Dear Doctor,
Its humbling that you liked the presentation and would like to use it for your purpose. Kindly find your requested presentation attached with this email.
The shortlink for your future reference is http://go.drankush.com/PolioFinal
We would always appreciate if you would place this reference as a due credit in your work and while sharing for others use.
Ankush, Amroskar S, Bhamaikar V, Barreto J. "Polio Final Presentation" Accessed from http://go.drankush.com/PolioFinal
-----------------------------------------------------
As we near eradication of this dreaded disease - "POLIO", we would like to share the following presentation we made for our Pediatrics seminar in 2012.
Best attempts have been made to cover most of the topic, keeping the size under 100 slides.
Hope you like it.
Ankush
Shahin Amroskar
Varsha Bhamaikar
Joyce Barreto
4. History
Timeline Events
ANCIENT EGYPT An egyptian mummy
3.,700 B.C with probable polio
found.
1,209 B.C Mummy Giptah with
an equinus foot
Eighteenth century First known
1789 description by
underwood
Ninteenth century First epidemic of
1834 polio in island of St.
Helena
5. History
Timeline Events
1855 First description by
Duchenne of the
pathalogical process
Twentieth century Transmission of polio to
1908 a monkey by
Landsteiner
1949 Growth of virus on
tissue culture
1951 Three types of polio
virus isolated and
identified
1954 First large scale trial of
Salk
1958 First general use of
Sabin
9. Agent
Poliovirus
Structure:
Group- group IV ((+)ssRNA)
Genus- Enterovirus
Family- Picornaviridae
3 serotypes- type 1, type2, type 3
Composed of an RNA genome and a protein capsid.
Resistance:
In feces – for months at 40 C & years at -200 C
Inactivated by heat and chlorination
10. Agent
Host range
Natural infection occurs only in humans
Mode of transmission
Feco-oral route
In early stage of disease- through inhalation or entry
through conjunctiva of droplets of respiratory
secretion of patient.
Period of communicability
7 to 10 days before and after the onset of symptoms
11. Host
Age
Most vulnerable- 6 months to three years
Sex
M: F ratio 3:1
Immunity
First 6 months maternal antibody
Acquired through infection with the wild virus
Immunization
12. Environment
Seasonal
More during rainy season
Environmental sources of infection
Contaminated water and food
Flies
Overcrowding and poor sanitation
13. Pathogenesis
Incubation period: 7-10 days (4- 35 days)
Feco-oral
Inhalational Portal of entry- Local Minor/Primary
mouth multiplication Viremia
infects the pharynx
and intestinal mucosa.
Gains entry by Multiplies in To spinal cord Major/Secondary
neurons and brain Viremia
binding to an
immunoglobulin-like
receptor, known as the
poliovirus receptor or Lesions are mostly
in anterior horns of DESTROYS
CD155, on the cell spinal cord causing
THEM!
membrane flaccid paralysis
14. Pathogenesis
Portal of entry- Local Minor/Primary
mouth multiplication Viremia
Epithelial
cells of GIT
Multiplies in To spinal cord Major/Secondary
neurons and brain Viremia
Lymphatic
tissue- from
tonsils to Lesions are mostly
DESTROYS
in anterior horns of
Peyer’s spinal cord causing
flaccid paralysis
THEM!
patches
15. Pathogenesis
Spreads to Portal of entry- Local Minor/Primary
mouth multiplication Viremia
regional lymph
nodes
Multiplies in To spinal cord Major/Secondary
Enters blood neurons and brain Viremia
stream -
primary viremia Lesions are mostly
in anterior horns of DESTROYS
spinal cord causing
flaccid paralysis
THEM!
16. Pathogenesis
Multiplies in
Portal of entry- Local Minor/Primary
reticulo- mouth multiplication Viremia
endothelial
systems
Multiplies in To spinal cord Major/Secondary
Enters blood neurons and brain Viremia
stream again -
secondary
Lesions are mostly
viremia in anterior horns of DESTROYS
spinal cord causing
flaccid paralysis
THEM!
17. Pathogenesis
Carried to spinal cord & brain
Portal of entry- Local Minor/Primary
mouth multiplication Viremia
Multiplies in To spinal cord Major/Secondary
Bloodstream Direct neurons and brain Viremia
(Tonsillectomy
trauma
IM injections
fatigue ) Lesions are mostly
in anterior horns of DESTROYS
spinal cord causing
flaccid paralysis
THEM!
