Scrambling birds’ brains: Could this toxic algae offer clues to human diseases?
By Lindsey Konkel
Environmental Health News
Part 12 of Winged Warnings
September 23, 2014
J. STROM THURMOND LAKE, Ga. – From their perch in a loblolly pine, two bald eagles swoop low over a floating flock of wintering coots. Most of the water birds scatter, but a few are left struggling on the surface. They flail on their backs, their wings twitching. They sense danger, but they cannot flee. Choosing its prey, an eagle dives over one of the sick coots, skewering it with sharp talons.
A mysterious toxin – with no name and no cure – lurking in lakes in the South has drilled holes in the brains of these waterbirds, rendering them unable to swim, eat and fly. In turn, this poison likely will also destroy the brain of the eagle that ate the coot.
Lacy holes that look like soap bubbles dot the tightly knit meshwork of the coots’ brain tissues, blocking the neurological signals transmitted between regions of their brains.
Since avian vacuolar myelinopathy, or AVM, was discovered in 1994, 76 dead eagles and hundreds of coots and other water birds at Thurmond Lake alone have been attributed to the disease. The full toll is unknown, but thousands of dead ducks, geese and even an owl have been recovered at 19 lakes across six states: Georgia, the Carolinas, Arkansas, Texas and Florida.
Researchers have found that the poison is attached to a newly discovered type of blue-green algae that grows on ubiquitous, invasive waterweeds.
“It may be an indicator of a larger ecological problem in which birds are the sentinels,” said Dr. John Fischer, director of the Southeast Cooperative Wildlife Disease Study in Athens, Ga.
In humans, researchers suspect that a neurotoxin may be linked to Lou Gehrig’s disease, or amyotrophic lateral sclerosis (ALS), a lethal neurodegenerative disease that destroys parts of the brain. No one knows whether any human neurological diseases are related to the bird disease, but new clues about the poisoned birds are emerging.
Hydrilla toxin beckons hungry coots
In a few weeks the cacophony of waterfowl will fill the Savannah River Basin as countless migrants alight on Thurmond Lake. But for now, on this August day, it’s muggy and still except for a dragonfly skimming the water’s surface.
Researcher Susan Wilde, an AVM expert from the University of Georgia, and her student Brigette Haram take turns tossing a metal rake over the side of a boat, slowly dragging it through the water on a rope. They pull up pounds of hydrilla – a plant that grows up through the water like plump fingers, beckoning thousands of hungry coots.
Imported from Asia, hydrilla was introduced to southern waterways in the 1960s. It can now be found from Texas to New York and appears to be spreading. Natural resource managers spend millions of dollars each year trying to control the invader, which outgrows native plants.
Wilde plucks a clump and examines it closely. “Look there,” she said, pointing to the tiny black dots speckled on the hydrilla’s leaves.
Those dark spots – a type of cyanobacteria or blue-green algae that lives on hydrilla – have been found at all lakes where the disease has been seen, she explains. Those spots contain the poison that is making the birds sick. It’s taken nearly a decade, but Wilde and her colleagues have identified the novel blue-green algae and are now trying to determine what neurotoxic compounds they harbor.
Hungry coots devour the hydrilla and become sick. Clumsy and unable to fly, they are easy targets for hunting eagles, which also develop neurological problems after eating the coots.
“They can’t fly, can’t swim well, can’t eat, and generally die fairly fast,” Fischer said.
Laboratory experiments have confirmed their suspicions about the hydrilla. In North Carolina, researchers conducted field trials by placing them in lakes known to have AVM. Wilde and colleagues at the University of Georgia followed up with a series of feeding trials in mallards and chickens. They found that the dark specks, harboring an unidentified toxin, appeared to be the culprit.
A combination of factors – including stress from migration, other contaminants with known neurotoxic elements such as lead or mercury – may be working together to exacerbate the debilitating outbreaks.
Past threats to people
Cyanobacteria occur almost anywhere on the planet where there’s moisture. Some are known to produce neurotoxic compounds that can harm the nervous systems of people and wildlife.
