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Epidemiology of Poliomyelitis Epidemiology of Poliomyelitis

Epidemiology of Poliomyelitis - PowerPoint Presentation

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Epidemiology of Poliomyelitis - PPT Presentation

Dr Ali Jafar Abedi MD DCH 1 Polio also called Poliomyelitis is a highly infectious disease caused by a virus The virus invades the nervous system and can cause permanent paralysis Polio is spread through ID: 928062

case polio cases paralysis polio case paralysis cases poliomyelitis virus poliovirus infection vaccine afp surveillance onset clinical days flaccid

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Slide1

Epidemiology of Poliomyelitis

Dr. Ali Jafar AbediMD, DCH

1

Slide2

Polio (also called Poliomyelitis) is a highly infectious disease caused by a virus

The virus invades the nervous system and can cause permanent paralysis Polio is spread through person-to-person contact and can spread rapidly through a community

Most infected people (90%) have no symptoms or very mild symptomsHowever, one in 200 infections leads to permanent paralysis (can’t move parts of the body) and even death

What

is polio disease?

www.immune.org.nz

2

Slide3

Poliomyelitis

The words polio (grey) and myelon (marrow, indicating the spinal cord) are derived from the Greek. It is the effect of poliomyelitis virus on the spinal cord that leads to the classic manifestation of paralysis.

3

Slide4

The disease of poliomyelitis has a long history. The first example may even have been more than 3000 years ago. An Egyptian stele dating from the 18th Egyptian dynasty (1580 - 1350 BCE) shows a priest with a deformity of his leg characteristic of the flaccid paralysis typical of poliomyelitis.

.

First described by Michael Underwood in 1789

4

Slide5

Introduction

A viral infection most often recognized by acute onset of flaccid paralysis.

Infection with poliovirus results in a spectrum of clinical manifestations from inapparent infection to non-specific febrile illness, aseptic meningitis, paralytic disease, and death.

Poliomyelitis is a highly infectious disease caused by three serotypes of poliovirus.

5

Slide6

Two phases of acute poliomyelitis can be distinguished: a non-specific febrile illness (minor illness) followed, in a small proportion of patients, by aseptic meningitis and/or paralytic disease (major illness).

The ratio of cases of inapparent infection to paralytic disease ranges from 100:1 to 1000:1.

6

Slide7

Outcomes of poliovirus infection

7

Slide8

Epidemiological pattern

The epidemiological pattern of polio depends upon the degree of the socioeconomic development and health care services of a country. The pattern of the disease has been considerably modified by widespread immunization.

8

Slide9

Causative organism

Poliovirus: belongs to “Picorna” viruses which are small RNA-containing viruses.

Polioviruses have three antigenically distinct types, giving no cross immunity:Type I: “Leon”; the commonest in epidemics

Type II: “Berlinhide”; the prevailing type in endemic areas.

Type III: “Lansing”; occasionally causes epidemics.

Polioviruses are relatively resistant and survive for a long time under suitable environmental conditions, but are readily destroyed by heat (e.g. pasteurization of milk, and chlorination of water).

9

Slide10

Types of polioviruses

99% reduction

in cases of wild poliovirus since

1988

Type 1 (

341

cases

as of 20 November 2013†

)

Type 2 (eliminated worldwide in 1999)

Type 3 (none detected since November 2012)

Wild

Vaccine derived polioviruses (VDPV)

Most are circulating VDPVs (

cVDPVs

)*

~49-184 per year since 2008 (through 20 Nov 2013)

Type

2

cVDPVs

account

for

97%

of

cVDPVs

VDPVs*

Vaccine-associated paralytic poliomyelitis (VAPP)**

Estimated ~250-500 globally per year

Type

2

accounts

for about 40% of VAPP

VAPP**

More up-to-date numbers can be found at

http

://www.polioeradication.org/Dataandmonitoring/Poliothisweek.aspx

*Other extremely rare VDPVs include primary immunodeficiency VDPVs (

iVDPVs

) and ambiguous VDPVs (

aVDPVs

)

**Refers

to spontaneous reversion to

neurovirulence of one of the attenuated viruses in OPV. VAPP occurs in OPV recipients or their close contacts in contrast to cVDPVs which are widely transmitted in a community and are not likely to be related to contact with a recent vaccine recipient.

OPV related

10

Slide11

Reservoir of infection

Man is the only reservoir of infection of poliomyelitis.

