Description

Between 2000 and 2005, the U.S. Fish and Wildlife Service Service and partners conducted an investigation of avian vacuolar myelinopathy AVM, an unusual neurological disease which has killed more than 100 bald eagles Haliaeetus leucocephalus since and thousands of coots Fulica americana wintering in Arkansas, Georgia, North Carolina, and South Carolina. By light microscopy, affected birds show diffuse, spongy degeneration of central nervous system white matter; by electron microscopy, the lesion is characterized as vacuoles formed in the myelin sheaths. The study was conducted to elucidate the etiology of AVM with a focus on 1 pathway identification through field and lab trials to reproduce the disease; and 2 toxicant identification through chemical analyses of birds and other media at affected and unaffected sites. Lake Surf also known as Woodlake, North Carolina, was the site for most of the work. We posed these specific study questions to address aspects of the disease not understood in 2000: Do birds arrive with the disease upon migration or get sick upon arrival? When is disease onset and what is its duration? Do birds with AVM always die, or can they recover? What at the lakes with AVMaffected birds might be causing the disease? Components of the study have been summarized in five peer reviewed publications and these papers provide detailed methods and study results. Some key findings include: Exposure to the causative agent of AVM is sitespecific birds get the disease locally, Exposure to the causative agent is seasonal, autumn to early winter; onset of disease can be rapid, within as little as 5 days postexposure; mallards Anas platyrhynchos can be effectively used as sentinels to monitor the disease; the severity of clinical signs does not appear closely linked with the severity of brain lesions; some birds with no clinical signs had lesions described as severe and several birds with obvious neurologic impairment had brain lesions described as mild; clinicallyaffected birds could regain function with supportive veterinary care; AVM was not transmitted by direct contact between affected birds and healthy birds; feeding studies were inconclusive although others have since experimentally reproduced the disease through feeding; and neither the sediments nor tissues analyzed show any compounds that are present in all of AVM positive lakes but not present or of low abundance in AVM negative lakes This study and others have not defined a specific cause. Currently, the cause is thought to be a naturally produced toxin associated with something in or on aquatic plants at the affected sites. Results of our study have been routinely cited in the work of others, indicating that the cooperative assessment provided advances in understanding of the disease.

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