Regional distribution of rabies viral antigen in central nervous system of human encephalitic and paralytic rabies

Tirawatnpong, Suranan; Hemachudha, Thiravat; Manutsathit, Sathaporn; Shuangshoti, Samruay; Phanthumchinda, Kammant; Phanuphak, Praphan

doi:10.1016/0022-510x(89)90178-0

Cited by 64 publications

(45 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, furious rabies patients had electrophysiologic and pathological evidence of anterior horn cells dysfunction. Our previous studies showed that rabies virus localization on autopsy or MRI pattern of involvement or specific rabies virus variant did not predict whether a patient was to have paralytic or furious rabies [2,17,18,28]. The findings of peripheral nerve, rather than anterior horn cell involvement in paralytic rabies, suggests that another mechanism other than direct viral infection may be involved in the paralysis.…”

Section: Discussionmentioning

confidence: 90%

See 1 more Smart Citation

Difference in neuropathogenetic mechanisms in human furious and paralytic rabies

Mitrabhakdi

Shuangshoti

Wannakrairot

et al. 2005

Journal of the Neurological Sciences

Self Cite

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 90%

“…Once in the CNS, the exact pathway of virus propagation is not known [15,16]. Postmortem examination in human rabies patients showed the brainstem and spinal cord as preferential sites of virus infection regardless of clinical types, as determined by immunohistochemistry [17].…”

Section: Introductionmentioning

confidence: 99%

Difference in neuropathogenetic mechanisms in human furious and paralytic rabies

Mitrabhakdi

Shuangshoti

Wannakrairot

et al. 2005

Journal of the Neurological Sciences

Self Cite

View full text Add to dashboard Cite

“…Previous reports have indicated large variations in the amount of inflammation and neuronopathic changes in the spinal cord and demyelinating and axonal injury in peripheral nerves of cases with paralytic rabies. 10,11 The pathogenetic basis of paralysis in rabies remains unclear. 12 One possibility raised by this case is that axonal (neuronal process) degeneration could be the first morphological consequence of rabies virus infection of neuronal perikarya.…”

Section: Fig 2 Confocal Images From Ventral Root (A-c) Axons Showinmentioning

confidence: 99%

Overlap of pathology in paralytic rabies and axonal Guillain–Barré syndrome

Sheikh

Ramos-Alvarez²,

Jackson

et al. 2005

Annals of Neurology

View full text Add to dashboard Cite

We describe clinical and pathological features of a case of paralytic rabies with acute axonal neuropathy that closely resembled axonal Guillain-Barre syndrome. This case emphasizes that there is overlap of both clinical and pathological features in paralytic rabies and axonal Guillain-Barre syndrome. These findings raise the possibility that infectious and autoimmune etiologies can lead to similar morphological changes in the nerves.

show abstract

“…Clinical signs include severe agitation, depression, hydrophobia, and paralysis followed by impaired consciousness and coma (9). Patients eventually die of circulatory insufficiency, cardiac arrest, and respiratory failure (9,23). Despite the dramatic and severe clinical course, postmortem examination of rabies patients reveals only a few pathological lesions, such as cerebral edema (18).…”

mentioning

confidence: 99%

Degeneration of Neuronal Processes after Infection with Pathogenic, but Not Attenuated, Rabies Viruses

Li¹,

Sarmento²,

2005

J Virol

View full text Add to dashboard Cite

The structural alterations of neuronal processes in mice were investigated after the mice were infected with rabies virus (RV). Silver staining of infected brain sections showed severe destruction and disorganization of neuronal processes in mice infected with pathogenic RV but not with attenuated RV. However, neuronal bodies showed very little pathological changes. Electron microscopy revealed the disappearance of intracellular organelles, as well as the disappearance of synaptic structures and vesicles. Infection of primary neurons with pathogenic, but not attenuated, RV resulted in the destruction of neuronal processes and disappearance of microtubule-associated protein 2 and neurofilament immunoreactivity, which suggests that pathogenic RV causes degeneration of neuronal processes possibly by interrupting cytoskeletal integrity.Despite extensive investigation, the mechanism by which rabies virus (RV) infection causes neurological disease and death is still not completely understood (3). RV enters the peripheral nervous system at the bite site by binding to one or more specific neural receptors (14,22,25) with or without local replication (19,21). Once inside neurons, RV is spread by retrograde transport to the spinal cord and then to the brain (4, 12). Clinical signs include severe agitation, depression, hydrophobia, and paralysis followed by impaired consciousness and coma (9). Patients eventually die of circulatory insufficiency, cardiac arrest, and respiratory failure (9, 23). Despite the dramatic and severe clinical course, postmortem examination of rabies patients reveals only a few pathological lesions, such as cerebral edema (18). Inflammatory reactions and other histological lesions are mild with relatively little neuronal loss (15, 18). These observations led to the hypothesis that fatal rabies may result from neuronal dysfunction rather than neuronal damage (24).Studies of neuronal dysfunction have revealed electroencephalographic abnormalities, including the disappearance of rapid eye movement sleep and the development of pseudoperiodic facial myoclonus (6). Brain electrical activity terminated about 30 min before cardiac arrest, indicating that cerebral death in experimental rabies occurs prior to failure of vegetative functions (6, 7). RV infection of neurons also induces dysfunction of ion channels, for example, reduction in sodium channels and inward rectifier potassium channels (10, 11), which could prevent infected neurons from firing action potentials and generating synaptic potentials, resulting in functional impairment. Decreased binding of serotonin (particularly the subtype 5-HT 1D ) to its receptors has also been reported (2). Recent studies of the release of norepinephrine, dopamine, and serotonin in the hippocampi of rats infected with RV indicated that at the terminal stage of the disease, neurons are no longer capable of releasing neurotransmitters at the synaptic junctions (5). Hence, there is evidence of impaired release of neurotransmitters and binding of neurotransmitters to th...

show abstract

Regional distribution of rabies viral antigen in central nervous system of human encephalitic and paralytic rabies

Cited by 64 publications

References 9 publications

Difference in neuropathogenetic mechanisms in human furious and paralytic rabies

Difference in neuropathogenetic mechanisms in human furious and paralytic rabies

Overlap of pathology in paralytic rabies and axonal Guillain–Barré syndrome

Degeneration of Neuronal Processes after Infection with Pathogenic, but Not Attenuated, Rabies Viruses

Contact Info

Product

Resources

About