18. Pathogenesis
Multiplies in neurons
Degeneration of Portal of entry- Local Minor/Primary
mouth multiplication Viremia
Nissl’s body
(chromatolysis)
Nuclear changes Multiplies in To spinal cord Major/Secondary
follows neurons and brain Viremia
When degeneration
irreversible Lesions are mostly
in anterior horns of DESTROYS
phagocytosed by spinal cord causing
flaccid paralysis
THEM!
leucocytes or
macrophages
19. Pathogenesis
Lesions are in anterior
horn of spinal cord
Flaccid paralysis Portal of entry- Local Minor/Primary
mouth multiplication Viremia
Can cause
encephalitis involving
• Brainstem Multiplies in To spinal cord Major/Secondary
• Motor & neurons and brain Viremia
Premotor areas of
cerebral cortex
Lesions are mostly
in anterior horns of DESTROYS
spinal cord causing
flaccid paralysis
THEM!
20. Pathogenesis
Portal of entry- Local Minor/Primary
mouth multiplication Viremia
Multiplies in To spinal cord Major/Secondary
neurons and brain Viremia
Lesions are mostly
in anterior horns of DESTROYS
spinal cord causing
flaccid paralysis THEM!
26. Head drop sign
Method
Hand placed under patient’s shoulder and
trunk is raised
Observation
Head lags behind limply
27. Kiss the knee test
Method
knees kept down
child asked to kiss his knees
Observation
Cannot do the maneuver due to stiffness spine
May draw up the knees sharply
28. Neck rigidity
Method
In uncooperative child-place childs head beyond the
edge of table
Observation
True involuntary neck rigidity persists
Voluntary stiffening of muscles disappears
29. Paralytic poliomyelitis
0.5 – 1% of infections
2 PHASES - Minor
Major
Minor- same as abortive polio
Major- muscle pain ,spasm and return of fever
Followed by rapid onset flaccid paralysis
complete within 72hrs
32. Spinal paralytic poliomyelitis
Most common
80% of cases
Results from lower motor neuron lesion of anterior
horn cells of spinal cord
Affects muscles of legs, arms and/or trunk
Severe cases – quadriplegia , paralysis of trunk
abdominal and thoracic muscles
33. Spinal paralytic poliomyelitis
Paralysis – asymmetrical ( legs > arms), descending
paralysis
Muscles – floppy
Reflexes diminished
Sensation normal
Residual paralysis after 60 days
34.
35. Bulbar polio
2% of cases
Life threatening
Cranial nerve lesion - vagus
Symptoms
o Nasal twang and hoarseness of voice
o Nasal regurgitation
o Dyspnea
o Dysphagia
o Child refuses to feed
o Secretions accumulate in pharynx - aspiration
36. Bulbar polio
• Involvement of
respiratory centre - Shallow , irregular respiration
Vasomotor centre - BP rises then falls
• pulse – rapid weak thready
• Skin – dusky red mottled
• Restless , confused and comatose
38. Polio Encephalitis
Occurs in rare cases
Symptoms
Irritability
Delirium
Disorientation
Tremors
Convulsions
Paralysis is of upper motor neuron type
39. Residual paralysis
Acute phase of illness lasts for 0-4weeks
Recovery –variable
At 60 days mild to severe residual paresis
Maximum recovery – first 6 months
Slow recovery upto 2 yrs
After 2 yrs post polio residual paralysis persists
throughout life
41. Stool examination
Collection of sample
Two samples 24 hr apart
Within 14 days of onset of paralysis
8-10 grams or thumb size
Collected in a clean wide mouth bottle – plastic or glass
with screw cap
Sample stored below 8°C
No dessication or leakage till received at WHO
Accredited Lab
If paralysis detected after 2 wks sample taken upto 60
days from onset
42. Stool examination
Contact sampling
Done when child has died without adequate stool
sampling
5 children in close contact with the child are taken
Single stool sample collected
44. Serological tests
3 types of antibodies
Neutralizing antibodies (IgG)
Antibodies to C antigen (IgM)
Anti-D antibodies
Complement fixation test – detects IgM and Anti-D
antibodies
Identifies exposure to poliovirus not for type- specific
diagnosis
Less often employed
45. Differential diagnosis
• Most common
GB syndrome
Transverse myelitis
• Others
Traumatic neuritis
Meningitis
Encephalitis
Toxin – diphtheria and
botulism
47. Treatment
Symptomatic and supportive
Rest in bed
Relief of pain and spasm of muscles
Neutral positioning of the limbs
Physiotherapy
Good nursing
48. Bed Rest
Essential during acute phase
Physical activity & trauma increases risk of paralytic polio
Posture to be changed every 2-3 hrs.