Man: cases and carriers

Cases: all clinical forms of disease

Carriers: all types of carriers (e.g. incubatory, convalescent, contact and healthy) except chronic type. In endemic areas, healthy carriers are the most frequent type encountered.

11

Slide12

Foci of infection

Pharynx: the virus is found in the oropharyngeal secretions.Small intestine: the virus finds exit in stools.

12

Slide13

Modes of transmission

Since foci of infection are the throat and small intestines, poliomyelitis spreads by two routes:

Oral-oral infection: direct droplet infection

Faeco

-oral infection:

Food-borne (ingestion) infection through the ingestion of contaminated foods. Vehicles include milk, water, or any others that may be contaminated by handling, flies, dust….Hand to mouth infection.

(polio virus has the ability to survive in cold environments. Overcrowding and poor sanitation provide opportunities for exposure to infection.)13

Slide14

Poliovirus infection is

highly contagiousPoliovirus is spread mostly by the fecal-oral routePrimary mode of transmission – passage of the virus in stool to the mouth of another childCan also be spread through saliva or droplets from a sneeze or cough

How does poliovirus spread?

Virus transferred to objects from hands

Virus transferred to another child’s hands

Virus transferred ingested

Next cycle of infection

Child excretes virus in stool

14

Slide15

Period of infectivity

Contact and healthy carriers: about 2 weeks

Cases: the cases are most infectious 7 to 10 days before and after the onset of symptoms. In the feaces, the virus is excreted commonly for 2 to 3 weeks, sometimes as long as 3 to 4 months.

In polio cases, infectivity in the pharyngeal foci is around one week, and in the intestinal foci 6-8 weeks.

Incubation Period: 7-14 days

15

Slide16

Susceptibility

Age: more than 95% reported in infancy and childhood with over 50% of them in infancy.

Sex: no sex ratio differences, but in some countries, males are infected more frequently than females in a ratio 3:1.

Risk factors: (provocative factors of paralytic polio in individuals infected with polio virus): fatigue, trauma, intramuscular injections, operative procedures, pregnancy, excessive muscular exercise…

Immunity: The maternal antibodies gradually disappear during the first 6 months of life. Immunity following infection is fairly solid, although infection with other types of polio virus can still occur.

16

Slide17

Sequelae of polio infection

Polio infection

Inapparent infection

Clinical poliomyelitis

Abortive polio

(minor illness)

Involvement of CNS

(major illness)

Paralytic polio

Non-paralytic

polio

Spinal polio

Bulbar polio

Bulbospinal polio

17

Slide18

Inapparent infection

Incidence is more than 100 to 1000 times the clinical cases. No clinical manifestations, but infection is associated with acquired immunity, and carrier state.

18

Slide19

Clinical poliomyelitis

Abortive polio (minor illness):

The majority of clinical cases are abortive, with mild systemic manifestations for one or two days only, then clears up giving immunity. Some abortive cases may be so mild to pass unnoticed.

Manifestations:

Moderate fever

Upper respiratory manifestations: pharyngitis and sore throatGastrointestinal manifestations: vomiting, abdominal pain, and diarrhea.

19

Slide20

Clinical poliomyelitis (cont.)

II. Involvement of the CNS (major illness):

Affects a small proportion of the clinical cases, and appears few days after subsidence of the abortive stage. It takes two forms: nonparalytic and paralytic polio.

Nonparalytic polio is manifested by fever, headache, nausea, vomiting, and abdominal pain. Signs of meningeal irritation (meningism), and aseptic meningitis (pain and stiffness in the neck back and limbs) may also occur.

The case either recovers or passes to the paralytic stage, and here the nonpralytic form is considered as a “preparalytic stage”.

20

Slide21

Clinical poliomyelitis (cont.)

Paralytic poliomyelitis:

Paralysis usually appears within 4 days after the preparalytic stage (around 7-10 days from onset of disease).

The case shows fever, headache, irritability, and different paralytic manifestations according to the part of the CNS involved, with destruction of the motor nerve cells, but not the sensory nerve cells.

Forms: spinal, bulbar, and bulbospinal.

21

Slide22

Spinal polio

Different spinal nerves are involved, due to injury of the anterior horn cells of the spinal cord, causing tenderness, weakness, and flaccid paralysis of the corresponding striated muscles.

The lower limbs are the most commonly affected.

22

Slide23

Bulbar polio

Nuclei of the cranial nerves are involved, causing weakness of the supplied muscles, and maybe encephalitis.

Bulbar manifestations include dysphagia, nasal voice, fluid regurgitation from the nose, difficult chewing, facial weakness and diplopia

Paralysis of the muscles of respiration is the most serious life-threatening manifestation.

