Epizootic avian vacuolar myelinopathy (AVM) was first recognized as a neurologic disease in bald eagles (Haliaeetus leucocephalus) and American coots (Fulica americana) in Arkansas, USA in 1994 and 1996, respectively, but attempts to identify the etiology of the disease have been unsuccessful to date. Between 1998 and 2001, wing clipped sentinel birds (wild American coots and game farm mallards [Anas platyrhynchos]) were released at Lake Surf, North Carolina, a lake with recurrent outbreaks of AVM, in order to gain a better understanding of the epizootiology of the disease. As early as 5–7 days post-release, sentinel coots and mallards showed neurologic signs of disease and were confirmed with AVM upon histologic examination of their brains. Serial releases of sentinel mallards during the summer, fall, and winter of 2000–01 demonstrated that exposure to the causative agent at a threshold sufficient to manifest disease was seasonal and occurred over about a 2 mo period, during November and December. Our findings that disease onset can be very rapid (5–7 days) and that exposure to the causative agent of AVM is site-specific, seasonal (late fall to early winter), and occurs over a relatively short duration (several months) supports the hypothesis that the disease is caused by a chemical substance, most likely of natural origin.
EPIZOOTIOLOGIC STUDIES OF AVIAN VACUOLAR MEYLINOPATHY IN WATERBIRDS
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Tonie E. Rocke, Nancy J. Thomas, Tom Augspurger, Kimberli Miller; EPIZOOTIOLOGIC STUDIES OF AVIAN VACUOLAR MEYLINOPATHY IN WATERBIRDS. J Wildl Dis 1 October 2002; 38 (4): 678–684. doi: https://doi.org/10.7589/0090-3558-38.4.678
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