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Category: Viruses and Viral Pathogenesis
7 Pathology of Allergic Forms of Encephalomyelitis, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817831/9781555812409_Chap07-1.gif /docserver/preview/fulltext/10.1128/9781555817831/9781555812409_Chap07-2.gifAbstract:
The concept of allergic damage to the nervous system arose with Pasteur's vaccine against rabies, first used in 1884. This vaccine was prepared from the dried and fixed spinal cord of an experimentally infected rabbit. Experiments on the effects of injecting uninfected brain tissue into animals showed that this procedure alone was capable of producing similar changes. The same pathological state has also been described after nonspecific upper respiratory tract infections and in the absence of overt preceding infection. Regardless of the setting in which allergic encephalitis occurs, the pathology is quite similar. The white matter of the centrum ovale is almost invariably severely involved, and in most cases the changes extend into the brain stem and spinal cord. Cases presenting clinically as acute transverse myelitis may show more severe pathology in the spinal cord than in the brain. The demyelination takes the form of a narrow sleeve around inflamed perivenous and perivenular spaces. Most clinicians and pathologists are impressed by the very close similarities in time course and histopathology between these inflammatory diseases and experimental allergic encephalomyelitis (EAE). The pathology consists initially of perivenular inflammatory cell infiltration with lymphocytes, plasma cells, and macrophages within the CNS, particularly in the white matter.
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Macroscopic appearance of coronal slice from a case of PVE. Vascular markings are prominent, and lateral and third ventricles are reduced in size.
Macroscopic appearance of coronal slice from a case of PVE. Vascular markings are prominent, and lateral and third ventricles are reduced in size.
Low-power view of cerebral white matter from a case of PVE. Myelin stain shows loss of myelin around veins.
Low-power view of cerebral white matter from a case of PVE. Myelin stain shows loss of myelin around veins.
Inflammatory cells in perivenous space and immediately surrounding white matter from a case of PVE. Hema toxylin and eosin stain.
Inflammatory cells in perivenous space and immediately surrounding white matter from a case of PVE. Hema toxylin and eosin stain.
Immunostaining inflammatory cells in perivenous space and adjacent white matter from a case of PVE showing (a) macrophages stained for CD68 and (b) leukocytes (mainly lymphocytes) stained for leukocyte common antigen. Both counterstained with hematoxylin
Immunostaining inflammatory cells in perivenous space and adjacent white matter from a case of PVE showing (a) macrophages stained for CD68 and (b) leukocytes (mainly lymphocytes) stained for leukocyte common antigen. Both counterstained with hematoxylin
Electron micrograph of cerebrum (a) and spinal cord (b) from two autopsy cases of PVE. Complete (a) or incomplete (b) vesicular dissolution of myelin with axons remaining intact. Lead citrate and uranyl acetate stain. Magnification, × 19,800.
Electron micrograph of cerebrum (a) and spinal cord (b) from two autopsy cases of PVE. Complete (a) or incomplete (b) vesicular dissolution of myelin with axons remaining intact. Lead citrate and uranyl acetate stain. Magnification, × 19,800.
Macroscopic appearance of coronal slice from a case of AHLE. Vascular markings and swelling are even more marked than in Fig. 7.1, and there are foci of petechial hemorrhage (white arrows).
Macroscopic appearance of coronal slice from a case of AHLE. Vascular markings and swelling are even more marked than in Fig. 7.1, and there are foci of petechial hemorrhage (white arrows).
Perivascular cells from a case of AHLE. Note that many are polymorphonuclear leukocytes. Hematoxylin counterstain on preparation immunostained for leukocyte common antigen.
Perivascular cells from a case of AHLE. Note that many are polymorphonuclear leukocytes. Hematoxylin counterstain on preparation immunostained for leukocyte common antigen.
Immunostain for β-amyloid precursor protein to mark damaged axons in a case of AHLE. Perivenous axons are selectively damaged. Counterstained with hematoxylin.
Immunostain for β-amyloid precursor protein to mark damaged axons in a case of AHLE. Perivenous axons are selectively damaged. Counterstained with hematoxylin.
Steps envisaged as occurring in development of PVE, based on experimental studies of EAE, and interventions that are effective in preventing or reducing clinical expression of the disease
Steps envisaged as occurring in development of PVE, based on experimental studies of EAE, and interventions that are effective in preventing or reducing clinical expression of the disease