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Rabies
Rhabdovirus
Dr.T.V.Rao MD
Early Rabies
 Rabies has been recognized in India since
the Vedic period (1500–500 BC) and is
described in the ancient Indian scripture
Atharvaveda,
 Rabies is endemic in India, a vast country
with a population exceeding 1.02 billion
and a land area of 3.2 million km.
RABIES (RHABDOVIRUS)
Rabies widely spread in Asia and
Africa
 Rabies is widely distributed across the
globe. More than 55 000 people die of
rabies each year. About 95% of human
deaths occur in Asia and Africa.
 Most human deaths follow a bite from an
infected dog. Between 30% to 60% of the
victims of dog bites are children under the
age of 15.
What is Rabies
 Rabies is a zoonotic disease (a disease that is
transmitted to humans from animals) that is
caused by a virus. Rabies infects domestic and
wild animals, and is spread to people through
close contact with infected saliva (via bites or
scratches). The disease is present on nearly
every continent of the world but most human
deaths occur in Asia and Africa (more than
95%). Once symptoms of the disease
develop, rabies is fatal.
Rabies - Common facts
 Mad Dog biting Humans lead to Rabies.
 Latin Rabhas means Frenzy.
 Hydrophobia Fear of Water, Saliva of Rabid
dogs
 Pasture’s success – Vaccination
Fixed virus from Rabbit injected into
Joseph Meister
Injected 13 injection of the cord vaccine.
7
Rabies- A Zoonotic Disease
 Rhabdovirus family;
genus Lyssavirus
 Enveloped, bullet-shaped
virions
 Slow, progressive
zoonotic disease
 Primary reservoirs are
wild mammals; it can be
spread by both wild and
domestic mammals by
bites, scratches, and
inhalation of droplets.
Rabies – A fatal Zoonotic Disease
Rabies in USA
 Most of the recent
human rabies cases in
the United States
have been caused by
rabies virus from
bats. Awareness of
the facts about bats
and rabies can help
people protect
themselves, their
families, and their
pets.
Rhabdoviruses
 A Bullet shaped virus/
Enveloped
 Contains ss RNA virus
 Rhabdoviridae – infects
mammals.
 Important virus
Lyssa virus- Rabies
virus
Lyssa means Rage.
Rabies virus
 Bullet shaped virus
 Size is 180 x 75 nm
 Has Lipoprotein
envelop
 Knob like spikes
/Glycoprotein S
 Genome un
segmented
 Linear negative sense
RNA
What is a Fixed Virus
 One whose virulence and
incubation period have
been stabilized by serial
passage and remained
fixed during further
transmission.
 Rabies virus that has
undergone serial passage
through rabbits, thus
stabilizing its virulence
and incubation period and
called as fixed virus
What is a Street Virus
 Virus from a naturally
infected animal, as
opposed to a laboratory-
adapted strain of the
virus.
 The virulent rabies virus
from a rabid domestic
animal that has
contracted the disease
from a bite or scratch of
another animal, and
called as street virus.
Any mammal can get rabies.
 Raccoons,
skunks, foxes and
bats
 Dogs, cats,
cattle and
ferrets
 Humans too
What kind of animals
get Rabies?
 The rabies virus can infect all
mammals.
 Mammals are warm-blooded
animals that have hair and
mammary glands to produce
milk for their babies.
 Animals like frogs, birds, and
snakes do not get rabies.
Man’s best friend
but can spread Rabies if not vaccinated
Rabies viruses are sensitive to
common Chemicals
 The virus is sensitive to
Ethanol
Iodine
Soap / Detergents
Ether, Chloroform, Acetone
Destroyed at 500 c in 1 hour
at 600 c in 5 minutes.
Antigenic properties
 Surface spikes
composed of
Glycoprotein G
 Produces
Pathogenicity by
binding to Acetyl
choline receptors in
the neural tissue
 Stimulate T
lymphocytes Cytotoxic
effect.
Transmission
 Abrasions or scratches on skin.
 Mucous membrane exposed to saliva.
 Most frequently via deep penetrating bite
wounds.
 Other routes.
Inhalation in bat infected caves.
Ingestion of dead /infected animal
meat
Corneal transplantation
RABIES (RHABDOVIRUS)
Pathogenesis of Rabies
 Bite by Rabid dog or other animals
 Virus are carried in saliva virus deposited
on the wound site.
