that blooms with depressed pigment levels can still be a risk to nearby drinking water sources or recreational activities. These results provide insight on the timeline (up to one week) required for monitoring the potential release of MCs after algicide application.

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Biodegradation of multiple microcystins and cylindrospermopsin in clarifier sludge and a drinking water source: Effects of particulate attached bacteria and phycocyanin

Cited by 24 publications

References 31 publications

Delayed Release of Intracellular Microcystin Following Partial Oxidation of Cultured and Naturally Occurring Cyanobacteria

Delayed Release of Intracellular Microcystin Following Partial Oxidation of Cultured and Naturally Occurring Cyanobacteria

Toxic Cyanobacterial Bloom Triggers in Missisquoi Bay, Lake Champlain, as Determined by Next-Generation Sequencing and Quantitative PCR

Impact of Hydrogen Peroxide and Copper Sulfate on the Delayed Release of Microcystin

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