Pathogenesis of Rhabdo (rabies) virus

  • The bite of rabid animal is the usual portal of entry which contains the infected saliva that is introduced into the depths of the wound.
  • The virus may gain access through a pre-existing scratch or abrasion occasionally if this has been contaminated with the saliva.
  • The virus multiplies locally in the tissues, invades adjacent nerve fibers, and spreads centrally to infect the neurons in the brain and spinal cord.
  • It is also thought that the virus may enter and travel along the neurons of peripheral nerves.
  • Bite wounds are taken as usual route of entry but sometimes it may enter through unusual route.
  • Rare examples of infection have been reported like by inhalation in bat infested caves where there was bat-rabies and also by ingestion through eating of rabies infected cattle.
  • Fox and coyote are highly susceptible that have been experimentally infected by inhalation from exposures in caves.

Incubation period

  • It varies from 10 days to 2 years after the rabid animals have bitten to the person.
  • It depends on the distance of the viruses from the brain where the viruses have been introduced.
  • Incubation period might be 60 days for bite on the legs, 40 days on the arm, 30 days on the head region.
  • This period is shorter in children as compared to adult.
  • Incubation period is short in the condition where severely lacerated wounds of the heads and shoulders have been heavily infected.
  • The virus is carried to the brain via the bloodstream in this case.

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 Pathological change

  • Degeneration of nerve cells occurs in cortex, mid-brain, basal ganglia, pons and medulla.
  • Histopathological examination of brain shows Negri inclusion bodies in the neurons of cerebellum and hippocampus.

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  • In addition to the above, a polio-encephalitis affecting usually the brain stem and spinal cord characterized by perivascular cuffing with lymphocytes and plasma cells, parenchymal microglial response and sometimes neuronophagia may be seen.
  • The inflammatory reaction appears early whereas the Negri bodies are more commonly found, in cases with a long illness.
  • From the neurons which show little or no cytopathic effect, the virus may spread to other tissues including the salivary glands.
  • In the tissues, the virus multiplies in acinar cells, the adrenals, kidneys, pancreas and myocardium.
  • Sometime, conjunctiva and cornea are also affected due to which the examination of exudate or corneal impression smears may be useful in immune-fluorescence for diagnostic procedure.


Clinical features

  • Sub-clinical disease is not known to occur in human.
  • Headache, fever, a profound sense of apprehension, and a feeling of irritation at the site of bite are the initial symptoms.
  • Patient will have dry throat and thirst, but they won’t drink.
  • High fever, difficulty in swallowing and the consequent fear of water become the dominant symptoms.
  • Due to this the disease is also called hydrophobia.
  • The attempts of drinking water after thirst provoke violent contraction of diaphragm and inspiratory muscles.
  • Thereafter, mere site or sound of water precipitates distressing muscular spasm.
  • The patient develops focal and generalized seizures, disorientation and delirium as the disease progresses.
  • 10- 20% of patients exhibit flaccid paralysis.
  • The patients become comatose later, which lasts for 2-10 days.
  • Death results from neurological and pulmonary failure.




Pathogenesis of Rhabdo (rabies) virus