 If untreated 50% will Develop rabies.
 Rabies can be produced by licks and
corneal transplantation.
 Virus multiply in the muscle ,connective
tissue, nerves after 48 – 72 hours.
 Penetrated nerve endings.
PATHOGENESIS
Live virus Epidermis, Mucus membrane
Peripheral nerve
CNS ( gray matter )
Other tissue (salivary glands,…)
centripetally
centrifugally
RABIES (RHABDOVIRUS)
RABIES (RHABDOVIRUS)
RABIES (RHABDOVIRUS)
Spread of Virus
 From Brain virus
spread to
Salivary glands,
Conjunctival cell
released into tears
Kidney
Lactating glands
and Milk after
pregnancy
RABIES (RHABDOVIRUS)
Pathogenesis
 Virus travels through axoplasam toward
the spinal cord, at the rate of 3 mm/hour,
 Towards the brain
 Spread from brain centrifugally to various
parts of the body.
 Multiplies in the salivary glands and shed
in the saliva.
 Cornea, facial tissues skin.
Pathogenesis
 Incubation 1 – 3 months.
 May be average from 7 days to 3
years.
 Stages of the disease.
Prodrome
Acute encephalitis.
Coma / Death.
Broad category - Presentations
 Furious Rabies
 Dumb ( Rage
tranquille )
 (Landry/Guillain-
Barre Syndrome
Category - WHO
 Category I: touching or feeding suspect
animals, but skin is intact
 Category II: minor scratches without
bleeding from contact, or licks on broken
skin
 Category III: one or more bites, scratches,
licks on broken skin, or other contact that
breaks the skin; or exposure to bats
Clinical Findings
 Bizarre behavior.
 Agitation
 Seizures.
 Difficulty in drinking.
 Patients will be able to eat solids
 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.
 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
Symptoms
CLINICAL MANIFESTATIONS
1 – Non specific prodrome
2 – Acute neurologic encephalitis
Acute encephalitis
Profound dysfunction of brainstem
3 – Coma
4 - Death ( Rare cases  recovery )
CLINICAL MANIFESTATIONS
Non specific prodrome
1 - 2 days  1 week
Fever, headache, sore throat
Anorexia, nausea, vomiting,
Agitation, depression
Parenthesis or fasciculation's at
or Around the site of inoculation of
virus.
Acute Neurologic Encephalitis
 1 – 2 days to < 1 week
 Excessive motor activity, Excitation,
Agitation
 Confusion, Hallucinations, Delirium,
 Bizarre aberrations of thought, Seizures,
 Muscle spasms, Meningismus,
 Opisthotonic posturing
 Mental aberration ( Lucid period  coma )
 Hypersalivation, Aphasia, Pharyngeal spasms
 Incordination, Hyperactivity
Acute Neurologic Encephalitis
Phase - Presentations
 Fever T > 40.6
 Dilated irregular pupils
 Lacrimation, Salivation & Perspiration
 Upper motor neuron paralysis
 Deep tendon reflexes
 Extensor plantar responses ( as a rule )
 Hydrophobia or Aerophobia (50 -70% )
Rabies can present as Grave
condition
Majority will succumb to
Disease
Clinical presentation – Leads
the clues in Diagnosis
 In most cases, human rabies is diagnosed
primarily on the basis of clinical symptoms
and signs, and a corroborative history of
or evidence of an animal bite, death of an
animal, and incomplete or no vaccination
following exposure. The facility for
laboratory diagnosis and confirmation of
rabies, be it in humans or in animals, is
available premortem in only a few
institutions in India. T
Common confirmatory test -
Rabies
1. The standard
premortem test is
a fluorescent
antibody test to
demonstrate the
presence of viral
antigen. The standard
postmortem test is
biopsy of the patient's
brain and examination
for Negri bodies.
Autopsies are rarely performed.
DIAGNOSIS
•Laboratory finding: ( CBC, CSF )
•Exclusion of other etiologies
•Pathology:
Formation of cytoplasmic inclusions:
( Negri bodies )
( Ammon’s horn, Cerebral cortex,
Brainstem, Hypothalamus,
The Purkinje cells of cerebellum,
Dorsal spinal ganglia )
Laboratory Diagnosis
 Survival possible. May need Laboratory Diagnosis
 Clinical differentiation other cases of Encephalitis.
