4. OUTLINE
ā¢Definition of AFP , causes and significance
ā¢Poliomyelitis ā Pathogenesis, clinical features,
Treatment and Prevention
ā¢Differential diagnosis of AFP
ā¢Polio vaccines
ā¢AFP Surveillance
ā¢Polio eradication
5. ACUTE FLACCID PARALYSIS (AFP)
Definition and relevance
ā¢ Rapid onset of weakness with reduced muscle tone progressing to maximum
severity within days to weeks
ā¢ Clinical significance
ā¢ Epidemiological significance
ā¢ WHO Epidemiological definition for Global Polio Eradication Programme
āAFP in any child less than 15 years or any paralytic illness at any
age when polio is suspectedā
8. POLIOMYELITIS
ā® āpoliosā - grey āmyelosā ā marrow [Ancient Greek]
ā® From prehistory
Major epidemics were unknown before 20th century
ā® 1916 US epidemic - 27,000 cases and more than 6,000 deaths due to polio in
the with over 2,000 deaths in New York City alone
āThousands fled the city to nearby mountain resorts; movie theaters were
closed, meetings were canceled, public gatherings were almost nonexistent,
and children were warned not to drink from water fountains, and told to avoid
amusement parks, swimming pools, and beachesā
ā® Worst epidemics in 1940ās and 1950ās
9. ā John Enders ā cultivated poliovirus in human tissue
ā Jonas Salk ā April 12, 1955 ā Inactivated polio vaccine (IPV)
ā Albert Sabin ā 1962 ā Oral polio vaccine (OPV)
10. ETIOLOGY
āPositive stranded RNA virus
āPicorna viridae ā Family ; Genus ā Enterovirus ; Species ā Entrovirus C
ā3 different Antigenic serotypes ā 1, 2, 3
All types cause paralysis
Type 1 most frequently causes epidemic
Type 2 most common cause for vaccine derived poliomyelitis
11. TRANSMISSION
āFecoāoral route predominates where sanitation is low
oral to oral route where sanitation is high
āHighly communicable āOne infected individual will infect all nonāimmune persons
in a household
āHumans are the only known reservoir
āVirus excretion
intermittently excreted for 6ā8 weeks after infection
Majority of viral excretion just prior to paralysis onset and up to first two
weeks ,dramatically tapers off after 4 weeks
12. PATHOGENESIS
ā Entry via CD 155 receptor positive cells lining
mucosa
ā Regional LN (Cervical and mesenteric LN)
ā Primary and transient viremia
ā Seeds extra neural tissue [ RES, brown fat and
skeletal muscle]
ā Secondary viremia
ā Direct seeding of CNS or
Retrograde spread via nerves
13. PATHOGENESIS (Contd..)
āPrimarily infects motor neuron cells (Anterior horn cells) in
spinal cord and brain stem (motor cranial nerve nuclei)
āClinical signs of paralysis occur when >50% motor neurons
supplying muscle are destroyed ( as there is overlap in muscle
innervation)
āIn brain less extensive lesions can cause paralysis
āVital centre involvement ā death
14. PATHOLOGY
āPerineuronal inflammation
āMixed inflammatory raction
āExtensive neuronal destruction
āPetechial hemorrhage and considerable inflmmatory edema in
affected areas
āInflammatory edema can also occur in RES ā Hyperplastic
lymphocytic follicles
15. CLINICAL FEATURES
ā¢ INCUBATION PERIOD 8-12 days (5-35 days)
Asymptomatic /
Inapparent infection
ā¢ 90-95%
ā¢ No symptoms
ā¢ No sequelae
Non paralytic
ā¢ 5%
ā¢ Abortive (4-8%)
ā¢ Aseptic
meningitis(1-2%)
Paralytic
ā¢ 0.1%
ā¢ Bulbar
ā¢ Spinal
ā¢ Bulbo spinal
ā¢ Encephalitic
16. āINAPPARENT INFECTION
āŖ Accounts for approximately 95% of cases
