Acute flaccid paralysis and Surveillance 2018

Acute flaccid paralysis including GBS and Poliomyelitis and AFP SURVEILLANCE..PULSE POLIO....POLIO END GAME STRATEGy

1. Acute Flaccid Paralysis ( GBS and Poliomyelitis ) Dr. Raghav Kakar

2. Introduction Acute flaccid paralysis (AFP) is defined as onset of paralysis ( <4 weeks ) in a child (age < 15 years) for which no obvious cause has been found; or, a paralysis in a person of any age in whom polio is suspected. The Paralysis is associated with loss of muscle tone and loss of reflexes. Reporting of all AFP cases less than 15 years of age is mandatory in India. All AFP cases should be investigated within 48 hours.

3. Anatomical localization and Etiolgical agents in Acute Flaccid Paralysis Anatomical site Etiology Anterior Horn Cell Poliovirus, Japanese B Encephalitis Dorsal root ganglia HSV, CMV, rabies Spinal Cord Acute transverse myelitis , trauma, space occupying lesions, Parasitic infestations Peripheral nerves GBS, Chronic inflammatory demyelinating polyneuropathy , Vit b12 deficiency, diphtheria, rabies, Heavy metals, Hypokalemia Neuromuscular junction Myasthenia crisis, organophosphorus poisoning, botulism Muscle Polymyositis , SLE, Lyme diseas , toxoplasmosis

4. Initial approach to a child with AFP A child with AFP is a medical emergency. The key steps in management are as follows: Respiratory care : It is essential to check for respiratory involvement in the form of rapid breathing, shallow or paradoxical respiratory efforts and use of accessory muscles. Early support and intubation is critical in final outcome of these patients. 2. Bulbar weakness detection and management : Patient should be monitored for pooling of secretion, ineffective or weak cough, nasal regurgitation of feeds.

5. 3. Managing Cardiovascular instability : Under ideal circumstances, ECG electrodes should be attached to all AFP patients. 4. Rule out dyselectrolytemia and snake envenomation : As they have treatment implications, these should be ruled out.

6. Onset of Paralysis Etiology Within hours to few days GBS, traumatic neuritis, t ransverse myelitis , myasthenia crisis, viral myositis Within 2-3 weeks Polio, Japanese B Encephalitis, Tick bite paralysis Weeks to months Lyme disease, Post diphtheritic polyneuropathy Months to years Rabies Once a patient with AFP is stabilized, a detailed clinical evaluation is obligatory to reach to a definite diagnosis. Clinical assessment

7. Progression of paralysis Disease Maximum Deficit at onset Traumatic neuropathy Hours to few days Poliomyelitis, Japanese B encephalitis Up to 2-4 weeks GBS, Varicella zoster, Tick bite paralysis Few weeks to months Lyme disease and polymyositis Topography Disease Assymetric involvement Poliomyelitis, Japanese B encephalitis, Traumatic neuropathy Symmetric involvement GBS, Transverse myelitis , rabies, botulism.

8. Clinical Feature Disease Sensory features Neuropathy secondary to neurotropic viruses (Rabies, varicella zoster) GBS Transverse myelitis Lyme disease Traumatic neuropathy DTR- Areflexia Diseases of AHC, peripheral nerves and in spinal shock phase of cord diseases Bladder Bowel involvement Transverse myelitis Fever at onset of paralysis Polio and non polio enteroviruses , other neurotropic viruses and occasionaly with transverse myelitis , viral myositis

9. Investigations Serum Potassium MRI Spine with contrast NCS, NST and EMG CSF Examination Serum Creatinine phosphokinase Urine for porphobilinogen Lyme’s serology

10. Guillain-Barre Syndrome

11. Introduction It is an acute inflammatory demyelinating polyradiculoneuropathy . It is an acute diffuse post-infective disease causing generalized paralysis and areflexia . The average age of incidence is 4-8 years, and rare below 2 years There are two major varieties: AMAN : Acute Motor Axonal Neuropathy AIDP : Acute Inflammatory Demyelinating Polyneuropathy

12. Antecedent causes  70% cases –post infectious . Viral infections : EBV, Measles, Mumps, CMV, HIV , Hep B. 20-30% cases –Campylobacter jejuni Mycoplasma pneumoniae  Immunosuppression .  Can be seen in patients with lymphoma, SLE.