Child to be placed on stomach for short periods each day, to
prevent pneumonia
49. Optimum position for limbs
Hip – slight flexion
Knee – 5 degree flexion
Foot – 90 degree support against the sole
Pain Relief
Sister Kenny’s treatment
Hot moist packs applied to the muscles to relieve pain and
spasm
analgesics
50. Physiotherapy
Method
• Joints & paralysed muscles – moved passively through full
range
• For 10 min , 2-3 times/day
Benefits
• Prevents deformities and contracture
• Promote development of muscle power in non-paralysed
muscles
52. Good nursing
Team approach is essential
Nursing staff is an imp part
Diet
Nutritious , balanced & wholesome
In non paralytic polio- normal diet
In paralytic
Fed by Ryles tube
Calories/kg body wt.
53. Good Nursing
In dysphagia pt. nursed in prone position with foot end raised – gravity
drainage of pooled secretions in pharynx
Or intermittent suction
Tracheostomy
Respiratory failure – assisted respiration with mechanical ventilator
54. Treatment
Indications for hospitalization
Paralysis of upper limbs <3 days duration
Progression of paralysis
Bulbar involvement
Respiratory distress
Marked drowsiness
Complications
60. Prognosis
Non paralytic cases – complete recovery
Paralytic polio – permanent weakness in 2/3rd cases
Worse – older children
sudden onset of illness with high fever
61. Post – polio syndrome
Observed in people who had polio during their childhood.
Affects about 25-50 % of the polio survivors.
More common in females
General fatigue
muscular weakness
joint pains
& breathing problems are seen in affected
63. Immunisation
• History
• Sabin’s Live Polio Vaccine
I. Preparation
II. Storage and transport
III. Administration
IV. Dosage
V. Development of Immunity
VI. Advantages and Disadvantages
VII. Complications and Contraindications
• Salk’s Killed Polio Vaccine
I. Preparation
II. Dosage
• Sabin Vs Salk
• Pulse Polio Immunization
64. History
• Earliest vaccines-
a. Crude suspensions of spinal cord from infected monkeys -Ineffective
b. Inactivated with Formalin (Brodie and Park) -Often dangerous
Ricinoleate (Kolmer) causing vaccination
poliomyelitis
• By 1953
a. Salk had developed a killed vaccine
b. Almost simultaneously, Koprowsky, Cox and Sabin independently developed live
attenuated vaccines
65. Sabin’s Live Polio Vaccine
• Sabin’s attenuated strains are employed
• Developed by plaque selection in MKTC
• Preparation
a. Attenuated strains grown in MKTC
b. Stringent precautions to ensure freedom from SV40 and B virus.
c. Use of molar MgCl2 or sucrose stabilises the vaccine against heat
inactivation
66. Sabin’s Live Polio Vaccine
• Criteria for selection
a. Should not be neurovirulent as tested by intraspinal inoculation in
monkeys
b. Should be able to set up
intestinal infection following feeding & induce immune
response
c. Should be stable &
not acquire neurovirulence after serial enteric passage
d. Should posses stable
genetic markers enabling differentiation from wild
virulent strians.