āŖ Virus stays in intestinal tract and does not attack the nerves
āŖ No symptoms, no sequelae
āŖ Virus is shed in the stool so infected individual is still able to
infect others
17. āABORTIVE POLIOMYELITIS
āŖ About 5% infections
āŖ Non specific flu like syndrome ( fever, mlaise, anorexia, headache)
sorethroat, abdominal pain, myalgia, irregular vomiting 1-2 weeks
after infection
āŖ O/E, non specific pharyngitis, abdominal/muscle tenderness, and
weakness
āŖ Lasts for 2-3 days
āŖ Recovers without sequelae
18. āNON PARALYTIC ASEPTIC MENINGITIS
āŖ In about 1%
āŖ Biphasic illness
1st phase -Symptoms similar to abortive poliomyelitis but more intense
- short symptom free interval
2nd phase ā CNS disease major illness
Soreness, stiffness of posterior muscles of neck, trunk, limbs
O/E ā nuchal rigidity, spinal rigidity
AF ā tense/bulging
19. PARALYTIC POLIOMYELITIS
3 clinically recognisable syndromes
āSPINAL PARALYTIC TYPE
āŖ Most common form of paralytic poliomyelitis; (79% of all paralytic cases)
āŖ Attacks motor neurons and causes paralysis of muscles innervated by spinal nerve
āŖ Biphasic illness
1st phase ā similar to abortive PM
symptom free for 2-5 days
2nd phase ā severe fever, headache, exacerbration of previous symptoms
severe muscle pain and neurological symptoms (paresthesias, hyperaesthesias,
fasiculation, spasm)
20. āŖ O/E, Neck stiffness, muscle tenderness
within 72 hours , asymmetric flaccid paralysis established
āŖ Most commonly affected muscle groups are
āQuadriceps, tibialis anterior, peroneal
āDeltoid, biceps, triceps
āAbdominal muscles, intercostal and diaphragm
āŖ Respiratory muscle paralysis can cause life threatening impairment of
ventilation
āŖ Superficial reflexes (abdominal, cremasteric, gluteal) are the first to
decrease, 12-24 hrours before onset of weakness
āŖ Deep tendon reflexes change 8-24 hours after superficial reflexes, it pretells
evolving paralysis (decreased or absent)
21. ā¢ Bowel, bladder dysfunction ( transient urinary retention, later incontinence,
constipation)
ā¢ Developing countries, biphasic illness may not be apparent
ā¢ Paralysis do not progress once fever comes down
ā¢ RESIDUAL PARALYSIS
22. āFACTORS FAVOURING PARALYSIS
ā¢ Male children
ā¢ Female adults
ā¢ Pubertal age group
ā¢ Pregnancy
ā¢ Tonsillectomy
ā¢ I M injections
ā¢ Increased physical activity and fatigue
23. āDistinguishing features
āŖ Asymmetric flaccid paralysis āproximal > distal
āŖ deep tendon reflexes diminished or absent
āŖ fever at onset, muscle pain
āŖ rapid progression to paralysis 2ā3 days
āŖ preservation of sensory nerve function
āŖ residual paralysis after 60 days
24. āBULBAR PARALYTIC TYPE
āŖ Less than 1% of paralytic polio
āŖ Dysfunction of Cranial nerves and medullary centres dominate clinical picture
Commonly involved cranial nerves are: ā
III to VII nerve nuclei ā good prognosis ā
IX to XII nerve nuclei ā poor prognosis ā¢
Vital centre involvement
āŖ Inability to swallow
āŖ Pooling of secretions
āŖ Nasal regurgitation
āŖ Nasal twang of voice/cry
āŖ Irregular respiration (pooling of
secretions in pharynx, vocal cord
paralysis
āŖ Deviation of palate/uvula/tongue
ā¢ Impairment of respiratory center ā
may lead to respiratory failure
ā¢ Impairment of circulatory center
(autonomic nervous system) ā
leading to hypertension and
peripheral circulatory failure
ā¢ Delirium, coma
25. ā¢ ROPE SIGN
