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Dr. Divija Ramachandran
Associate Professor
Department of Community Medicine
Sree Gokulam Medical College and Research Foundation
Dogs ….. Man’s BEST friend !
BEWARE OF RABIES ……..!
Introduction
• Zoonotic disease of carnivorous animals ; dogs-enzootic
• CNS ( Brain and spinal cord) - Acute fatal encephalomyelitis
• Caused by RNA virus - Lyssavirus - Family : Rhabdovirideae
• Most important viral zoonoses of warm blooded animals
• Variable incubation period, short period of illness and most characteristic feature
is “fear of water” – painful spasms of muscles of deglutition followed by
respiratory paralysis, delirium, asphyxia and death.
Sir Louis Pasteur and the Anti-RabiesVaccine
Pasteur Institute , Paris
Etiology
• Caused by a bullet shaped ,single stranded, non segmented, RNAVirus.
• The virus has spikes all over and contain glycoprotein which is the antigenic
substance
Pathophysiology
• Neurotropic virus - tendency to affect the CNS
• The spike like projections help the virus to establish
itself in the axoplasm (cytoplasm of the nerve cells)
• In the neurons of the brain, these viral particles are
seen as inclusion bodies , called ‘ Negri Bodies’ which
is pathognomonic of rabies.
• Absence of Negri bodies however does not rule out
rabies.
• Virus are often found in various body fluids like saliva,
milk, urine, lymph of rabid animals,and in saliva,
semen, sweat and tears among affected persons.
Characteristics of rabies virus
• Lipid content of the sheath – inactivated by fat solvents like disinfectants such as
Dettol, Savlon ,Tincture Iodine
• Inactivated by UV Rays, heating for 30 seconds , and 40% alcohol.
• The virus is highly resistant against cold, dryness, decay
• Virus remains infectious for weeks in cadavers.
STREETVIRUS
• Wild virus in saliva of rabid animals – StreetVirus
• Highly pathogenic – virulent to both man and animals
• Capable of producing Negri Bodies in neurons
• Incubation period: 3 weeks to 3 months
FIXEDVIRUS
• Successive passage of the street virus through the brain of lab animals , the street
virus is made to lose it’s pathogenicity and capacity to produce Negri bodies. ,
however retaining its antigenicity.
• Hence the incubation period becomes short and fixed – 5-6 days in lab animal.
• Modified virus is called Fixed virus – avirulent to man
• Antigenicity present, no capacity to invade
• Cannot multiply or produce Negri Bodies.
Reservoir of infection
• The principal reservoir of infection are the rabid animals like dogs, wolves, foxes
etc.
• No carriers among humans. Carrier state among animals is not conclusively
established.
• Cases of hydrophobia constitute potential source of infection.
• Vampire bats serve as constant source of infection for humans and wild animals
and enables the virus to be present in nature.
• Dogs are principal reservoirs in India
Period of infectivity
• Humans are infectious during period of illness
• Rabid animal infectious during last 3 to 5 days of incubation period and during
entire period of illness 12 to 15 days
• All warm blooded animals are susceptible
• ONLY 15 -20% get the disease as the virus is excreted intermittently through the
saliva of rabid animals.
Modes ofTransmission
• Lick of bite of rabid animal.
• Sylvatic cycle in wild animals
• Urban cycle in domestic animals
• And accidentally to human beings from animals
• Human to human transmission does not occur as saliva doesn’t have optimum
number of virus and humans do not have biting tendency. Rabies in man is a ‘dead
end disease’. Can spread through transplantation.
Furious Rabies (Mad dog syndrome)
• 80 to 90% of cases
• Dog behaves abnormally – goes to dark corners ,
restless and shows agitation, run amuck
• Bites man and animals without provocation
• Paralysis of lower jaw, protruded tongue, drooling saliva,
paralysis of vocal cord, limbs and trunk.
• Death due to respiratory paralysis and convulsions.
