This study in Minnesota shows that aeration does not reduce lake muck. We will report on all studies which show both positive and negative results to help members understand all alternatives.
To view this study, please click below:
This study in Minnesota shows that aeration does not reduce lake muck. We will report on all studies which show both positive and negative results to help members understand all alternatives.
To view this study, please click below:
THIS IS A STUDY OF LAKE AND POND MUCK CONTROL IN WISCONSIN. NOTE THE REDUCTION IN MUCK AS WELL AS NUTRIENTS. TO VIEW THE REPORT, PLEASE CLICK BELOW:
THIS STUDY SHOWS THE SUCCESSFUL REDUCTION OF LAKE MUCK WITH AN AERATION SYSTEM. TO VIEW THE STUDY, PLEASE CLICK BELOW:
Aerobic Bacteria: Nature’s Rapid Muck Digesters
Deepen Your Lake Without Dredging
Home / Aerobic Bacteria: Nature’s Rapid Muck Digesters
Aerobic Bacteria: Nature’s Rapid Muck Digesters
Posted on: 03-22-2013 by: jtucci
Get Rid of the Compost Pile at the Bottom of Your Lake
The “muck” that accumulates at the lake-bottom is organic compost that cannot be broken down fast enough. This is a sign that your lake is overloaded with nutrients and simply can’t keep up with the amount of decaying weeds, algae, leaves, feces and other organic material piling up on the bottom every year.
Muck is a sign that your lake is severely out of balance. The first step in restoring that balance is to increase dissolved oxygen in the water column and to the “compost pile” at the bottom. The second step is to biologically accelerate the healthy (and normal) decomposition of the muck.
Nature again provides the answer in the form of beneficial aerobic bacteria that can literally eat the muck and convert it into more bacteria, carbon dioxide and water. These bacteria are then eaten by other micro-organisms and insects which, in-turn, are eaten by fish.
This is a healthy natural process that can deliver results quickly. We are consistently reducing lake-bottom muck by one foot per season by unleashing these powerful “bottom-cleaners” in combination with Lake Bottom Aeration. The end result is a clean lake-bottom and bigger healthier fish!
“Good” Bacteria Versus “Bad” Bacteria
There are essentially two ways that a lake digests the organic muck coating the bottom – aerobic digestion and anaerobic digestion. Aerobic digestion is fast and it’s good for the lake. Anaerobic digestion is not only bad for the lake; it’s harmful to fish and other beneficial organisms and potentially harmful to humans.
Oxygen makes a rapid muck reduction possible.
When there is sufficient oxygen at the bottom of the lake, aerobic bacteria and other microorganisms that feed on organic muck thrive. In fact, oxygenating the lake-bottom binds up to 97% of the phosphorus and nitrogen in the water to the bottom sediment where it becomes food for beneficial, muck consuming bacteria and insects. Without oxygen these beneficial organisms can’t survive to do the work of rapid muck reduction. This is why Lake Bottom Aeration is the critical first step in reviving your lake.
We accelerate the lake’s natural muck digestion process by adding aerobic bacteria which immediately and exponentially increases their population on the bottom of the lake.
Once the population of aerobic bacteria is boosted and supported by Lake Bottom Aeration, we make it easier for them to digest/metabolize phosphorous and nitrogen by adding vegetable-based enzymes which soften/break down the tough cellular walls of dead organic matter. In fact, we put aerobic digestion of muck – and the reduction of phosphorous and nitrogen which fuel weed and algae growth – into hyperdrive.
Our Rapid Muck Reduction Bio-Augmentation Products
Clean & Clear Concentrated Enzymes™
Clean & Clear Concentrated Enzymes is a special blend of non-toxic vegetable enzymes from nature that acts as a catalyst to biodegrade non-living organic matter and reduce available nutrients in the water, thus improving water quality. Clean & Clear softens the cell walls of dead organic matter making it easier for beneficial bacteria to feed. In essence, these enzymes give the bacteria a “jump start” in digesting lake-bottom muck. Clean & Clear also reduces odor caused by toxic gases from pathogenic (disease-type) bacteria, including hydrogen sulfide, ammonia, amines and mercaptans. Clean & Clear provides the following benefits:
Accelerates bio-degradation of organic matter
Helps beneficial aerobic bacteria compete with anaerobic bacteria, thereby reducing phosphorus and nitrogen which fuel weed and algae growth. Helps liquefy organic waste.
