Pathophysiology of The Rabies

Pathophysiology of the Rabies
The main source of rabies virus is in saliva and may be present in the saliva only sporadically
(Smith, 1996) for several days before the onset of clinical signs of rabies (Charlton, 1988).
Virus may also be found in other tissues, which may therefore also potentially act as a source
of the virus.
Rabies virus is most commonly transmitted through the bite of an infected mammal although
transmission has been rarely documented via other routes such as contamination of mucous
membranes (i.e., eyes, nose, mouth), aerosol transmission, and corneal and organ
transplantations (Centers for Disease Control and Prevention, 2011). The virus may enter the
peripheral nervous system directly and replicate in muscle tissue after entering the host,
remaining at or near the site of introduction for most of the incubation period. However, the
precise sites of viral sequestration remain unknown, since neither antigen nor virus can
usually be found in any organ during this phase.
Virus may enter the peripheral nervous system via the neuromuscular junctions, and moves
rapidly centripetally to the central nervous system for replication and may developed
symptoms shortly thereafter. The virus then begins to pass centrifugally to many tissues and
organs, such as the salivary glands. At this point of time, the animal becomes infectious and
can transmit the disease through a bite and will not appear to be sick.
Forms of Rabies
There will be two forms of rabies which is almost invariably fatal disease that can present as
classic furious rabies or paralytic rabies. Patient with furious rabies have shorter survival of
patients compared with those with paralytic rabies. It may be due to closely corresponds to
the greater amount of virus and lower immune response in the CNS of patients with the
furious form (Hemachudha et al., 2013). People with furious rabies exhibit signs of
hyperactivity, excited behaviour, hydrophobia (fear of water) and sometimes aerophobia (fear
of flying). After a few days, death occurs by cardiorespiratory arrest. While, paralytic rabies
accounts for about 30% of the total number of human cases. The muscles gradually become
paralyzed, starting at the site of the bite or scratch. A coma slowly develops, and eventually
death occurs due to respiratory failure. The paralytic form of rabies is often misdiagnosed,
contributing to the under-reporting of the disease.
Signs and symptoms
Usually patient that were infected with rabies may developed signs and symptoms
which are divided into three stage. The first stage was prodromal stage where the symptoms
appeared was mild and non-specific such as fever, chills, malaise, headache, anorexia,
nausea, sore throat which is the beginning of hydrophobia that experienced by 17% to 80% of
rabies patients. In this stage there are forceful, painful muscle spasms of the throat, which
expel any liquids administered orally. This stage may last for 2-10 days. A specific early
symptom is local or radiating pain, burning, or itching, a sensation of cold, and/or tingling at
the inoculation bite.
The second stage was acute neurological or excitation phase that will last for 2 to 7 days.
Patients may shiwed signs of nervousness, anxiety, agitation, marked restlessness,
apprehension, irritability, hyperesthesia, sensitivity to loud noises, hydrophobia, excessive
salivation (1 to 1.5 liters in 24 hours), lacrimation (secretion of tears), and perspiration. The
signs also include the asymmetrical dilation of constriction of the pupils, absence of corneal
reflexes, weakness of facial muscles and hoarseness as the virus replicating in the brain and
impaired the cranial nerve.
The last stage was the terminal stage characterised by coma. There will be
generalized flaccid paralysis and eventually, the patient experiences peripheral
vascular collapse, coma, and death.
References:
1. Campbell, J.B. & Charlton, K.M. (1988). The Pathogenesis of Rabies. Kluwer
Academic Publishers, Boston, Massechusetts, USA. Washington D.C. American
Society for Microbiology.
2. Smith, J.S. (1996). New aspects of rabies with emphasis on epidemiology, diagnosis,
and prevention of the disease in the United States. Kluwer Academic Publishers,
Boston, Massechusetts, USA. Washington D.C. American Society for Microbiology.
3. Centers for Disease Control and Prevention (2011). How is rabies transmitted?.
Centers
for
Disease
Control
and
Prevention
National Center for Emerging and Zoonotic Infectious Diseases (NCEZID)
Division of High-Consequence Pathogens and Pathology (DHCPP)
4. Hemachudha T et al,. (2013). Human rabies: neuropathogenesis, diagnosis, and
management. 12(5):498-513. US National Library of MedicineNational Institutes of
Health.

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