67. Sabin’s Live Polio Vaccine
Genetic Markers:
• D Marker
• Rct 40
• MS
• Mcbride’s intratypic antigenic marker
Molecular Epidemiological Methods:
• Monoclonal antibodies specific to vaccine strains
• Oligonucleotide finger printing
• Nucleic acid sequencing
68. Sabin’s Live Polio Vaccine
• Storage
i. Stabilised vaccine: 1 year at 4 °C
1 month at room temperature
ii. Non-stabilised vaccine: -20 °C in deep freeze (In the freezer
compartment of refrigerator)
• During transport, keep the vaccine under
i. Dry ice (solid carbon dioxide)
ii. Freezing mixture (equal quantities of wet ice and ammonium chloride)
• At vaccination clinic
i. Shouldn’t be frozen and thawed repeatedly deleterious effect on
potency
ii. Keep vaccine in ice during administration
69. Sabin’s Live Polio Vaccine
• OPV in India, trivalent, contains
a. Type 1- 1 lakh TC ID 50
b. Type 2- 2 lakh TC ID 50 per 0.5 ml
c. Type 3- 3 lakh TC ID 50 (2 drops in India)
• Administration- 2 drops
• Use the dropper supplied
a. Tilt the child’s back
b. Gently squeeze the cheeks/
pinch the nose make the mouth open
c. Let the drops fall from the dropper onto the tongue.
70. Sabin’s Live Polio Vaccine
• National Immunization Schedule
Age Dose
At birth OPV-0
At 6 weeks OPV-1
At 10 weeks OPV-2
At 14 weeks OPV-3
16-24 months OPV
71. Sabin’s Live Polio Vaccine
• Indian Academy of Paediatrics recommendation
Age Dose
At birth OPV-0
At 6 weeks OPV-1+IPV
At 10 weeks OPV-2+IPV
At 14 weeks OPV-3+IPV
16-24 MONTHS OPV+IPV
5 years OPV
72. Development of Immunity
Infects intestinal epithelial cells
Replicates transported to Peyer’s patches Stimulates
production of IgA antibodies
Secondary multiplication d subsequent viremia (LOCAL IMMUNITY)
Spreads to other parts of body Prevents infection of
GIT with wild strains
Production of circulating antibodies Vaccine progeny
excreted in feces
Prevents dissemination of virus to nervous system
Non-immunized
persons immunized
Prevents paralytic polio
(SYSTEMIC IMMUNITY) HERD IMMUNITY
73. Sabin’s Live Polio Vaccine
• Advantages
i. Oral easily admin no need of highly trained personnel
ii. Induces both humoral and systemic immunity
iii. Antibodies quickly produced*
iv. Vaccinees excrete virus herd immunity
v. Useful in epidemics
vi. Relatively inexpensive
• Disadvantages
i. Instability at high temperatures
ii. Frequent vaccine failures even with fully potent vaccines
iii. Very small residual neurovirulence in OPV
74. Sabin’s Live Polio Vaccine
• Complications
a. Mutation (esp. type 3[1] /2[2])
b. WHO estimated the risk of
i. vaccine-associated paralysis : 1 case/million vaccinees
ii. Risk of close contact of vaccinee : 1 case/5 million doses of vaccine
developing paralytic polio
Contraindications
a. Immunocompromised individuals leukemics, malignacy, those
receiving corticosteroids.
b. Pregnant mothers OPV should be delayed until after pregnancy unless
immediate protection is required, when IPV is indicated.
c. Premature Babies
75. ALERT!
DIARRHOEA NOT A CONTRAINDICATION
But a dose of OPV given at that time shouldn't be considered as part of the
series and should receive another at earliest opportunity.
76. Salk’s Killed Polio Vaccine
Formalin inactivated preparation
Three types of polio virus grown in monkey kidney tissue culture(MKTC)
•Procedure for Preparation
3 types of PVs Adequate titre Inactivated with
Standard virulent
grown separately filtered to remove formalin at 37°C
strains used
in MKTC debris and clumps FOR 12-15 DAYS
Stringent tests to Further tests for
Three types are
ensure complete safety and Issued for use
further pooled
inactivation potency
77. Salk’s Killed Polio Vaccine
• 1954 nationwide field trial (USA)- 80 -90% protection
• 1955 – ‘Cutter incident’; over 100 cases of paralytic poliomyelitis occurred
in vaccines and their contacts following insufficiently inactivated vaccine.
78. Salk’s Killed Polio Vaccine
• Injectable Polio Vaccine (IPV)
a. 1st dose given at 6 weeks.
b. Immunity sustained by booster doses every 3-5 years thereafter
c. Vaccination of choice among HIV, other immunocompromised states,
pregnant mothers.