Improves water quality
Reduces odors, including animal manure odors; improves air quality
Safe to use; no health problems
Safe in the environment; no pollution concerns
Safe around animals
Easy to apply economical to use
C-FLO Living Organisms
Description: C-FLO is a special formulation of beneficial microorganisms that feed on organic sediment (muck) at the bottom of ponds and lakes. These organisms are found in the woods feeding on dead leaves, bark, weeds and other dead matter. When you walk through the woods, you step on as many as 300,000,000 of these tiny organisms with every step. C-FLO is comprised of healthful organisms that are natural food for aquatic insects. C-FLO multiplies as it feeds on organic sediment, and insects grow and multiply as they feed on C-FLO. Fish then feed on the insects and grow rapidly.
What C-FLO does: C-FLO feeds on bottom organic muck, ooze, and peat, digesting and converting it to carbon dioxide and water. As C-FLO feeds on bottom muck, the lake will deepen, creating a better environment for fish, and less opportunity for weeds to grow. Cattails and lilies will gradually disappear. This process replaces dredging the organic material at a tiny fraction of the cost. C-FLO is harmless to fish, wildlife, pets, humans, and the environment when used as directed. As mentioned above, the sediment decomposition process is accelerated by the addition of oxygen breathing microorganisms. These organisms have been exempted from the need to be registered for use in lakes by the U.S. Environmental Protection Agency because of their beneficial and harmless nature.
Where it can be used: C-FLO will only work in ponds and lakes that are continuously oxygenated and rid of hydrogen sulfide (rotten egg smell when the bottom is stirred up). If oxygen runs out or hydrogen sulfide rises for even a few days, the organisms may die and your pond or lake will need a new application. Therefore, for best results C-FLO should be used with Clean & Clear Concentrated Enzymes and Lake Bottom Aeration.
Lack of Oxygen Produces “Bad” Bacteria that can Kill Your Lake
When the bottom of the lake is layered with dead organic matter (muck) and weeds and algae choke the surface of the lake, it means there is not enough oxygen on the lake-bottom to sustain a thriving and productive population of aerobic bacteria. In fact, when oxygen is absent, anaerobic bacteria take over.
Anaerobic bacterial digestion breaks down organic matter much slower and produces acids which not only decrease water quality, but also cause a massive release of phosphorus and nitrogen from the organic sediment – the two major nutrients which fuel excess weed and algae growth. Anaerobic bacteria also produce toxic gases such as ammonia, methane, and hydrogen sulfide (the rotten egg smell).
If your lake-bottom sediment smells like rotten eggs or “swamp gas” it’s a sure sign anaerobic bacterial digestion is at work. Worse, anaerobic bacteria include pathogenic (disease-producing) bacteria. These diseases include cholera, scabies, typhoid, shigella, salmonella, botulism and miscellaneous bacteria that cause infectious boils and sores.
This is an article from the University of New Hampshire Magazine on what in our lakes may be dangerous to human health.
Could there be a connection between blue-green algae and clusters of deadly neurological disease near our lakes?
By Virginia Stuart ’75 ’80G
David Hersey spends most of his time propped up in bed in his living room these days. “I have one arm that still works,” the former parachute rigger and skydiving enthusiast notes wryly as he extends his left hand to a visitor. It’s been three years since he heard a neurologist say, in so many words, “You have ALS, there’s no known treatment, and you’re going to die.” The doctor was only confirming what Hersey had already figured out from his own research after noticing that he kept stubbing his toe. Before that, the 58-year-old Deerfield, N.H., resident had never heard of amyotrophic lateral sclerosis, otherwise known as Lou Gehrig’s disease.
Ever since, he’s been watching it gradually creep upward, rendering his limbs useless while his sense of touch and mental abilities remain intact. “I will eventually die of respiratory failure,” he says. Hersey, however, likes to point out that there is no typical ALS patient. He, for one, has little use for self-pity. “I don’t have a list of things I didn’t do,” he explains. “I did them as I went along.”
