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Massive Necrosis of the Brain in Rabies

Published online by Cambridge University Press:  18 September 2015

C.L. Dolman  and
K.M. Charlton
C.L. Dolman*
Affiliation:
Department of Pathology, University of British Columbia and Vancouver General Hospital, Vancouver
K.M. Charlton
Affiliation:
Pathology Section & Rabies Unit, Animal Diseases Research Institute, Nepean, Ontario
*
Pathology Laboratory, Vancouver General Hospital, 855 W. 12th Ave., Vancouver, B.C., Canada V5Z 1M9
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Abstract:

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A young man developed virologically proved hydrophobic rabies three months after being scratched on the cheek by a bat in Northern Alberta. He became comatose after 8 days and died 5 weeks after vigorous therapy with immune globulin, interferon and Vidarabine, and excellent maintenance of oxygenation. Electroencephalographic deterioration was gradual. At postmortem examination, the brain showed widespread loss of nerve cells, mild diffuse inflammatory changes and no Negri bodies. The lesions of massive laminar necrosis of the cerebral cortex, total loss of Purkinje cells with preservation of the granule cell layer, and severe softening of the amygdala are attributed to direct viral action rather than to anoxia or brain swelling with respirator brain.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 14 , Issue 2 , May 1987 , pp. 162 - 165
Copyright
Copyright © Canadian Neurological Sciences Federation 1987

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