 Post mortem Diagnosis by
By demonstration of Negri bodies.
Isolation of virus fro Mice brain
inoculation.
tissue culture on culture lines
W 138, BHK,
PCR emerging method.
IF methods corneal impression method.
Diagnostic methods
 Antigen detection by specific Immuno
fluorescence.
Ante-mortem - Conjunctival,skin biopsy
from nape of neck.
Postmortem impression from surfaces of
salivary glands Hippocampus,
Histological examination
ELISA specific antibody detection.
PCR
Negri bodies – A gold standard
in Diagnosis
 Inclusion bodies
called Negri bodies
are 100%
diagnostic for
rabies infection,
but found only in
20% of cases
Negri bodies
in Brain Tissue
 Negri bodies round or
oval inclusion bodies seen
in the cytoplasm and
sometimes in the
processes of neurons of
rabid animals after death.
 Negri bodies are
Eosinophilic, sharply
outlined, pathognomonic
inclusion bodies (2-10 µm
in diameter) found in the
cytoplasm of certain
nerve ..
Emerging Methods in Diagnosis
 The reference method for diagnosing rabies is
by performing PCR or viral culture on brain
samples taken after death. The diagnosis can
also be reliably made from skin samples taken
before death. It is also possible to make the
diagnosis from saliva, urine and cerebrospinal
fluid samples, but this is not as sensitive.
Inclusion bodies called Negri bodies are
100% diagnostic for rabies infection, but
found only in 20% of cases.
DIFFERENTIAL DIAGNOSIS
Other viral encephalitis
Hysteria reaction to animal bite
Landry/Guillan-barre syndrome
Poliomyelitis
Allergic encephalomyelitis ( rabies vaccine )
PREVENTION
Preexposure Prophylaxis
Postexposure Prophylaxis
Ist Vaccine for Rabies
 Prepared by Pasteur
by drying various
periods pieces of
spinal cord of Rabbits
infected with fixed
virus
 1885 Joseph
Meister 9 year boy
vaccinated 13
injections were given
 Patient saved
Preexposure vaccination
 Indicated in
Laboratory
workers.
Veterinarians
and technical staff.
Bat handlers.
Supporting care in
Animal/Dog Bites
Basic care in Animal bites
 Before exposure to infection
In Veterinary surgeons animal handlers.
Specific Prophylaxis
After exposure to Dog bite.
Local treatment
Cauterization
Scrub with Soap and clean.
Use cetavalon, tincture of Iodine
Antirabic serum don't suture
 Tell an health care
worker immediately
 Wash the wound out
with soap and water
 Inform the doctor
right away
If you are bitten or
scratched
POSTEXPOSURE PROPHYLAXIS
1 – Wound cleaning & treatment
RABIES (RHABDOVIRUS)
RABIES (RHABDOVIRUS)
Post exposure vaccination
 Anti Rabis vaccines are given when person
is
1 Bitten
2 Scratched
3 Licked
By Rabid animal
animal to be kept for 10 days ?
Vaccines
 Semple vaccine
Contain 5 % suspension. Of infected
Sheep brain, ( Infected with fixed virus )
Inactivated with Phenol at 370c
Vaccines available after inactivation with Beta
propiolactone Used in India
Vaccine contains Nucleic capsid antigen,
Small quantities of Glycoprotein G
Used in Developed countries Neural
complications.
Neural Vaccines*
 Class I slight risk
 Class II Moderate risk
 Class III Great risk
 Nerual vaccines may cause Neuroparlytic
complications, Laundry’s type ascending
paralysis
• Dose is regulated according to grade/class of bites
• Many countries do not use in view of neurological complications
HUMAN RABIES Cell culture Vaccines
Vaccine:
Human diploid cell vaccine (HDCV)
Developed by Koprowsky,Wiktor,and Plotkin
Purified chick embryo cell vaccine (PCEC)
Purified Vero cell vaccine (PVRV)
Purified duck embryo vaccine (PDEV)
Post exposure Prophylaxis
 The vaccination is
given on
0, 3, 7, 14, 30,
and 90th day
Immunity lasts for 5
years
Injected on deltoid
region IM/SC
Not to be given in the
gluteal region
POSTEXPOSURE PROPHYLAXIS
3 – Active immunization
Cell culture Vaccines in –
commonly prescribed
1 Human diploid cell
vaccine.