As his condition has progressed, his pursuits have taken an intellectual bent—learning Italian, exploring the Internet, and reading about ALS research, which, he’s convinced, has made little progress since Yankees slugger Gehrig was diagnosed with the disease in 1939.
Elijah Stommel, a neurologist and researcher at Dartmouth-Hitchcock Medical Center, has been known to lie awake at night puzzling over possible causes of ALS. A few years ago, he started to notice clusters of ALS patients near lakes. At Mascoma Lake in Enfield, N.H., for example, he was seeing an occurrence of the disease roughly 25 times higher than expected. Around the same time, he read about a controversial theory linking ingestion of a toxin produced by blue-green algae to neurodegenerative diseases like ALS, Alzheimer’s and Parkinson’s. His search for a field biologist who could help him explore a possible connection between algae in lakes and ALS in lakeside residents led to Jim Haney, a UNH expert on aquatic organisms and the toxins they produce. Haney was also intrigued by the new theory.
One November day in 2007, Haney and graduate student Amanda Murby ’06,’10G canoed out onto Mascoma Lake to get samples of the water and sediment. At the UNH Biotoxins Lab, the sediment revealed high levels of microcystin, a well-studied liver toxin produced by certain algae. Exposure through swimming can cause rashes and gastroenteritis, and ingestion of contaminated water has been blamed for animal and human deaths around the world. The neurotoxin suspected of causing ALS, the amino acid BMAA, has yet to be found in the lake. Although it is harder to identify and less well studied than microcystin, BMAA is produced by the same species of algae which was found in abundance in Mascoma. Later Murby mapped the algae in the lake, showing how currents could circulate the organisms toward the public beach in warm weather. Last summer, the N.H. Department of Environmental Services issued 17 advisories for harmful blue-green algae blooms at freshwater beaches, including Mascoma’s.
Now Stommel asks all his new patients where they live and how long they have lived there. Using sophisticated geographical software, he and his colleague, neurologist Tracie Caller, have documented a significant statistical increase in the incidence of ALS cases near water bodies with a history of toxic algae blooms. They have also identified patients near these lakes who have developed some symptoms of ALS but not the full-blown disease.
In April, Haney and Stommel applied for a federal grant to study ALS clusters in northern New England and algae blooms in nearby lakes and waterways. If the research adds to the mounting evidence of a link between the disease and the algae, it could help light the way to a cure. But even if it doesn’t, the researchers hope to raise awareness of a known health threat and to motivate the public to take better care of a beloved and valuable natural resource.
Jim Haney and his colleagues at the Biotoxins Lab, John Sasner and Mike Ikawa, were already experts on the deadly “red tide” algae when they got a call in 1997 from Silver Lake State Park in Hollis, N.H. Children who had been swimming in the lake were getting stomach ailments. Haney was surprised to find that water samples from the lake looked like a pure culture of the kind of algae that produces microcystin—in concentrations among the highest ever detected worldwide. He urged the state to keep children out of the water whenever the scum of an algae bloom formed. At the same time, he recognized “an unbelievable opportunity,” and began to study blue-green algae.
Haney has a sort of scientific love-hate relationship with these microscopic organisms, which are actually bacteria and technically called cyanobacteria. They were here if not at the very dawn of life on Earth, then “only” about a billion years later. In fact, they were the first organisms to develop photosynthesis—producing the oxygen that enabled the rest of life as we know it to unfold.
Today blue-green algae can be found virtually anywhere on the globe—in the middle of the ocean, a handful of desert sand, the fur of a sloth, a dietary supplement, a glass of water, or a leaf of lettuce. Viewed through a microscope, they reveal a beautiful symmetry in delicate spirals or straight chains like opened bracelets. To the naked eye, however, an algae bloom can resemble pea soup, green latex paint, white flakes or brown scum.
In 2003, New Hampshire became one of the first states to test for blue-green algae in its freshwater beach inspection program, which is directed by biologist Sonya Carlson ’06G, a former student of Haney’s. The state issues an advisory when algae levels at a public beach exceed the World Health Organization standards for drinking water. The beach manager must then post a sign and decide whether to close the beach for the duration of the bloom.
