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Clinical features of avian vacuolar myelinopathy in American coots

R. Scott LarsenEnvironmental Medicine Consortium, Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606.
North Carolina Zoological Park, Asheboro, NC 27203.

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Felicia B. NutterEnvironmental Medicine Consortium, Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606.

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Tom AugspurgerUnited States Fish and Wildlife Service, Raleigh Field Office, Raleigh, NC 27636.

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Tonie E. RockeUS Geological Survey, Biological Resources Division, National Wildlife Health Center, Madison, WI 53711.

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Lindsay TomlinsonMicrobiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606.
Present address is the Department of Pathology, Bristol-Myers Squibb Co, 1 Squibb Dr, New Brunswick, NJ 08903.

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Nancy J. ThomasUS Geological Survey, Biological Resources Division, National Wildlife Health Center, Madison, WI 53711.

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Michael K. StoskopfEnvironmental Medicine Consortium, Departments of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606.

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 DVM, PhD, DACZM

Abstract

Objective—To characterize clinical features of avian vacuolar myelinopathy (AVM) in American coots.

Design—Case-control study.

Animals—26 AVM-affected American coots and 12 unaffected coots.

Procedures—Complete physical, neurologic, hematologic, and plasma biochemical evaluations were performed. Affected coots received supportive care. All coots died or were euthanatized, and AVM status was confirmed via histopathologic findings.

Results—3 severely affected coots were euthanatized immediately after examination. Seventeen affected coots were found dead within 7 days of admission, but 5 affected coots survived > 21 days and had signs of clinical recovery. Abnormal physical examination findings appeared to be related to general debilitation. Ataxia (88%), decreased withdrawal reflexes (88%), proprioceptive deficits (81%), decreased vent responses (69%), beak or tongue weakness (42%), and head tremors (31%), as well as absent pupillary light responses (46%), anisocoria (15%), apparent blindness (4%), nystagmus (4%), and strabismus (4%) were detected. Few gross abnormalities were detected at necropsy, but histologically, all AVM-affected coots had severe vacuolation of white matter of the brain. None of the control coots had vacuolation.

Conclusions and Clinical Relevance—Although there was considerable variability in form and severity of clinical neurologic abnormalities, clinical signs common in AVM-affected birds were identified. Clinical recovery of some AVM-affected coots can occur when supportive care is administered. Until the etiology is identified, caution should be exercised when rehabilitating and releasing coots thought to be affected by AVM. (J Am Vet Med Assoc 2002;221: 80–85)

Abstract

Objective—To characterize clinical features of avian vacuolar myelinopathy (AVM) in American coots.

Design—Case-control study.

Animals—26 AVM-affected American coots and 12 unaffected coots.

Procedures—Complete physical, neurologic, hematologic, and plasma biochemical evaluations were performed. Affected coots received supportive care. All coots died or were euthanatized, and AVM status was confirmed via histopathologic findings.

Results—3 severely affected coots were euthanatized immediately after examination. Seventeen affected coots were found dead within 7 days of admission, but 5 affected coots survived > 21 days and had signs of clinical recovery. Abnormal physical examination findings appeared to be related to general debilitation. Ataxia (88%), decreased withdrawal reflexes (88%), proprioceptive deficits (81%), decreased vent responses (69%), beak or tongue weakness (42%), and head tremors (31%), as well as absent pupillary light responses (46%), anisocoria (15%), apparent blindness (4%), nystagmus (4%), and strabismus (4%) were detected. Few gross abnormalities were detected at necropsy, but histologically, all AVM-affected coots had severe vacuolation of white matter of the brain. None of the control coots had vacuolation.

Conclusions and Clinical Relevance—Although there was considerable variability in form and severity of clinical neurologic abnormalities, clinical signs common in AVM-affected birds were identified. Clinical recovery of some AVM-affected coots can occur when supportive care is administered. Until the etiology is identified, caution should be exercised when rehabilitating and releasing coots thought to be affected by AVM. (J Am Vet Med Assoc 2002;221: 80–85)