Press – Athens, Ga. – The alarm bells began to ring when a dozen eagles were found dead near a lake in Arkansas.
The death – and, later, the death of other waterfowl, amphibians and fish – was due to a brain disease that caused holes in the white matter of the brain. Site and laboratory research over nearly three decades has established the key clusters needed to unravel this wildlife mystery: Eagle and waterfowl deaths occur in late autumn and winter within reservoirs with excessive water weeds, and birds can die within five days of arrival.
But until recently, the poison that caused the infection, vacuolar myelinopathy, was unknown.
Now, after years of identifying toxic blue-green algal species (cyanobacteria) and separating the toxic fertilizer, an interdisciplinary research group from the University of Georgia and international colleagues on the structure of the toxin to prove this. The results were recently published in the journal Science.
The cyanobacteria grow on the leaves of an invasive aquatic plant, Hydrilla verticillata, under certain conditions: in human lakes when bromide is present. The bacteria – and the animal deaths caused by it – have been recorded in waters throughout the southeastern United States. That’s why it’s important for anyone in the outdoors – anglers, hunters, birdwatchers and more – to be aware of the symptoms of this neurological disease and to avoid eating animals. contagious.
“We want people to recognize it before taking birds or fish from these lakes,” said Susan Wilde, an associate professor of water science at Warnell School of Forestry and Natural Resources who first discovered the cyanobacteria. In some animals, such as birds, turtles, salamanders and even beavers, the disease manifests as irregular movements or movements. Anglers need to be even more careful, however, as it is impossible to detect toxin in fish without obvious symptoms.
“For fish, it’s sad. I avoided fish with sores or deformities of some kind; we see fish affected by slow swimming speeds, but anglers can’t see that, ”said Wilde. “We want people to know the lakes where this disease was recorded and to be careful about eating birds and fish from those lochs.”
Wilde and Warnell graduate students studying the cyanobacteria have compiled maps and a list of affected watercourses.
The latest study details a new mapping of the genome of the bacteria, a final piece in the puzzle to understand how it develops and survives. Wilde and others have been studying the cyanobacteria since 2001, when bald eagles began to die in Georgia, South Carolina and North Carolina. In later decades the cyanobacteria themselves, Aetokthonos hydrillicola (Latin for “killing an eagle that grows on Hydrilla”), were discovered, and links were made between the invasive aquatic plant and the animals that eat it.
But until recently, Professor Timo Niedermeyer of the Martin Luther Halle-Wittenberg University Pharmacy Institute in Germany said that the origin of the degenerative disease in the brain was a mystery.
Niedermeyer, who has been working with natural cyanobacteria products for years, wanted to help put the pieces together. He contacted Wilde and offered to cooperate. Samples of Hydrilla collected in the field were sent to him, and his lab nurtured the cyanobacteria in the laboratory and sent them back to UGA for further testing. But the tests came back negative: The cyanobacteria from the laboratory did not transmit the disease.
“It wasn’t just the birds that were going crazy, we were too. We wanted to prove this, ”said Niedermeyer. Again, he had settled pages sent to him from UGA.
Steffen Breinlinger, a doctoral student in his research group, used a new imaging beauty spectrometer to study the combination of the plant’s leaf-molecular, molecular-to-molecular surface. He discovered a new material that only occurs on the leaves where the cyanobacteria grows but is not extracted in the cyanobacteria cultures. His studies on the chemical structure of the isolated molecule showed five bromine atoms.
“The structure is amazing,” Breinlinger said. The unusual properties for molecules are created by cyanobacteria, and they explain why the poison did not form under laboratory conditions, where bromide is not present. “We then added bromide to our laboratory cultures, and the cyanobacteria began to release the toxin. ”
After nearly a decade of testing the peripheral molecule and collaboration between the laboratories in Germany and Georgia, they had the proof: the molecule causes vacuolar myelinopathy. The researchers call their discovery aetokthonotoxin, “a poison that kills the eagle.”
“Ultimately, not only did we catch the assassin, but we also mentioned the weapon that the cyanobacteria would use to kill these eagles,” Wilde said.
The neurological disease has not yet occurred in Europe, and no example of the toxin-producing cyanobacterium has been reported. It is not yet known that humans suffer from vacuolar myelinopathy, although the study found a successful effect on chickens with the toxin, and Wilde continues to test fish and waterfowl such as ducks and coots for the disease.
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This message can be found online at https://news.uga.edu/international-investigation-discovers-bald-eagles-killer/