Introduction
It is anacute fatal disease in man & other warm blooded animals
Characterized by:
Abnormal behavior,
Nervous disturbances such as motor nerve irritability,
Mania,
An attacking complex,
Inability to swallow,
Excessive salivation,
Impairment of consciousness,
Progressive ascending paralysis &
Death due to respiratory paralysis
4.
• Rabies claimsnearly 55000 human deaths, worldwide
• Mostly children
• Presently the efforts at rabies control have enabled a marginal
reduction of rabies deaths from 30,000 to 20,000 in India annually
Introduction
5.
Lyssa virus
Family: Rhabdoviridae
RNAvirus,
Bullet shaped (180 nm X 75 nm in dia.)
Highly fragile viruses
susceptible to standard disinfectants
Sunlight & moderate heat destroy the virus
There are 25 viruses in this genus, of which closely related rabies
viruses are called “Classical rabies viruses”
Etiology
6.
Serotypes of rabiesviruses are:
1. Lagos bat virus,
2. Mokola virus,
3. Duvenhage virus,
4. European bat lyssa virus I (EBL I),
5. European bat lyssa virus II (EBL II) &
6. Australian bat lyssa virus
Etiology
7.
• Based onantigenicity, the virus is classified as fixed or street rabies
virus
Etiology
Sl. No. Fixed rabies virus Street rabies virus
1. The virus is passaged by serial
intradermal route in rabbits
It is from naturally occurring infection
2. Incubation period is fixed and shorter
(6-7 days)
Incubation period is variable (11-47
days)
3. It does not produce Negri bodies It produces Negri bodies
(Intracytoplasmic inclusion bodies)
4. No shedding of virus in the saliva Shedding of virus in the saliva
5. The virus is not virulent and self-
limiting. Used for vaccine production.
The virus is virulent and not self-
limiting. Pathogenic to warm blooded
animals.
8.
• Worldwide distribution
•Primary reservoirs:
Foxes, bats, raccoons, skunks, dogs, cats & cattle
• Transmission:
From fresh saliva via bite, scratch or abrasion by an rabid animal
Rabid dogs shed virus in saliva 5-7 days before showing signs
Cat does so for only 3 days before signs
Contamination of skin wounds by fresh saliva from infected animals
also a source of infection
Source & Transmission
9.
• Central nervoussystem disturbances
• The clinical course especially (in dogs)
• Can be divided into 3 phases:
▫ The prodromal form
▫ The excitative form
▫ The paralytic form
Prodromal period: 1-3 days, animals either show signs of paralysis
or become vicious
Disease in animals
10.
1. In dogs
Furiousform (changes in behaviour & stage of
excitement)
Tendency to bite either inanimate/animate objects
till death
Travel to long distance
Shows imaginary catching stance
Attempt to lick water but unable to drink water due
to the paralysis of pharyngeal & laryngeal muscles
Drooling of saliva
Photophobia
Changes in barking due to paralysis of vocal chords
Finally, dropped jaw & tongue will protrude & head
will drop down
Disease in animals
11.
1. In dogs
Dumpform or paralytic form:
Isolated themselves in dark places
Paralysis of lower jaw (dropped jaw ), tongue, larynx &
hindquarters
Not capable to bite
2. In cats
Furious form is more common
Disease in animals
12.
3. In cattle
Furiousform is more common:
Violently attack other animals or
Attack to inanimate objects,
loud bellowing,
Incoordination of gait,
Excessive salivation,
Behavioral changes,
Muzzle tremor,
Aggression,
Sexual excitement,
Hyper excitability &
Pharyngeal paralysis
Disease in animals
Paralytic form:
Knuckling of hind fetlock,
Sagging & swaying of hind
quarter while walking,
Deviation of tail to one side,
Drooling of saliva & yawing
movement
• In horse:
Muscletremors are frequent & common,
pharyngeal paralysis,
ataxia & lethargy,
Sudden onset of lameness in one limb followed by recumbency &
violent head tossing
• In pigs:
Twitching of nose,
excessive salivation,
chronic convulsion,
rapid chewing movement & may walk backward
Disease in animals
15.
