POLIOMYELITIS
Dr. Sushrit A. Neelopant
Assistant Professor,
Department of Community Medicine
RIMS, Raichur
INTRODUCTION
• Polio – Grey, Muellos – marrow ( Greek )
• Acute viral infection, occurs mainly in children
• Caused by RNA virus
• Primarily infection of GIT
• It may infect CNS in < 1 %
– May cause varying degree of paralysis
• First described - Michael Underwood -1789
• First outbreak described in U.S. -1843
• 21,000 paralytic cases reported- U. S. - 1952
• Global eradication in near future
HISTORY
• Heine - described Polio in 1840
• Medin - in 1890
• Hence called as Heine-Medin disease
• Landsteiner & Popper – Identified the virus in 1909
• Enders, Robbibs, Waller– Cultivated the virus - Nobel
• Salk vaccine – Killed vaccine 1955
• Sabin vaccine – Live attenuated vaccine in 1959
PROBLEM STATEMENT- WORLD
• Pre vaccination - found all countries
• Since extensive use from 1955 – eliminated from developed
countries
• Still endemic in
– Pakistan, Afghanistan
INDIA
27-03-2014
CONTD…..
• 2002- 1600 cases in 159 Districts
• 2003 – 225 cases in 87 Districts
• 2004 – 136 cases in 44 Districts
• 2005 – 66 cases in 35 Districts
• 2006 – 383 cases – Western UP , Bihar
EPIDEMIOLOGY - TREND
• It can occur sporadically, Endemically & Epidemically
• Earlier it was a sporadic disease
• Evolved as epidemic disease
• Earlier it was disease of infants, later started affecting
older age group
• Earlier seen in temperate climate now in tropical
climate also
AGENT
• Poliovirus – 3 serotypes 1, 2 & 3
– Type 1– Brunhilde, 2 – Lansing, 3 - Loen
• Most outbreaks - type 1 virus
• It can survive outside the human body for 4 months
in cold season, 6 months – faeces
• Rapidly destroyed by pasteurization, chemical,
physical agents, drying (not available in freeze dried
form )
RESERVOIR OF INFECTION
• Man is the only source of infection
• Most cases – Mild, sub clinical – Play an imp. role in
spread of the infection
• For every clinical case of Polio – 1000 sub clinical
cases in children & 75 in adults
• Period of communicability – 7–10 days before & after
the onset of symptoms
HOST
• Age – Infants & children
• Most vulnerable age – 6 months–3 years
• Sex – 3 males to 1 female
• Maternal antibody– Protect 6 months after birth
• Infection– Confers long lasting immunity, but no
protection against another strain
FACTORS– PROVOCATE LATENT
INFECTION
• Injection
– DPT (Vascularisation part spinal cord)
• Fatigue
– Trauma, Excercise
• Surgery
– Head & Neck region
ENVIRONMENT
• Likely to occur rainy season
• In India – 60 % cases – June–September
• Environmental sources – Contaminated water, food,
through flies
• Over crowding, poor sanitation – Opportunity for
infection
MODE OF TRANSMISSION
• Transmitted – Droplet infection, faeco–oral route
Acute phase
• Faeco oral route – Later phase
– Fluids
– Foods
– Fruits & Vegetables
– Fomites
– Fingers
– Flies
PATHOGENESIS
• Portal of entry- Oral route. Adheres to the epithelial
cells and replicates. Passes to the submucosa and
replicates in Peyer`s patches & tonsils
• Travels to regional L.N. and gives rise to initial
viraemia.
• Localization and replication occurs in R.E.Cells
• A second viraemia occurs with localization in
different organs
PATHOGENESIS
• CNS infection- most likely to occur during viraemia
either through muscle end plate or blood stream
• Virus detectable in oro-pharynx up to 3 weeks and in
stool up to 12 weeks and up to 1 year in immuno-
deficient patients
• In GIT, during replication, the oral polio virus can
undergo mutation and convert into more neuro
virulent phenotype
SUMMARY - PATHOGENESIS
• Entry into mouth
• Replication in pharynx, GI tract,
local lymphatics
• Hematologic spread to lymphatics and central
nervous system
• Viral spread along nerve fibers
• Destruction of motor neurons
CLINICAL SPECTRUM
Infection with Polio virus
Sub clinical
infection
95 %
Abortive
infection 4 %
Aseptic menin
1 %
Paralytic
< 1 %
ASEPTIC MENINGITIS
• 1% cases
• CSF findings - raised proteins, normal sugar,
pleocytosis (<1000 cells, Polymorphonuclear
predominance)
• Lasting for 2-10 days.