23

Slide24

Bulbospinal polio

Combination of both spinal and bulbar forms

24

Slide25

Complications and case fatality

Respiratory complications: pneumonia, pulmonary edema

Cardiovascular complications: myocarditis, cor pulmonale.

Late complications: soft tissue and bone deformities, osteoporosis, and chronic distension of the colon.

Case fatality: varies from 1% to 10% according to the form of disease (higher in bulbar), complications and age ( fatality increases with age).

25

Slide26

Case definition

The following case definition for paralytic poliomyelitis has been approved by CDC (1997)

Clinical case definition Acute onset of a flaccid paralysis of one or more limbs with decreased or absent tendon reflexes in the affected limbs, without other apparent cause, and without sensory or cognitive loss.

26

Slide27

Case classification

Probable: A case that meets the clinical case definition.

Confirmed: A case that meets the clinical case definition and in which the patient has a neurologic deficit 60 days after onset of initial symptoms, has died, or has unknown follow-up status.

Confirmed cases are then further classified based on epidemiologic and laboratory criteria. Only confirmed cases are included in the

Morbidity and Mortality Weekly Report (MMWR)

.Indigenous case: Any case which cannot be proved to be imported.

Imported case: A case which has its source outside the country. A person with poliomyelitis who has entered the country and had onset of illness within 30 days before or after entry

27

Slide28

HOT CASE

A case of AFP with any of the following set of conditions

-Age < 5 year plus H/O fever at onset plus asymmetrical proximal paralysis.

Age < 5 year with rapidly progressive paralysis leading to bulbar involvement (cranial nerves affected) & death.

Any case which in the opinion of SMO/DIO looks like polio.

28

Slide29

Diagnosis

The diagnosis of paralytic poliomyelitis is supported by: (i) clinical course, (ii) virological

testing, and (iii) residual neurologic deficit 60 days after onset of symptoms. Laboratory testing, such as the measurement of antibodies (especially pre- and post-onset of paralysis), and other studies, such as magnetic resonance imaging, electromyography, and/or nerve conduction tests, can help strengthen or exclude the diagnosis of poliomyelitis.

29

Slide30

WHO uses a sensitive screening case definition for the identification of AFP cases and for investigation of any case of AFP in a person younger than 15 years or in a person of any age in whom poliomyelitis is suspected.

However, virological examination is essential for confirmation of the diagnosis of poliomyelitis; this involves detection of poliovirus from the stools of patients with AFP and further characterization of the isolated poliovirus to determine whether it is vaccine-associated, vaccine-derived or wild virus.

30

Slide31

Molecular diagnostics such as polymerase chain reaction are used to differentiate WPV, VDPV, and Sabin-like poliovirus.

In addition all discordant poliovirus isolates are partially sequenced to determine their origin and relatedness to other isolates. According to the laboratory results and review by national polio expert committees, cases are further classified as confirmed, polio-compatible, or polio-negative.

The AFP surveillance is supplemented by environmental surveillance which involves testing sewage or other environmental samples for the presence of poliovirus

31

Slide32

Diagnosis and laboratory testing (cont.)

Serologic testing A four-fold titer rise between the acute and convalescent specimens suggests poliovirus infection.

Cerebrospinal fluid (CSF) analysis

The cerebrospinal fluid usually contains an increased number of leukocytes—from 10 to 200 cells/mm3 (primarily lymphocytes) and a mildly elevated protein, from 40 to 50 mg/100 ml.

32

Slide33

Prevention

General prevention:Health promotion through environmental sanitation.

Health education (modes of spread, protective value of vaccination).

33

Slide34

Prevention

Seroprophylaxis by immunoglobulins: Not a practical way of giving protection because it must be given either or before or very shortly after exposure to infection.

(0.3 ml/kg of body weight).

34

Slide35

an armoury of five different vaccines to stop polio transmission:

Oral polio vaccine (OPV)Monovalent oral polio vaccines (mOPV1 and mOPV3)Bivalent oral polio vaccine (

bOPV)Inactivated polio vaccine (IPV)

35

Slide36

prevention

Active immunization:Salk vaccine (intramuscular polio trivalent killed vaccine).Sabin vaccine (oral polio trivalent live attenuated vaccine).

