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Dr.k yashoda rabies presentation
1. RABIES
By
Dr. K .Yashoda
P.G Scholar
Under the guidance of
Proff. K. Laxmikantham
Department of Kaya Chikitsa,
DR.B.R.K.R, Govt . Ayurvedic Medical college,
Erragadda, Hyderabad . TS.
1
3. DEFINITION
Rabies is a viral disease that causes
acute encephalitis (inflamm ation of
the brain) in warm- blooded animals
Rabies is a zoonotic disease
(a disease that is transmitted to humans
from animals) that is caused by a virus
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5. INTRODUCTION
The disease infects domestic and wild animals, and is
spread to people through close contact with infected
saliva via bites or scratches.
Dogs are the source of 99% of humanrabies deaths
Once symptoms of the diseasedevelop, rabies is
nearly always fatal.
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6. •Rabies is estimated to cause
59 000 human deaths annually
in over 150 countries, with
95% of cases occurring in
Africa and Asia.
•Dogs are responsible for 99
% of rabies cases, and the
burden of disease is
predominantly borne by rural
poor communities, with nearly
half of cases due to children
under the age of 15.
•Non bite exposure :
•Exposure to aerosols in the
laboratory, caves containing
millions of bats, rarely
transmit rabies corneal tissue
transplantation
Epidemiology and burden of disease
8. SOURCE OF INFECTION
The source of infection to man is the saliva of rabid
animals.
In dogs & cats, the virus may be present in the saliva
for 3-4 days before the clinical onset & during the
course of illness till death.
3 – 5% of Human
cases
Cause > 90% of the
Human cases
10. INCUBATION PERIOD
• It is highly variable in man, commonly 1- 3 Months
following exposure.
•The closer the bite to the brain, the shorter the incubation.
• Rabies virus travels 100-400 mm per day.
•Rare cases are as short as 2 weeks or greater than 1 Year
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11. Pathogenesis
⚫ Incubation period : 1-3 months.
⚫ STAGES:
1) Virus inoculated by bite.
2) Replication in muscles: virus binds to nicotinic acetylcholine receptors on
post synaptic membranes at NMJ.
3) Retrograde axonal transport :Spreads centripetally along peripheral nerves
towards CNS( 100-400 mm/day) through local dorsal root ganglion, spinal
cord.
4) CNS dissemination/ spreading
5) Centrifugal spread along sensory & autonomic nerves
Virus is shed even in infected human’s saliva but human to human
transmission is not conformed
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12. ⚫ Most characteristic pathologic findings:
⚫ Brain
i. Mononuclear cell infiltration ,
ii. Perivascular cuffing of lymphocytes,
iii. Babes nodules consisting of glial cells,
⚫ Negri body
i. Eosinophilic cytoplasmic inclusion in neurons composed of rabies
virus proteins & viral RNA.
ii. Not observed in all cases of rabies.
iii. Commonly seen in hippocampus & cerebellum.
⚫ Basis for behavioural changes including aggressive behaviour is not
well understood.
⚫ Lack of prominent degenerative neuronal changes has led to concept that
neuronal dysfunction (rather than neuronal death) responsible for clinical
disease in rabies.
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15. SIGN & SYMPTOMS
• Bizarre behavior.
• Agitation
• Seizures.
• Difficulty in drinking.
. Afraid of water - Hydrophobia.
• Even sight or sound of water disturbs
the patient.
• But suffer with intense thirst.
• Spasms of Pharynx produces choking
• Death in 1 -6 days.
• Respiratory arrest / Death / Some may survive.
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16. Conti….
• Headache, fever, sore throat
• Nervousness, confusion
• Pain or tingling at the site of the bite
• Hallucinations
• Seeing things that are not really there
• Hydrophobia
• “Fear of water" due to spasms in the throat
• Paralysis
• Unable to move parts of the body
• Coma and death
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20. Prognosis
•People
•Nearly 100% treatable if exposure is known and post-
exposure treatment begins before signs of disease
•Nearly 100% fatal once symptoms occur
Only 6 people have ever survived (with brain damage )
when treated after clinical sins began
•Once symptoms began death with in 2 weeks
-Often with in days
-Usually with in 1 week
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23. PRE EXPOSURE PROPHYLAXIS
• Provided to subjects at risk before
occupational or vocational exposure to
rabies.
