Polio final presentation

POLIOMYELITIS andACUTE FLACCID PARALYSIS

TopicsIntroductionHistoryEpidemiologyPathogenesisClinical featuresDiagnosisTreatmentPrognosisPreventionProgrammes

IntroductionSynonyms Infantile paralysisDefinition Acute viral infectious disease Caused by enterovirus Route – feco – oralGreek poliós - "grey" myelós - "spinal cord"

History Timeline Events ANCIENT EGYPT An egyptian mummy 3.,700 B.C with probable polio found. 1,209 B.C Mummy Giptah with an equinus foot Eighteenth century First known 1789 description by underwood Ninteenth century First epidemic of 1834 polio in island of St. Helena

History Timeline Events 1855 First description by Duchenne of the pathalogical process Twentieth century Transmission of polio to 1908 a monkey by Landsteiner 1949 Growth of virus on tissue culture 1951 Three types of polio virus isolated and identified 1954 First large scale trial of Salk 1958 First general use of Sabin

EpidemiologyIncidence(2011)India: 5 cases- 1 Wild polio, 4 VAPP(2010)Global: 332 confirmed casesIndia: 42 confirmed casesLast case detected in Goa in 1997

Agent PoliovirusStructure: Group- group IV ((+)ssRNA) Genus- Enterovirus Family- Picornaviridae 3 serotypes- type 1, type2, type 3 Composed of an RNA genome and a protein capsid.Resistance: In feces – for months at 40 C & years at -200 C Inactivated by heat and chlorination

AgentHost range Natural infection occurs only in humansMode of transmission Feco-oral route In early stage of disease- through inhalation or entry through conjunctiva of droplets of respiratory secretion of patient.Period of communicability 7 to 10 days before and after the onset of symptoms

HostAge Most vulnerable- 6 months to three yearsSex M: F ratio 3:1Immunity First 6 months maternal antibody Acquired through infection with the wild virus Immunization

EnvironmentSeasonal More during rainy seasonEnvironmental sources of infection Contaminated water and food Flies Overcrowding and poor sanitation

Pathogenesis Incubation period: 7-10 days (4- 35 days)Feco-oralInhalational Portal of entry- Local Minor/Primary mouth multiplication Viremiainfects the pharynxand intestinal mucosa.Gains entry by Multiplies in To spinal cord Major/Secondary neurons and brain Viremiabinding to animmunoglobulin-likereceptor, known as thepoliovirus receptor or Lesions are mostly in anterior horns of DESTROYSCD155, on the cell spinal cord causing THEM!membrane flaccid paralysis

Pathogenesis Portal of entry- Local Minor/Primary mouth multiplication Viremia Epithelial cells of GIT Multiplies in To spinal cord Major/Secondary neurons and brain Viremia Lymphatic tissue- from tonsils to Lesions are mostly DESTROYS in anterior horns of Peyer’s spinal cord causing flaccid paralysis THEM! patches

Pathogenesis Spreads to Portal of entry- Local Minor/Primary mouth multiplication Viremia regional lymph nodes Multiplies in To spinal cord Major/Secondary Enters blood neurons and brain Viremia stream - primary viremia Lesions are mostly in anterior horns of DESTROYS spinal cord causing flaccid paralysis THEM!

Pathogenesis Multiplies in Portal of entry- Local Minor/Primary reticulo- mouth multiplication Viremia endothelial systems Multiplies in To spinal cord Major/Secondary Enters blood neurons and brain Viremia stream again - secondary Lesions are mostly viremia in anterior horns of DESTROYS spinal cord causing flaccid paralysis THEM!

PathogenesisCarried to spinal cord & brain Portal of entry- Local Minor/Primary mouth multiplication Viremia Multiplies in To spinal cord Major/SecondaryBloodstream Direct neurons and brain Viremia (Tonsillectomy trauma IM injections fatigue ) Lesions are mostly in anterior horns of DESTROYS spinal cord causing flaccid paralysis THEM!

Pathogenesis Multiplies in neurons Degeneration of Portal of entry- Local Minor/Primary mouth multiplication Viremia Nissl’s body (chromatolysis) Nuclear changes Multiplies in To spinal cord Major/Secondary follows neurons and brain Viremia When degeneration irreversible  Lesions are mostly in anterior horns of DESTROYS phagocytosed by spinal cord causing flaccid paralysis THEM! leucocytes or macrophages

Pathogenesis Lesions are in anterior horn of spinal cord Flaccid paralysis Portal of entry- Local Minor/Primary mouth multiplication Viremia Can cause encephalitis involving • Brainstem Multiplies in To spinal cord Major/Secondary • Motor & neurons and brain Viremia Premotor areas of cerebral cortex Lesions are mostly in anterior horns of DESTROYS spinal cord causing flaccid paralysis THEM!

