Avian vacuolar myelinopathy (AVM) is a fatal neurological disease that affects various waterbirds and raptors. It is most common in the bald eagle and American coot, and it is known in the killdeer, bufflehead, northern shoveler, American wigeon, Canada goose, great horned owl, mallard, and ring-necked duck. [1] [2] Avian vacuolar myelinopathy is a newly discovered disease that was first identified in the field in 1994 when dead bald eagles were found near DeGray Lake in Arkansas in the United States. Since then, it has spread to four more states and infested multiple aquatic systems including 10 reservoirs. [3] [4] The cause of death is lesions on the brain and spinal cord. [2] [5] A neurotoxin called aetokthonotoxin produced by cyanobacteria causes the disease. [6]
Clinical signs have been recorded from research studies where individual birds were intentionally given the disease and from wild specimens and dead birds recovered from the field. [7] [8] [9]
In 2021, researchers found that the cause of the disease is a neurotoxin produced by the cyanobacterium Aetokthonos hydrillicola . [6] This particular cyanobacterium grows very well on the invasive species hydrilla (Hydrilla verticillata), covering 20–90% of leaf surfaces. [8] These invasive hydrilla plants often take over any aquatic system to which they are introduced. [3] Waterfowl then consume the hydrilla, ingesting the cyanobacteria. Some raptors, like bald eagles, prey upon the diseased waterfowl and contract identical clinical symptoms from consuming toxin-containing tissues. [3] The toxin causes widespread vacuolation of the white matter of the brain and spinal cord of intoxicated birds. [2]
Birrenkott et al. (2004) [4] attempted a study in 2004 to determine linkage between the invasive aquatic plant Hydrilla verticillata and the outbreak of AVM among waterfowl after it was observed that only lakes containing excess amounts of hydrilla harbored infected birds. In this study, adult mallards and northern bobwhites were divided by species into multiple sections to observe the effects of hydrilla when it was ingested by the birds, and also by physical contact or drinking of water containing hydrilla. The results of this study found that drinking water or physical contact with hydrilla or areas in which it was present had no noticeable effect on test birds. However, when fed a diet of over 50% hydrilla, the birds developed AVM. Wilde et al. (2005) [8] performed a study to determine the cause of AVM by conducting food trials in areas affected by AVM. Disease-free mallards were fed cyanobacteria from hydrilla and observed daily. Birds that developed symptoms were captured and euthanized. By the conclusion of the study, 15 of the 20 study mallards had been recovered, and all had AVM. In 2021, after 25 years of research on this disease, its cause was finally identified to be a novel tryptophan derived alkaloid known as Aetokthonotoxin that is produced by the aforementioned bacteria. [6]
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Aetokthonotoxin (AETX), colloquially known as eagle toxin, is a chemical compound that was identified in 2021 as the cyanobacterial neurotoxin causing vacuolar myelinopathy (VM) in eagles in North America. As the biosynthesis of aetokthonotoxin depends on the availability of bromide ions in freshwater systems and requires an interplay between the toxin-producing cyanobacterium Aetokthonos hydrillicola and the host plant it requires to live, it took more than 25 years to identify aetokthonotoxin as the VM-inducing toxin after the disease has first been diagnosed in bald eagles in 1994. The toxin cascades through the food-chain: Among other animals, it builds up in fish and waterfowl such as coots or ducks which feed on hydrilla colonized with the cyanobacterium. Aetokthonotoxin is transmitted to raptors, such as the bald eagle, as they prey on AETX poisoned animals. The total synthesis of AETX was achieved in 2021, the enzymatic functions of the 5 enzymes involved in AETX biosynthesis were described in 2022.