Pathogenesis of Rhabdo (rabies) virus

August 11, 2018

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.

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.

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.

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I am Shailesh Koirala