PathogenesisPortal of entry- Local Minor/Primary mouth multiplication Viremia Multiplies in To spinal cord Major/Secondary neurons and brain Viremia Lesions are mostlyin anterior horns of DESTROYSspinal cord causing flaccid paralysis THEM!

Clinical Features Abortive polio Inapparent (90- 95%) Non- paralyticInfection aseptic Apparent (5- meningitis 10%) Paralytic poliomyelitis Polio encephalitis

Abortive polio 4 – 8% of infections Minor illness Symptoms low grade fever sore throat vomiting abdominal pain Loss of appetite malaise Recovery – complete, no paralysis

Non paralytic aseptic meningitis 1- 2 % of infections Symptoms headache nausea vomiting pain and stiffness of back and legs

Non paralytic aseptic meningitis Signs Tripod sign Kiss the knee test Head drop sign Neck rigidity Recovery within 2 – 10 days

Tripod sign

Head drop sign Method Hand placed under patient’s shoulder and trunk is raised Observation Head lags behind limply

Kiss the knee test Method knees kept down child asked to kiss his knees Observation Cannot do the maneuver due to stiffness spine May draw up the knees sharply

Neck rigidity Method In uncooperative child-place childs head beyond the edge of table Observation True involuntary neck rigidity persists Voluntary stiffening of muscles disappears

Paralytic poliomyelitis 0.5 – 1% of infections 2 PHASES - Minor Major Minor- same as abortive polio Major- muscle pain ,spasm and return of fever Followed by rapid onset flaccid paralysis complete within 72hrs

Paralytic poliomyelitis Spinal paralytic poliomyelitis Paralytic Bulbar polioPoliomyelitis Bulbo-spinal polio

Spinal paralytic poliomyelitis Most common 80% of cases Results from lower motor neuron lesion of anterior horn cells of spinal cord Affects muscles of legs, arms and/or trunk Severe cases – quadriplegia , paralysis of trunk abdominal and thoracic muscles

Spinal paralytic poliomyelitis Paralysis – asymmetrical ( legs > arms), descending paralysis Muscles – floppy Reflexes diminished Sensation normal Residual paralysis after 60 days

Bulbar polio 2% of cases Life threatening Cranial nerve lesion - vagus Symptomso Nasal twang and hoarseness of voiceo Nasal regurgitationo Dyspneao Dysphagiao Child refuses to feedo Secretions accumulate in pharynx - aspiration

Bulbar polio• Involvement of respiratory centre - Shallow , irregular respiration Vasomotor centre - BP rises then falls• pulse – rapid weak thready• Skin – dusky red mottled• Restless , confused and comatose

Bulbo-spinal poliomyelitis 20% cases Combination of spinal paralytic and bulbar polio

Polio Encephalitis Occurs in rare cases Symptoms Irritability Delirium Disorientation Tremors Convulsions Paralysis is of upper motor neuron type

Residual paralysis Acute phase of illness lasts for 0-4weeks Recovery –variable At 60 days mild to severe residual paresis Maximum recovery – first 6 months Slow recovery upto 2 yrs After 2 yrs post polio residual paralysis persists throughout life

DiagnosisHistoryClinical examinationStool examinationCSF examinationSerological tests

Stool examination Collection of sample Two samples 24 hr apart Within 14 days of onset of paralysis 8-10 grams or thumb size Collected in a clean wide mouth bottle – plastic or glass with screw cap Sample stored below 8°C No dessication or leakage till received at WHO Accredited Lab If paralysis detected after 2 wks sample taken upto 60 days from onset

Stool examination Contact sampling Done when child has died without adequate stool sampling 5 children in close contact with the child are taken Single stool sample collected

CSF examinationCharacteristics Observations Appearance Clear / slightly turbid Cells Leucocytosis (mainly lymphocytes) Proteins Normal / slightly raised glucose Normal