13. Pathophysiology It is immune mediated with involvement of both humoral and cell mediated mechanism. Triggers are the common enviornmental pathogens ( C.jejuni -commonest, EBV, CMV). These triggers activate CD 4+ T-cells against variety of endogeneously produced antigens like GQ1B, GM1 etc

14. Resembelance of the triggering factor to the antigen on peripheral nerves leads to an overzealous autoimmune response mounted by T-cells and Macrophages Activated T-cells stimulate the B-cells to produce specific antigangliosidic antibodies. Cytokines and chemokines released by activated T-cells may increase capillary permeability and results in more myelin or axonal injury.

15. Pathophysiology

16. Clinical Features A progressive ascending, symmetrical paralysis coming on over hours, days to a few weeks is the hallmark of GBS. Pain and refusal to walk are the presenting symptoms. Frequent radicular involvement is manifested by the positive straight leg raising sign . ( Lasègue's sign) Cranial nerve involvement in 50% cases. Autonomic manifestations seen in one third patients

17. Motor weakness : Begins in lower limbs and progressively involves trunk, upper limbs, diaphragm, respiratory, pharyngeal and laryngeal muscles. May also involve lower cranial nerves Proximal muscles involved more in limbs. Progression of paralysis for 4-10 days. Areflexia

18. Higher functions : Consciousness is normal Cranial Nerves: 7 th nerve bilateral involvement is frequently seen. Sensory symptoms No objective sensory loss. There may be distal impairment of vibration and position sense in some.

19. Acute Motor Axonal Neuropathy Children ,young adults Seasonal variation Rapid in evolution Anti GD1a and Anti GM1 antibodies First attack on motor nodes of Ranvier Macrophage activation Axonal damage is variable

20. Acute Inflammatory Demyelinating Polyneuropathy Adults > children Lack of seasonal variation Rapid recovery Less severe Anti gen involved in AIDP still remains unknown Demyelinating First attack on Schwann cell surface Widespread myelin damage

21. Miller Fischer Syndrome Adults,children Uncommon Anti GQ 1 b anitbodies >90% (Not seen in other forms of GBS) Cause conduction block Pupillary paralysis Distal Paresthesia seen. Only 5% GBS 25-50% show limb weakness (MFS- GBS overlap syndrome)

22. Atypical Variants Bickerstaff’s Brainstem Encephalitis Rare variant Characterized by : Ophthalmoplegia Ataxia Symptoms of brainstem involvement like drowsiness and altered consciousness. Polyneuritis Cranialis Acute disorder with multiple cranial neuropathy B/l 7 th nerve palsy with high CSF protein Slowed Nerve Conduction Velocities Associated with previous CMV infections

23. Acute Motor and Sensory Axonal Neuropathy Similar to AMAN with sensory and bulbar involvement and severe course. 4 . Pharyngo -cervical-Brachial variant Paralysis involves bulbar, neck and upper limb muscles Locked-in state Patient may look comatose due to severe quadriplegia and pan-cranial neuropathy Patient doesnt respond to stimuli Acute Pandysautonomia pure sensory variant Predominant autonomic or sensory involvement.

24. Lab Features CSF : Normal pressure Xanthochromic appearance Raised CSF protein 1-10 g/l (100-1000mg/dl) ALBUMINOCYTOLOGICAL DISSOSCIATION Cell count normal, no pleocytosis Proteins : elevated, twice the normal limit Glucose : Normal Culture : Sterile

25. Nerve conduction velocity studies: s/o either axonal or demyelinating neuropathy. Axonal neuropathy has worst prognosis Electromyography: Evidence of acute denervation is present Sural Nerve Biopsy may show: Segmental demyelination Focal inflammation Wallerian degeneration Serum Creatinine kinase may be normal to elevated

26. Asbury criteria for diagnosis of GBS REQUIRED : 1.  A reflexia 2.  I nclude in differential and rule out other causes 3.  D uration < 4 weeks 4.  P rogressive weakness of 2 or more limbs due to neuropathy Features supportive of diagnosis: 1.  A febrile 2.  I nvolvement: Mild sensory involvement Facial or other cranial nerve involvement 3.  D emyelinating electrophysiologic evidence 4.  P rotein in CSF High + Low WBC ( Albumino-cytologic dissociation) 5.  S ymmetrical distribution relatively