The incubationperiod: few months (usually 30 to 60 days),
Depending on
The distance of bite,
Severity of bite,
Amount of virus inoculated
Aggressive status of the rabid animal
Infection reaches to CNS symptoms begin to show
The infection is effectively untreatable & usually fatal within days
Death almost invariably results 2-10 days after first symptoms
Drinking cause extremely painful laryngeal spasm
Patient refuses to drink (hydrophobia-fear of water)
Muscle spasm, laryngospasm & extreme excitability are present
Disease in human
16.
Convulsions occur
Thick tenacious saliva
Increased lacrimation,
Frequent micturition
Increased perspiration.
The initial symptoms of rabies are often mild fever & pain or paresthesia
at the wound site
Furious rabies is rapidly fatal: hydrophobia or aerophobia, phobia
towards sound, hyperactivity and fluctuating consciousness
Flaccid paralysis ascending with pain in the affected muscles & mild
sensory disturbances will precede death from respiratory paralysis
Disease in human
17.
Classification of exposurebased involvement
of risk
Class I-
Slight or negligible risk
Licks on healthy/ unbroken
skin
Scratches without oozing of
blood
Class II-
Definite but moderate risk
Consumption of unboiled milk from
suspected animals
Licks on fresh cuts
Scratches with oozing of blood
All bites except on head, neck, face, palm
and fingers
Minor wounds less than five in number
Class III-
Severe/ grave risk
Licks on mucosa
Bites on head, Neck, face,
palm & fingers
Lacerated wounds on any
part of the body
Bites from wild animals
18.
1. Sign &symptoms
2. Fluorescent antibody test (FAT)
▫ Corneal impression smear, as well as brain
▫ Highly specific & rapid test (99.9%)
▫ Detects different strains using monoclonal antibody
▫ The identifiable strains correlate well with species & geographic
distributions observed
3. Identification of Negribodies (intracytoplasmic inclusion bodies) in the
brain impression smear by Seller's staining technique
4. Virus isolation from body fluid or brain tissue
5. Molecular techniques
Diagnosis
Negri bodies
19.
Post-exposure care toprevent rabies includes:
Washing & scrubbing the wound with phenolic soap and/or plenty of
running tape water
Application of antiseptics
Avoiding bandaging or suturing of wound, or point of contact
Administering anti-rabies immunizations as soon as possible
Anti-rabies vaccine should be given for category II & III exposures
(follow post exposure schedule)
Treatment
20.
• Post exposureschedule
If the animal is not previously immunized,
Post exposure vaccination on
0-day (the day starts within 24 hours after bite), 3rd
, 7th
, 14th
, 28th
& if
necessary, on 90th
day (Essen's schedule)
If the animal is immunized annually 0 day, 3rd
and 7th
day, put the
animal under observation for 10 days
If the animal dies, should follow the full regimen (5 doses)
Treatment
21.
Pre-exposure schedule
• Typeof vaccine:
Inactivated (from cell culture or embryonated egg vaccine)
• Number of doses:
Three: 0, 7th
& 21st
or 28th
day given by IM or ID route (vaccine should not
be given in the gluteal region)
Booster: After one year then every five years
• Contraindication:
Severe reaction to previous dose
• Adverse reactions:
Mild local or systemic reactions; rare neuroparalytic reactions reported
• Special precautions:
Do not use animal-brain-derived vaccines
Vaccination
22.
• Postexposure immunization:
Upto50% of human rabies immune globulin is infiltrated around the
wound; the rest is administered IM
(ERIG or HRIG: anti-rabies antibody)
• Human Diploid Cell Vaccine (HDCV):
5 injections IM at days 0, 3, 7, 14, & 28
• Vaccination of domestic animals
• Enforced animal control measures (Animal Birth Control and Anti-
rabies vaccination programme: ABC-AR)
• Controlling stray dog population
• Proper immunization of household dogs (ABC-AR programme)
• Vaccination of high risk personnel
• Awareness programme among public
Prevention