Serological tests 3 types of antibodies Neutralizing antibodies (IgG) Antibodies to C antigen (IgM) Anti-D antibodies Complement fixation test – detects IgM and Anti-D antibodies Identifies exposure to poliovirus not for type- specific diagnosis Less often employed

Differential diagnosis • Most common  GB syndrome  Transverse myelitis • Others  Traumatic neuritis  Meningitis  Encephalitis  Toxin – diphtheria and botulism

TREATMENT

Treatment Symptomatic and supportive Rest in bed Relief of pain and spasm of muscles Neutral positioning of the limbs Physiotherapy Good nursing

Bed Rest Essential during acute phase Physical activity & trauma increases risk of paralytic polio Posture to be changed every 2-3 hrs. Child to be placed on stomach for short periods each day, to prevent pneumonia

 Optimum position for limbs Hip – slight flexion Knee – 5 degree flexion Foot – 90 degree support against the sole Pain Relief Sister Kenny’s treatment Hot moist packs applied to the muscles to relieve pain and spasm analgesics

Physiotherapy Method• Joints & paralysed muscles – moved passively through full range• For 10 min , 2-3 times/day Benefits• Prevents deformities and contracture• Promote development of muscle power in non-paralysed muscles

Physiotherapy

Good nursing Team approach is essential Nursing staff is an imp part Diet Nutritious , balanced & wholesome In non paralytic polio- normal diet In paralytic Fed by Ryles tube Calories/kg body wt.

Good Nursing In dysphagia pt. nursed in prone position with foot end raised – gravity drainage of pooled secretions in pharynx Or intermittent suction Tracheostomy Respiratory failure – assisted respiration with mechanical ventilator

TreatmentIndications for hospitalization Paralysis of upper limbs <3 days duration Progression of paralysis Bulbar involvement Respiratory distress Marked drowsiness Complications

Rehabilitation

Rehabilitation Physical Emotional and Psychological Social

RehabilitationEmotional support to thechild helps prepare himselffor better adjustment inlife despite the handicap

Complications Myocarditis Hypertension Pulmonary edema Pneumonia Urinary tract infections Skeletal deformities - equinus foot scoliosis osteoporosis bone fractures Compression neuropathy

Prognosis Non paralytic cases – complete recovery Paralytic polio – permanent weakness in 2/3rd cases Worse – older children sudden onset of illness with high fever

Post – polio syndrome Observed in people who had polio during their childhood. Affects about 25-50 % of the polio survivors. More common in females General fatigue muscular weakness joint pains & breathing problems are seen in affected

PREVENTION

Immunisation• History• Sabin’s Live Polio Vaccine I. Preparation II. Storage and transport III. Administration IV. Dosage V. Development of Immunity VI. Advantages and Disadvantages VII. Complications and Contraindications• Salk’s Killed Polio Vaccine I. Preparation II. Dosage• Sabin Vs Salk• Pulse Polio Immunization

History• Earliest vaccines-a. Crude suspensions of spinal cord from infected monkeys -Ineffectiveb. Inactivated with Formalin (Brodie and Park) -Often dangerous Ricinoleate (Kolmer) causing vaccination poliomyelitis• By 1953a. Salk had developed a killed vaccineb. Almost simultaneously, Koprowsky, Cox and Sabin independently developed live attenuated vaccines

Sabin’s Live Polio Vaccine• Sabin’s attenuated strains are employed• Developed by plaque selection in MKTC• Preparationa. Attenuated strains grown in MKTCb. Stringent precautions to ensure freedom from SV40 and B virus.c. Use of molar MgCl2 or sucrose stabilises the vaccine against heat inactivation

Sabin’s Live Polio Vaccine• Criteria for selectiona. Should not be neurovirulent  as tested by intraspinal inoculation in monkeysb. Should be able to set up intestinal infection  following feeding & induce immune responsec. Should be stable & not acquire neurovirulence  after serial enteric passaged. Should posses stable genetic markers  enabling differentiation from wild virulent strians.

