COLLEGE OF HEALTH SCIENCES
DEPARTMENT OF MEDICINE
PRESENTATION ON RABIES
BY
NEUROLOGY UNIT
3RD MARCH, 2025.
MODERATOR:
OUTLINE
• INTRODCUTION
• EPIDEMIOLGOY
• RISK FACTORS
• MICROBIOLOGY OF THE CAUSATIVE AGENT
• TRANSMISSION AND INCUBATION PERIOD
• PATHOPHYSIOLOGY
• CLINICAL PRESENTATION
• INVESTIGATIONS
• TREATMENT AND PREVENTION
INTRODUCTION
• Rabies is a viral disease that primarily affects mammals such as dogs,
cats, livestock and wildlife, including humans
• Rabies is a very serious public health problem in over 150 countries
and territories, mainly in Asia and Africa with an estimated 55,000
deaths per year worldwide.
• Established infection is almost invariably fatal; there are only a
handful of recorded cases of survival from clinical rabies.
EPIDEMIOLOGY
• Rabies remains a major public health problem ,particularly in
developing countries.
• It is estimated that 59,000 people die from rabies annually world
wide ,with the vast majority of the cases occurring in Africa and Asia
• India has the highest number of rabies related deaths ,accounting for
approximately 35%of the global total
• Other countries includes China, Parkistan, Indonesia, Bangladesh.
RISK FACTORS
• People in rural areas; particularly in low income countries,where
domestic dog vaccination and access to rabies post exposure
prophylaxis maybe limited
• Animal handlers and veterinarians
• Travelers
• Children
MICROBIOLOGY OF RABIES
• Rabies is caused by Rhabdovirus
• Rhabdovirus is a single stranded RNA virus of the genus Lyssavirus
• the virus is bullet-shaped and has spike-like structures arising from
its surface containing glycoproteins that cause the host to produce
neutralizing, hemagglutination-inhibiting antibodies
• The virus has a marked affinity for central nervous tissue and salivary
glands of a wide range of mammals .
• Established infection is invariably fatal.
TRANSMISSION AND INCUBATION
• Mode of infection: By saliva usually through the bites or licks of an
infected animal on abrasions or on intact mucous membranes. Other
forms of transmission (aerosolized exposure in bat infested caves, post
organ transplant) are rare.
• Source of infection: Humans are usually infected from dogs/fox
(rarely cats) and bats.
• Incubation period in humans: Varies from few weeks to several
months. Unusually average is 1–3 months. In general, severe bites
(especially on the head or neck), are associated with shorter incubation
periods than those elsewhere.
Pathogenesis of Rabies
• Incubation period ranges from 20-90 days
• The virus binds to nicotinic acetylcholine receptor on the postsynaptic
membranes at the neuromuscular junctions
• Rabies virus spread along the peripheral nerves toward the spinal cord
or the brainstem via a retrograde fast axonal transport
• The pathological changes are more compared to the clinical severity and
fatal outcome of the disease.
• The most characteristic pathologic finding in rabies is the Negri body
• These inclusion bodies are commonly observed in the purkinje cells of
the cerebellum.
PATHOGENESIS OF RABIES VIRUS IN HUMANS
CLINICAL PRESENTATION
• Clinical varieties: There are two distinct clinical varieties of rabies in humans:
I. Furious rabies (the classic variety)
II. Dumb rabies (the paralytic)
• The only characteristic feature in the initial prodromal period is the pain and
tingling (paresthesia) at the site of the bite. There may be fever, malaise and
headache.
• After a prodromal period of 1–10 days, marked anxiety, agitation or depressive
features, hallucinations, and paralysis may develop. It may be accompanied by
spitting, biting and mania, with lucid intervals in which the patient is markedly
anxious
CLINICAL PRESENTATION CONT’
• Hyperexcitability is the hallmark and is precipitated by auditory or visual
stimuli. The characteristic ‘hydrophobia’ (fear of water) develops in 50% of
patients. In hydrophobia, though the patient is thirsty, attempts at drinking
(or to eat) provoke violent/severe contractions of the diaphragm and other
inspiratory (pharyngeal) muscles. Aerophobia (fear of air) is pathognomonic
of rabies.