2 Purified chick
embryo cell
vaccine
3.Purified Vero cell
vaccine
Human Diploid Cell
Vaccine
 Koprowsky, Viktor,
Plokin discovered
 Inactivated in
Betaproprionate.
 No serious side
effects.
 Human Diploid cell
vaccines purified .
 Sub Unit vaccines in
progress/developed.
Human Diploid Cell Vaccines
 Dosage
 Preexposure prophylaxis
0 – 7 – 21 – or 28 – 56 days
A booster after 1 year,
Repeat once in 5 days,
Post exposure Prophylaxis
Sex doses
0 -3 -7-14 – 30 - 90 days
Given IM or SC in the Deltoid region
Don't inject inGluteal region.
Preexposure prophylasixis
doses
 Given on the following
days
0, 7, 21,or 28
and 56th day
Generally given to
Vet nary personal
Passive Immunization
 Human Rabies
Immunoglobulin HRIG
 High Risk bitten on
face and neck
 Given a dose of 20 IU
/Kg wt
 Half at the site of bite
and rest IM route.
 Active immunization
should be initiated with
passive immunization.
Future of Rabies Vaccines
 A number of experimental vaccines are
under development that may provide
alternative safe and potent but less
expensive vaccine options. These include
DNA vaccines, recombinant viral
vaccines, and recombinant protein
vaccines. Further testing is needed to
determine if and which one of these novel
vaccines will make their way into mass
production and application in the future.
Subunit or Genetically Engineered
vaccines for Rabies
 A viral immunizing agent
that has been treated to
remove traces of viral
nucleic acid so that only
protein subunits remain.
The subunits have less
risk of causing adverse
reactions.
 Several trails in
progress
Epidemiology
 No Danger of Nursing Rabies patients
but do take precautions
 Any animal bite can cause Rabies except
Mice
 BATS in caves in spread he disease by
respiratory disease.
 India around 30,000 die with Rabies.
 Vaccination of the Dogs and
Licensing of the Dogs
In spite of Health Education several die due
to Rabies infection in Developing world
World's Rabies Day (on September 28)
 World Rabies Day is a
cooperative global
event planned to
reduce the suffering
from rabies. This day
celebrates Dr. Louis
Pasteur’s vision of a
rabies free world.
Created by Dr.T.V.Rao MD for ‘e’
learning Programme in developing
world
Email
doctortvrao@gmail.com

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RABIES (RHABDOVIRUS)

  • 2. Early Rabies  Rabies has been recognized in India since the Vedic period (1500–500 BC) and is described in the ancient Indian scripture Atharvaveda,  Rabies is endemic in India, a vast country with a population exceeding 1.02 billion and a land area of 3.2 million km.
  • 4. Rabies widely spread in Asia and Africa  Rabies is widely distributed across the globe. More than 55 000 people die of rabies each year. About 95% of human deaths occur in Asia and Africa.  Most human deaths follow a bite from an infected dog. Between 30% to 60% of the victims of dog bites are children under the age of 15.
  • 5. What is Rabies  Rabies is a zoonotic disease (a disease that is transmitted to humans from animals) that is caused by a virus. Rabies infects domestic and wild animals, and is spread to people through close contact with infected saliva (via bites or scratches). The disease is present on nearly every continent of the world but most human deaths occur in Asia and Africa (more than 95%). Once symptoms of the disease develop, rabies is fatal.
  • 6. Rabies - Common facts  Mad Dog biting Humans lead to Rabies.  Latin Rabhas means Frenzy.  Hydrophobia Fear of Water, Saliva of Rabid dogs  Pasture’s success – Vaccination Fixed virus from Rabbit injected into Joseph Meister Injected 13 injection of the cord vaccine.
  • 7. 7 Rabies- A Zoonotic Disease  Rhabdovirus family; genus Lyssavirus  Enveloped, bullet-shaped virions  Slow, progressive zoonotic disease  Primary reservoirs are wild mammals; it can be spread by both wild and domestic mammals by bites, scratches, and inhalation of droplets.
