The document summarizes key information about acute poliomyelitis including its clinical diagnosis, cycle of infection, transmission, pathogenesis, immunity, risk factors, types of infection, treatment, vaccines, and strategies for eradication. Poliomyelitis is caused by three serotypes of poliovirus and spreads primarily through the fecal-oral route. It can cause abortive infection or paralytic disease. Treatment focuses on supportive care and vaccines aim to build immunity to stop transmission and eradicate the virus globally through high vaccination coverage and surveillance.

1. ACUTE POLIOMYELITIS DR. NATARAJ PL

3. Clinical Diagnosis (WHO case definition)“ A case of poliomyelitis is defined as any child under fifteen years of age with acute flaccid paralysis or any person with paralytic illness at any age when polio is suspected”

4. Cycle of infectionAgentPoliovirus : three serotypes (P1, P2, P3) with different antigenicity

5. The virus can live in water for three months and in the faeces for six months.

6. The poliovirus is rapidly inactivated by heat, formaldehyde, chlorine and ultraviolet light. Reservoir Cases : clinical & subclinical plays a role in the spread of infectionCarriers: faecal temporary. There is no chronic carrier.Source of infection:Faeces and pharyngeal secretions of the infected person

7. PersonAge and sex:In developing countries Poliomyelitis is a disease of young children and adolescentsIn developed countries adults were affected more commonly than children with increased both the disease severity and deaths.Sex difference have been noticed in the ratio of three male to one female

8. TimePoliovirus infection typically peaks in the summer months. Man is the only reservoir

9. Time course of poliovirus infection

10. Mode of transmission1-Feaces (feco-oral): in areas with lack of personal hygiene especially in young children in developing countries. It results in infection not paralysis.2-Droplet:in developed countries with high standard of sanitation, droplet is common mode of transmission during the acute phase of the disease when the virus is in the throat.3-Direct contact with respiratory discharge4- Common vehicle: ingestion of food or drink contaminated with faeces5- Indirect contact with articles contaminated with pharyngeal discharge of infected person. InletThe mouth and nose

11. Pathogenesis of Polio Virus Infection

12. Immunity in PolioTransplacentally acquired passive immunityAfter natural infectionAfter immunisationLocal immunity

13. Immunity to Poliovirus InfectionExposure to poliovirus initiates a complex process that eventually results in both humoral (systemic) and mucosal (local) immunity. Poliovirus infection provides lifelong immunity against the disease, but this protection is limited to the particular type of poliovirus involved (Type 1, 2, or 3) Thus, infection with one type does not protect an individual against infection of the other two types. IgMand IgG antibodies are detected in the serum as early as 1-3 days following natural infection but disappears after 2-3 months.

14. Poliomyelitis: Risk FactorsImmune deficiencyPregnancyPoor sanitation and hygiene Poverty Unimmunized status, especially if <5 yearsTonsillectomy: a risk factor for bulbar paralysis.Intramuscular injections or truamaGenetics:No genetic susceptibility has been identified.

15. Response to Infection

16. Abortive poliomyelitis5% casesInfluenza like symptoms 1-2 weeks laterLasts only for 2-3 daysClinical examination unremarkableComplete recovery

17. Non paralytic poliomyelitis1% casesInitial minor illness-headache, nausea, vomiting, soreness and stiffness of neck muscles, fleeting paralysis of bladder and constipationShort symptom free interludeMajor illness

18. Non paralytic poliomyelitisNuchal and spinal rigidity are hallmarkTripod sign, Kiss the kneeNeck rigidity, Kernigs signHead dropReflexes usually normalChanges in reflex indicate impending paralysis

19. Paralytic poliomyelitis-spinal2nd phase of the illnessSpotty paralysisAsymmetric flaccid paralysisOne leg most common followed by one armAbsent DTRs

20. Paralytic poliomyelitis-spinalAbsent DTRsNo sensory deficitsFull picture by 3 days. Usually no further progressionBowel and bladder dysfunctionOlder age and provocation paralysis the biphasic illness is not seen

21. Paralytic poliomyelitis-spinalRecovery is slow starting after several weeks of the disease, but usually within 6 monthsIf not then residual paralysisRecovery may continue for as long as 18 monthsAtrophy, deformity and failure to grow

22. Paralytic poliomyelitis-BulbarNasal twang to voice and nasal regurgitation of foodInability to swallow and pooling of oral secretionsPalatal and tongue involvementVocal cord palsy

23. Paralytic poliomyelitis-BulbarVital centers in medulla being involvedAscending paralysisAutonomic disturbancesRecovery is variable

24. Paralytic poliomyelitis-EncephalitisInvolvement of higher centersSeizures,coma,spastic paralysisPeripheral & cranial nerve palsiesRespiratory paralysis-due to variety of possibilities

26. Clinical Evolution

27. Poliomyelitis: ComplicationsUrinary tract infectionSkin ulcersTraumatic injuries to affected limb(s)Atelectasis & PneumoniaMyocarditisPostpoliomyelitis progressive muscular atrophy.Postpoliomyelitis motor neuron disease.Respiratory muscle involvement and death

28. Poliomyelitis: Diagnosis Based on the clinical presentation.Cerebrospinal Fluid: Leukocytosis, Increased protein, Normal glucose. Virus recovery from stool, throat washing, blood.Virus recovery from stool is essential to diagnosis.