Similar lesions had been found in the 1970s in the brains of stillborn and dying infants who had been washed with the chemical hexachlorophene, once widely used as a disinfectant. Tests, however, showed that the brain lesions were likely caused by a natural toxin, not a manmade pollutant.
Cyanobacteria are becoming more abundant in the world’s water bodies, fed largely by nutrients from urban and agricultural runoff. In August, toxins from an algae bloom in Lake Erie were found in Toledo, Ohio’s water supply, leavings hundreds of thousands of people without tap water for days. The toxin can cause diarrhea, intestinal pain and even liver problems.
Wilde wondered whether another well-known toxin, called BMAA, could be causing the holes in the birds’ brains. In the 1960s, researchers on the island of Guam discovered BMAA in the brains of villagers suffering high rates of neurodegenerative diseases such as ALS, Parkinson’s and dementia. It was produced by cyanobacteria on the seeds of cycad trees. The neurotoxin made its way up the food web to humans through flying foxes, deer and pigs that foraged the seeds and were then hunted by people. More recently, researchers found BMAA in the brain tissue of eight Canadian Alzheimer’s patients, but not in the brains of people who had died of other causes.
|Brigette Nelson Haram|
BMAA’s presence has been documented in algal blooms throughout North America. It’s been found in the brains of beached dolphins in Florida, said Deborah Mash, a neuroscientist at the University of Miami, and at high concentrations in northern New England lakes, where researchers suspect it may play a role in the ALS clusters that have developed in people living near some lakes in New Hampshire and Vermont.
Wilde and her students have detected BMAA in some samples of the new species of algae, which she has named “eagle killer that lives on hydrilla,” Aetokthonous hydrillicola, but not in other samples. This suggests that BMAA may not be causing the birds’ brain lesions.
“We can’t really rule too much out at this point. But I think we’re looking at a novel toxin here,” Wilde said.
Solving the mystery in birds may help scientists find the cause of human diseases, said Mash, who studies ALS and other neurodegenerative diseases.
“More now than at any other part in human history, our environment has become a toxic soup. Sorting out which ones cause disease is what’s ultimately going to inform the human condition,” she said.
Jeopardizing eagle comeback?
At Thurmond Lake, a comeback of bald eagles coincided with the arrival of hydrilla in the mid-90s.
Five to six pairs of nesting eagles used to inhabit the Georgia side of the lake, with another one or two on the South Carolina side, said Jim Ozier, a wildlife biologist with the Georgia Department of Natural Resources. Now the only successful nest is located in the extreme north corner where the hydrilla doesn’t reach.
The eagles still arrive en masse early in the fall (last November, Wilde and Haram counted 17), following the coots. They set up nesting sites, but by January, when they should be hatching eggs and tending young, the nests are vacant.
|Brigette Nelson Haram|
Some eagles have been recovered dead in nests or on the ground near nesting trees, surrounded by coot feet. Most are never found. But it’s unclear whether they are dying of the disease or moving on from Thurmond Lake for other reasons.
Bald eagles have high nest site fidelity and tend to return to the same territories year after year, so relocating to another lake entirely would be unusual for nesting adults, Haram said. This fall, she will fit five eagles with radio-tracking devices to monitor their movements and if they become ill, to track and recover their bodies to determine the cause of death.
AVM has been “a blow” to the eagle population at Thurmond, Ozier said, although statewide, as in much of the country, eagles appear to be thriving.
In Georgia last year, more than 200 bald eagles fledged. “The overall impact could be big if it spreads, but thankfully, we haven’t seen that,” Ozier said.
The Army Corps of Engineers, which manages Thurmond Lake, is discussing ways to control hydrilla. At some AVM-positive lakes, including DeGray Lake in Arkansas, where the disease was first found, getting rid of hydrilla has reduced bird deaths.
It’s not known whether the disease, or the toxin itself, could be transmitted from birds to humans. Fischer said it doesn’t appear to be a human disease concern. Tests feeding sick coots to pigs, raccoons, and muskrat produced no brain lesions in the mammals.
But more research is needed to understand the health risks, Wilde and Haram said.
“Until we know what this toxin is, we don’t know what the implications are for human health,” Haram said.
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