  • 8. Rabies – A fatal Zoonotic Disease
  • 9. Rabies in USA  Most of the recent human rabies cases in the United States have been caused by rabies virus from bats. Awareness of the facts about bats and rabies can help people protect themselves, their families, and their pets.
  • 10. Rhabdoviruses  A Bullet shaped virus/ Enveloped  Contains ss RNA virus  Rhabdoviridae – infects mammals.  Important virus Lyssa virus- Rabies virus Lyssa means Rage.
  • 11. Rabies virus  Bullet shaped virus  Size is 180 x 75 nm  Has Lipoprotein envelop  Knob like spikes /Glycoprotein S  Genome un segmented  Linear negative sense RNA
  • 12. What is a Fixed Virus  One whose virulence and incubation period have been stabilized by serial passage and remained fixed during further transmission.  Rabies virus that has undergone serial passage through rabbits, thus stabilizing its virulence and incubation period and called as fixed virus
  • 13. What is a Street Virus  Virus from a naturally infected animal, as opposed to a laboratory- adapted strain of the virus.  The virulent rabies virus from a rabid domestic animal that has contracted the disease from a bite or scratch of another animal, and called as street virus.
  • 14. Any mammal can get rabies.  Raccoons, skunks, foxes and bats  Dogs, cats, cattle and ferrets  Humans too
  • 15. What kind of animals get Rabies?  The rabies virus can infect all mammals.  Mammals are warm-blooded animals that have hair and mammary glands to produce milk for their babies.  Animals like frogs, birds, and snakes do not get rabies.
  • 16. Man’s best friend but can spread Rabies if not vaccinated
  • 17. Rabies viruses are sensitive to common Chemicals  The virus is sensitive to Ethanol Iodine Soap / Detergents Ether, Chloroform, Acetone Destroyed at 500 c in 1 hour at 600 c in 5 minutes.
  • 18. Antigenic properties  Surface spikes composed of Glycoprotein G  Produces Pathogenicity by binding to Acetyl choline receptors in the neural tissue  Stimulate T lymphocytes Cytotoxic effect.
  • 19. Transmission  Abrasions or scratches on skin.  Mucous membrane exposed to saliva.  Most frequently via deep penetrating bite wounds.  Other routes. Inhalation in bat infected caves. Ingestion of dead /infected animal meat Corneal transplantation
  • 21. Pathogenesis of Rabies  Bite by Rabid dog or other animals  Virus are carried in saliva virus deposited on the wound site.  If untreated 50% will Develop rabies.  Rabies can be produced by licks and corneal transplantation.  Virus multiply in the muscle ,connective tissue, nerves after 48 – 72 hours.  Penetrated nerve endings.
  • 22. PATHOGENESIS Live virus Epidermis, Mucus membrane Peripheral nerve CNS ( gray matter ) Other tissue (salivary glands,…) centripetally centrifugally
  • 26. Spread of Virus  From Brain virus spread to Salivary glands, Conjunctival cell released into tears Kidney Lactating glands and Milk after pregnancy
  • 28. Pathogenesis  Virus travels through axoplasam toward the spinal cord, at the rate of 3 mm/hour,  Towards the brain  Spread from brain centrifugally to various parts of the body.  Multiplies in the salivary glands and shed in the saliva.  Cornea, facial tissues skin.
  • 29. Pathogenesis  Incubation 1 – 3 months.  May be average from 7 days to 3 years.  Stages of the disease. Prodrome Acute encephalitis. Coma / Death.
  • 30. Broad category - Presentations  Furious Rabies  Dumb ( Rage tranquille )  (Landry/Guillain- Barre Syndrome
  • 31. Category - WHO  Category I: touching or feeding suspect animals, but skin is intact  Category II: minor scratches without bleeding from contact, or licks on broken skin  Category III: one or more bites, scratches, licks on broken skin, or other contact that breaks the skin; or exposure to bats
  • 32. Clinical Findings  Bizarre behavior.  Agitation  Seizures.  Difficulty in drinking.  Patients will be able to eat solids  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.
  • 33.  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 Symptoms
  • 34. CLINICAL MANIFESTATIONS 1 – Non specific prodrome 2 – Acute neurologic encephalitis Acute encephalitis Profound dysfunction of brainstem 3 – Coma 4 - Death ( Rare cases  recovery )
  • 35. CLINICAL MANIFESTATIONS Non specific prodrome 1 - 2 days  1 week Fever, headache, sore throat Anorexia, nausea, vomiting, Agitation, depression Parenthesis or fasciculation's at or Around the site of inoculation of virus.