27. Features casting doubt on the diagnosis Asymmetrical weakness Persistent bladder and bowel dysfunction Bladder or bowel dysfunction at onset >50 mononuclear leukocytes/mm 3  or presence of polymorphonuclear leukocytes in CSF Distinct sensory level. Features that rule out the diagnosis Hexacarbon abuse Abnormal porphyrin metabolism Recent diphtheria infection Lead intoxication

28. Treatment Supportive care : Ventilation, physiotherpary IVIG : best given within 3-4 days of onset of weakness. Indications: Acute GBS of less than 2 weeks Inability to walk unaided Bulbar weakness Dose : 0.4mg/kg/day for 5 days or 1g/kg/day for 2 days

29. Plasmapharesis In cases of rapid progression Not much benificial after 3 weeks Dose : 200-250 ml/kg/bodyweight of plasma is removed on alternate days in 4-6 sittings for 8-12 days Complications: CVS complication Dysautonomia Hepatitis and AIDS Prevention of secondary infections

30. Plasmapheresis f/b IVIG is not superior to IVIG or PE alone Oral steroids (methyl prednisolone ) may delay recovery, however a short course is very useful in management of radicular pain Some patients show worsening after initial treatment---the so called Treatment-related clinical fluctuations . If these fluctuations occur more than 3 times or if the recovery has not occurred 9 weeks into illness, one must consider Acute variant of Chronic Inflammatory Demyelinating Polyneuropathy (A-CIDP)

31. Treatment-related clinical fluctuations : Worsening of at least one grade on the GBS disability scale after initial stabilization or improvement within first 8 weeks after treatment. In a recent study, more TRF were observed in the 2 day IVIg treatment group (1g/kg for 2 days) than in the 5 day treatment group ( 0.4g/kg for 5 days ) TRFs provide evidence that the treatment in a specific patient is effective, although not lasting long enough, and that the patient will probably respond again after repeating the same treatment. It is rational to retreat the patient with IVIg or PE.

32. Treatments other than PE and IVIg Brain derived neurotrophic factor. Interferon Beta-1a According to cochrane review, the numbers in the study of above mentioned modalities were too small and larger sequential RCTs might be more promising Tripterygium polyglycoside —a chinese herbal medicine I t showed a significant improvement in disabillity scale 8 weeks after onset of symptoms.

33. Prognosis The clinical course is usually benign, and recovery begins within 2-3 weeks. Some patient might be left with residual weakness. Tendon reflexes are usually last to recover. Improvement usually follows a gradient opposite the direction of involvement. 3 clinical features are predictive of poor outcome: Cranial nerve involvement Intubation and Max disability at the time of presentation

34. Easy fatigue is one of the most common chronic symptom. Axonal form of GBS has slower recovery, some requiring upto years. 10% may have persistent neurological symptoms 5% may show recurrence.

35. Poliomyelitis

36. Introduction Greek poliós = "grey", myelós = marrow , and the suffix - itis = inflammation First described by British physician Micheal Underwood in 1799 referring to it as "debility of the lower extremities.“ A viral infection most often recognized by acute onset of flaccid paralysis. Primarily an infection of human alimentary tract, but may infect CNS in very small no. ( i.e <1%) Infection results in a spectrum of clinical manifestations.

37. Problem statement World A worldwide problem in pre vaccination era With the wide use of polio vaccine from 1954, it is being eliminated from most of the developed countries In 1988 WHA resolved to eradicate the disease globally, GPEI was estabilished . Polio cases have decreased by over 99% since 1988, from an estimated 3,50,000 cases to only less than 100 in 2014 globally

38. In 2016, only 3 countries in the world remain polio endemic. A total of 35 cases of paralytic poliomyelitis due to WPV Type 1 were reported in 2016 from these 3 countries Failure to eradicate polio from these 3 countries could result in as many as 200,000 new cases every year within 10 yrs, all over the world. India In India, Vaccination against polio started in 1978 with e xtended programme on immunization.

39. Pulse Polio Immunization launched in 1995. In 2009, India had half the number of polio cases in the world. By 2011, in less than two years’ time, India brought polio infections to the zero level. India’s last reported polio case was a 2-year-old girl in the Howrah district of West Bengal, on 13 January 2011. India removed from list of polio-endemic countries in 2012. South East Asia region was declared polio free on March 27th 2014.