• Enhanced potency IPV
a. Produced in human diploid cells
b. Two s.c. Does, 4-8 weeks apart, third
may be 6-12 months later.
c. Better seroconversion
79. Sabin Vs Salk
Feature Sabin’s Vaccine (live) Salk’s Vaccine (killed)
Strain Live attenuated virus Killed formalised vaccine
Administration Oral (preferred in mass Injectable (adv. can be
campaigns) given with DPT)
Factors affecting Diarrhoeal disease preventing Not affected by these
efficacy colonisation by vaccine virus factors
Safety Safe Safe
But, cases of vaccine induced
paralysis reported
80. Sabin Vs Salk
Feature Sabin’s Vaccine (live) Salk’s Vaccine (killed)
Economical More Less (because, virus
content is 10,000 times
more, hence costlier)
Nature of Local and systemic Only systemic, no
immunity intestinal immunity No
herd immunity
Duration Life long Periodic booster doses
required
Use in epidemic Ideal Not very ideal- May
promote multiplication
on 7 dissemination of
wild virus.
81. Pulse Polio Immunization
Largest public health campaign ever conducted in a single country
• Occurs as two rounds 4-6 wks apart during low transmission season of
polio- Nov to Feb
• First round- 9th Dec ‘95 and 20th Jan ‘96
• Sudden, simultaneous, mass administration of OPV on a single day
• To all children 0-5 years
• Regardless of previous immunization
• Extra doses which supplement
• Do not replace the doses during routine immunization
• Children/infants should receive all their schedules OPV doses.
82. WE NEED JUST ONE
MORE THING TO END
POLIO FOREVER
“YOU”
84. Introduction
Case definition
• Child less than 15 yrs with acute onset flaccid paralysis for which
no obvious cause is found
• Acute - onset paralysis < 4 wks
• Flaccid - floppy or limp paralysis
• Background rate of AFP
• One case of AFP per year for every one lakh population of children
less than 15 years
85. Conditions causing AFP
Site Conditions
Muscle Myoglobinuric myopathy
Hypokalemic paralysis
Toxic paralysis
Myopathy of intensive care
Neuromuscular junction Myasthenia gravis
Botulism
Hypermagnesemia
Peripheral nerve Guillian barre syndrome
Diphtheric neuropathy
Porphyria
Lead neuropathy
Hypophosphatemia
Cobalamin deficiency
Anterior horn cells Poliomyelitis
Other enteroviruses
86. Differential Diagnosis of AFP
Feature Poliomyelitis G.B. Syndrome Transverse Traumatic
myelitis neuritis
History
Progression to 24-48 hrs Hours to days Hours to 4 days Hours to 4 days
full paralysis
Fever onset High always No Present before No
present at onset paralysis
of paralysis
Bladder Absent Transient Present Never
dysfunction
87. Feature Poliomyelitis G.B. Syndrome Transverse Traumatic
myelitis neuritis
Differential Diagnosis of AFP
Examination
Flaccidity Acute, Acute, Acute, Acute, assymetric
assymetrical, symmetrical, symmetrical,
proximal distal, ascending lower limb
Muscle tone Diminished Diminished Diminished in Diminished
lower limbs
Deep tendon Decrease or Absent Absent early, Decreased or
reflexes absent hyperreflexia late absent
Sensation Severe myalgia Cramps, tingling, Anesthesia of Pain in gluteal
and backache, no hypo anesthesia lower limb with region
sensory changes of palms and sensory level
soles
Cranial nerves Only when Often present Absent Absent
bulbar and affecting nerves
bulbo-spinal VII,IX,X,XI,XII
Respiratory Only when bulbo In severe cases Sometimes Absent
insufficiency and bulbo-spinal
88. Feature Poliomyelitis G.B. Syndrome Transverse Traumatic
myelitis neuritis
Differential Diagnosis of AFP
Investigations
CSF examination High Less than 10 Cellular or Normal
leucocytosis; leucocytes: high acellular; normal
normal or slightly protein or slighly
increased protein increased protein
EMG at three Abnormal Normal Normal May show
weeks abnormality
Nerve Normal Abnormal, Normal Abnormal
conduction demylination or
velocity at 3 axonal damage
weeks
Sequlae at 3 months
Severe, Symmetrical Diplegia, atrophy Moderate
assymetrical atrophy of distal after years, atrophy in the
