Lynn A. Lewis-Weis, MS; R.W. Gerhold, DVM; John R. Fischer, DVM, PhD
Southeastern Cooperative Wildlife Disease Study, College of Veterinary Medicine, University of Georgia, Athens, GA, USA
Abstract
Avian vacuolar myelinopathy (AVM) was first recognized as a cause of bald eagle mortality in 1994 in Arkansas and has since caused more than 90 bald eagle and numerous American coot mortalities in five southeastern states. The cause of AVM remains undetermined but is suspected to be a natural toxicant. In this study, chickens and swine were evaluated as potential animal models for AVM research. Chickens that consumed a mixture of tissues from coots with AVM for 28 days developed brain lesions consistent with those of AVM, as did chickens that received only the gastrointestinal tracts of affected coots in a subsequent trial. Additionally, chickens that consumed submerged vegetation (hydrilla) collected from a lake during an AVM outbreak developed brain lesions. Chickens that consumed only coot liver, kidney, brain, muscle, or adipose tissue did not develop brain lesions, nor did chickens that consumed submerged vegetation (hydrilla) from a lake where AVM’s absence has been documented for several years. Brain lesions were not apparent in young pigs that consumed a mixture of tissues from affected coots for 28 days. Results of these studies indicate that chickens can serve as useful animal models for AVM research and that the cause of AVM is associated with the gastrointestinal tracts of affected coots, apparently as a consequence of consuming submerged vegetation from lakes during AVM outbreaks.