40. Epidemiology Poliovirus: belongs to “ Picorna ” viruses which are small RNA-containing viruses. Non Enveloped. Three serotypes- 1, 2 & 3 giving no cross immunity Human is the only reservoir. It multiplies in the intestine and spreads via faeco -oral route. The maximum excretion of virus occurs just before the onset of paralysis and during the first 2 weeks after the onset of paralysis. However, virus is intermittently excreated for upto 2 months after infection

41. Etiopathogenesis Three antigenically distinct serotypes. Type1, 2 and 3 Polio virus can remain active for several days at room temperature and can be stored indefinitely at -20 degree C Inactivated by Heat, Chlorine and UV rays. Most frequent cause of epidemic polio is Type 1 followed by type 3. The primary site of replication is small intestine and regional lymph nodes.

42. Poliovirus accesses the CNS via peripheral nerves and primarily infects motor neuron cells in the spinal cord (the anterior horn cells) and the medulla oblongata. Infants born to mothers with few antibodies are protected for a few weeks. Active immunity after natural infection ( including inapparent and mild infection ) is probably lifetime but protects against the infecting serotype only.

43. HOST FACTORS Age: All age groups; children(6 MONTHS TO 3 YEARS most susceptible) 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: Fatigue, trauma, im injections, tonsillectomy, immunizing agents like alum containing DPT vaccine and excessive muscular exercise…

44. Clinical manifestations

45. Abortive polio : Occurs in 4-8% of infections Low grade fever, sore throat Vomiting, abdominal pain Loss of weigh, malaise Recovery is complete and rapid. There is no paralysis

46. 2. Non Paralytic Polio : 1-2% population Non specific illness Pre paralytic polio Back stiffness, Muscle tenderness, Head lag and Nuchal rigidity Nuchal - Spinal signs present Sensory system normal Child fully conscious IM injection, physical activities should be avoided Reflexes : In early stages DTR may be exaggerated. Depression of DTRs is an indication of impending paralysis Recovery within 2-10 days

47. Paralytic Polio 0.5-1% of infections Symptoms occur in two phases : Minor : similar to abortive polio Major : begins with muscle pain, spasms and fever. This is followed by rapid onset of flaccid paralysis that is usually complete within 72 hours. There are 3 types of paralytic poliomyelitis : Spinal Paralytic poliomyelitis Bulbar polio Bulbospinal Polio

48. Spinal Paralytic polio Most common , seen in 80% cases of paralytic polio Results from lower motor neuron lesion of the AHC of the spinal cord and affects muscles of legs, arms and/or trunk The affected muscles are Flaccid, and reflexes are diminished. There is no sensory involvement Paralysis is often asymmetric, with lower limbs more involved Involvement of diaphragm causes respiratory difficuty . Descending paralysis is seen. Severe cases may develop quadriplegia. Autonomic involvement- Urinary retention and constipation. Residual flaccid paralysis is usually present after 60 days

49. b) Bulbar Polio 2% of paralytic polio cases Due to weakness of motor part of cranial nerve. 9 th and 10 th CN involvement :Inability to swallow, Nasal twang, Nasal regurgitation, pooling of saliva, hoarseness of voice Irregular and shaloow respiration Cardiac arrhythmias Pulse is rapid, weak and thready . Patient becomes restless, confused, delirious and comatose. Bulbospinal Polio 20% of paralytic cases Combination of both spinal and bulbar component.

50. Residual Paralysis Acute phase of illness subsides by 4 weeks and the recovery begins in paralysed muscles The extent of recovery is variable depending upon extent of damage caused to neurons. Max recovery takes place in the first 6 months but slow recovery continues till 18-24 months. After 2 years, no more recovery is expected and the child is said to have “Post Polio Residual Paralysis” which remains as such through out the life

51. Post Polio Syndrome Clinical deterioration occurs in survivors after several decades. H/o recent muscle weakness, poor endurance, fatigue and joint pain. Attributed to combination of ageing process and distal muscle degeneration due to increased metabolic demands

52. Complications 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).

53. Diagnosis and Lab testing Laboratory studies critical to rule out or confirm the diagnosis of paralytic poliomyelitis. Virus isolation The likelihood of poliovirus isolation is highest from stool specimens, Intermediate from pharyngeal swabs, and very low from blood or spinal fluid. Serologic testing A four-fold titre rise between the acute and convalescent specimens suggests poliovirus infection.