29. Obtain stool, blood and throat samples for viral serology, demonstrating a four fold rise in IgG is helpful but not always easy.

30. Positive IgM is diagnostic. Polymerase chain reaction amplification of poliovirus RNA from CSF or serologically, by comparing viral titers in acute and convalescent sera.

31. Diagnosis…cont Electrodiagnostic investigations reveal normal sensory nerve studies. Motor nerve studies: show normal to mildly slowed conduction velocities and low to normal amplitudes. MRI may be helpful to evaluate involvement of anterior horn of the spinal cord or other findings.

32. Differential diagnosisGuillain-Barre syndromeDiphtheric paralysisBotulismMyasthenia GravisPolymyositis & Viral myositisTransverse MyelitisSpinal cord compressionHypokalemic periodic paralysis

34. Treatment-AbortiveAnalgesics & sedativesBed restNutritionAvoid exertion & IM injections

35. Treatment-non paralyticAbove mentioned methodsHot packs & hot tub bathsFirm bedFoot board or splintGentle physical therapy

36. Treatment-ParalyticCare of bowel & bladderIncreased fluid intakeCare of airway & secretionsMonitor vital signsVentilationTracheostomy

38. Outcome Complete recovery in abortive & non paralytic polio60% mortality in bulbar polio & 5% in spinal polioRecovery beyond 6 months is unlikely

39. Four different oral polio vaccines are available to stop polio transmission. From left to right: mOPV3, mOPV1, bOPV and OPV

40. Oral polio vaccineContains 3 serotypes of vaccine virus Grown on monkey kidney (Vero) cellsContains magnesium sulfate, phenolphthaleinHeat sensitive – to be stored at –200 cStored at 2-80 c during administration VVM on the vial

41. Oral polio vaccineShed in stool for up to 6 weeks following vaccination – Herd immunitySeroconversion rates of 73%, 90% and 70% for 1, 2, 3 serotypes after 3 doses4 doses in the first year of life and boosters-IAP recommendationType 2 serotype disappears first with immunisationUsed in pulse polio programme

42. Oral polio vaccine-Adverse reactionsVaccine associated paralytic poliomyelitis(VAPP)-250 to 800 cases annually-1/5 million dosesMost common by type2 (type 3 as per Nelson and Park)Circulating vaccine derived polio viruses (cVDPV)-out breaks of paralytic polio

46. VACCINE VIAL MONITORX3 = bad:Don’t Utilize1 = good:UtilizeX2 = good:Utilize4 = bad:Don’t UtilizeThe central square is equal to, or darker than the surrounding circleThe central square is lighter than the surrounding circle

47. Polio is suitable to be eradicated for the following reasonsPolio only affects humans, there are no known animal reservoirsAn effective, inexpensive vaccine is available: Oral Polio Vaccine (OPV) Immunity is life long There are no chronic carriersHalf life of excreted virus in the sewage is 48hrs ( spread occurs only during this period)

48. AFP surveillanceAFP is defined as sudden onset of weakness and floppiness in any part of body in a child <15 years or paralysis in a person of any age in whom polio is suspectedBackground rate of AFP 1/1,00,000 children is minimum

49. AFP surveillanceCase notification and investigation –within 48 hours2 stool samples 24 hours apart within 2 weeks (upto 60 days)Outbreak response immunizationActive case searchingHot cases identification

50. AFP surveillanceCollection of stool samplesTransportation Eight national laboratories60 day follow up

51. AFP surveillance – strategiesHigh coverage of routine immunizationSupplemental doses of OPVSurveillance of AFP casesConducting mop-up vaccination campaigns

52. AFP surveillance – virological classification

53. Before a WHO region can be certified polio-free, three conditions must be satisfied:There are at least three years of zero polio cases due to wild poliovirus;Disease surveillance efforts in countries meet international standards; andEach country must illustrate the capacity to detect, report and respond to “imported” polio cases

54. What is Post Polio Syndrome ?It is the late manifestation of acute paralytic polio.25-40% of people who had paralytic polio15-40yr previously. They show symptoms of muscle and joint pain, general fatigue and weakness. Three indications of PPS: A. Previous diagnoses of polio B. Long interval following recovery: people usually live long but effect can occur during 30-35 years after the diagnoses. C. Gradual onset: weakness that tends to be perceptible until it interferes with daily activities.