36

Slide37

Inactivated Polio Vaccine

Contains 3 serotypes of vaccine virusGrown on monkey kidney (Vero) cells

Inactivated with formaldehydeContains 2-phenoxyethanol, neomycin, streptomycin, polymyxin B

37

Slide38

Oral Polio Vaccine

Contains 3 serotypes of vaccine virusGrown on monkey kidney (Vero) cells

Contains neomycin and streptomycinShed in stool for up to 6 weeks following vaccination

38

Slide39

Salk versus Sabin vaccine

IPV (Salk)

OPV (Sabin)

killed formolised virus

Given SC or IM

Induces circulating antibodies, but not local (intestinal immunity)

Prevents paralysis but does not prevent reinfection

Not useful in controlling epidemics

More difficult to manufacture and is relatively costly

Does not require stringent conditions during storage and transportation. Has a longer shelf life.

live attenuated virus

given orally

immunity is both humoral and intestinal. induces antibody quickly

Prevents paralysis and prevents reinfection

Can be effectively used in controlling epidemics.

Easy to manufacture and is cheaper

Requires to be stored and transported at subzero temperatures, and is damaged easily.

39

Slide40

Polio Vaccination of Unvaccinated Adults

IPVUse standard IPV schedule if possible (0, 1-2 months, 6-12 months)

May separate doses by 4 weeks if accelerated schedule needed

40

Slide41

Polio Vaccine Adverse Reactions

Rare local reactions (IPV)No serious reactions to IPV have been documentedParalytic poliomyelitis (OPV)

41

Slide42

What is vaccine-derived polio?

Vaccine-derived polioviruses (VDPVs) are rare strains of poliovirus that have genetically mutated from the strain contained in the oral polio vaccine.

42

Slide43

VDPV can Cause Sustained Person-to-Person Spread and Reintroduction of Poliovirus

VDPVs are classified into 3 categories:Circulating VDPVs (cVDPVs)

Emerge in areas with inadequate OPV coverageMay lead to sustained person-to-person spread Immunodeficient-associated VDPVs (

iVDPVs

)

Isolated from persons with primary immunodeficiencies who exhibit prolonged VDPV infection after OPV exposure Potential source of PV reintroduction in the future; they may excrete virus for up to 20 years Ambiguous VDPVs (aVDPVs) Clinical isolates from persons with no known immunodeficiency orEnvironmental isolates with unidentified source

WHO. WER, 2006 . McLennan, et al. Lancet, 2000

Slide44

VAPP: Rare But Serious

Vaccine-Associated Paralytic Polio:Defined as those cases of AFP from whose stool samples, vaccine-related poliovirus but no wild polio virus is isolated

Caused by mutation of vaccine virus during replication in the gut of vaccinee (reversion to neurovirulence)

VAPP is indistinguishable from naturally occurring polio

Same incubation period, range of severity and Case Fatality Rate

May affect both vaccinees & close contacts.

Sutter et al. Vaccines. 2008. Paul. Vaccine

, 2004 .John. Bull of the WHO

, 2004.44

Slide45

B. Control of patient, contacts and the immediate environment:

Report to local health authority: Obligatory case report of paralytic cases as a Disease under surveillance by WHO, Class 1.

2) Isolation: Enteric precautions in the hospital for wild virus disease; of little value under home conditions because many household contacts are infected before poliomyelitis has been diagnosed.

3) Concurrent disinfection: Throat discharges, feces and articles soiled therewith. Terminal cleaning.

4) Quarantine: Of no community value.

45

Slide46

5) Protection of contacts: Immunization of familial and other

close contacts is recommended but may not contribute to

immediate control; the virus has often infected susceptibleclose contacts by the time the initial case is recognized.

6) Investigation of contacts and source of infection:

Occurrence

of a single case of poliomyelitis due to wild poliovirus must

be recognized as a public health emergency promptingimmediate investigation and planning for a large-scale response.

A thorough search for additional cases of AFP in thearea around the case assures early detection, facilitates

control and permits appropriate treatment of unrecognized

and unreported cases.

7) Specific treatment: None; however, Physical therapy is used to attain maximum function after paralytic poliomyelitis.

46

Slide47

C. Epidemic measures:

In any country, a single case of poliomyelitis must now be considered a public health emergency, requiring an extensive supplementary immunization response over a large geographic area.

47

Slide48

D. Disaster implications:

Overcrowding of non-immune groups and collapse of the sanitary infrastructure pose an epidemic threat.

48

Slide49

E. International measures:

Poliomyelitis is a Disease under surveillance by WHO and is targeted for eradication by 2005.

National health administrations are expected to inform WHO immediately of individual cases and to supplement these reports as soon as possible with details of the nature and extent of virus transmission.