With the support of a federal grant, Haney and his colleagues have tested levels of microcystin in 80 of New Hampshire’s 959 lakes, using the highly sensitive ELISA (enzyme-linked immunosorbent assay) method. “It’s misleading to talk about lakes having toxic cyanobacteria or not,” he says. “It’s a matter of how much they have.” He’s seen a thousandfold difference in levels from the lowest to highest concentrations.
Paul Cox, a world-renowned ethnobotanist, visited UNH recently to tell about his efforts to solve one of the great medical mysteries. Why has the native population of Chamorros on Guam had an incidence of a fatal ALS-like disease up to 100 times higher than normal? At its peak in the 1950s, 25 to 30 percent of the population succumbed to the ailment, in the largest cluster of the disease ever documented. The culprit, Cox concluded, was the Chamorros’ predilection for a local delicacy, the giant fruit bat—which they devoured fur, head, and all.
When analysis of the preserved brains of victims of the disease revealed high levels of BMAA, Cox saw a classic case of biomagnification. In a “House That Jack Built” sort of chain of causality, the Chamorro are the people who ate the bats, who ate the cycad seeds, which contain the BMAA, which is produced by the blue-green algae, which live symbiotically in cycad roots.
The surprising discovery of BMAA in the brains of some of Cox’s controls—who were victims of Alzheimer’s disease—strengthened his hypothesis that blue-green algae toxins may cause neurodegenerative disease in susceptible people.
When Cox published his findings in Neurology in 2002, some neurologists welcomed his scientific crossover, but others were skeptical, particularly scientists who had promoted other theories about the Chamorro mystery. Some of his results have been confirmed independently, however, and scientists at the University of Miami have just published a study in which high levels of BMAA were detected in 49 out of 50 brain samples from North American ALS and Alzheimer’s victims.
If BMAA does somehow cause neurodegenerative diseases—by damaging glutamate receptors in the brain, perhaps, or replacing normal amino acids in brain proteins—scientists believe the process would only occur in people who have a genetic predisposition to accumulate the toxin.
Haney and Stommel plan to explore the possible correlation between ALS and algae through patient interviews, tests of water and fish, and sophisticated mapping and statistical analysis. Cox’s lab will assist with analysis of hair and brain samples from victims. Lake-bottom cores can give clues to past levels of contamination. Haney found, for example, that a sudden jump in toxin levels revealed the point when a state fish hatchery came online 70 years ago and started polluting a Berlin, N.H., lake with nutrients. In the seemingly upside-down world of lake management, “nutrients” and “feeding” are not nice words.
On a Thursday night in May, several pairs of UNH students presented the results of a semester-long study of the water quality in local lakes before a small audience. It was the culmination of Haney’s lake management course, which provides a service to the state while training students from a variety of majors.
Although each lake was different, the recommendation for maintaining or improving water quality was invariably the same: reduce or prevent the flow of nutrients into the lake. Nutrients such as phosphate from fertilizers, animal wastes and detergents can lead to overgrowth of aquatic organisms. The solution is to maintain a buffer of vegetation along the shore, reduce or eliminate use of fertilizer adjacent to the lake, keep septic systems well maintained and resist the pressure to pave over swaths of land in the lake’s watershed.
An important goal of the algae and ALS project is to raise public awareness. The N.H. Department of Environmental Services and UNH Cooperative Extension will play key roles in this part of the project. New Hampshire already has 900 citizen volunteers monitoring the water quality of lakes across the state under the guidance of UNH and Cooperative Extension, and 500 more, under N.H. Department of Environmental Services’ supervision, are watching for invasive weeds. Members of both monitoring programs have already started to learn about signs of algae problems in lakes. Other efforts will be aimed at informing veterinarians and medical doctors so that they can be on the lookout for algae-related illness.
In the meantime, the experts recommend several ways to avoid getting sick from algae toxins. The most obvious caveat is to avoid drinking contaminated water, which can happen inadvertently while swimming during a bloom. Haney cautions that the toxins in blue-green algae are not destroyed, and may even be intensified, by boiling. They can also concentrate in shellfish or finfish in contaminated lakes, bays, rivers or oceans. “Aerosolization,” a documented means of transmission of toxins such as red tide, could theoretically spread contaminants through wind, or the spray created by waterskiing. And perhaps it goes without saying that you won’t find blue-green algae supplements on the kitchen shelves of any of these researchers.