• Non paralytic polio
PARALYTIC POLIO
• <1% of cases.
• Occurring one or more days after symptoms of
aseptic meningitis
• Sudden onset fever, vomiting, anorexia
• Back & neck muscle pain
• Followed by lower motor neuron paralysis (Flaccid)
CONTD…..
• Mild cases- Few muscles paralysed
• More proximal than distal
• Severe cases entire limb paralysed
• No sensory loss ( DD- GBS )
• DTR – Diminished
• 2-3 days full paralysis (Asymmetrical)
• Residual paralysis
BULBAR POLIOMYELITIS
• Fever, weakness swallowing, coughing
• Paralysis of pharynx
• Collection of secretion in the throat
• Inability to swallow threatens life
• Recovery good but slow ( If they survive )
POST POLIO SYNDROME
• New occurence of weakness, fatigue, fasciculations
and pain with atrophy of groups of muscles involved
in initial episode of paralysis
• May occur after 20-40 years
• May extend over 1-10 years
• Due to dysfunction and exhaustion of motor neurons
that compensated for the neurons lost and not due
to re-infection or reactivation
DIAGNOSIS
• Isolation of the virus- Stool
• Virus cannot be grown in culture- from throat swab,
CSF or Blood
• Rise in antibody titer – Confirmatory
• Aseptic meningitis- 1%.
– With CSF revealing raised proteins, normal sugar,
pleocytosis (<1000 cells, PMN predominance)
Lasting for 2-10 days
POLIO VIRUS – ELECTRON
MICROSCOPE
MANAGEMENT
• General supportive care
– Isolation
– Concurrent disinfection – Stool – 10 % Cresol
– Bed rest – avoid stress on affected muscles
– Paracetamol – Fever, Pain
– Prophylactic oral antibiotics
– Splints – to prevent deformity
– Fluid & electrolyte balance ( Oral )
– Physiotherapy – After acute phase of illness – 6
weeks
DIFFERENTIAL DIAGNOSIS FOR POLIO
• Transverse myelitis
– No fever, symmetrical paralysis lower extremity,
marked sensory loss, in children > 4 yrs., CSF – N
• Traumatic neuritis
– H/O IM injection, paralysis of limb with pain, Limb
affected below knee, foot drop, slow recovery, any
age group
DIFFERENCE – POLIO & GB SYNDROME
POLIO MYELITIS
• Caused – virus
• Common – Infants, < 5 yrs
• Acute onset
• Fever present
• Flaccid, asymmetrical
• Descending
• No sensory deficit
• No cranial nerve involvement
GB SYNDROME
• Demyelinating dis.
• Rare – Infants, 1-4 yrs
• Chronic
• Fever- 2-3 weeks prior
• Flaccid, symmetrical
• Ascending
• Sensory deficit present
• Cranial nerves involved – 7,9
PREVENTION
• Immunization is the only way to protect children
against polio
• All children by the age of 6 months– Fully immunized
• Both Killed & Live vaccines are available
POLIO VACCINE
• 1955 Inactivated vaccine
• 1959 Live attenuated vaccine
• 1987 Enhanced-potency IPV (IPV)
– It can be given with DPT, sero-conversion is better
compared to OPV after 3 doses
– It can also prevent the multiplication of virus in
the pharynx
INACTIVATED KILLED VACCINE
• Also known as Salk Vaccine
• Contains all 3 types – Polio virus
• 4 doses required – 1st 3 when child 6 weeks old with
1-2 months interval
• 4th dose – 6- 12 months after the 3rd dose
• Additional doses every 5 years till the age of 18 years
CONTD…..
