1.
POLIOMYELITIS
and
ACUTE FLACCID PARALYSIS

2.
Topics
Introduction
History
Epidemiology
Pathogenesis
Clinical features
Diagnosis
Treatment
Prognosis
Prevention
Programmes

3.
Introduction
Synonyms
Infantile paralysis
Definition
Acute viral infectious disease
Caused by enterovirus
Route – feco – oral
Greek
poliós - "grey"
myelós - "spinal cord"

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

6.
Epidemiology
Incidence
(2011)
India: 5 cases- 1 Wild polio, 4 VAPP
(2010)
Global: 332 confirmed cases
India: 42 confirmed cases
Last case detected in Goa in 1997

7.
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

8.
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

9.
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

10.
Environment
Seasonal
 More during rainy season
Environmental sources of infection
 Contaminated water and food
 Flies
 Overcrowding and poor sanitation

11.
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

12.
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

13.
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!

14.
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!

15.
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!

16.
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

17.
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!

18.
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!

19.
Clinical Features
Abortive polio
Inapparent (90-
95%) Non- paralytic
Infection aseptic
Apparent (5- meningitis
10%)
Paralytic
poliomyelitis
Polio
encephalitis

20.
Abortive polio
 4 – 8% of infections
 Minor illness
 Symptoms
low grade fever
sore throat
vomiting
abdominal pain
Loss of appetite
malaise
 Recovery – complete, no paralysis

21.
Non paralytic aseptic meningitis
 1- 2 % of infections
 Symptoms
headache
nausea
vomiting
pain and stiffness of back and legs

22.
Non paralytic aseptic meningitis
Signs
 Tripod sign
 Kiss the knee test
 Head drop sign
 Neck rigidity
Recovery within 2 – 10 days

23.
Tripod sign

24.
Head drop sign
 Method
Hand placed under patient’s shoulder and
trunk is raised
 Observation
Head lags behind limply

25.
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

26.
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

27.
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

28.
Paralytic poliomyelitis
Spinal paralytic
poliomyelitis
Paralytic
Bulbar polio
Poliomyelitis
Bulbo-spinal
polio

29.
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

30.
Spinal paralytic poliomyelitis
 Paralysis – asymmetrical ( legs > arms), descending
paralysis
 Muscles – floppy
 Reflexes diminished
 Sensation normal
 Residual paralysis after 60 days

31.
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

32.
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

33.
Bulbo-spinal poliomyelitis
 20% cases
 Combination of spinal paralytic and bulbar polio

34.
Polio Encephalitis
Occurs in rare cases
Symptoms
 Irritability
 Delirium
 Disorientation
 Tremors
 Convulsions
 Paralysis is of upper motor neuron type

35.
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

36.
Diagnosis
History
Clinical examination
Stool examination
CSF examination
Serological tests

37.
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

38.
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

39.
CSF examination
Characteristics Observations
Appearance Clear / slightly turbid
Cells Leucocytosis (mainly
lymphocytes)
Proteins Normal / slightly raised
glucose Normal

40.
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

41.
Differential diagnosis
• Most common
 GB syndrome
 Transverse myelitis
• Others
 Traumatic neuritis
 Meningitis
 Encephalitis
 Toxin – diphtheria and
botulism

42.
TREATMENT

43.
Treatment
Symptomatic and supportive
 Rest in bed
 Relief of pain and spasm of muscles
 Neutral positioning of the limbs
 Physiotherapy
 Good nursing

44.
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

45.
 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

46.
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

47.
Physiotherapy

48.
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.

49.
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

50.
Treatment
Indications for hospitalization
 Paralysis of upper limbs <3 days duration
 Progression of paralysis
 Bulbar involvement
 Respiratory distress
 Marked drowsiness
 Complications

51.
Rehabilitation

52.
Rehabilitation
 Physical
 Emotional and Psychological
 Social

53.
Rehabilitation
Emotional support to the
child helps prepare himself
for better adjustment in
life despite the handicap

54.
Complications
 Myocarditis
 Hypertension
 Pulmonary edema
 Pneumonia
 Urinary tract infections
 Skeletal deformities -
equinus foot
scoliosis
osteoporosis
bone fractures
 Compression neuropathy

55.
Prognosis
 Non paralytic cases – complete recovery
 Paralytic polio – permanent weakness in 2/3rd cases
 Worse – older children
sudden onset of illness with high fever

56.
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

57.
PREVENTION

58.
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

59.
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

60.
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

61.
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.

62.
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

63.
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

64.
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.

65.
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

66.
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

67.
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

68.
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

69.
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

70.
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.

71.
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

72.
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.

73.
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

74.
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

75.
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.

76.
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.

77.
WE NEED JUST ONE
MORE THING TO END
POLIO FOREVER
“YOU”

78.
Acute Flaccid
Paralysis

79.
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

80.
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

81.
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

82.
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

83.
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

84.
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

85.
Case investigation
• Stool sample collection
• Stool sample result
• 60 days follow up
• Special investigations if indicated
• Final classification

86.
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

87.
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

88.
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

89.
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

90.
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

91.
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.

92.
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/

93.
Contact
• For distribution and discussion:
Dr. Ankush
Goa Medical College, Goa
drankush1989@gmail.com