Submitted to: Journal of Veterinary Diagnostic Investigation
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/16/2001
Publication Date: N/A
Citation: N/A Interpretive Summary: Raccoons are highly adaptable omnivores and have managed to survive and increase their numbers in many urban and suburban areas. For this reason, they have been used as monitors of zoonotic diseases and environmental contamination. Under free ranging situation, these animals may get access to animal carcasses that may have died of naturally occurring transmissible espongiform encephalopathies (TSEs) such as scrapie, transmissible mink encephalopathies (TME), and chronic wasting disease (CWD). Experimental evidence indicates that raccoons can be readily infected by TME. Therefore, raccoons can be considered as useful experimental animal models for the study of TSEs of livestock. However, since there is paucity of published information on diseases of raccoons (especially those affecting the brain), documentation of naturally occurring diseases and lesions in this species is of paramount importance. In the present study, microscopic evidence of degeneration of brain cells (neurons) was seen in 17/39 (47% prevalence in adults) of raccoons from Iowa. These degenerative changes are in some respects similar to those seen in TSEs. However, confirmatory tests for the presence of this disease were negative. The findings were probably related to advancing age. However, because of the apparent geographic restriction of this condition in Iowa, factors other than age (such as genetic, nutrition, and/or environment) have to be considered. Major impact of this study will be on veterinary diagnostic pathologists who for the first time will be aware of this TSE-like lesion in raccoons. They will need to perform a specific test for TSEs on such cases to rule out the possibility of a TSE disease.
Technical Abstract: During a 12-month period (1998-1999) microscopic evidence of neuroaxonal degeneration in medulla of raccoons (Procyon lotor) was seen in 17/39 (47% prevalence in adults) from Iowa, USA. Three of the animals were kits (< 3 months), 26 were between 1 and 2 years, and 10 were over 7 years. Lesions were not seen in the medulla of the 3 kits. In young adults, the lesions were mild and were seen in 7 animals. More severe lesions were present in the 10 older raccoons. Grossly, the brains were unremarkable. Microscopically, neuroaxonal degeneration was confined to the dorsal caudal medulla where certain nuclei (predominantly gracilis and cuneate) were bilaterally affected. Severely affected animals had vacuolar degeneration of neurons, often resulting in complete disappearance of neuronal cells and resulting in extensive areas of spongiosis. Tests for the presence of PrPres in the brain were negative. In less affected cases, axonal spheroids, with or without amphophilic PAS positive granular material, was seen within some of the degenerate neurons and axons. In positive cases, there was a paucity of inflammatory cells in the affected areas. Since lesions were not present in kits, were either absent or mild in young adults, and severe in older raccoons, the findings may be related to advancing age. However, because of the apparent geographic restriction of this condition, factors other than age (genetic, nutrition, and/or environment) may influence the process of degenerative changes in the brains of raccoons in Iowa.