“We all teamed up to hunt the eagle killer!”
At first, the scene at DeGray Lake in Arkansas looked like a massacre. In 1994, 29 bald eagles were found dead nearby. It was the biggest undiagnosed die-off of bald eagles in history, and it was only getting started.
By 1996, at least 70 eagles had died across several Arkansas reservoirs. Two years later, conditions continued to deteriorate as dead birds of different species turned up at ten sites across six states.
The birds had died from a disease called avian vacuolar myelinopathy (AVM) that attacks their brains, causing them to fly erratically or swim in circles before succumbing. Now, almost two decades later, scientists finally know what causes it.
In a paper published Thursday in Science, scientists describe the chain of events that leads to AVM. It’s a deadly three-part process that requires invasive plants, abundant bacteria, and chemicals in the environment.
It starts with the invasive plant called Hydrilla verticillata, or waterthyme, first introduced to the United States when home aquariums were dumped into local waterways in the 1960s. This plant is an especially attractive home to cyanobacteria called Aetokthonos hydrillicola, which isn’t deadly to waterbirds on its own. However, when these cyanobacteria are exposed to the chemical bromide it produces a dangerous neurotoxin called aetokthonotoxin.
That’s the toxin that causes AVM inside a bird’s body, according to this new paper.
Ultimately AVM is a plague of our own making, explains Steffen Breinlinger, the study’s first author. Breinlinger is a doctoral student at the Martin Luther University Halle-Wittenberg in Germany. Two out of the three ingredients needed to produce the neurotoxin — the invasive plants and the bromide present in ponds, lakes, and reservoirs — came together because of human intervention, he explains.
“We really have to tread carefully and pay more attention to our environment,” Breinlinger tells Inverse. “We often do not realize how complex ecosystems are and only afterward we realize what we have done.”
The background — Not all birds with AVM are found dead. Infected eagles have been spotted overshooting their perches or flying into rock walls. American coots, waterbirds often mistaken for ducks, sometimes swim in circles on their backs or refuse to fly at all.
Analysis of these birds’ brains showed that their tissue contained tiny lumps called vacuoles that spread along their nerve cells in the brain and spinal cord. Those lumps are a tell-tale sign of AVM. Sometimes brains reveal more than lumps: Analysis of the 1994 bald eagles revealed holes.
“Birds of prey are an unfortunate sentinel telling us something is dangerous in this reservoir.”
By 2005, research conducted by Susan Wilde, this study’s senior author and a professor at the University of Georgia, determined that birds with AVM often came from bodies of water filled with waterthyme.
“Birds of prey are an unfortunate sentinel telling us something is dangerous in this reservoir,” Wilde tells Inverse.
Those plants were home to an “unidentified” cyanobacteria that covered as much as 95 percent of the surface area on those leaves. By 2014, Wilde clarified that this bacteria might be A. hydricolla. However, when chickens were force-fed the bacteria, they didn’t develop the disease, suggesting that was only part of the story.
Meanwhile, eagles, coots, Canada geese, owls, and other birds have continued to die of the disease. By 2019, at just one lake in Georgia, a total of 105 eagle deaths had been confirmed. But as the Associated Press reported, the total is likely much higher as bird carcasses aren’t always recovered.
What’s new — In this new study, Wilde worked with pharmacologist Timo Niedermeyer and Breinlinger, both of whom had also been tackling AVM from the bacterial side at Martin Luther University of Halle Wittenberg in Germany. Their earlier work revealed a missing link in the environment that wasn’t present in the lab: bromide.
Some bromide is naturally found in seawater, but it is also released in large quantities through human activities. Bromide can drain into waterways from road salts, flame retardants, municipal waste incinerators, herbicides (some actually used to kill waterthyme), coal-fired power plants, and other industries.
For this paper, the team introduced bromide into cyanobacteria and found it produced the neurotoxin they had seen in wild waterthyme. When they exposed the neurotoxin to zebrafish, they had seizures. When they exposed chickens to the neurotoxin manufactured in the lab, or neurotoxin gleaned from the environment, none of the groups developed spastic symptoms. But those who received the toxin developed the characteristic vacuoles on their brainstems.
Breinlinger explains the chickens may not have developed symptoms because, in nature, animals are exposed to this toxin far longer than they would be in one lab experiment. But for now, it seems clear that the toxin, spurred on by bromide, is behind the disease.
As Breinlinger puts it: “We all teamed up to hunt the eagle killer!”
What can we do about it? — Monitoring bromide in the environment isn’t easy because environments aren’t stagnant, but it could be a key way to control the spread of AVM.
Waterthyme leaves contain about 20 times more bromide than sediment, and between 500 and 1000 times more bromide than the water itself. In the fall, waterthyme dies and water levels mix, effectively dousing the environment (and the cyanobacteria within it) with the bromide needed to make the toxin.
We could try to eliminate or at least control the invasive plants, Wilde suggests. But the plants are extremely widespread and have been reported in at least 31 states. Even once weeded out waterthyme can regrow from roots or plant fragments left behind. That’s why Breinlinger calls controlling waterthyme a “Sisyphean task.”
Still, Wilde believes it can be done. “If more people recognize invasive species and report them, we can rapidly respond and better manage or eradicate harmful species,” she says.
But even that might not be enough unless we also address the bromide that ends up in waterways through herbicides.
“Much like the butterfly that causes a hurricane on the other side of the planet, we cannot just throw a herbicide in a reservoir because we want to get rid of one particular invasive plant and expect nothing else to happen,” Breinlinger says.
Abstract: Vacuolar myelinopathy is a fatal neurological disease that was initially discovered during a mysterious mass mortality of bald eagles in Arkansas in the United States. The cause of this wildlife disease has eluded scientists for decades while its occurrence has continued to spread throughout freshwater reservoirs in the southeastern United States. Recent studies have demonstrated that vacuolar myelinopathy is induced by consumption of the epiphytic cyanobacterial species Aetokthonos hydrillicola growing on aquatic vegetation, primarily the invasive Hydrilla verticillata. Here, we describe the identification, biosynthetic gene cluster, and biological activity of aetokthonotoxin, a pentabrominated biindole alkaloid that is produced by the cyanobacterium A. hydrillicola. We identify this cyanobacterial neurotoxin as the causal agent of vacuolar myelinopathy and discuss environmental factors—especially bromide availability—that promote toxin production