• Mortality is 100 percent.
Dumb Rabies ( Paralytic Rabies )
• 10 to 20% of rabies
• Dog becomes silent and withdraws itself
• Death from general paralysis
• HYDROPHOBIA not a feature
Clinical Features
• Prodromal stage : Headache, restlessness, Fever,Tingling and numbness at the
site of bite and malaise.
Clinical Features
• Stage of convulsions:
• Sensory system – Sensitive to senses of touch , cold, hot – can get convulsions
• Motor system – Increased tone and spasticity of muscles- exaggerated reflexes,
jerks
• Sympathetic system- Excessive perspiration, lacrimation, salivation
• Aerophobia and photophobia
Clinical Features
• Stage of paralysis: Difficulty and pain in swallowing food – choking sensation-
painful spasms
Lab diagnosis ( Antemortem)
• Nuchal skin biopsy
• Saliva –Virus isolation or RTPCR
• Serum and spinal fluid for antibodies
Lab diagnosis (Postmortem)
• Brain biopsy and Seller’s stain for Negri Bodies.
• Flourescent AntibodyTest
Management of Hydrophobia
• Isolation in quiet room
• Sedatives, antipyretics, analgesics, anti-histaminics and anticonvulsants
• IV rehydration, steroids, osmotic diuretics like mannitol
• Expert nursing care
• Mechanical ventilation of lung
• Medical attendants should receive pre exposure prophylaxis with antirabies
vaccines and are advised to wear glasses, masks, gloves, shoes, plastic apron.
They should avoid contact with saliva, urine, tears of patient.
Principles of Post Exposure Prophylaxis
• To reduce viral load
• To neutralise virus at point of entry
• Prevent nerve infection
• To induce systemic immunity
Post Exposure Prophylaxis
• Wound treatment
• Observation of the animal
• Antirabies immunization - Antirabies vaccine and Immnunoglobulin
• Advice to patient
1.WoundTreatment (First AidTreatment)
• Thorough washing of wound with soap and running tap water for 10 mins
• Application of virucidal agents like povidone iodine and tincture iodine
• Deep wounds exploration and debridement must be carried out
• Suturing of wounds must be avoided. (If required – only after administering Ig)
• Bandaging must not be done
• Immunisation for tetanus must be carried out
• Analgesics and anti-inflammatory, antibiotics to prevent secondary infection
2. OBSERVETHE BITTENANIMAL FOR
10 DAYS
• CHANGE IN BEHAVIOUR
• WITHDRAWING
• RUNAMUCK
• CHANGE IN BARK
• DEATH
WHO Guidelines for Post Exposure Prophylaxis
Active Immunization
• All anti rabies vaccines are killed vaccines.
• Virus is killed or inactivated by Beta PropionoLactone (BPL)
• They are broadly classified into 3 categories:
 NERVETISSUEVACCINES (NTV)
DUCK EMBRYOVACCINE (DEV)
MODERNTISSUE OR CELL CULTUREVACCINES (TCVs OR CCVs)
Cell CultureVaccines
• Human diploid cell vaccine (HDCV),
• Purified Vero cell rabies vaccine (PVRV),
• Purified chick-embryo cell vaccine (PCECV)
• Purified duck embryo vaccine (PDEV).