Planning a large-scale immunization response must begin immediately and, if epidemiologically appropriate, in coordination with bordering countries.

49

Slide50

E. International measures (cont.):

Once a wild poliovirus is isolated, molecular epidemiology can often help trace the source.

Countries should submit monthly reports on case of poliomyelitis AFP cases and AFP surveillance performance to their respective WHO offices.

International travelers visiting areas of high prevalence must be adequately immunized.

50

Slide51

51

Slide52

Polio Eradication

Last case in United States in 1979Western Hemisphere certified polio free in 1994

Last isolate of type 2 poliovirus in India in October 1999Global eradication goal

52

Slide53

WHY POLIO IS A CANDIDATE FOR ERADICATION ?

MAN IS THE ONLY RESERVIORNO LONG TERM CARRIER STATEROUTE OF TRANSMISSION IS FAECO-ORAL

HALF LIFE OF EXCRETED VIRUS IN SEWAGE SAMPLE IN TROPICAL CLIMATE LIKE INDIA IS 48 HOURS.POTENT AND EFFECTIVE VACCINE.

53

Slide54

FOUR KEY STRATEGIES FOR POLIO ERADICATION

RI-PROGRAMME [ UIP ] MASS IMMUNIZATION(PPI) CAMPAIGNS

APF SURVEILLANCE MOPING UP IN FOCAL AREAS

54

Slide55

55

Slide56

56

Slide57

Surveillance

Acute Flaccid Paralysis (AFP) surveillanceNationwide AFP (acute flaccid paralysis) surveillance is the gold standard for detecting cases of poliomyelitis.

57

Slide58

The four steps of surveillance are:

finding and reporting children with acute flaccid paralysis (AFP)transporting stool samples for analysisisolating and identifying poliovirus in the laboratorymapping the virus to determine the origin of the virus strain.

58

Slide59

WHY OPV ?

ALSO KNOWN AS SABIN VACCINEPOTENT LIVE VACCINEGIVES GUT IMMUNITYGIVES HERD IMMUNITY- INTERRUPT’s TRANSMISSION CYCLEEASY TO ADMINISTER

COST EFFECTIVE59

Slide60

WHAT IS PULSE POLIO ?

TO IMMUNIZE ALL THE KIDS< 5YRS NATION WIDE ON A SINGLE DAY IN THE SHORTEST POSSIBLE TIME WITH OPV & THAT THE ENVIRONMENT WILL GET SATURATED WITH THE VACCINE VIRUS SO THAT IT WILL REPLACE THE WILD VIRUS AND THUS INTERUPT THE TRANSMISSION OF WILD VIRUS .

60

Slide61

WHY AFP SURVEILLANCE INSTEAD OF

POLIO SURVEILLANCE ?

SURVEILLANCE OF A POLIO CASE ALONE IS NOT SUFFICIENT BECAUSE IT IS IMPOSSIBLEE TO PRECISELY IDENTIFY ALL CASES OF POLIO CLINICALLY DUE TO CONFUSING AND AMBIGUOUS CLINICAL SIGNS AND VARIABLE CLINICAL KNOWLEDGE & SKILLS OF DOCTOR.

CLINICALLY POLIO IN ACUTE STAGE, IS DIFFICULT TO DISTINGUISH FROM OTHER CAUSES OF ACUTE ONSET OF FLACCID PARALYSIS.-----

61

Slide62

The principle of AFP surveillance is to identify children below 15 years with the syndrome of Acute Flaccid Paralysis

Acute-Rapid progression or short, brief duration Flaccid-Floppy or soft and yielding to passive stretching at any time during illness Paralysis–Loss of motor strength

Severe loss of motor strength is called paralysis or plegia

Paresis-indicates slight loss of motor strength

62

Slide63

All cases of acute flaccid paralysis should be reported, irrespective of diagnosis, within 6 months of onset

All cases with flaccid paralysis should be reported and their stools must be collected within 14 days of onset. If it is not possible to collect stool specimens within 14 days, the specimens should still be collected up to 60 days after onset of paralysis.

63

Slide64

Include every case with

: Current flaccid paralysis History of flaccid paralysis in the current illness Borderline or ambiguous clinical signs.

64

Slide65

A case should not be included as AFP if

there is no evidence of acute flaccid paralysis at the time of examination or anytime during the course of illness or if the onset of paralysis is more than 6 months prior to notification.

