Rabies

• Bullet shaped, enveloped, helical nucleocapsid and a negative-sense RNA

virus.
• Knob-like envelope glycoproteins elicit neutralizing and hemagglutination
antibodies
• Strains from different sources (animals) are antigenically heterogeneous
• G protein binds to the acetylcholine or NCAM receptor on target cells.
• Rabies virus negative-sense RNA genome replicates in the cytoplasm by
using viral RNA-dependent RNA polymerase
• G protein-containing lipoprotein envelope acquired from plasma membrane
Electron micrograph of the rabies virus
(yellow) (×36 700). Note the bullet shape.
The external surface of the virus contains spike-
like glycoprotein projections that bind
specifically to cellular receptors.
Transmission
In most cases the disease is transmitted via the bite of rabid animals which
shed infectious virus with their saliva. The virus enters the body through
transdermal inoculation (i.e. wounds) or direct contact of infectious material (i.e.
saliva, cerebrospinal liquid, nerve tissue) to mucous membranes or skin lesions.
The virus can not penetrate intact skin.
PATHOGENESIS
• Replicates initially in muscle at the site of entry and then enters peripheral nervous system
• Spreads to CNS and replicates exclusively in gray matter
• Passes centrifugally along autonomic nerves to reach tissues, including salivary glands,
adrenal medulla, kidneys, and lungs
• Presence of the virus in salivary glands (of animals) facilitates further transmission
• The Negri bodies found in neurons
• The incubation period for rabies ranges from 10 days to 1 year, depending on the amount
of virus introduced, the amount of tissue involved, the host immune mechanisms, the
innervation of the site, and the distance that the virus must travel from the site of
inoculation to the CNS. Thus, the incubation period is generally shorter with face wounds
than with leg wounds.
• Immunization early in the incubation period frequently aborts the infection.
Sequential steps (1-8) in the pathogenesis of rabies
virus infection are shown in the diagram.
CLINICAL ASPECTS MANIFESTATIONS
SIGNS
After (bite) exposure with a rabid animal, initial symptoms of rabies are of non-specific nature and may
be very similar to those of other infectious diseases including general weakness or discomfort, fever,
or headache. A first specific clinical sign is neuropathic pain or a prickling or itching sensation at the
site of the bite. Signs rapidly progress and include cerebral dysfunction, anxiety, confusion, agitation,
delirium, abnormal behavior, hallucinations, and insomnia. Once clinical signs of rabies appear,
without intensive care, death occurs within 2 weeks after onset of symptoms. There is no treatment
available.
DIAGNOSIS
• Viral RNA, antigen and antibody are detected ante mortem in saliva, neck biopsy, serum and CSF,
and brain biopsy (if available) to rule out rabies
• Viral antigen detected in brain tissue of human postmortem or animals
• The Negri bodies by histologic examinations
TREATMENT
• No specific treatment is available
• Vaccination immediately after animal bites to prevent rabies disease