The scientists want to convey concern, but not alarm, about the algae in New Hampshire lakes. In general, the lakes have tested below the WHO drinking-level standards, except during active blooms. “I’d be thrilled to own a cottage on a New Hampshire lake,” says Cox, whose Institute for Ethnomedicine is based in Wyoming. In fact, northern New England has less of a problem with blue-green algae blooms than many states with more development, more farming or a warmer climate.
David Hersey has his own, rather metaphysical, theory as to why he may have contracted ALS. In the year 2000, virtually everyone he had ever been close to died, one after another, of unrelated diseases, mostly cancer. Can it be a coincidence, he muses, that someone could suffer such a devastating series of losses, and then contract a disease where “everything is gradually disappearing”?
Hersey isn’t part of an ALS cluster, although he did spend many a summer afternoon swimming in a local lake as a boy and also lived for more than 20 years near (and often rollerbladed along) the Charles River in Boston, which has also had algae blooms. “I do feel like the neurotoxic effect of these algae blooms is a piece of the puzzle,” he says.
Even if they don’t receive the National Institute of Environmental Health grant, says Haney, the researchers will find the money to continue working on this puzzle. “We think we live in this Garden of Eden world and assume everything out there is there for us to use, that lakes are free of problems,” he warns. “But there are problems out there that we don’t know about.”
And whether the result of algae toxins is just an upset stomach or one of mankind’s most dread diseases, this is one of those times when what we don’t know can hurt us. ~
The following article is more specific about the relationship of lake algae and ALS.
Are Algae Blooms Linked to Lou Gehrig’s Disease?
Medical researchers are now uncovering clues that appear to link some cases of ALS to people’s proximity to lakes and coastal waters
By Lindsey Konkel, Environmental Health News on December 11, 20143
In New England, medical researchers are now uncovering clues that appear to link some cases of the lethal neurological disease to people’s proximity to lakes and coastal waters. Credit: Jeff Reutter / Ohio Sea Grant via Flickr
For 28 years, Bill Gilmore lived in a New Hampshire beach town, where he surfed and kayaked. “I’ve been in water my whole life,” he said. “Before the ocean, it was lakes. I’ve been a water rat since I was four.”
Now Gilmore can no longer swim, fish or surf, let alone button a shirt or lift a fork to his mouth. Earlier this year, he was diagnosed with Amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease.
In New England, medical researchers are now uncovering clues that appear to link some cases of the lethal neurological disease to people’s proximity to lakes and coastal waters.
About five years ago, doctors at a New Hampshire hospital noticed a pattern in their ALS patients—many of them, like Gilmore, lived near water. Since then, researchers at Dartmouth-Hitchcock Medical Center have identified several ALS hot spots in lake and coastal communities in New England, and they suspect that toxic blooms of blue-green algae—which are becoming more common worldwide—may play a role.
Now scientists are investigating whether breathing a neurotoxin produced by the algae may raise the risk of the disease. They have a long way to go, however: While the toxin does seem to kill nerve cells, no research, even in animals, has confirmed the link to ALS.
No known cause
As with all ALS patients, no one knows what caused Bill Gilmore’s disease. He was a big, strong guy—a carpenter by profession. One morning in 2011, his arms felt weak. “I couldn’t pick up my tools. I thought I had injured myself,” said Gilmore, 59, who lived half his life in Hampton and now lives in Rochester, N.H.
Three years and many doctors’ appointments later, Gilmore received the news in June that the progressive weakening in his limbs was caused by ALS.
Neither Hampton nor Rochester is considered a hot spot for ALS. Gilmore is one of roughly 5,600 people in the United States diagnosed each year with the disease. The average patient lives two to five years from the time of diagnosis.
There is no cure, and for the majority of patients, no known cause. For 90 to 95 percent of people with ALS, there’s no known genetic mutation. Researchers assume that some unknown interaction between genes and the environment is responsible.
In recent years, some of this research has focused on blue-green algae, also known as cyanobacteria.
“There’s a growing awareness of the importance of gene/environment interactions with neurodegenerative diseases. There is more interest in examining environmental exposures, including exposures to cyanobacteria, as possible risk factors for sporadic ALS,” said Paul Alan Cox, director of the nonprofit Institute of Ethnomedicine in Wyoming, which focuses on treatments for ALS and other neurodegenerative diseases.