  • 36. Acute Neurologic Encephalitis  1 – 2 days to < 1 week  Excessive motor activity, Excitation, Agitation  Confusion, Hallucinations, Delirium,  Bizarre aberrations of thought, Seizures,  Muscle spasms, Meningismus,  Opisthotonic posturing  Mental aberration ( Lucid period  coma )  Hypersalivation, Aphasia, Pharyngeal spasms  Incordination, Hyperactivity
  • 37. Acute Neurologic Encephalitis Phase - Presentations  Fever T > 40.6  Dilated irregular pupils  Lacrimation, Salivation & Perspiration  Upper motor neuron paralysis  Deep tendon reflexes  Extensor plantar responses ( as a rule )  Hydrophobia or Aerophobia (50 -70% )
  • 38. Rabies can present as Grave condition
  • 39. Majority will succumb to Disease
  • 40. Clinical presentation – Leads the clues in Diagnosis  In most cases, human rabies is diagnosed primarily on the basis of clinical symptoms and signs, and a corroborative history of or evidence of an animal bite, death of an animal, and incomplete or no vaccination following exposure. The facility for laboratory diagnosis and confirmation of rabies, be it in humans or in animals, is available premortem in only a few institutions in India. T
  • 41. Common confirmatory test - Rabies 1. The standard premortem test is a fluorescent antibody test to demonstrate the presence of viral antigen. The standard postmortem test is biopsy of the patient's brain and examination for Negri bodies. Autopsies are rarely performed.
  • 42. DIAGNOSIS •Laboratory finding: ( CBC, CSF ) •Exclusion of other etiologies •Pathology: Formation of cytoplasmic inclusions: ( Negri bodies ) ( Ammon’s horn, Cerebral cortex, Brainstem, Hypothalamus, The Purkinje cells of cerebellum, Dorsal spinal ganglia )
  • 43. Laboratory Diagnosis  Survival possible. May need Laboratory Diagnosis  Clinical differentiation other cases of Encephalitis.  Post mortem Diagnosis by By demonstration of Negri bodies. Isolation of virus fro Mice brain inoculation. tissue culture on culture lines W 138, BHK, PCR emerging method. IF methods corneal impression method.
  • 44. Diagnostic methods  Antigen detection by specific Immuno fluorescence. Ante-mortem - Conjunctival,skin biopsy from nape of neck. Postmortem impression from surfaces of salivary glands Hippocampus, Histological examination ELISA specific antibody detection. PCR
  • 45. Negri bodies – A gold standard in Diagnosis  Inclusion bodies called Negri bodies are 100% diagnostic for rabies infection, but found only in 20% of cases
  • 46. Negri bodies in Brain Tissue  Negri bodies round or oval inclusion bodies seen in the cytoplasm and sometimes in the processes of neurons of rabid animals after death.  Negri bodies are Eosinophilic, sharply outlined, pathognomonic inclusion bodies (2-10 µm in diameter) found in the cytoplasm of certain nerve ..
  • 47. Emerging Methods in Diagnosis  The reference method for diagnosing rabies is by performing PCR or viral culture on brain samples taken after death. The diagnosis can also be reliably made from skin samples taken before death. It is also possible to make the diagnosis from saliva, urine and cerebrospinal fluid samples, but this is not as sensitive. Inclusion bodies called Negri bodies are 100% diagnostic for rabies infection, but found only in 20% of cases.
  • 48. DIFFERENTIAL DIAGNOSIS Other viral encephalitis Hysteria reaction to animal bite Landry/Guillan-barre syndrome Poliomyelitis Allergic encephalomyelitis ( rabies vaccine )
  • 50. Ist Vaccine for Rabies  Prepared by Pasteur by drying various periods pieces of spinal cord of Rabbits infected with fixed virus  1885 Joseph Meister 9 year boy vaccinated 13 injections were given  Patient saved
  • 51. Preexposure vaccination  Indicated in Laboratory workers. Veterinarians and technical staff. Bat handlers.