ā¢ LANDRY TYPE PARALYSIS ā Ascending paralysis culminating in bulbar
involvement
ā¢ Death, partial recovery, full recovery
ā¢ Cranial nerve involvement is seldom permanent
26. āBULBOSPINAL POLIO
āŖ Accounts for 19% of paralytic cases
āŖ Has mixed features; i.e. features of both spinal as well as bulbar
forms
āŖ Affects extremities and cranial nerves
āŖ Leads to severe respiratory involvement
27. āPOLIOENCEPHALITIS
āŖ Very rare
āŖ Causes inflammation of gray matter of brain
āŖ Signs/symptoms include agitation, confusion, stupor, and coma
āŖ Autonomic dysfunction is common and it has a high mortality
29. DIAGNOSIS
āIsolating virus from stool sample
āŖ 2 samples collected 24-48 hours apart
āŖ Each 8-10 g (one adult thumb size)
āŖ Within 14 days of onset of paralysis (may be collected upto 60 days)
āŖ Transported in clean, dry, screw capped container to WHO accredited lab
āŖ In REVERSE COLD CHAIN
āŖ Virus grown in 2 cell lines (Human rhabdomyosarcoma cells, L20B cells)
āŖ Cytopathic effects looked for
āŖ Serotyping and identifying
30. āCSF study
āŖ Normal in minor illness
āŖ CNS involvement- pleiocytosis (20-300 cells/micro L), initially PMNL, later
mononuclear cells. Count normal by 2nd week
āŖ CSF protein normal initially, increase by 2nd week
āSEROCONVERSION
āŖ 4 fold rise in antibodies by 3-6 weeks
31. TREATMENT
ā¢ Limit progression
ā¢ Prevent ensuing deformities
ā¢ Preparing child and family for prolonged treatment
ā All I M Injections and surgical procedures are contraindicated in acute
phase of poliomyelitis (PROVOCATIVE POLIOMYELITIS)
32. INDICATIONS FOR HOSPITALISATION
ā¢ Progression of paralysis
ā¢ Respiratory distress
ā¢ Bulbar involvement
ā¢ Paralysis of upper limbs of less than 3 days
ā¢ Marked drowsiness
33. TREATMENT
ā¢ Bed rest ā Physical activity increases risk of paralysis.
ā¢ Pain relief āAnalgesics, sister Kennedy's method, mild sedative in spinal form, not
to be used in bulbar form, encephalitis.
ā¢ Neutral position of limbs. ( feet at right angles to legs, knees slightly flexed, hips
and spine straight )
ā¢ Physiotherapy prevents deformity
ā¢ Bowel ā manage constipation
ā¢ Bladder ā for retention Parasympathetic stimulant (Betanechol), manual
compression, cathetrisation carefully ( lasts for less than few days)
ā¢ Good diet, high fluid
34. TREATMENT (Contd..)
āBULBAR POLIOMYELITIS
ā¢ Maintain airway, avoid aspiration
ā¢ BP monitoring
ā¢ Tracheostomy (Vocal cord paralysis, constriction of hypopharynx)
ā¢ Most recover with little residual impairment
36. PROGNOSIS
ā¢ Inapparent infection
ā¢ Abortive poliomyelitis Good outcome
ā¢ Aseptic meningitis syndrome
ā¢ Paralytic disease ā depends on CNS involvement
ā¢ Severe bulbar disease ā mortality 60%
Less severe bulbar/ spinal ā mortality 5-10%
37. POST POLIO SYNDROME
ā¢ In 25-50% survivors of wPV infection
ā¢ 15-30 years after infection
ā¢ Muscle pain and exacerbration of existing weakness or appearance of new
weakness
ā¢ RISK FACTORS
- increased time since infection
- permanent residual impairment after recovery from acute illness
- Female sex
40. GUILLEIN BAREE SYNDROME
ā¢ Most common cause of AFP in post polio era
ā¢ Infection triggered immune mediated attack on the nerve axons or myelin
ā¢ Antecedant respiratory or gastrointestinal illnesses
ā¢ AIDP most common, AMAN also in Indian children
ā¢ pain, paraesthesia, or weakness in the limbs which spreads proximally.