54. Treatment The aim of the treatment is to promote recovery and to minimize residual paralysis and disability. Children with bulbospinal polio and respiratory paralysis would require hospitalization Children with isolated limb paralysis should be advised complete bed rest Proper positioning The child should be made to lie on a firm bed and maintain limbs in neutral position. Trunk and hip should be straight with slight flexion at the knees and feet at right angle at ankle. External rotation should be prevented.

55. Pain Relief Warm moist fomentation should be given. Massage and IM injections should be avoided during the acute phase of illness Bowel and Bladder Laxatives should be avoided Intermittent catheterization may be done. Physiotherapy to be started once the acute phase subsides. Contractures and fixed deformities may require orthopedic surgery, to be done after 2 years.

56. Prognosis The outcome of inapperent and abortive polio is relatively good. It is bad for older children and those with sudden onset of illness with high fever. In severe bulbar polio, mortality may be as highg as 60%, whereas in less severe bulbar or spinal polio, mortality varies from 5-10% Type-1 has the greatest propensity for natural poliomyelitis, whereas Type-3 has a predilection for VDPV.

57. ACTIVE IMMUNIZATION Oral (Sabin) Polio Vaccine 1961 by Albert Sabin, Live attenuated vaccine. Provide both humoral and Mucosal (Gut) immunity . Mucosal intestinal immunity prevent infection with wild polio virus. Intestinal immunity is the main reason why mass campaigns with OPV can rapidly stop person to person transmission of wild polio virus. Immunity probably lifelong Shed in stool for up to 6 weeks following vaccination

58. Risks associated with use of OPV Vaccine Associated Paralytic Poliomyelitis Those cases of AFP, which have residual weakness 60 days after onset of paralysis and from whose stool samples, vaccine related poliovirus is isolated. In some recipient of OPV, there is genetic change ( <1%), in the VP1 gene of vaccine virus. This minor change turns the vaccine virus virulent. Causes paralysis in recipient (recipient VAPP) or among unimmunized close contacts (contact VAPP) 1 case of VAPP occurs after 2.3 million first doses, and after 12 million subsequent doses.

59. Vaccine derived Poliovirus There is a greater genetic change (1-15%) in the VP1 gene of the vaccine virus. It has potential for human infection and paralysis. Types of VDPV : 1) cVDPV (Circulating vaccine derived polio virus ) : A cVDPV is associated with sustained person to person transmission and is circulating in the community under conditions of low population immunity, with evidence of causing 2 or more paralytic cases.

60. iVDPV ( Immununo deficiency –related vaccine –derived polio virus) reported in immunodeficient patients who have prolonged infections after exposure to OPV. 3) aVDPV (ambiguous vaccine derived polio virus) currently have unclassified source (i.e., a single isolate from a healthy or non- immunodeficient person; environmental isolates without an associated AFP case). Among these 3 types, cVDPV causes sustained circulation. Due to the risks of this OPV must be phased out to secure a lasting polio- free world.

61. AFP Surveillance Bulletin – India. Report for week 46, ending 18 November 2017

62. Inactivated (Salk) vaccine Developed in 1955 by Dr Jonas Salk. Consists of inactivated polio strains of all three types. Excellent humoral immunity. Gives Mucosal protection but not mucosal immunity. No risk of VAPP or VDPV. 0.5 ml IM or SC or a fractional dose of 0.1ml Intradermal .

63. Vaccination Schedule National Immunization Schedule : bOPV at birth,6-10-14 weeks followed by booster at 15-18month. IPV at 14 week (0.5ml) In some states Fractional doses of IPV at 6 and 14 weeks instead of IM dose The IAP Schedule : ‘ Sequential IPV-OPV schedule ’ bOPV at birth IPV at 6-10-14 weeks bOPV at 6 and 9 month IPV at 15-18 month bOPV at 5 year

64. Pulse Polio Immunization (PPI) Program Following the Global Polio Eradication Initiative of WHO in 1988, GOI conducted the first round of PPI consisting of 2 immunization days 6 wks apart on 9 th dec 1995 and 20 th jan 1996. Encounters and challenges faced by the innovators: The size of the campaign (6.5 lakh polio booths; ~125 million children to be administered on each immunization day; cold chain and vaccine management) The attitudinal diversity (diverse religious, socioeconomic and cultural background) Management of Human Resources (Doctors, Nurses, Health, Anganawadi Workers, Volunteers, NGOs)

65. Strategy adopted : The basic strategy for eradicating polio consisted of: Immunizing every child below 1 year with at least 3 doses of OPV. National Immunization Days during which every child below 5 years gets 2 additional doses of OPV on 2 days separated by 4 to 6 weeks. Surveillance of AFP to identify all reservoirs of wild poliovirus transmission. Extensive house-to-house immunization mopping -up campaigns in the final stages where wild poliovirus transmission persists.