• Sabin 1957
• Contains live attenuated virus ( all 3 types )
• Ideal to give each type as monovalent vaccine
• Administrative purpose trivalent vaccine given
• Vaccine contains – 3 lakh TCID 50 of type 1, 1 lakh
TCID 50 of type 2 & 3 lakh TCID 50 of type 3 (TCID –
Tissue culture infective dose)
DIFF. BETWEEN IPV & OPV
• IPV ( Salk )
– Killed ,
– IM, Cold chain not req
– Systemic immunity
– Doesn’t protect gut – Re-
inf. With wild virus
– Not useful – to control
epidemics / Eradication
– Trained person req.
– Imm. Shorter – 5 years
– No vaccine associated
paralysis
• OPV ( Sabin )
– Live attenuated
– Oral, Cold chain req.
– Local & Systemic imm.
– Protects gut from re inf.
With wild virus
– Useful – Control
epidemics / Eradication
– Trained person not req
– Immunity – Lifelong
– Vaccine associated
paralysis can occur
NATIONAL IMMUNIZATION SCHEDULE
• Soon after birth – Zero dose polio
• 1st dose – 6 weeks
• 2nd dose 10 weeks
• 3rd dose 14 weeks
• 1st booster 18 months
• 2nd booster – 4 years 6 months - 5 years
• Dose – 2 drops
• Vaccine associated paralytic polio esp with type 3
virus due to mutation
REASON FOR VACCINE FAILURE
• Incomplete schedule
• Use of date expired vaccine
• Instability of vaccine
• Lack of cold chain maintenance
– Vaccine vial monitor -
• Vaccine associated paralytic polio
VACCINE VIAL MONITOR
ERADICATION OF POLIOMYELITIS
• A country is said to be free from polio – Zero
incidence for continuous 3 years
• Why eradicate polio ?
– Humans – only reservoir
– No chronic carrier state
– Half life – excreted wild polio virus in sewage – 48
hours
– Potent vaccine is available
– Lifelong immunity if schedule is completed
correctly
CONTD…..
• Last case in United States in 1979
• Western Hemisphere certified polio free in 1994
• Last isolate of type 2 poliovirus in India in October
1999
• Global eradication goal
Wild Poliovirus 1988
Wild Poliovirus 2008
PULSE POLIO IMMUNIZATION
• GOI – introduced 1995
• Supplementary programme – Routine imm.
• PPI started - in-spite of good routine immunization
coverage, because 10 % remained unimmunized
• For 100 % Immunization coverage < 3 yrs
• Later on it was extended to < 5 yrs children
• PPI on NID on 2 occasions with 4-6 weeks gap
HOW PPI HELPS TO ERADICATE POLIO
• Wild polio virus requires un immunized gut for its
multiplication within 1-2 days of its excretion
• Immunized children’s gut doesn’t allow
multiplication of wild polio virus
• Hence if all children < 5years get immunized against
polio, on PPI day, wild polio virus can’t survive
STRATEGIES OF POLIO ERADICATION
• High level routine immunization coverage
• Pulse polio immunization
• Acute flaccid paralysis surveillance
• Mop up immunization
AFP SURVEILLANCE
• Introduced– 1997 in India
• To detect final reservoir of wild polio virus
• AFP– Sudden onset of paralysis of the limb <4 weeks
duration in child <15 years
• AFP surveillance– Detecting all cases of acute
paralysis not only polio cases, it ensures that polio
cases are not missed
• Hence AFP surveillance is tool to detect suspected
polio cases
OBJECTIVES OF AFP SURVEILLANCE
• To detect high risk areas– to plan immunization
• To monitor progress of AFP surveillance
• To certify country polio free
• It is an indicator of sensitivity of surveillance
system
EVENTS AFTER DETECTING AFP CASE
(60 days FU)
AFP case–
2 stool
samples
Wild Polio
virus
Confirmed
case
No wild
polio virus
Discard
Inadequate
sample
Residual
weakness
Died, Lost - FU
Confirm
No residual
weakness
Discard
REPORTING OF AFP CASES
• All AFP cases reported to District immunization
officer – DIO, as early as possible
• In case no AFP cases- Zero reporting is must
– Initial phase AFP required – detecting polio virus