ā¢ Paralysis ā Symmetric, Ascending, progressing over days to weeks
ā¢ Lower cranial nerve involvement
ā¢ Bladder dysfuction may be present initially, transient
ā¢ Autonomic signs
ā¢ Respiratory insufficiency severe cases
41. ā¢ CSF STUDY : Albumino cytological dissociation
ā¢ NERVE CONDUCTION STUDIES : slowed conduction, decreased motor
amplitude
ā¢ TREATMENT : Supportive care
IvIg 2g/kg over 2-5 days
Plasmapheresis
42. TRANSVERSE MYELITIS
ā¢ an acute demyelinating disorder of the spinal cord
ā¢ acute phase of spinal shock (over hours to 4 days)
flaccid paraparesis or quadriparesis (symmetric)
urinary retention or incontinence (persistent)
absent reflexes and mute plantars
sensory loss/level
ā¢ Autonomic signs present
ā¢ After a few weeks, the signs of UMN dysfunction appear, in the form of spasticity,
and hypereflexia
43. ā¢ CSF study ā Normal or mild pleiocytosis
ā¢ Nerve conduction velocity ā Normal
ā¢ MRI spine ā to R/o Trauma, Epidural abscess, hematoma, Anterior spinal aretery
syndrome
ā¢ TREATMENT : Supportive care
Methyl prednisolone I/V 10-30 mg/kg/day for 5 days followed by oral
44. TRAUMATIC NEURITIS
ā¢ Follows IM injection
ā¢ one limb involvement and definite history of injection in that limb (usually less
than 24 h) before the onset of paralysis.
ā¢ Associated with pain and hypothermia of affected limb
ā¢ sensory deficits and lack of CSF pleocytosis favor the diagnosis of traumatic
neuritis
ā¢ NERVE CONDUCTION STUDY ā Sensory motor axonal neuropathy
45.
46. āNon polio enteroviral myelitis
āŖ most common ā Enterovirus 71
āŖ frequently is associated with aseptic meningitis, hand, foot and mouth disease
and hemorrhagic conjunctivitis
āŖ Other viruses - Rabies, JE
āŖ Hypokalemic paralysis
47. When child comes with flaccid paralysis
always seeā¦
ā respiratory muscle weakness
ā bulbar weakness
āCardiovascular instability
āDyselectrolemia and toxemia
āSpinal compression
49. āNATURAL IMMUNITY
ā¢ Circulating and mucosal antibodies (secretory IgA)
ā¢ Serotype specific and no cross immunity
ā¢ Mucosal immunity decreases viral replication and shedding
ā¢ More chance of paralytic polio in B cell immunodeficiency
50. ORAL POLIO VACCINE (OPV)
ā¢ Developed by Dr Albert Sabin and first used in 1961
ā¢ LIVE ATTENUATED VACCINE
ā¢ licensed formulations of OPV:
(i) monovalent OPVs against type 1 (mOPV1), type 2 (mOPV2) or type 3
(mOPV3);
(ii) bivalent OPV (bOPV) containing types 1 and 3; and
(iii) trivalent (tOPV) containing types 1, 2 and 3
ā¢
51. ā¢ Vaccine virus multiplies in intestinal mucosa (ātakeā of vaccine)- wPV if
encountered infection rate less, excretion less
ā¢ During the first 4ā6 weeks following OPV vaccination, the vast majority of non-
immune vaccine recipients shed Sabin poliovirus in nasopharyngeal secretions and
faeces.
