Current Neurology and Neuroscience Reports

, Volume 6, Issue 6, pp 460–468



    • Neurology Division, Department of MedicineChulalongkorn University Hospital
  • Supaporn Wacharapluesadee
  • Jiraporn Laothamatas
  • Henry Wilde

DOI: 10.1007/s11910-006-0047-2

Cite this article as:
Hemachudha, T., Wacharapluesadee, S., Laothamatas, J. et al. Curr Neurol Neurosci Rep (2006) 6: 460. doi:10.1007/s11910-006-0047-2


Despite increases in our understanding of rabies pathogenesis, it remains an inevitably fatal disease. Lack of awareness, low level of political commitment to rabies control, and failure to recognize and correlate clinical, laboratory, and neuroimaging features contribute to continuing deaths. Clinical symptomatology, once believed to be unique, may be variable, even in patients associated with lyssaviruses of the same genotype. This article discusses virus transport, the role of virus and host response mechanisms in relation to protean clinical manifestations, and mechanisms responsible for relative intactness of consciousness in human rabies. Differential involvement of the anterior horn cell in furious rabies and the peripheral nerve in paralytic rabies is summarized. Escape mechanisms from host defenses explain why a fatal outcome is unavoidable regardless of therapy. Neuroprotective treatment, using a coma-induction regimen, proves not to be beneficial. Survival of patients with excellent recovery relies on early innate and adaptive immunity plus adequate intensive care support.

Copyright information

© Current Science Inc. 2006