– Later stages – to prove the absence of polio virus
• AFP – Public health emergency
LINE LISTING OF CASES
• Reporting of every case of AFP in a prescribed
proforma
• It includes
– Name, age, sex, address, imm. Status, date of
onset of paralysis, clinical findings etc
• Helps in avoiding duplication of case
• Follow up of the case
• Identify high risk areas
• Implement control measures
MOP UP IMMUNIZATION
• Last stage in polio eradication
• Door to door immunization of all children in high risk
area – circulation of wild polio virus is reported or
suspected
• All children within 5 km area immunized
• About 2000- 3000 children are immunized
• Started within 48 hrs of reporting a case of AFP and
to complete within 7 days
INTENSIVE PULSE POLIO IMMUNIZATION- IPPI
• In- spite of PPI, AFP cases do occur
• GOI – 1999 intensified PPI
• 3 days programme
• 1st day – Children immunized in Booth
• 2nd day – House to house survey
– X mark if child not immunized, non co-operation,
locked houses
– P mark if child is immunized ( GV mark on the
finger of the child indicate immunization )
CONTD…..
• 3rd day – Only X marked houses are visited
– Children are immunized with OPV
– X mark is wiped
– P mark is put on the door
• Purpose of IPPI – not to miss even single child
SUPPLEMENTARY IMMUNIZATION ACTIVITIES-
SNID
• In some states – UP , Bihar
• To supplement PPI, 2 more round of OPV from
October - January
• Better coverage of children
• Consistency in vaccine coverage
• To maintain high level of AFP surveillance
SUMMARY
• Poliomyelitis is an acute, highly infectious disease of
children
• One of the diseases to be eradicated
• High routine immunization, Pulse polio
immunization, AFP surveillance, Mop up
immunization – Help in the eradication of the disease
10/2/2020 55

20180319 poliomyelitis

  • 1.
    POLIOMYELITIS Dr. Sushrit A.Neelopant Assistant Professor, Department of Community Medicine RIMS, Raichur
  • 2.
    INTRODUCTION • Polio –Grey, Muellos – marrow ( Greek ) • Acute viral infection, occurs mainly in children • Caused by RNA virus • Primarily infection of GIT • It may infect CNS in < 1 % – May cause varying degree of paralysis • First described - Michael Underwood -1789 • First outbreak described in U.S. -1843 • 21,000 paralytic cases reported- U. S. - 1952 • Global eradication in near future
  • 3.
    HISTORY • Heine -described Polio in 1840 • Medin - in 1890 • Hence called as Heine-Medin disease • Landsteiner & Popper – Identified the virus in 1909 • Enders, Robbibs, Waller– Cultivated the virus - Nobel • Salk vaccine – Killed vaccine 1955 • Sabin vaccine – Live attenuated vaccine in 1959
  • 4.
    PROBLEM STATEMENT- WORLD •Pre vaccination - found all countries • Since extensive use from 1955 – eliminated from developed countries • Still endemic in – Pakistan, Afghanistan
  • 5.
  • 6.
    CONTD….. • 2002- 1600cases in 159 Districts • 2003 – 225 cases in 87 Districts • 2004 – 136 cases in 44 Districts • 2005 – 66 cases in 35 Districts • 2006 – 383 cases – Western UP , Bihar
  • 7.
    EPIDEMIOLOGY - TREND •It can occur sporadically, Endemically & Epidemically • Earlier it was a sporadic disease • Evolved as epidemic disease • Earlier it was disease of infants, later started affecting older age group • Earlier seen in temperate climate now in tropical climate also
  • 8.
    AGENT • Poliovirus –3 serotypes 1, 2 & 3 – Type 1– Brunhilde, 2 – Lansing, 3 - Loen • Most outbreaks - type 1 virus • It can survive outside the human body for 4 months in cold season, 6 months – faeces • Rapidly destroyed by pasteurization, chemical, physical agents, drying (not available in freeze dried form )
  • 9.