ā¢ In unvaccinated populations, these vaccine viruses are easily transmitted within
and to a lesser degree outside households, thereby vaccinating and inducing
immunity in persons not reached directly by immunization programmes.
ā¢ In addition, such transmission may boost intestinal immunity in some persons and
help to increase community protection if virulent viruses are introduced.
52. ā¢ MgCl2 stabilising agent
ā¢ 2 drops orally
ā¢ Stored at 2 to 8 degree Celsius ( can be frozen for prolonged storage)
ā¢ Pink colour is due to phenol red as pH indicator ( no relation with potency)
ā¢ VACCINE VIAL MONITOR (VVM)
53. ā¢ SCHEDULE
National Immunisation Schedule ā birth dose (0 dose)
6,10, 14 weeks ( OPV 1,2,3)
16-24 weeks (OPV B1)
(vaccine take and seroconversion lower in developing countries)
ā¢ Seroconversion after 3 doses 90%
ā¢ Protection is life long
ā¢ Catch up vaccination can be given up to 5 years
54. āCONTRAINDICATIONS
ā® Inherited or acquired immunodeficiency
ā®malignant neoplasm treated with chemotherapy,
ā®recent haematopoietic stem cell transplantation,
ā®drugs with known immunosuppressive or immunomodulatory properties
(e.g. high dose systemic corticosteroids, alkylating drugs, antimetabolites,
TNF-Ī± inhibitors, IL-1 blocking agent, or other monoclonal antibodies
targeting immune cells),
ā®current or recent radiation therapies targeting immune cells.
ā®Pregnant women
ā®Household contacts of immunodeficient patients
ā®Breast feeding and mild diarrhoea are NOT contraindications
55. āADVERSE EFFECTS
ā¢ VACCINE ASSOCIATED PARALYTIC POLIO (VAPP)
- due to spontaneous neurovirulence of one of the viruses in the OPV
- occurs in approximately 1 in 106 doses of OPV (2-4 cases/million birt cohort)
- disease indistinguishable from wPV infection, within 4-40 days
- vaccine virus is typically not mutated.
- B cell immunodeficiencies have a 2000-3000 fold increased risk for VAPP
- In industrialised countries, more with early doses
In low income countries, more with later doses (lower immune responsiveness, high maternal
antibodies)
Recepient VAPP or contact VAPP
56. ā¢ VACCINE DEPENDENT POLIO VIRUS (VDPV)
- The attenuated viruses ,through prolonged replication in an individual or in a
community, re-acquire the neurovirulence and transmissibility characteristics of
WPV
- 90% due to type 2
- genetically divergent forms of the original Sabin vaccine virus conventionally
defined by
>1% genetic divergence (or >10 nucleotide [nt] changes) for PV1 and PV3
>0.6% (or >6 nt changes) for PV2.
57. ā¢ 3 categories
ā¢ (1)Circulating VDPV(cVDPVs) - evidence of person-to-person transmission in the
community exists
ā¢ (2) immunodeficiency associated VDPVs (iVDPVs) -isolated from some people
with primary B-cell or combined immunodeficiency disorders (with defects in
antibody production) who may have prolonged VDPV infections and
ā¢ (3) ambiguous VDPVs (aVDPVs), which are either clinical isolates from persons
with no known immunodeficiency, or sewage isolates of unknown origin
ā¢ āpersistent cVDPVā cVDPVs that continue to circulate for >6 months following
detection.
58. ā¢ epidemiological characteristics of cVDPVs are similar or identical to those of WPVs
ā¢ cause similar paralytic disease
ā¢ capacity for sustained person-to-person transmission
ā¢ lost the original attenuating mutations
ā¢ can replicate at 39.5 Ā°C
ā¢ usually recombinants with other species of enterovirus.
ā¢ Can circulate in undervaccinated community also can be imported to and cause
outbreaks in previously controlled areas
ā¢ most advanced antiviral agent, pocapavir (V-073), a capsid inhibitor, has been
shown to shorten poliovirus excretion following a challenge with OPV.