• Higher potency, safe and provide longer immunity
Intramuscular Regimens (2 types)
• Essen Regimen
• Zagreb Regimen
Essen Regimen
• 5 doses / 5 vials
Ig
0 3 7 14 28
Essen Regimen
• First 3 doses should be given on indicated days else vaccine failure
• If animal is healthy, can be stopped after 3 doses
• Immunity developed after 8 to 10 Days
Zagreb Regimen (2-1-1)
• 2 doses on first day
0 7 21
Ig
Zagreb regimen
• Early antibody response
• Less vials and visits needed
Intradermal schedule (UpdatedThai
Regimen)
ARV : Deltoid or Anterolateral aspect of thigh
Human Ig = 20 IU/ kg (on day 0)
0 3 7 28
0.1ml Id/ site x 2
Ig
Intradermal schedule
• Total of 4 visits, less vaccine required
• Useful in resource limited settings
• However skilled personnel needed
• Not given in immunosuppressed patients
• DO NOT GIVE MIXED SCHEDULES
Immunoglobulin
• Rabies Ig : In all category 3 patients
• Immediate protection
• Given on Day 0
• Irrespective of interval between exposure and beginning of treatment
• Serum alone not to be administered
Immunoglobulin
• ERIG – Ionorab (Intradermal test needed) – 40 IU /kg bodywt
• HRIG –Rabivax - 20 IU/kg body wt
Rabies Immunoglobulin
• As much as possible inject Ig into the depth of the wound and also infiltrated
around the wound.
• Remaining RIG should be administered intramuscularly into the gluteal region in
single dose on day 0 along with active immunisation , followed by complete
course.
• Has local virucidal effect. And prevents virus from entering susceptible nerve
cells.
4. Advice to patient
• Proper follow up and complete treatment
What to do in case of reexposure?
• If patient has received complete course of preexposure or post exposure
prophylaxis by IM or ID requires only 2 doses of vaccine
• On day 0 and 3 by IM.
PRE EXPOSURE PROPHYLAXIS
• Veterinarians
• Animal handlers
• Lab personnel
• Pet owners
• 3 doses ofTCV on days 0,7 and 28
Personal protection against rabies
• Do not touch animal bitten wounds with bare hands
• Do not provoke any animal
• Avoid contact with secretions of hydrophobia patient
• Take pre exposure immunisation if you belong to at risk group
• Vets to wear masks and gloves while examining rabid animals
REFERENCES
• ParksTextbook of Public Health 23rd Edition
• Community Medicine with recent advances by AH Suryakantha
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Rabies.pptx

  • 1. Dr. Divija Ramachandran Associate Professor Department of Community Medicine Sree Gokulam Medical College and Research Foundation
  • 2. Dogs ….. Man’s BEST friend !
  • 3. BEWARE OF RABIES ……..!
  • 4. Introduction • Zoonotic disease of carnivorous animals ; dogs-enzootic • CNS ( Brain and spinal cord) - Acute fatal encephalomyelitis • Caused by RNA virus - Lyssavirus - Family : Rhabdovirideae • Most important viral zoonoses of warm blooded animals • Variable incubation period, short period of illness and most characteristic feature is “fear of water” – painful spasms of muscles of deglutition followed by respiratory paralysis, delirium, asphyxia and death.
  • 5.
  • 6. Sir Louis Pasteur and the Anti-RabiesVaccine
  • 8. Etiology • Caused by a bullet shaped ,single stranded, non segmented, RNAVirus. • The virus has spikes all over and contain glycoprotein which is the antigenic substance
  • 9. Pathophysiology • Neurotropic virus - tendency to affect the CNS • The spike like projections help the virus to establish itself in the axoplasm (cytoplasm of the nerve cells) • In the neurons of the brain, these viral particles are seen as inclusion bodies , called ‘ Negri Bodies’ which is pathognomonic of rabies. • Absence of Negri bodies however does not rule out rabies. • Virus are often found in various body fluids like saliva, milk, urine, lymph of rabid animals,and in saliva, semen, sweat and tears among affected persons.
  • 10. Characteristics of rabies virus • Lipid content of the sheath – inactivated by fat solvents like disinfectants such as Dettol, Savlon ,Tincture Iodine • Inactivated by UV Rays, heating for 30 seconds , and 40% alcohol. • The virus is highly resistant against cold, dryness, decay • Virus remains infectious for weeks in cadavers.