  • 53. Basic care in Animal bites  Before exposure to infection In Veterinary surgeons animal handlers. Specific Prophylaxis After exposure to Dog bite. Local treatment Cauterization Scrub with Soap and clean. Use cetavalon, tincture of Iodine Antirabic serum don't suture
  • 54.  Tell an health care worker immediately  Wash the wound out with soap and water  Inform the doctor right away If you are bitten or scratched
  • 55. POSTEXPOSURE PROPHYLAXIS 1 – Wound cleaning & treatment
  • 58. Post exposure vaccination  Anti Rabis vaccines are given when person is 1 Bitten 2 Scratched 3 Licked By Rabid animal animal to be kept for 10 days ?
  • 59. Vaccines  Semple vaccine Contain 5 % suspension. Of infected Sheep brain, ( Infected with fixed virus ) Inactivated with Phenol at 370c Vaccines available after inactivation with Beta propiolactone Used in India Vaccine contains Nucleic capsid antigen, Small quantities of Glycoprotein G Used in Developed countries Neural complications.
  • 60. Neural Vaccines*  Class I slight risk  Class II Moderate risk  Class III Great risk  Nerual vaccines may cause Neuroparlytic complications, Laundry’s type ascending paralysis • Dose is regulated according to grade/class of bites • Many countries do not use in view of neurological complications
  • 61. HUMAN RABIES Cell culture Vaccines Vaccine: Human diploid cell vaccine (HDCV) Developed by Koprowsky,Wiktor,and Plotkin Purified chick embryo cell vaccine (PCEC) Purified Vero cell vaccine (PVRV) Purified duck embryo vaccine (PDEV)
  • 62. Post exposure Prophylaxis  The vaccination is given on 0, 3, 7, 14, 30, and 90th day Immunity lasts for 5 years Injected on deltoid region IM/SC Not to be given in the gluteal region
  • 63. POSTEXPOSURE PROPHYLAXIS 3 – Active immunization
  • 64. Cell culture Vaccines in – commonly prescribed 1 Human diploid cell vaccine. 2 Purified chick embryo cell vaccine 3.Purified Vero cell vaccine
  • 65. Human Diploid Cell Vaccine  Koprowsky, Viktor, Plokin discovered  Inactivated in Betaproprionate.  No serious side effects.  Human Diploid cell vaccines purified .  Sub Unit vaccines in progress/developed.
  • 66. Human Diploid Cell Vaccines  Dosage  Preexposure prophylaxis 0 – 7 – 21 – or 28 – 56 days A booster after 1 year, Repeat once in 5 days, Post exposure Prophylaxis Sex doses 0 -3 -7-14 – 30 - 90 days Given IM or SC in the Deltoid region Don't inject inGluteal region.
  • 67. Preexposure prophylasixis doses  Given on the following days 0, 7, 21,or 28 and 56th day Generally given to Vet nary personal
  • 68. Passive Immunization  Human Rabies Immunoglobulin HRIG  High Risk bitten on face and neck  Given a dose of 20 IU /Kg wt  Half at the site of bite and rest IM route.  Active immunization should be initiated with passive immunization.
  • 69. Future of Rabies Vaccines  A number of experimental vaccines are under development that may provide alternative safe and potent but less expensive vaccine options. These include DNA vaccines, recombinant viral vaccines, and recombinant protein vaccines. Further testing is needed to determine if and which one of these novel vaccines will make their way into mass production and application in the future.
  • 70. Subunit or Genetically Engineered vaccines for Rabies  A viral immunizing agent that has been treated to remove traces of viral nucleic acid so that only protein subunits remain. The subunits have less risk of causing adverse reactions.  Several trails in progress
  • 71. Epidemiology  No Danger of Nursing Rabies patients but do take precautions  Any animal bite can cause Rabies except Mice  BATS in caves in spread he disease by respiratory disease.  India around 30,000 die with Rabies.  Vaccination of the Dogs and Licensing of the Dogs
  • 72. In spite of Health Education several die due to Rabies infection in Developing world
  • 73. World's Rabies Day (on September 28)  World Rabies Day is a cooperative global event planned to reduce the suffering from rabies. This day celebrates Dr. Louis Pasteur’s vision of a rabies free world.
  • 74. Created by Dr.T.V.Rao MD for ‘e’ learning Programme in developing world Email doctortvrao@gmail.com