65

Slide66

Causes of AFP

Poliomyelitis

Gullain Barre Syndrome

Traumatic neuritis

Transverse

MyelitisAny other flaccid/lower motor presentation66

Slide67

AFP SURVEILLANCE

STEPS

FOR EACH AFP CASECASE INVESTIGATION

2 STOOL SPECIMENS,COLLECTED 24 HOURS APART,AND WITHIN 14 DAYS OF ONSET OF PARALYSIS

SENT FOR CULTURES TO LAB TO ISOLATE POLIO VIRUS

ORI ACTIVITY & SEARCH FOR MORE AFP CASES IN THE AREA60 DAYS FOLLOW-UP EXAMINATION AFTER ONSET.

67

Slide68

Onset of paralysis

Investigation of suspected case

(

48 hours of report)

2 stool specimens collected (

14 days since onset of paralysis)

24 hours apart

Outbreak response immunization additional case finding

60-day follow-up exam

Specimens arrive at national laboratory

Results reported from national laboratory

Poliovirus isolates send to regional reference laboratory for intratypic differentiation

Final classification of the case by the expert committee (

12 weeks since onset of paralysis)

Flow diagram of case investigation,

stool specimen collection and

outbreak response immunization

 

≤ 3 Days

≤ 24 Days

≤ 7 Days

68

Slide69

VIROLOGIC CLASSIFICATION SCHEME

NO WILD POLIOVIRUS

AFP

WILD POLIOVIRUS

INADEQUATE

STOOL SPECIMENS

TWO ADEQUATE*

STOOL SPECIMENS

NO RESIDUAL WEAKNESS

CONFIRM

COMPATIBLE

DISCARD

DISCARD

RESIDUAL WEAKNESS, DIED OR LOST TO F/U

DISCARD

EXPERT REVIEW

69

Slide70

Surveillance indicators

Indicator

Minimum levels for certification standard surveillance

Completeness of reporting 

At least 80% of expected routine reports should be received on time (inc. zero reports)

The distribution of reporting sites should be representative of the geography and demography of the country

Sensitivity of surveillance

At least one case of non-polio AFP should be detected annually per 100 000 population aged less than 15 years.

In endemic regions this rate should be two per 100 000.

Completeness of case investigation

All cases should have a full clinical and virological investigation with at least 80% of AFP cases having ‘adequate’ stool specimens collected.

Completeness of follow-up

At least 80% of AFP cases should have a follow-up examination for residual paralysis at 60 days after the onset of paralysis

Laboratory performance

All AFP case specimens must be processed in a WHO-accredited laboratory within the Global Polio Laboratory Network (GPLN)

70

Slide71

Environmental surveillance

Environmental surveillance involves testing sewage or other environmental samples for the presence of poliovirus. Environmental surveillance often confirms wild poliovirus infections in the absence of cases of paralysis.

71

Slide72

Systematic environmental sampling (e.g. in Egypt and Mumbai, India) provides important supplementary surveillance data.

Ad-hoc environmental surveillance elsewhere (especially in polio-free regions) provides insights into the international spread of poliovirus.

72

Slide73

Certification of polio eradication

Certification is done for WHO Regions and not for individual countriesWHO Regions that have been certified polio free:Americas: 20 August 1994

Western Pacific: 29 October 2000Europe: 21 June 2002

73

Slide74

Certification of a region is considered only when

All countries in the area demonstratethe absence of wild poliovirus transmission for at least three consecutive yearspresence of certification standard surveillanceglobal action plan for laboratory containment of wild poliovirus

74

Slide75

Certification standard surveillance

Non-polio AFP rate: ≥2 per 100,000 population aged less than 15 years annuallyAdequate stool specimens : ≥80%All stool specimens tested for poliovirus at a WHO-accredited laboratory

Additional CriteriaInvestigation of AFP cases within 48 hours of initial notification: ≥80%

Timeliness of weekly AFP surveillance reports: ≥80%

75

Slide76

Laboratory containment of WPV

To minimize the risk of reintroduction of WPV into the community from a laboratoryWHO action plan comprises three phases:Phase 1: laboratory survey and inventory

Phase 2: global certification: implement appropriate biosafety measuresPhase 3: post global certification: more stringent, will be prepared when there is global strategy to stop OPV

For regional certification evidence that phase 1 has been implemented

76

Slide77

Rukhsar Khatoon last case of WPV detected in India (Jan 2011), her mother Shabida Bibi in Shahapar village, WB

77

Slide78

Tommorows lecture

End game polio

78

Slide79

Thank You

79