Cyanobacteria—some of the oldest organisms on the planet—can occur wherever there is moisture. Blooms are fed largely by nutrients in agricultural and urban runoff.
Some cyanobacteria produce toxic compounds that can sicken people. In August, hundreds of thousands of people in Toledo, Ohio, were left without tap water for days when toxins from an algal bloom in Lake Erie were found in the water supply.
While the cyanobacteria toxin that prompted the Toledo water crisis can cause diarrhea, intestinal pain and liver problems, other toxins produced by the blue-green algae can harm the nervous systems of humans and wildlife.
Scientists have long suspected that a cyanobacteria toxin could play a role in some forms of ALS. After World War II, U.S. military doctors in Guam found that many indigenous Chamorro suffered from a rapidly progressing neurological disease with symptoms similar to both ALS and dementia. Years later, scientists found the neurotoxin BMAA in the brains of Chamorro people who died from the disease. Cyanobacteria that grow on the roots and seeds of cycad trees produce the toxin.
Cox, a researcher in Guam in the 1990s, hypothesized that BMAA worked its way up the food chain from the cycad seeds to bats to the Chamorro who hunted them. But Cox and his colleagues also found BMAA in the brains of Canadian Alzheimer’s patients who had never dined on Guam’s fruit bats. In patients who had died from other causes, they found no traces of it. The source of the BMAA in the Canadians remains unknown.
Some researchers have suggested that fish and shellfish from waters contaminated with cyanobacteria blooms may be one way that people ingest BMAA. In southern France, researchers suspect ALS cases may be linked to consumption of mussels and oysters. Lobsters, collected off the Florida coast near blooms, also have been found with high levels of BMAA.
Scientists around the world are investigating how the neurotoxin gets into the body and whether it contributes to disease.
“We don’t really know what exposure routes are most important,” Cox said.
New England’s ALS hot spots
In New Hampshire, Dartmouth neurologist Elijah Stommel noticed that several ALS patients came from the small town of Enfield in the central part of the state. When he mapped their addresses, he saw that nine of them lived near Lake Mascoma.
Around the lake, the incidence of sporadic ALS—cases for which genetics are not a likely cause—is approximately 10 to 25 times the expected rate for a town of that size.
“We had no idea why there appeared to be a cluster around the lake,” Stommel said.
Based on the link between ALS and the neurotoxin in other parts of the world, Stommel and his colleagues hypothesize that the lake’s cyanobacteria blooms could be a factor.
Across northern New England, the researchers have continued to identify ALS hot spots—a large one in Vermont near Lake Champlain and a smattering of smaller ones among coastal communities in New Hampshire and Maine.
Earlier this year, the researchers reported that poorer lake water quality increased the odds of living in a hot spot. Most strikingly, they discovered that living within 18 miles of a lake with high levels of dissolved nitrogen—a pollutant from fertilizer and sewage that feeds algae and cyanobacteria blooms—raised the odds of belonging to an ALS hot spot by 167 percent.
The findings, they wrote, “support the hypothesis that sporadic ALS can be triggered by environmental lake quality and lake conditions that promote harmful algal blooms and increases in cyanobacteria.”
How people in New England communities could be ingesting the neurotoxin remains largely a mystery. While fish in the lakes do contain it, not everyone in the Dartmouth studies eats fish.
“We’ve sent questionnaires to patients and there’s really no common thread in terms of diet or activities,” Stommel said. “The one common thing that everybody does is breathe.”
In other words, it’s possible that a boat, jet ski or even the wind could stir up tiny particles of cyanobacteria in the air, where people then breathe it in.
Testing the air for a neurotoxin
Last August, at Lake Attitash, Jim Haney, a University of New Hampshire biologist, waded knee-deep into swirling green water. Cyanobacteria were blooming at the small lake in the northeastern corner of Massachusetts. Haney had rigged up three vacuum-like devices with pipes, plastic funnels and paper to suck up and filter air near the lake’s surface.
He took the filter papers back to his laboratory and measured the cyanobacteria cells, BMAA and other toxins stuck to them.