59. INACTIVATED POLIO VACCINE (IPV)
ā¢ KILLED VACCINE
ā¢ made from selected WPV strains
- Mahoney or Brunhilde (type 1)
- MEF-1 (type2)
- Saukett (type 3)
ā¢ inactivation of cell culture derived polioviruses with formaldehyde
ā¢ Potency measured by D antigen content
eIPV ā 40D, 80D, 32D units of types 1, 2 and 3 polioviruses
60. ā¢ highly effective in eliciting humoral antibody responses to poliovirus in both high
income and low-income settings
ā¢ Seroconversion 90-95% ( 2 doses 2 months apart after 8 weeks) 99% ( 3 doses 4
weeks apart )
ā¢ less effective than OPV in inducing intestinal mucosal immunity in previously
unvaccinated individuals.
ā¢ IPV can reduce the quantity and duration of virus shedding in faeces, which may
contribute to a reduction in transmission
61. ā¢ Can be given i/m or sub cutaneously
ā¢ STORAGE at 2-8 degree Celsius, not frozen
ā¢ SCHEDULE
National Immunisation Schedule 2 doses of fractional IPV (0.1 ml) at 6 and 14 weeks
ā¢ SIDE EFFECTS
transient minor local erythema (0.5%ā1%)
induration (3%ā11%)
tenderness (14%ā29%)
ā¢ Vaccine of choice in
patients with immunodeficiency including symptomatic HIV
siblings and close contacts of immunodeficient
62. āIntroduction of IPV
āŖ induce an immunity base that could be rapidly boosted should there be an outbreak
of polio due to poliovirus type 2 after the removal of type 2 virus from OPV
āŖ reduce risks for the development of VAPP
āŖ could boost both humoral and mucosal immunity against poliovirus types 1 and 3 in
vaccine recipients.
ātOPV to bOPV switch in April 2016
ā®In polio endemic countries and high risk of importation 3 doses of bOPV with atleast
1 dose IPV
ā®In countries with high vaccination coverage (e.g. 90%ā95%) and low importation
risk sequential IPVābOPV schedule.
ā®n countries with sustained high vaccination coverage and very low risk of both WPV
importation and transmission IPV only schedule
64. āTo identify and investigate every single case of acute flaccid paralysis that can be
polio.
āAIMS
ā®To detect areas where wPV transmission is occurring
ā®To identify priority areas for immunisation
ā®To measure the quality and impact of polio immunisation activities
ā®For polio free certification (zero WPV for 3 years)
āNPSP established in 1997 (WHO and Ministry of H&FW, GoI)
65. āSELECTION OF CASES
ā¢ Sudden onset of weakness and floppiness in any part of the body in a child < 15
years of age or paralysis in a person of any age in which polio is suspected
ā¢ Irrespective of diagnosis
ā¢ Within 6 months of onset
āCASE NOTIFICATION
ā¢ All cases to be reported to District Immunisation Officer (DIO)
66. āCASE INVESTIGATION
ā¢ All cases should be verified and investigated within 48 hours of notification
ā¢ Case Investigation Form (CIF) ā history and physical examination
ā¢ Assign an EPID number
ā¢ Travel history or history of visits within 35 days , cross reporting SOS
ā®SAMPLE COLLECTION
ā¢ Two stool samples at minimum interval of 24 hours within 14 days of onset of
paralysis
ā¢ Can be collected up to 60 days
ā¢ Each specimen about 8 grams ( 1 adult thumb size)
ā¢ Stored and transported under cold chain to WHO accredited lab within 72 hours
(REVERSE COLD CHAIN) at 2-8 degree Celsius
67.
68. ā¢ Adequate stool:
ā¢ Two specimens
ā¢ collected within 14 days of paralysis onset and at least 24 hours apart;
ā¢ each specimen must be of adequate volume (8-10 grams) and
ā¢ arrive at a WHO-accredited laboratory in good condition (i.e., no desiccation, no leakage,
with adequate documentation and evidence that the cold chain was maintained.