66. Key Points : Targeted all children upto 3 yrs later on WHO increased the age upto 5 yrs. PPI occurs in two rounds about 4-6 wks apart during low transmission season of polio , i.e. Between nov to feb . These doses are extra dose which supplements and do not replace the doses received during immunization services. There is no minimum interval between PPI and scheduled OPV doses

67. Polio Eradication & Endgame Strategic Plan 2013-2018

68. On 26 May 2012, the World Health Assembly declared the completion of poliovirus eradication to be a “ programmatic emergency for global public health ” and called for the development of comprehensive polio endgame strategy. In response to this directive, the GPEI developed Polio Eradication & Endgame Strategic Plan (PEESP) 2013-2018 . This strategy shall prevent circulating VDPV by augmenting the immunity induced by earlier doses of trivalent OPV. By 2019 there shall be complete cessation of OPV

69. Three distinct steps of polio endgame strategy . Switch tOPV to bOPV Withdraw bOPV & routine OPV use Before end 2015 2016 2019-2020 Introduce atleast one dose of IPV in RI On going strengthening of routine immunization

70. .

71. AFP-SURVEILLANCE Nationwide AFP (acute flaccid paralysis) surveillance is the gold standard for detecting cases of poliomyelitis. Surveillance identifies new cases and detects importation of wild poliovirus The four steps of surveillance are: Finding and reporting children with AFP Transporting stool samples for analysis Isolating and identifying poliovirus in the laboratory Mapping the virus to determine the origin of the virus strain.

72. Finding and reporting children with acute flaccid paralysis (AFP) surveillance: The first links in the surveillance chain are staff in all health facilities- from district health centres to large hospitals. They must promptly report every case of AFP in any child under 15 years of age. The number of AFP cases reported each year is used as an indicators of a country’s ability to detect polio-even in countries where disease no longer occurs. A country’s surveillance system needs to be sensitive enough to detect at least one case of AFP for every 100,000 children under 15- even in absence of polio.

73. Transporting stool samples for analysis Two stool specimens should be collected at an interval of 24 to 48 hours apart and within 14 days of onset of paralysis. However, when AFP cases are seen late (i.e. greater than 2 weeks after paralysis onset), stool specimen may be collected up to 60 days after onset of paralysis. The specimen should be placed in a clean container such as wide mouth plastic or glass bottle with screw on cap. It need not be autoclaved, but should be cleaned. At least ‘one thumb sized’ 8 gm of stool is required. Stool sample should be adequate and in good condition accompanied by all details as required by laboratories

74. Isolating Poliovirus If poliovirus is isolated the next step is to distinguish between wild and vaccine related. If wild polio virus is isolated then identify which of the two surviving types of wild virus is involved.

75. Mapping The Virus Once wild poliovirus has been identified further tests are carried out to determine where the strain may have originated. By determining the genetic makeup of virus, wild virus can be compared to others and classified into genetic families which cluster in defined geographic areas. When polio has been pinpointed to a precise geographical area, it is possible to identify the source of importation of poliovirus- both long range and cross border.

76. 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. Systematic environmental sampling provides important supplementary surveillance data. Ad-hoc environmental surveillance elsewhere (especially in polio-free regions) provides insights into the international spread of poliovirus.

77. Surveillance Indicators .

78. .

79. The Ministry of Health has sponsored the formation of a network of laboratories some of which are located at: Sanjay Gandhi Postgraduate Institute, Lucknow National Institute of Communicable Diseases, New Delhi ERC , Mumbai NIV , Bengaluru BJMC, Ahmedabad Enterovirus Research Institute, Kasauli Pasteur Institute of India, Coonoor

80. Albert Sabin Jonas Salk George Guillain Jean Barre Charles Miller Fischer Jean Baptiste Landry Thank You.