“We want to know what level lake residents may be exposed to through airborne particles,” said Haney, who is sampling the air at Massachusetts and New Hampshire lakes in collaboration with the Dartmouth team.
Stommel said,“it’s very compelling to look at the filter paper and see it just coated with cyanobacteria.”
At this point, Haney and graduate students are trying to understand under what conditions the toxins might be coming out of the lake and whether the airborne particles are an important route of exposure.
Preliminary findings suggest that BMAA and other cyanobacteria cells are being aerolized. “There is potentially a large quantity of cyanobacteria that could be inhaled,” Haney said. He noted, however, that the measurements were taken about eight inches above the water’s surface, making it likely that concentrations would be much lower farther away.
While the toxins are likely to be most abundant in the air around lakes, they exist all over the planet, even in deserts.
In 2009, BMAA was even detected in the sands of Qatar. Crusts containing cyanobacteria may lie dormant in the soil for most of the year, but get kicked up during spring rainstorms. Cox and colleagues hypothesized that breathing in toxins from dust might be a trigger for a doubling of ALS incidence in military personnel after Operation Desert Storm.
Near Haney’s workstation at Lake Attitash, a child splashed in the shallow water off a dock. Haney scooped up a cupful of water. He peered at the tiny green particles in the cup that reflect the sunlight, making the mixture resemble a murky pea soup.
“We’ve developed this view of nature as idyllic, which is wonderful, but not everything in nature is benign,” he said. “Rattlesnakes are natural and you wouldn’t get too close to one of those.”
“Proximity does not equal causality”
The hypothesis that exposure to BMAA may trigger the disease in some people remains controversial.
Researchers have evidence that people living close to lakes with blooms may be at increased risk for ALS. They’ve even found BMAA in the diseased brain tissue of people who have died of neurodegenerative diseases. Nevertheless, “proximity does not equal causality,” said Deborah Mash, a neuroscientist at the University of Miami in Florida.
The big, unanswered question is whether the toxin can actually cause the disease. So far, there’s little evidence to show how it could induce the type of brain changes seen in people with ALS.
Tests of human cells have found that BMAA kills the motor neurons—nerve cells that control muscles—implicated in ALS. Primates fed high levels of BMAA in the 1980s showed signs of neurological and muscular weakness. But the toxin did not kill their motor neurons.
“What is lacking at this point is a clear animal model that demonstrates that BMAA exposure results in ALS-like neuropathy,” Cox said.
So what is a possible mechanism for how the toxin may lead to the disease? The body may mistake BMAA for the amino acid L-serine, a naturally occurring component of proteins. When the toxin is mistakenly inserted into proteins, they become “misfolded,” meaning they no longer function properly and can damage cells.
Cox and colleagues soon will test two drugs in FDA-approved clinical trials. They’re about to enter second-phase testing with L-serine. The idea, explained Sandra Banack, a researcher at the Institute for Ethnomedicine, is that large doses of L-serine may be able to “outcompete” low levels of BMAA in the body, preventing it from becoming incorporated into proteins.
For ALS patients like Gilmore, the research can’t come soon enough. “If they can figure out a cause, then hopefully they can find a cure,” Gilmore said.
This article originally ran at Environmental Health News, a news source published by Environmental Health Sciences, a nonprofit media company.
ABOUT THE AUTHOR(S)
Lindsey Konkel is a freelance science journalist based in Monmouth County, New Jersey.
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Environmental Health News
updated 9/28/2007 2:36:21 PM ET
PHOENIX — It sounds like science fiction but it’s true: A killer amoeba living in lakes enters the body through the nose and attacks the brain where it feeds until you die.
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Even though encounters with the microscopic bug are extraordinarily rare, it’s killed six boys and young men this year. The spike in cases has health officials concerned, and they are predicting more cases in the future.
“This is definitely something we need to track,” said Michael Beach, a specialist in recreational waterborne illnesses for the Centers for Disease Control and Prevention.
“This is a heat-loving amoeba. As water temperatures go up, it does better,” Beach said. “In future decades, as temperatures rise, we’d expect to see more cases.”