  • 11. STREETVIRUS • Wild virus in saliva of rabid animals – StreetVirus • Highly pathogenic – virulent to both man and animals • Capable of producing Negri Bodies in neurons • Incubation period: 3 weeks to 3 months
  • 12. FIXEDVIRUS • Successive passage of the street virus through the brain of lab animals , the street virus is made to lose it’s pathogenicity and capacity to produce Negri bodies. , however retaining its antigenicity. • Hence the incubation period becomes short and fixed – 5-6 days in lab animal. • Modified virus is called Fixed virus – avirulent to man • Antigenicity present, no capacity to invade • Cannot multiply or produce Negri Bodies.
  • 13. Reservoir of infection • The principal reservoir of infection are the rabid animals like dogs, wolves, foxes etc. • No carriers among humans. Carrier state among animals is not conclusively established. • Cases of hydrophobia constitute potential source of infection. • Vampire bats serve as constant source of infection for humans and wild animals and enables the virus to be present in nature. • Dogs are principal reservoirs in India
  • 14. Period of infectivity • Humans are infectious during period of illness • Rabid animal infectious during last 3 to 5 days of incubation period and during entire period of illness 12 to 15 days • All warm blooded animals are susceptible • ONLY 15 -20% get the disease as the virus is excreted intermittently through the saliva of rabid animals.
  • 15. Modes ofTransmission • Lick of bite of rabid animal. • Sylvatic cycle in wild animals • Urban cycle in domestic animals • And accidentally to human beings from animals • Human to human transmission does not occur as saliva doesn’t have optimum number of virus and humans do not have biting tendency. Rabies in man is a ‘dead end disease’. Can spread through transplantation.
  • 16. Furious Rabies (Mad dog syndrome) • 80 to 90% of cases • Dog behaves abnormally – goes to dark corners , restless and shows agitation, run amuck • Bites man and animals without provocation • Paralysis of lower jaw, protruded tongue, drooling saliva, paralysis of vocal cord, limbs and trunk. • Death due to respiratory paralysis and convulsions. • Mortality is 100 percent.
  • 17. Dumb Rabies ( Paralytic Rabies ) • 10 to 20% of rabies • Dog becomes silent and withdraws itself • Death from general paralysis • HYDROPHOBIA not a feature
  • 18. Clinical Features • Prodromal stage : Headache, restlessness, Fever,Tingling and numbness at the site of bite and malaise.
  • 19. Clinical Features • Stage of convulsions: • Sensory system – Sensitive to senses of touch , cold, hot – can get convulsions • Motor system – Increased tone and spasticity of muscles- exaggerated reflexes, jerks • Sympathetic system- Excessive perspiration, lacrimation, salivation • Aerophobia and photophobia
  • 20. Clinical Features • Stage of paralysis: Difficulty and pain in swallowing food – choking sensation- painful spasms
  • 21. Lab diagnosis ( Antemortem) • Nuchal skin biopsy • Saliva –Virus isolation or RTPCR • Serum and spinal fluid for antibodies
  • 22. Lab diagnosis (Postmortem) • Brain biopsy and Seller’s stain for Negri Bodies. • Flourescent AntibodyTest
  • 23. Management of Hydrophobia • Isolation in quiet room • Sedatives, antipyretics, analgesics, anti-histaminics and anticonvulsants • IV rehydration, steroids, osmotic diuretics like mannitol • Expert nursing care • Mechanical ventilation of lung • Medical attendants should receive pre exposure prophylaxis with antirabies vaccines and are advised to wear glasses, masks, gloves, shoes, plastic apron. They should avoid contact with saliva, urine, tears of patient.
  • 24.