ā¢ LABORATORY METHODS
ā¢ Primary isolation of virus in cell culture
RD cell lines ( all enteroviruses) L20B cell lines ( poliovirus)
Serotyping
ā¢ Intratypic Differentiation (WPV or vaccine virus)
ā¢ Genetic sequencing ( genetic relationship and temporal origin)
69. āOUTBREAK RESPONSE IMMUNISATION
ā¢ Usually 500 children below 5 years from the locality or village given bOPV
ā¢ May be also done in places where the kid has travelled
āACTIVE CASE SEARCH IN THE COMMUNITY
ā¢ Active house to house search for AFP
āIDENTIFICATION OF āHOT CASEā
ā¢ Age less than 5 years +history of fever at onset of paralysis +asymmetrical proximal
paralysis or patchy paralysis.
ā¢ Age less than 5 years with rapidly progressive paralysis leading to bulbar
involvement and death.
70. āCROSS NOTIFICATION AND TRACKING OF CASES
ā60 DAY FOLLOW UP EXAMINATION
ā®AFP cases with inadequate stool specimen collection
ā®AFP cases with isolation of wild poliovirus
ā®AFP cases with isolation of vaccine-type (Sabin-type) poliovirus.
ā¢ Verify history
ā¢ Examine for residual paralysis
ā¢ Send the feed back
72. āSurveillance System Performance Indicators.
ā¢ 1. Non Polio AFP rate per 100,000 1/100,000, operational target for India >2/100,000)
ā¢ 2. Reported AFP cases with 2 stool specimens collected within14 days of onset of
paralysis (target >80%)
ā¢ 3. Notification of AFP cases within 10 days of onset of paralysis (target >80%)
ā¢ 4. Reported AFP cases investigated within 48 hours of notification (target >80%)
ā¢ 5. Timeliness of weekly reporting (target >80%)
ā¢ 6. Completeness of weekly reporting (target >90%)
ā¢ 7. Stool specimens reaching a WHO accredited laboratory within 72 hours of being sent
(target >80%)
ā¢ 8. Stool specimens reaching laboratory in good condition (target >80%)
ā¢ 9. Stool specimens with a turn around time 80%)
ā¢ 10.Stool specimens from which non-polio enteroviruses were isolated (target >10%).
74. āPOLIO IS ERADICATABLE because
ā¢ Man is the only reservoir
ā¢ Effective vaccine is available
ā¢ Immunity is lifelong
ā¢ Virus cannot survive long outside body
ā¢ First effective vaccine ā IPV ā used since 1955
ā¢ Oral Polio vaccine ā in use since 1961 ā was the game changer
ā¢ By 1970 Polio vaccine was in routine immunisation worldwide
75. ā¢ 1988 ā World Health Assembly resolved to eradicate polio by 2000 and Global Polio
Eradication Initiative (GPEI) was launched
ā¢ GPEI is a PPP led by national governments with 5 partners
ā®Attaining high rates of routine immunisation
ā®National immunisation Days (NID)
ā®Mopping up immunisation
ā®AFP surveillance
76. 1988 ā 125 endemic
countries, 3.5 lac cases,
paralysing 1000 children
daily
1994 ā Americas
2000 ā Western Pacific
2002- European region
2014- South East Asian region
CERTIFIED POLIO FREE
Last case of type 2 in 1999
Declared eradicated on September 2015
Last case of type 3 in November 2012
Declared eradicated on October 2019
77. POLIO IN INDIA tOPV introduced in EPI in 1979
In 1988, 23800 cases
1995, Pulse Polio Immunisation
1997, NPSP
2009, 756 cases, 60% of total cases
in the world
ā® Last case reported from
Howrah, West Bengal
on January 13, 2011
ā® On Feb 25, 2012
removed from endemic
countries
ā® On 27 march 2014, India
declared polio free