    RESERVOIR OF INFECTION •Man is the only source of infection • Most cases – Mild, sub clinical – Play an imp. role in spread of the infection • For every clinical case of Polio – 1000 sub clinical cases in children & 75 in adults • Period of communicability – 7–10 days before & after the onset of symptoms
  • 10.
    HOST • Age –Infants & children • Most vulnerable age – 6 months–3 years • Sex – 3 males to 1 female • Maternal antibody– Protect 6 months after birth • Infection– Confers long lasting immunity, but no protection against another strain
  • 11.
    FACTORS– PROVOCATE LATENT INFECTION •Injection – DPT (Vascularisation part spinal cord) • Fatigue – Trauma, Excercise • Surgery – Head & Neck region
  • 12.
    ENVIRONMENT • Likely tooccur rainy season • In India – 60 % cases – June–September • Environmental sources – Contaminated water, food, through flies • Over crowding, poor sanitation – Opportunity for infection
  • 13.
    MODE OF TRANSMISSION •Transmitted – Droplet infection, faeco–oral route Acute phase • Faeco oral route – Later phase – Fluids – Foods – Fruits & Vegetables – Fomites – Fingers – Flies
  • 14.
    PATHOGENESIS • Portal ofentry- Oral route. Adheres to the epithelial cells and replicates. Passes to the submucosa and replicates in Peyer`s patches & tonsils • Travels to regional L.N. and gives rise to initial viraemia. • Localization and replication occurs in R.E.Cells • A second viraemia occurs with localization in different organs
  • 15.
    PATHOGENESIS • CNS infection-most likely to occur during viraemia either through muscle end plate or blood stream • Virus detectable in oro-pharynx up to 3 weeks and in stool up to 12 weeks and up to 1 year in immuno- deficient patients • In GIT, during replication, the oral polio virus can undergo mutation and convert into more neuro virulent phenotype
  • 16.
    SUMMARY - PATHOGENESIS •Entry into mouth • Replication in pharynx, GI tract, local lymphatics • Hematologic spread to lymphatics and central nervous system • Viral spread along nerve fibers • Destruction of motor neurons
  • 17.
    CLINICAL SPECTRUM Infection withPolio virus Sub clinical infection 95 % Abortive infection 4 % Aseptic menin 1 % Paralytic < 1 %
  • 18.
    ASEPTIC MENINGITIS • 1%cases • CSF findings - raised proteins, normal sugar, pleocytosis (<1000 cells, Polymorphonuclear predominance) • Lasting for 2-10 days. • Non paralytic polio
  • 19.
    PARALYTIC POLIO • <1%of cases. • Occurring one or more days after symptoms of aseptic meningitis • Sudden onset fever, vomiting, anorexia • Back & neck muscle pain • Followed by lower motor neuron paralysis (Flaccid)
  • 20.
    CONTD….. • Mild cases-Few muscles paralysed • More proximal than distal • Severe cases entire limb paralysed • No sensory loss ( DD- GBS ) • DTR – Diminished • 2-3 days full paralysis (Asymmetrical) • Residual paralysis
  • 22.
    BULBAR POLIOMYELITIS • Fever,weakness swallowing, coughing • Paralysis of pharynx • Collection of secretion in the throat • Inability to swallow threatens life • Recovery good but slow ( If they survive )
  • 23.
    POST POLIO SYNDROME •New occurence of weakness, fatigue, fasciculations and pain with atrophy of groups of muscles involved in initial episode of paralysis • May occur after 20-40 years • May extend over 1-10 years • Due to dysfunction and exhaustion of motor neurons that compensated for the neurons lost and not due to re-infection or reactivation
  • 24.
    DIAGNOSIS • Isolation ofthe virus- Stool • Virus cannot be grown in culture- from throat swab, CSF or Blood • Rise in antibody titer – Confirmatory • Aseptic meningitis- 1%. – With CSF revealing raised proteins, normal sugar, pleocytosis (<1000 cells, PMN predominance) Lasting for 2-10 days
  • 25.