atrophy; skeletal muscles recovery recovery in affected limb
deformity appear in milder cases milder cases
late
89. AFP Surveillance
• All cases to be reported
• All reported cases classified as polio non polio
• High sensitivity of reporting will ensure detection of all cases
resulting in control measures to interrupt transmission
• Two critical indicators of quality of surveillance are -
a. rate of non polio AFP
b. proportion of AFP cases with two adequate stools collected
within 14 days of onset of paralysis
90. Case investigation
• Stool sample collection
• Stool sample result
• 60 days follow up
• Special investigations if indicated
• Final classification
91. Stool examination
Collection of sample
Two samples 24 hr apart
Within 14 days of onset of paralysis
8-10 grams or thumb size
Collected in a clean wide mouth bottle – plastic or glass with screw
cap
Sample stored below 8 C
No dessication or leakage till received at WHO Accredited Lab
If paralysis detected after 2 wks sample taken upto 60 days from
onset
92. Stool examination
Contact sampling
Done when child has died without adequate stool sampling
5 children in close contact with the child are taken
Single stool sample collected
93. Virological AFP
Compatible
Wild polio Confirm
virus expert
Residual
review
weakness, died
lost to follow up discard
AFP
Inadequate or No
no specimen residual discard
No wild
virus weakness
2 adequate stool specimen discard
94. Clinical AFP
Lost follow confirm
up
Residual
paralysis confirm
AFP Follow-up at
60 days
Positive for
confirm
wild polio
virus
No residual
paralysis discard
95. Sequence of action to be taken after
detecting a case of AFP
Acute onset of paralysis
Within 48 hrs
Investigate the suspected case Discard the case of traumatic /
electrolyte imbalance
Within 3 days
2 adequate stool specimen National lab to
collected report within 28 days
Outbreak response immunization
and active surveillance
Intratyping
60 days follow up (before 70 Final classification of
days) case within 90 days
96. Bibliography
Textbooks
1. M.D RMK, Stanton BF, Geme JS, Schor N, Behrman RE. Nelson Textbook
of Pediatrics: Expert Consult Premium Edition - Enhanced Online
Features and Print. Elsevier - Health Sciences Division; 2011.
2. Parthasarathy et al. Textbook of Pediatrics IAP. Jaypee Brothers
Publishers; 2005.
3. O.P. Ghai et al. Essential Pediatrics. CBS Publishers & Distributors; 2009.
4. Park JE. Textbook of preventive and social medicine: a treatise on
community health. Banarsidas Bhanot; 1972.
5. Fauci AS, Eugene B, M.D SLH, M.D DLL, J J, Joseph L. Harrison’s principles
of internal medicine. McGraw-Hill; 2008.
97. Bibliography
• Online Resources
• AFP Statistics:
i. National Polio Surveillance Project
http://www.npspindia.org/
• Image Courtesy:
i. Rotary International Foundation
http://www.rotary.org
ii. Bill and Melinda Gates foundation
http://www.gatesfoundation.org/
iii. Global Polio Eradication Initiative
http://www.polioeradication.org/
JI C, Cohen JI. Harrison’s Principles of Internal Medicine Chapter 175: Enteroviruses and Reoviruses. McGraw-Hill Professional; 2004. p. pp.&nbsp;1144.Chamberlin SL NB (eds ), Chamberlin SL, Narins B (eds.). The Gale Encyclopedia of Neurological Disorders. Detroit: Thomson Gale; 2005.
Rationale Risk of VAPP is extremely low as child receives OPV at a time when he is protected by VAPP by maternal antibodies.Subsequently he is protected from VAPP by IPV
Ghai’s Essential Paediatrics, Pradeep Seth, Surjit Singh, AditiSinhaImmunity and ImmunizationPg 167Park’s Textbook of Preventive and Social Medicine, K. Park, Epidemiology of Communicable diseases-Poliomyelitis Pg 181
Salk D. Eradication of Poliomyelitis in the United States. II. Experience with Killed Poliovirus Vaccine. Review of Infectious Diseases. 1980 Mar 1;2(2):243 -257. Lapinleimu K, Stenvik M. Experiences with polio vaccination and herd immunity in Finland. Dev. Biol. Stand. 1981;47:241-246.