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Understanding Drivers of Cyanotoxin Production in the Lake Okeechobee Waterway
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The U.S. Geological Survey (USGS) and other researchers combined field and laboratory approaches in two studies to understand the factors that drive cyanobacterial bloom development and associated cyanotoxin production in Lake Okeechobee, the St. Lucie River and Estuary, and the Indian River Lagoon in response to the large-scale Lake Okeechobee cyanobacteria bloom in 2016.
Cyanotoxins—natural toxins produced by cyanobacteria—are common in freshwater systems. Cyanotoxin exposures have been linked to illness and death in companion animals, livestock, and wildlife in the United States and are perceived as a health threat to humans through drinking water, inhalation or skin exposure during recreational activities, or consumption of fish or shellfish. Not all cyanobacteria produce cyanotoxins or produce them at high enough concentrations to cause noticeable health effects on humans or other organisms.
In two related studies, USGS scientists and their collaborators provide information on the factors driving the development of cyanobacterial blooms (sometimes referred to as harmful algal blooms [HABs]), and cyanotoxin production in Lake Okeechobee, the St. Lucie River and Estuary, and the Indian River Lagoon (the Lake Okeechobee Waterway) during a 2016 cyanobacterial bloom that resulted in a state of emergency declaration in the State of Florida.
In the first study, scientists from the National Oceanic and Atmospheric Administration’s Great Lakes Environmental Research Laboratory, Stony Brook University, the USGS, Bowling Green State University, and the University of Michigan used metagenomic analyses (measured genes) to determine if cyanobacteria in the bloom had the gene clusters that allow the organism to synthesize microcystin, saxitoxin, and cylindrospermopsin. The results indicated that microcystin and saxitoxin gene clusters were present and likely originated from the dominant cyanobacteria, Microcystis and Dolichospermum, respectively.
The presence of gene clusters that are linked to toxin synthesis does not always indicate there will be detectable cyanotoxins in the water. For example, in this study, microcystin, as well as the gene clusters capable of producing it, were present in the water, but saxitoxin was below detection in the water despite the presence of the gene clusters capable of producing it. The presence of gene clusters does indicate the potential for cyanotoxin production within an organism and represents an early indication of potential bloom toxicity. In this study, nitrogen was the nutrient most closely linked to microcystin concentration and microcystin synthase gene abundance.
In a follow-up laboratory exposure study, the USGS and U.S. Army Corps of Engineers researched salinity, which increases along the flow path from Lake Okeechobee to the ocean, to determine if it was an important factor controlling cyanobacterial growth and cyanotoxin production. Two cyanobacteria collected from Lake Okeechobee (Microsystis aeruginosa and Dolichospermum circinale) were exposed to varying levels of salinity to simulate how the organisms might respond when transported from freshwater in the lake to more saline waters in the estuary. The laboratory results show that a salinity of approximately half that of seawater (18 practical salinity units [psu]) led to a weakening of M. aeruginosa cell membranes and resulted in microcystin leaking from the cells. D. circinale, another common cyanobacterium in this system, did not tolerate salinities greater than 7.5 psu. This controlled laboratory study indicates that as freshwater cyanobacteria are transported to brackish and marine waters, there could be a loss of membrane integrity, which could lead to the release of cellular microcystin into the surrounding waterbody. However, follow up environmental studies would be necessary to confirm if these laboratory findings are applicable in the Lake Okeechobee Waterway or other environments where freshwater cyanobacteria are transported to brackish and marine waters.
Together, these studies provide important new insights into some of the drivers of cyanotoxin production along freshwater-to-estuarine gradients in the Lake Okeechobee Waterway. However, questions remain on the actual health risks of low-level cyanotoxin exposure and how to predict which blooms contain toxins. Without this information, public health officials often consider all visible cyanobacterial blooms as potentially toxic to protect public health. For example, a state of emergency was declared again by the State of Florida during summer 2018 owing to a cyanobacterial bloom in Lake Okeechobee.
Ongoing studies by the USGS Toxic Substances Hydrology and Contaminant Biology Programs and their partners will continue to provide the science to understand the health risks associated with low-level cyanotoxin exposure and define the drivers of cyanotoxin production. This information is necessary to maximize natural resource utilization while minimizing health risks.
The USGS Toxic Substances Hydrology and Greater Everglades Priority Ecosystem Programs, U.S. Army Corps of Engineers, Chicago Community Trust, National Oceanic and Atmospheric Administration Great Lakes Environmental Research Laboratory, and the University of Michigan Cooperative Institute for Great Lakes Research provided resources and funding for this research effort.
Kramer, B.J., Davis, T.W., Meyer, K.A., Rosen, B.H., Goleski, J.A., Dick, G.J., Oh, G., and Gobler, C.J., 2018, Nitrogen limitation, toxin synthesis potential, and toxicity of cyanobacterial populations in Lake Okeechobee and the St. Lucie River Estuary, Florida, during the 2016 state of emergency event: PLoS ONE, v. 13, no. 5, p. e0196278, doi:10.1371/journal.pone.0196278.
Rosen, B.H., Loftin, K.A., Graham, J.L., Stahlhut, K.N., Riley, J.M., Johnston, B.D., and Senegal, S., 2018, Understanding the effect of salinity tolerance on cyanobacteria associated with a harmful algal bloom in Lake Okeechobee, Florida: U. S. Geological Survey Scientific Investigations Report 2018-5092, 32 p.
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