    POLIO VIRUS –ELECTRON MICROSCOPE
  • 26.
    MANAGEMENT • General supportivecare – Isolation – Concurrent disinfection – Stool – 10 % Cresol – Bed rest – avoid stress on affected muscles – Paracetamol – Fever, Pain – Prophylactic oral antibiotics – Splints – to prevent deformity – Fluid & electrolyte balance ( Oral ) – Physiotherapy – After acute phase of illness – 6 weeks
  • 27.
    DIFFERENTIAL DIAGNOSIS FORPOLIO • Transverse myelitis – No fever, symmetrical paralysis lower extremity, marked sensory loss, in children > 4 yrs., CSF – N • Traumatic neuritis – H/O IM injection, paralysis of limb with pain, Limb affected below knee, foot drop, slow recovery, any age group
  • 28.
    DIFFERENCE – POLIO& GB SYNDROME POLIO MYELITIS • Caused – virus • Common – Infants, < 5 yrs • Acute onset • Fever present • Flaccid, asymmetrical • Descending • No sensory deficit • No cranial nerve involvement GB SYNDROME • Demyelinating dis. • Rare – Infants, 1-4 yrs • Chronic • Fever- 2-3 weeks prior • Flaccid, symmetrical • Ascending • Sensory deficit present • Cranial nerves involved – 7,9
  • 29.
    PREVENTION • Immunization isthe only way to protect children against polio • All children by the age of 6 months– Fully immunized • Both Killed & Live vaccines are available
  • 30.
    POLIO VACCINE • 1955Inactivated vaccine • 1959 Live attenuated vaccine • 1987 Enhanced-potency IPV (IPV) – It can be given with DPT, sero-conversion is better compared to OPV after 3 doses – It can also prevent the multiplication of virus in the pharynx
  • 31.
    INACTIVATED KILLED VACCINE •Also known as Salk Vaccine • Contains all 3 types – Polio virus • 4 doses required – 1st 3 when child 6 weeks old with 1-2 months interval • 4th dose – 6- 12 months after the 3rd dose • Additional doses every 5 years till the age of 18 years
  • 32.
    CONTD….. • Sabin 1957 •Contains live attenuated virus ( all 3 types ) • Ideal to give each type as monovalent vaccine • Administrative purpose trivalent vaccine given • Vaccine contains – 3 lakh TCID 50 of type 1, 1 lakh TCID 50 of type 2 & 3 lakh TCID 50 of type 3 (TCID – Tissue culture infective dose)
  • 33.
    DIFF. BETWEEN IPV& OPV • IPV ( Salk ) – Killed , – IM, Cold chain not req – Systemic immunity – Doesn’t protect gut – Re- inf. With wild virus – Not useful – to control epidemics / Eradication – Trained person req. – Imm. Shorter – 5 years – No vaccine associated paralysis • OPV ( Sabin ) – Live attenuated – Oral, Cold chain req. – Local & Systemic imm. – Protects gut from re inf. With wild virus – Useful – Control epidemics / Eradication – Trained person not req – Immunity – Lifelong – Vaccine associated paralysis can occur
  • 34.
    NATIONAL IMMUNIZATION SCHEDULE •Soon after birth – Zero dose polio • 1st dose – 6 weeks • 2nd dose 10 weeks • 3rd dose 14 weeks • 1st booster 18 months • 2nd booster – 4 years 6 months - 5 years • Dose – 2 drops • Vaccine associated paralytic polio esp with type 3 virus due to mutation
  • 35.
    REASON FOR VACCINEFAILURE • Incomplete schedule • Use of date expired vaccine • Instability of vaccine • Lack of cold chain maintenance – Vaccine vial monitor - • Vaccine associated paralytic polio
  • 36.
  • 37.
    ERADICATION OF POLIOMYELITIS •A country is said to be free from polio – Zero incidence for continuous 3 years • Why eradicate polio ? – Humans – only reservoir – No chronic carrier state – Half life – excreted wild polio virus in sewage – 48 hours – Potent vaccine is available – Lifelong immunity if schedule is completed correctly
  • 38.