According to the CDC, the amoeba called Naegleria fowleri (nuh-GLEER-ee-uh FOWL’-erh-eye) killed 23 people in the United States, from 1995 to 2004. This year health officials noticed a spike with six cases — three in Florida, two in Texas and one in Arizona. The CDC knows of only several hundred cases worldwide since its discovery in Australia in the 1960s.
In Arizona, David Evans said nobody knew his son, Aaron, was infected with the amoeba until after the 14-year-old died on Sept. 17. At first, the teen seemed to be suffering from nothing more than a headache.
“We didn’t know,” Evans said. “And here I am: I come home and I’m burying him.”
After doing more tests, doctors said Aaron probably picked up the amoeba a week before while swimming in the balmy shallows of Lake Havasu, a popular man-made lake on the Colorado River between Arizona and California.
Though infections tend to be found in southern states, Naegleria lives almost everywhere in lakes, hot springs, even dirty swimming pools, grazing off algae and bacteria in the sediment.
Beach said people become infected when they wade through shallow water and stir up the bottom. If someone allows water to shoot up the nose — say, by doing a somersault in chest-deep water — the amoeba can latch onto the olfactory nerve.
The amoeba destroys tissue as it makes its way up into the brain, where it continues the damage, “basically feeding on the brain cells,” Beach said.
People who are infected tend to complain of a stiff neck, headaches and fevers. In the later stages, they’ll show signs of brain damage such as hallucinations and behavioral changes, he said.
Once infected, most people have little chance of survival. Some drugs have stopped the amoeba in lab experiments, but people who have been attacked rarely survive, Beach said.
“Usually, from initial exposure it’s fatal within two weeks,” he said.
Researchers still have much to learn about Naegleria. They don’t know why, for example, children are more likely to be infected, and boys are more often victims than girls.
“Boys tend to have more boisterous activities (in water), but we’re not clear,” Beach said.
In central Florida, authorities started an amoeba phone hotline advising people to avoid warm, standing water and areas with algae blooms. Texas health officials also have issued warnings.
People “seem to think that everything can be made safe, including any river, any creek, but that’s just not the case,” said Doug McBride, a spokesman for the Texas Department of State Health Services.
Officials in the town of Lake Havasu City are discussing whether to take action. “Some folks think we should be putting up signs. Some people think we should close the lake,” city spokesman Charlie Cassens said.
Beach cautioned that people shouldn’t panic about the dangers of the brain-eating bug. Cases are still extremely rare considering the number of people swimming in lakes. The easiest way to prevent infection, Beach said, is to use nose clips when swimming or diving in fresh water.
“You’d have to have water going way up in your nose to begin with” to be infected, he said.
David Evans has tried to learn as much as possible about the amoeba over the past month. But it still doesn’t make much sense to him. His family had gone to Lake Havasu countless times. Have people always been in danger? Did city officials know about the amoeba? Can they do anything to kill them off?
Evans lives within eyesight of the lake. Temperatures hover in the triple digits all summer, and like almost everyone else in this desert region, the Evanses look to the lake to cool off.
It was on David Evans’ birthday Sept. 8 that he brought Aaron, his other two children, and his parents to Lake Havasu. They ate sandwiches and spent a few hours splashing around.
“For a week, everything was fine,” Evans said.
Then Aaron got the headache that wouldn’t go away. At the hospital, doctors first suspected meningitis. Aaron was rushed to another hospital in Las Vegas.
“He asked me at one time, ’Can I die from this?”’ David Evans said. “We said, ’No, no.”’
On Sept. 17, Aaron stopped breathing as his father held him in his arms.
“He was brain dead,” Evans said. Only later did doctors and the CDC determine that the boy had been infected with Naegleria.
“My kids won’t ever swim on Lake Havasu again,” he said.
This is a study on the feasibility for lake aeration at Cedar Lake, Michigan, for weed and sedimentation control. This article shows the appropriate science to support this approach. Cedar Lake is 155 acres.
To view this study, click below:
THIS YOUTUBE VIDEO SHOWS THE SUCCESS OF LAKE AERATION IN THE CONTROL OF MILFOIL AND ALGAE AND THE ELIMINATION OF MUCK.
WATCH THIS YOUTUBE VIDEO TO LEARN MORE ABOUT LAKE AERATION, A PROCESS TO MAKE A HEALTHY LAKE.