  • 25. Principles of Post Exposure Prophylaxis • To reduce viral load • To neutralise virus at point of entry • Prevent nerve infection • To induce systemic immunity
  • 26. Post Exposure Prophylaxis • Wound treatment • Observation of the animal • Antirabies immunization - Antirabies vaccine and Immnunoglobulin • Advice to patient
  • 27. 1.WoundTreatment (First AidTreatment) • Thorough washing of wound with soap and running tap water for 10 mins • Application of virucidal agents like povidone iodine and tincture iodine • Deep wounds exploration and debridement must be carried out • Suturing of wounds must be avoided. (If required – only after administering Ig) • Bandaging must not be done • Immunisation for tetanus must be carried out • Analgesics and anti-inflammatory, antibiotics to prevent secondary infection
  • 28. 2. OBSERVETHE BITTENANIMAL FOR 10 DAYS • CHANGE IN BEHAVIOUR • WITHDRAWING • RUNAMUCK • CHANGE IN BARK • DEATH
  • 29. WHO Guidelines for Post Exposure Prophylaxis
  • 30. Active Immunization • All anti rabies vaccines are killed vaccines. • Virus is killed or inactivated by Beta PropionoLactone (BPL) • They are broadly classified into 3 categories:  NERVETISSUEVACCINES (NTV) DUCK EMBRYOVACCINE (DEV) MODERNTISSUE OR CELL CULTUREVACCINES (TCVs OR CCVs)
  • 31. Cell CultureVaccines • Human diploid cell vaccine (HDCV), • Purified Vero cell rabies vaccine (PVRV), • Purified chick-embryo cell vaccine (PCECV) • Purified duck embryo vaccine (PDEV). • Higher potency, safe and provide longer immunity
  • 32. Intramuscular Regimens (2 types) • Essen Regimen • Zagreb Regimen
  • 33. Essen Regimen • 5 doses / 5 vials Ig 0 3 7 14 28
  • 34. Essen Regimen • First 3 doses should be given on indicated days else vaccine failure • If animal is healthy, can be stopped after 3 doses • Immunity developed after 8 to 10 Days
  • 35. Zagreb Regimen (2-1-1) • 2 doses on first day 0 7 21 Ig
  • 36. Zagreb regimen • Early antibody response • Less vials and visits needed
  • 37. Intradermal schedule (UpdatedThai Regimen) ARV : Deltoid or Anterolateral aspect of thigh Human Ig = 20 IU/ kg (on day 0) 0 3 7 28 0.1ml Id/ site x 2 Ig
  • 38. Intradermal schedule • Total of 4 visits, less vaccine required • Useful in resource limited settings • However skilled personnel needed • Not given in immunosuppressed patients • DO NOT GIVE MIXED SCHEDULES
  • 39. Immunoglobulin • Rabies Ig : In all category 3 patients • Immediate protection • Given on Day 0 • Irrespective of interval between exposure and beginning of treatment • Serum alone not to be administered
  • 40. Immunoglobulin • ERIG – Ionorab (Intradermal test needed) – 40 IU /kg bodywt • HRIG –Rabivax - 20 IU/kg body wt
  • 41. Rabies Immunoglobulin • As much as possible inject Ig into the depth of the wound and also infiltrated around the wound. • Remaining RIG should be administered intramuscularly into the gluteal region in single dose on day 0 along with active immunisation , followed by complete course. • Has local virucidal effect. And prevents virus from entering susceptible nerve cells.
  • 42. 4. Advice to patient • Proper follow up and complete treatment
  • 43. What to do in case of reexposure? • If patient has received complete course of preexposure or post exposure prophylaxis by IM or ID requires only 2 doses of vaccine • On day 0 and 3 by IM.
  • 44. PRE EXPOSURE PROPHYLAXIS • Veterinarians • Animal handlers • Lab personnel • Pet owners • 3 doses ofTCV on days 0,7 and 28
  • 45. Personal protection against rabies • Do not touch animal bitten wounds with bare hands • Do not provoke any animal • Avoid contact with secretions of hydrophobia patient • Take pre exposure immunisation if you belong to at risk group • Vets to wear masks and gloves while examining rabid animals
  • 46. REFERENCES • ParksTextbook of Public Health 23rd Edition • Community Medicine with recent advances by AH Suryakantha