• Cranial nerve lesions and autonomic instability is common.
• Examination: It shows hyperreflexia, spasticity and features of sympathetic
overactivity (pupillary dilatation and diaphoresis).
• Patient develops convulsions, respiratory paralysis and cardiac arrhythmias.
Death usually occurs within 10–14 days of the onset of symptoms.
INVESTIGATIONS
• Diagnosis is usually made on clinical grounds.
• Skin punch biopsy: To detect antigen with an immunofluorescent
• antibody test on frozen section.
• Reverse transcription polymerase chain reaction (RTPCR): Isolation of viral RNA
• Isolation of viruses: From saliva or the presence of antibodies in blood or CSF.
• Corneal smear test: It is unreliable.
• Classic Negri bodies: They can be demonstrated at postmortem in 90% of patients
with rabies. These are eosinophilic, cytoplasmic, ovoid bodies, 2– 10 nm in diameter,
found in large numbers in the neurons of the hippocampus and the cerebellum.
• Diagnosis on the biting animal: By using RTPCR, immunofluorescence assay (IFA)
or tissue culture of the brain
MANAGEMENT
• Established disease: Once the CNS disease is established, treatment is
symptomatic, as death is virtually inevitable.
• Only a few patients with established rabies survive.
• Intensive care: The patient should be isolated in a quiet, darkened room. Patients
who received some postexposure prophylaxis should be given intensive care
facilities to control cardiac and respiratory failure and nutritional support. Only
palliative treatment can be given once symptoms appeared.
• Heavy sedation: The patient should be heavily sedated with diazepam/ morphine,
supplemented by chlorpromazine if needed. Sedation should be done liberally in
patients who are excitable.
• Nutrition and fluids should be given intravenously or through a gastrostomy.
• Milwaukee Protocol using antivirals (Ribavirin and Amantidine) along with
ketamine and midazolam infusion has been tried.
MANAGEMENT OF RABIES
• There is no cure for rabies
• But if a patient has been exposed to the virus before the onset of symptoms ,post
exposure prophylaxis therapy can be performed
• This can achieve up to 99% survival rate
• Human Rabies Immunoglobulin[HRIG]; this is given to an individuals who
have not been vaccinated against rabies .it introduces sensitized immunoglobins
which help to destroy the virus before it reaches the central nervous system .
• Rabies Vaccination; unvaccinated patients are given 4 shots of 1.0ml injections
in a span of 14 days (0,3,7,and 14).
• Vaccinated patients are given 2 booster shots 1.0ml of rabies vaccine over a 3 day
span(on day 0 and 3).
PREVENTION
Pre-exposure prophylaxis
• High-risk individuals: Preexposure prophylaxis is indicated to individuals with a
high-risk of contracting rabies. These include laboratory workers (who work with
rabies virus), animal handlers (who handle potentially infected animals
professionally), veterinarians and those who live at special risk in rabies-endemic
areas.
• Method: – Three doses on days 0, 7 and 28 (1.0 mL) of human diploid (HDCV) or
chick embryo cell
• vaccine given by deep subcutaneous or intramuscular route.
• – A reinforcing dose after 12 months and additional reinforcing doses are given
every 3–5 years (depending on the risk of exposure)
CONCLUSION
• Rabies remains a significant global health issue ,particularly in countries with
insufficient access to vaccines and medical care
• In developed regions, rabies is less common due to successful vaccination and
control programs .
• The main strategy for control is prevention through widespread vaccination of
domestic animals and timely post exposure prophylaxis
• Efforts are ongoing to eliminate rabies as a public health problem ,with focus on
vaccination and education .
REFERENCES
• Kumar & Clark’s Clinical Medicine (10th ed.)
• Davidson’s principles & practice of medicine (24th ed.)
THANK YOU
