Bald Eagle Killer: Mysterious Suspect Finally Found After 25 Years

Scientists appear to have cracked the mystery of a neurological disorder that has been killing bald eagles and other birds in the United States after 25 years.

According to New Scientist, eagles might have consumed bromide-laced prey plucked from lakes. These species then developed a disease caused by a toxin released by blue-green algae from the lake.

Bald eagles died in large numbers in Arkansas in 1994. The predatory birds' navigation abilities will deteriorate until death, forcing them to crash into trees or even losing their ability to fly.

Killer Plant Spreading Across U.S.

When their brains were analyzed post-mortem, scientists discovered distinct lesions and gaps inside, giving the impression that the disease had eaten the brain away.

The condition was eventually determined to have been contracted by the eagles from the waterbirds they preyed on, who also showed similar symptoms before dying. Experts named the disorder Avian vacuolar myelinopathy (AVM).

For years, scientists believed AVM was contagious in some way, but the precise cause was unclear. More AVM outbreaks occurred along the way in the Southeastern United States, around lakes and other freshwater bodies. By the early 2000s, they had established a strong link between the spread of Hydrilla verticillata, an invasive aquatic species, and AVM.

Researchers discovered in 2015 that a particular photosynthetic bacteria called cyanobacteria that grows on this plant caused the AVM. The previously unknown species was given the name Aetokthonos hydrillicola, which means "eagle killer living on hydrilla" in Greek and Latin.

Cyanobacteria are also known as blue-green algae because of their color when clumped together in large numbers. Despite the nickname, they are not true algae. This type of algae is harmful to animals and humans because of the toxins it can create.

When scientists from the University of Georgia and other institutions attempted to examine A. hydrillicola in isolation, they discovered a problem. The bacteria they produced in their lab were harmless to birds. They seemed to be harmful only when they were growing on the vine.

Who is the Suspect Then? Did Bromides Kill Eagles?

Scientists from the University of Georgia collaborated with researchers from Germany and the Czech Republic to solve the AVM puzzle's final parts in a report.

They published the study, titled "Hunting the Eagle Killer: A Cyanobacterial Neurotoxin Causes Vacuolar Myelinopathy," in the journal Science on Thursday.

According to their findings, A. hydrillicola only creates the toxin that triggers AVM when it is also exposed to bromide, the negatively charged form of bromine.

The researchers were eventually able to trigger this toxin from their lab-grown samples of A. hydrillicola. They discovered that it could kill birds in the same way that AVM does in the wild after discovering this connection.

The bacteria's genetic analysis also revealed the unique bits of DNA that allow it to produce the toxin. Experts assigned their latest find the name aetokthonotoxin (AETX), which means "eagle poison."

In reviewing their results, the researchers said AETX is the agent of vacuolar myelinopathy.

Though they could have figured out the actual killing behind AVM, there are still some unanswered questions.

Specifically, where does the bromide that drives this toxin's development come from? Why does AVM tend to be confined to the United States?

Bromide can be used in various natural environments. Still, it's also found in various synthetic compounds that may end up in the marine world. Researchers can use it in herbicides to monitor the Hydrilla plant's spread around water treatment facilities and elsewhere, in particular. As a result, people likely contributed to the emergence of a new environmental catastrophe to solve one issue.

More study is required to validate the role of these herbicides and other human-made sources of bromide in triggering AVM outbreaks. However, the authors still warn against using them to manage Hydrilla populations. Since this toxin can develop in animals other than birds, such as rodents, fish, and amphibians, it has the potential to make mammals, including humans, ill.

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