2. • Rabies is a rapidly progressive, acute infectious
disease of the central nervous system (CNS) in
humans and animals that is caused by infection
with rabies virus.
• usually conveyed by saliva through bites or licks
on abrasions or on intact mucous membranes.
• Humans are most frequently infected from dogs
and bats.
Introduction
3. Etiologic Agent of Rabies
• family Rhabdoviridae.
• Two genera in this family, Lyssavirus and Vesiculovirus,
• Rabies virus is a lyssavirus
• single-strand RNA virus
4. Structure of Rabies Virus
Envelope Membrane
Matrix Protein Glycoprotein
Ribonucleoprotein
5. Pathogenesis of Rabies
• Incubation period of rabies is usually 20–90 days, but it may be
as short as a few days or >1 year.
• In muscles, the virus is known to bind to nicotinic acetylcholine
receptors on postsynaptic membranes at neuromuscular
junctions.
• Rabies virus spreads centripetally along peripheral nerves
toward the spinal cord or brainstem via retrograde fast axonal
transport.
• centrifugal spread along sensory and autonomic nerves to other
tissues, including the salivary glands, heart, adrenal glands, and
skin.
• Rabies virus replicates in acinar cells of the salivary glands and
is secreted in the saliva of rabid animals that serve as vectors of
the disease.
7. Negri Body
• the most characteristic pathologic finding
in rabies
• eosinophilic cytoplasmic inclusions in brain
neurons
• composed of rabies virus proteins and
viral RNA.
• commonly observed in Purkinje cells of the
cerebellum and in pyramidal neurons of
the hippocampus.
10. Two acute neurologic forms of rabies are seen
in humans
Encephalitic (furious) form in 80% and
Paralytic form in 20%.
• Autonomic dysfunction is common in rabies and may result in
hypersalivation, gooseflesh, cardiac arrhythmia, and priapism.
• encephalitic rabies, episodes of hyperexcitability are typically
followed by periods of complete lucidity that become shorter
as the disease progresses.
11. • Brainstem involvement –
• hydrophobia (involuntary, painful contraction of the diaphragm
and accessory respiratory, laryngeal, and pharyngeal muscles in
response to swallowing liquids) and
• aerophobia (the same features caused by stimulation from a draft
of air).
• Brainstem dysfunction progresses rapidly, and coma—followed
within days by death—is the rule unless the course is prolonged
by supportive measures.
• late complications can include cardiac and/or respiratory failure,
disturbances of water balance (syndrome of inappropriate ADH
secretion or diabetes insipidus), noncardiogenic pulmonary
edema, GI hemorrhage
Encephalitic Rabies
12. Hydrophobia- feature of
Encephalitic Rabies
Hydrophobic spasm of
inspiratory muscles associated
with terror in a patient with
encephalitic (furious) rabies who
is attempting to swallow water.
13. Paralytic Rabies
• Muscle weakness predominates and cardinal features of
encephalitic rabies (hyperexcitability, hydrophobia, and
aerophobia) are lacking.
• early and prominent flaccid muscle weakness,begins in
the bitten extremity and spreads to produce
quadriparesis and facial weakness. Sphincter
involvement is common,
• sensory involvement is usually mild, and these cases are
commonly misdiagnosed as Guillain-Barre syndrome
14. Diagnosis of Rabies
• Diagnostically useful specimens include serum,
CSF, fresh saliva, skin biopsy samples from the
neck, and brain tissue (rarely obtained before
death).
• Corneal impression smears - low diagnostic
yield ,generally not performed.
• Negative antemortem rabies-specific laboratory
tests never exclude a diagnosis of rabies, and
tests may need to be repeated after an interval
for diagnostic confirmation.
16. • There is no established treatment for rabies.
• Only a few patients with established rabies have
survived. All received some post-exposure prophylaxis
and needed intensive care facilities to control cardiac
and respiratory failure. Otherwise, only palliative
treatment is possible once symptoms have appeared.
• combination of antiviral drugs, ketamine, and therapeutic
(induced) coma .
• Nutrition and fluids should be given intravenously or
through a gastrostomy.
Treatment of Rabies
17. PREVENTION OF RABIES
Post-exposure Prophylaxis
Pre-exposure Prophylaxis
Post-exposure treatment of persons who have
have been vaccinated previously
21. Local wound care
Active immunization with Rabies
vaccine and
Passive immunization with RIG
Post-exposure Prophylaxis
22. Local wound care
• All bite wounds and scratches should be
washed thoroughly with soap and water
for atleast 15 minutes. Devitalized tissues
should be debrided.
• tetanus prophylaxis given, and antibiotic
treatment initiated whenever indicated.
• Wound care should not be delayed, even if
the initiation of immunization is postponed.
25. • 5 doses of rabies vaccine should be given IM in the deltoid
area. (The anterolateral aspect of the thigh also is acceptable
in children.) Gluteal injections, which may not always reach
muscle, should not be given and have been associated with
rare vaccine failures.
• Ideally, the first dose should be given as soon as possible
after exposure; failing that, it should be given without further
delay. The additional doses should be given on days 3, 7,14
and on day 28.
• Pregnancy is not a contraindication for immunization.
• Glucocorticoids and other immunosuppressive medications
may interfere with the development of active immunity and
should not be administered during PEP unless they are
essential.
Active immunization with Rabies
vaccine
26. • Routine measurement of serum neutralizing antibody
titers is not required, but titers should be measured 2–4
weeks after immunization in immunocompromised
persons.
• Local reactions (pain, erythema, edema, and pruritus)
and mild systemic reactions (fever, myalgias, headache,
and nausea) are common;
• anti-inflammatory and antipyretic medications may be
used, but immunization should not be discontinued
Active immunization with Rabies
vaccine
27. • Previously unvaccinated persons should be passively immunized
with rabies immune globulin (RIG).
• If RIG is not immediately available, it should be administered no
later than 7 days after the first vaccine dose.
• If anatomically feasible, the entire dose of RIG (HRIG- 20 IU/kg)
should be infiltrated at the site of the bite, and any RIG remaining
after infiltration of the bite site should be administered IM at a distant
site
• With multiple or large wounds, the RIG preparation may need to be
diluted in order to obtain a sufficient volume for adequate infiltration
of all wound sites.
• If the exposure involves a mucous membrane, the entire dose
should be administered IM.
• Rabies vaccine and RIG should never be administered at the same
site or with the same syringe
• Serious adverse effects of human RIG are uncommon.
• Local pain and low-grade fever may occur.
Passive immunization with
RIG
29. Pre-exposure Prophylaxis
• Pre-exposure rabies prophylaxis should be considered for
people with an occupational or recreational risk of rabies
exposures and also for certain travelers to rabies-endemic
areas.
• The primary schedule consists of three doses of rabies
vaccine given on days 0, 7, and 21 or 28.
• Serum neutralizing antibody tests help determine the need for
subsequent booster doses.
• When a previously immunized individual is exposed to rabies,
two booster doses of vaccine should be administered on days
0 and 3.
• Wound care remains essential.
• RIG should not be administered to previously vaccinated
persons.