    CONTD….. • Last casein United States in 1979 • Western Hemisphere certified polio free in 1994 • Last isolate of type 2 poliovirus in India in October 1999 • Global eradication goal
  • 39.
  • 40.
  • 41.
    PULSE POLIO IMMUNIZATION •GOI – introduced 1995 • Supplementary programme – Routine imm. • PPI started - in-spite of good routine immunization coverage, because 10 % remained unimmunized • For 100 % Immunization coverage < 3 yrs • Later on it was extended to < 5 yrs children • PPI on NID on 2 occasions with 4-6 weeks gap
  • 42.
    HOW PPI HELPSTO ERADICATE POLIO • Wild polio virus requires un immunized gut for its multiplication within 1-2 days of its excretion • Immunized children’s gut doesn’t allow multiplication of wild polio virus • Hence if all children < 5years get immunized against polio, on PPI day, wild polio virus can’t survive
  • 43.
    STRATEGIES OF POLIOERADICATION • High level routine immunization coverage • Pulse polio immunization • Acute flaccid paralysis surveillance • Mop up immunization
  • 45.
    AFP SURVEILLANCE • Introduced–1997 in India • To detect final reservoir of wild polio virus • AFP– Sudden onset of paralysis of the limb <4 weeks duration in child <15 years • AFP surveillance– Detecting all cases of acute paralysis not only polio cases, it ensures that polio cases are not missed • Hence AFP surveillance is tool to detect suspected polio cases
  • 46.
    OBJECTIVES OF AFPSURVEILLANCE • To detect high risk areas– to plan immunization • To monitor progress of AFP surveillance • To certify country polio free • It is an indicator of sensitivity of surveillance system
  • 47.
    EVENTS AFTER DETECTINGAFP CASE (60 days FU) AFP case– 2 stool samples Wild Polio virus Confirmed case No wild polio virus Discard Inadequate sample Residual weakness Died, Lost - FU Confirm No residual weakness Discard
  • 48.
    REPORTING OF AFPCASES • All AFP cases reported to District immunization officer – DIO, as early as possible • In case no AFP cases- Zero reporting is must – Initial phase AFP required – detecting polio virus – Later stages – to prove the absence of polio virus • AFP – Public health emergency
  • 49.
    LINE LISTING OFCASES • Reporting of every case of AFP in a prescribed proforma • It includes – Name, age, sex, address, imm. Status, date of onset of paralysis, clinical findings etc • Helps in avoiding duplication of case • Follow up of the case • Identify high risk areas • Implement control measures
  • 50.
    MOP UP IMMUNIZATION •Last stage in polio eradication • Door to door immunization of all children in high risk area – circulation of wild polio virus is reported or suspected • All children within 5 km area immunized • About 2000- 3000 children are immunized • Started within 48 hrs of reporting a case of AFP and to complete within 7 days
  • 51.
    INTENSIVE PULSE POLIOIMMUNIZATION- IPPI • In- spite of PPI, AFP cases do occur • GOI – 1999 intensified PPI • 3 days programme • 1st day – Children immunized in Booth • 2nd day – House to house survey – X mark if child not immunized, non co-operation, locked houses – P mark if child is immunized ( GV mark on the finger of the child indicate immunization )
  • 52.
    CONTD….. • 3rd day– Only X marked houses are visited – Children are immunized with OPV – X mark is wiped – P mark is put on the door • Purpose of IPPI – not to miss even single child
  • 53.
    SUPPLEMENTARY IMMUNIZATION ACTIVITIES- SNID •In some states – UP , Bihar • To supplement PPI, 2 more round of OPV from October - January • Better coverage of children • Consistency in vaccine coverage • To maintain high level of AFP surveillance
  • 54.
    SUMMARY • Poliomyelitis isan acute, highly infectious disease of children • One of the diseases to be eradicated • High routine immunization, Pulse polio immunization, AFP surveillance, Mop up immunization – Help in the eradication of the disease
  • 55.