• Subjects include diagnosticians,
laboratory & vaccine workers,
veterinarians, cavers, etc.
• Simplifies post exposure
management.
• Only vaccines used
.
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24. POST EXPOSURE PROPHYLAXIS
• Consists of wound care, rabies immune globulin,
and vaccine.
• Cleansing
• Chemical Treatment
• Anti-Rabies Serum
• Antibiotics & anti-tetanus measure
• Observe the animal for 10 days.
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26. Cont…
• Wash lesions well with soap and water
(tetanus booster)
• Infiltrate rabies immune globulin (20
IU/kg) into and around the margin of the
bites.
• Administer vaccine on days
•0,3,7,14, and 28. (90)
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27. RABIES IMMUNOGLOBULIN
• Two Human Rabies
Immunoglobulins are
available;
• Both supplied in vials at~150 IU/ml
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30. TREATMENT
•LOCAL WOUND TREATMENT
- Wash with soap/detergent and water preferably for 10
mins.
- Apply alcohol, povidone iodine/ any antiseptic
- Anti-Tetanus
•*Avoid suturing wounds
•*Don’t apply ointment, cream/ wound dressing
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31. • ANTIMICROBIAL
• Amoxicillin
• Cloxacillin
• Cefuroxime
• *For those instances where there’s no obvious signs of
infection( Amoxicillinas prophylaxis )
• ***Educate the public simple local wound treatment &
warn not to use procedures that may further contaminate
the wounds
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32. VACCINE ADMINISTRATION
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Type of Vaccine
CELL CULTURE VACCINES
• Human diploid cell vaccine (HDCV)
• Second generation tissue culture vaccine (non-Human)
Type: Killed viral vaccine
Dose: 1 ml IM Schedule: on 0, 3, 7, 14, 28 day,
booster on day 90
33. PASSIVE IMMUNIZATION
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• Horse Anti Rabies serum: 40 IU / kg at 0 day
• Human rabies immunoglobin (HRIG): 20 IU / kg
around the wound and rest in IM on 0 day
• Booster doses are essential whenever anti-rabies
serum is given with the vaccine
34. MANAGEMENT OF RABIES PATIENT
• Once symptoms start, treatment should center on comfort care, using
sedation & life support measures once diagnosis is certain
• MEDICATIONS
• Diazepam
• Midazolam
• Haloperidol + Dipenhydramine
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35. • SUPPORTIVE CARE
• Pts w/ confirmed rabies should receive adequate sedation &
comfort care in an appropriate medical facility.
• Once rabies diagnosis has been confirmed, invasive procedures must be
avoided
• Provide suitable emotional and physical support
• Discuss & provide important info. to relatives concerning transmission
of dse.
• Honest gentle communication concerning prognosis should be provided
to relatives of pt
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36. • INFECTION CONTROL
• Patient should be admitted in a quiet, draft-free, isolation room
• HLCR workers & relatives in contact w/ pt should wear proper
personal protective equipment (gown, gloves, mask, goggles)
•. DISPOSAL OF DEAD BODIES
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37. 37
CONCLUSION
•It's a fatal disease, and dangerous public health problem.
•Most European countries are saved from this disease by practicing prevention measures.
•Workshops on public health education should be coordinated to inform people about responsible
pet ownership and regular veterinary care.
•Prevention can be accomplished by avoiding exposure to stray animals. Alternatively, by
supplying affected people with timely local wound care in conjunction with the administration of
human rabies immune globulin and vaccine.
•Local governments should develop and sustain successful programs to ensure the vaccination of
all dogs, cats, and ferrets, as well as the elimination of trays.
