Avian vacuolar myelinopathy (AVM) was first recognized as a cause of bald eagle (Haliaeetus leucocephalus) mortality in 1994 in Arkansas (USA) and has since caused over 90 bald eagle and numerous American coot (Fulica americana) mortalities in five southeastern states. The cause of AVM remains undetermined but is suspected to be a biotoxin. Naturally occurring AVM has been limited to wild waterbirds, raptors, and one species of shorebird, and has been reproduced experimentally in red-tailed hawks (Buteo jamaicensis). In this study, chickens and swine were evaluated for susceptibility to vacuolar myelinopathy with the intent of developing animal models for research and to identify specific tissues in affected coots that contain the causative agent. Additionally, submerged, aquatic vegetation, primarily hydrilla (Hydrilla verticillata), and associated material collected from a reservoir during an AVM outbreak was fed to chickens in an effort to reproduce the disease. In two separate experiments, six 4-wk-old leghorn chickens and ten 5-wk-old leghorn chickens were fed coot tissues. In a third experiment, five 3-mo-old domestic swine and one red-tailed hawk, serving as a positive control, were fed coot tissues. In these experiments, treatment animals received tissues (brain, fat, intestinal tract, kidney, liver, and/or muscle) from coots with AVM lesions collected at a lake during an AVM outbreak. Negative control chickens and one pig received tissues from coots without AVM lesions that had been collected at a lake where AVM has never been documented. In a fourth experiment, eight 3-wk-old leghorn chickens were fed aquatic vegetation material. Four chickens received material from the same lake from which coots with AVM lesions were collected for the previous experiments, and four control chickens were fed material from the lake where AVM has never been documented. Blood was collected and physical and neurologic exams were conducted on animals before and once per week during the trials. All animals were sacrificed and necropsies were performed on Day 29 of feeding, with the exception of one treated chicken that was sacrificed and necropsied on Day 15 of feeding. Microscopic lesions of vacuolar myelinopathy were present in the red-tailed hawk and five chickens that received a mixture of all tissues and two chickens that received only gastrointestinal tissues of coots with AVM lesions. Three of four treated chickens in the aquatic vegetation trial developed vacuolar lesions. None of four treatment pigs or any of the negative control animals developed vacuolar lesions. Chickens are susceptible to AVM and may serve as a useful animal model for future studies. Swine may be refractory to AVM or not affected by AVM at the same dose as are chickens and red-tailed hawks. The causative agent of AVM in affected coots is associated with the gastrointestinal tissues. Furthermore, AVM can be reproduced in chickens via ingestion of aquatic vegetation and associated materials collected from a lake during an AVM outbreak. T...

ABSTRACT:Avian vacuolar myelinopathy (AVM) is a neurologic disease of unknown etiology that affects bald eagles (Haliaeetus leucocephalus), American coots (Fulica americana), and several species of waterfowl. An unidentified neurotoxin is suspected as the cause of AVM, which has been documented at several reservoirs in the southeastern United States. We conducted diagnostic and epidemiologic studies annually during October-March from 1998-2004 at Clarks Hill/Strom Thurmond Lake on the Georgia/South Carolina border to better understand the disease. Avian vacuolar myelinopathy was confirmed or suspected as the cause of morbidity and mortality of 28 bald eagles, 16 Canada geese (Branta canadensis), six American coots, two great-horned owls (Bubo virginianus), and one killdeer (Charadrius vociferus). Active surveillance during the outbreaks yielded annual average prevalence of vacuolar lesions in 17-94% of coots, but not in 10 beavers (Castor canadensis), four raccoons (Procyon lotor), and one gray fox (Urocyon cinereoargenteus) collected for the study. Brain lesions were not apparent in 30 Canada geese collected and examined in June 2002. The outbreaks at this location from 1998-2004 represent the most significant AVM-related bald eagle mortality since the Arkansas epornitics of 1994-95 and 1996-97, as well as the first confirmation of the disease in members of Strigiformes and Charadriiformes.

Implementation of the Conservation Reserve Program (CRP) altered the interspersion and abundance of patches of different land-cover types in landscapes of the southeastern United States. Because northern bobwhites (Colinus virginianus) are experiencing significant population declines throughout most of their range, including the Southeast, it is critical to understand the impacts of landscape-scale changes in habitat on their reproductive rates. Our objective was to identify components of landscape structure important in predicting nest site selection by bobwhites at different spatial scales in the Upper Coastal Plain of Georgia. We used a Geographic Information System (GIS) and spatial analysis software to calculate metrics of landscape structure near bobwhite nest sites. Logistic regression was used to model the relationship of nest sites to structure within the surrounding landscape at 4 spatial scales. We found that patch density and open-canopy planted pine were consistently important predictor variables at multiple scales, and other variables were important at various scales. The density of different patch types could be increased by thinning rows of pines in large monotypic stands of closed-canopy planted pine stands. Thinning and creating openings in CRP pine plantations should provide increased nesting opportunities for bobwhites. We interpret the support for other variables in our analysis as an indication that various patch configuration lead to different combinations of landscape structure that provide an acceptable range of habitat conditions for bobwhites. JOURNAL OF WILDLIFE MANAGEMENT 69(4):1528-1537; 2005

Avian vacuolar myelinopathy (AVM) was recognized in 1994 as a cause of wild bird mortality when 29 bald eagles (Haliaeetus leucocephalus) succumbed to the disease at DeGray Lake, Arkansas (USA). The cause of AVM and its source remain undetermined despite extensive diagnostic and research investigations. Two years later, when AVM killed 26 eagles in the same area in Arkansas, it became apparent that American coots (Fulica americana) had identical neurologic signs and lesions, and it was hypothesized that eagles acquired AVM via ingestion of affected coots. In order to test this hypothesis, we fed coot tissues (brain, liver, kidney, muscle, fat, and intestinal tract) to rehabilitated, non-releasable red-tailed hawks (Buteo jamaicensis). Five hawks received tissues from coots with AVM lesions, and one hawk received tissues from coots without brain lesions that had been collected at a site where AVM never has been documented. All hawks received 12-70 g/day (mean = 38 g) of coot tissues for 28 days. All six hawks remained clinically normal during the study. The birds were euthanatized on day 29 and microscopic lesions of AVM were found in all hawks that received tissues from affected coots, but not in the hawk that received tissues from unaffected coots. This marks the first time that AVM has been produced in birds under laboratory conditions and proves that birds of prey can acquire AVM via ingestion of tissues from affected coots.