Difference in neuropathogenetic mechanisms in human furious and paralytic rabies

Mitrabhakdi, Erawady; Shuangshoti, Shanop; Wannakrairot, Pongsak; Lewis, Richard A.; Susuki, Keiichiro; Laothamatas, Jiraporn; Hemachudha, Thiravat

doi:10.1016/j.jns.2005.05.004

Cited by 84 publications

(80 citation statements)

References 35 publications

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“…Rabies virus, which almost exclusively targets neurons, disproportionately affects cerebral over systemic perfusion by disrupting nNOS that causes cerebral artery spasm. It is believed that the morbidity and mortality burden of rabies stems from cerebral vasospasm or from dysautonomia through neuropathy [2,4]. The combination of drugs and treatment strategies in Milwaukee Protocol are aimed to reverse this process to allow latent immune mechanisms to clear rabies virus from the body.…”

Section: Discussionmentioning

confidence: 99%

Transcranial doppler findings in a case of rabies encephalitis

Sarwal¹,

Botdorf²,

Newey³

et al. 2014

J Med Disord

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Rabies encephalitis is a uniformly fatal disease with several hypothesis proposed to explain pathogenesis and mortality. One such theory premises deficiency of neuronal nitric oxide synthetase deficiency causing selective cerebral vasospasm. We present transcranial Doppler findings in a case of rabies that did not show imaging evidence of vasospasm. Transcranial Doppler in two published cases have reported occurrence of global vasospasm. Our case showed no sonographic vasospasm in middle cerebral arteries but consistently increased distal resistance indices likely due to cerebral edema. While vasospasm may occur in rabies, cerebral edema secondary to disease or pharmacological interventions confounds transcranial Doppler readings. Cerebral angiogram and multimodality monitoring is encouraged.

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Section: Discussionmentioning

confidence: 99%

Transcranial doppler findings in a case of rabies encephalitis

Sarwal¹,

Botdorf²,

Newey³

et al. 2014

J Med Disord

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“…In the encephalitic form, heightened immune response has been found with T-cell infiltrates, high serum concentrations of the interleukin (IL)-2 receptor and IL-6, and early mortality [78,79]. In contrast, patients with paralytic rabies have been reported to have defective immune responsiveness, lack of lymphocyte proliferative responses to rabies viral antigen, and lower levels of the serum cytokines, IL-6 and soluble IL-2 receptor [79][80][81].…”

Section: Bat Rabiesmentioning

confidence: 99%

“…In contrast, patients with paralytic rabies have been reported to have defective immune responsiveness, lack of lymphocyte proliferative responses to rabies viral antigen, and lower levels of the serum cytokines, IL-6 and soluble IL-2 receptor [79][80][81]. Pathological studies demonstrate peripheral nerve inflammation and demyelination as the prime pathological manifestation in cases of paralytic rabies and chromatolysis in anterior horn cells in encephalitic form [11,78,82].…”

Section: Bat Rabiesmentioning

confidence: 99%

“…Participation of autoantibodies against peripheral nerve antigens in the evolution of paralysis is also suggested by vivid enhancement of ventral and dorsal nerve roots on magnetic resonance imaging, similar to GBS [77,88]. However, neither neutralizing antibodies nor antiganglioside nor myelin basic protein antibodies have been consistently demonstrated in CSF in paralytic rabies [78,81,89].…”

Section: Bat Rabiesmentioning

confidence: 99%

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Perspectives in Diagnosis and Treatment of Rabies Viral Encephalitis: Insights from Pathogenesis

et al. 2016

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Rabies viral encephalitis, though one of the oldest recognized infectious disease of humans, remains an incurable, fatal encephalomyelitis, despite advances in understanding of its pathobiology. Advances in science have led us on the trail of the virus in the host, but the sanctuaries in which the virus remains hidden for its survival are unknown. Insights into host-pathogen interactions have facilitated evolving immunologic therapeutic strategies, though we are far from a cure. Most of the present-day knowledge has evolved from in vitro studies using fixed (attenuated) laboratory strains that may not be applicable in the clinical setting. Much remains to be unraveled about this elusive virus. This review attempts to re-examine the current advances in understanding of the pathobiology of the rabies virus that modulate the diagnosis, treatment, and prevention of this fatal disease.

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“…Looking back to the different manifestations of rabies in humans infected with a same RABV strain, it is reasonable to argue that the immune status of patients may be the Further evidence that favors an immune host-dependent modulation between paralytic/peripheral and furious/limbic rabies comes from studies on human rabies patients, which led to the conclusion that inflammatory demyelinating peripheral nerve dysfunction is the pathologic basis for paralysis (47).…”

Section: Viral and Host Factors Affecting Rabies Outcomesmentioning

confidence: 99%

On the interference of clinical outcome on rabies transmission an perpetuation

Brandão¹

2009

J. Venom. Anim. Toxins incl. Trop. Dis

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Rabies is a viral zoonotic infectious disease that affects mammals and is caused by genotypes/species of the Lyssavirus genus (Rhabdoviridae, Mononegavirales), with the genotype 1 (classic rabies virus -RABV) being the most prevalent. Despite continuous efforts, rabies is still an incurable disease that causes thousands of deaths amongst humans worldwide. Due to a wide range of hosts and the different evolutionary paths of RABV in each host, several host-specific variants have arisen in an ongoing process. The result of RABV replication in nervous tissues may lead to two opposite clinical outcomes, i.e., paralytic/dumb form and encephalitic/furious one. The paralytic form creates dead-end hosts mainly amongst herbivores, while the furious form of the disease allows for augmented transmission when manifested in gregarious carnivores, as their natural aggressive behavior is accentuated by the disease itself. The aim of this article is to propose a theoretical model intended to explore how the rabies virus intrinsically modulates the immune system of different host classes, the pathological changes that the virus causes in these animals and how these elements favor its own perpetuation in nature, thus providing a basis for better prediction of the patterns this disease may present.

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Difference in neuropathogenetic mechanisms in human furious and paralytic rabies

Cited by 84 publications

References 35 publications

Transcranial doppler findings in a case of rabies encephalitis

Transcranial doppler findings in a case of rabies encephalitis

Perspectives in Diagnosis and Treatment of Rabies Viral Encephalitis: Insights from Pathogenesis

On the interference of clinical outcome on rabies transmission an perpetuation

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