Sabin’s Live Polio VaccineGenetic Markers:• D Marker• Rct 40• MS• Mcbride’s intratypic antigenic markerMolecular Epidemiological Methods:• Monoclonal antibodies specific to vaccine strains• Oligonucleotide finger printing• Nucleic acid sequencing

Sabin’s Live Polio Vaccine• Storagei. Stabilised vaccine: 1 year at 4 °C 1 month at room temperatureii. Non-stabilised vaccine: -20 °C in deep freeze (In the freezer compartment of refrigerator)• During transport, keep the vaccine underi. Dry ice (solid carbon dioxide)ii. Freezing mixture (equal quantities of wet ice and ammonium chloride)• At vaccination clinici. Shouldn’t be frozen and thawed repeatedly deleterious effect on potencyii. Keep vaccine in ice during administration

Sabin’s Live Polio Vaccine• OPV in India, trivalent, containsa. Type 1- 1 lakh TC ID 50b. Type 2- 2 lakh TC ID 50 per 0.5 mlc. Type 3- 3 lakh TC ID 50 (2 drops in India)• Administration- 2 drops• Use the dropper supplied a. Tilt the child’s back b. Gently squeeze the cheeks/ pinch the nose  make the mouth open c. Let the drops fall from the dropper onto the tongue.

Sabin’s Live Polio Vaccine• National Immunization ScheduleAge DoseAt birth OPV-0At 6 weeks OPV-1At 10 weeks OPV-2At 14 weeks OPV-316-24 months OPV

Sabin’s Live Polio Vaccine• Indian Academy of Paediatrics recommendationAge DoseAt birth OPV-0At 6 weeks OPV-1+IPVAt 10 weeks OPV-2+IPVAt 14 weeks OPV-3+IPV16-24 MONTHS OPV+IPV5 years OPV

Development of ImmunityInfects intestinal epithelial cellsReplicates  transported to Peyer’s patches Stimulates production of IgA antibodiesSecondary multiplication d subsequent viremia (LOCAL IMMUNITY)Spreads to other parts of body Prevents infection of GIT with wild strainsProduction of circulating antibodies Vaccine progeny excreted in fecesPrevents dissemination of virus to nervous system Non-immunized persons immunizedPrevents paralytic polio(SYSTEMIC IMMUNITY) HERD IMMUNITY

Sabin’s Live Polio Vaccine• Advantagesi. Oral easily admin no need of highly trained personnelii. Induces both humoral and systemic immunityiii. Antibodies quickly produced*iv. Vaccinees excrete virus herd immunityv. Useful in epidemicsvi. Relatively inexpensive• Disadvantagesi. Instability at high temperaturesii. Frequent vaccine failures even with fully potent vaccinesiii. Very small residual neurovirulence in OPV

Sabin’s Live Polio Vaccine• Complicationsa. Mutation (esp. type 3[1] /2[2])b. WHO estimated the risk of i. vaccine-associated paralysis : 1 case/million vaccinees ii. Risk of close contact of vaccinee : 1 case/5 million doses of vaccine developing paralytic polioContraindicationsa. Immunocompromised individuals leukemics, malignacy, those receiving corticosteroids.b. Pregnant mothers OPV should be delayed until after pregnancy unless immediate protection is required, when IPV is indicated.c. Premature Babies

ALERT! DIARRHOEA NOT A CONTRAINDICATIONBut a dose of OPV given at that time shouldnt be considered as part of the series and should receive another at earliest opportunity.

Salk’s Killed Polio VaccineFormalin inactivated preparationThree types of polio virus grown in monkey kidney tissue culture(MKTC)•Procedure for Preparation 3 types of PVs Adequate titre Inactivated withStandard virulent grown separately filtered to remove formalin at 37°C strains used in MKTC debris and clumps FOR 12-15 DAYSStringent tests to Further tests for Three types areensure complete safety and Issued for use further pooled inactivation potency

Salk’s Killed Polio Vaccine• 1954 nationwide field trial (USA)- 80 -90% protection• 1955 – ‘Cutter incident’; over 100 cases of paralytic poliomyelitis occurred in vaccines and their contacts following insufficiently inactivated vaccine.

Salk’s Killed Polio Vaccine• Injectable Polio Vaccine (IPV)a. 1st dose given at 6 weeks.b. Immunity sustained by booster doses every 3-5 years thereafterc. Vaccination of choice among HIV, other immunocompromised states, pregnant mothers. • Enhanced potency IPV a. Produced in human diploid cells b. Two s.c. Does, 4-8 weeks apart, third may be 6-12 months later. c. Better seroconversion

Sabin Vs SalkFeature Sabin’s Vaccine (live) Salk’s Vaccine (killed)Strain Live attenuated virus Killed formalised vaccineAdministration Oral (preferred in mass Injectable (adv. can be campaigns) given with DPT)Factors affecting Diarrhoeal disease preventing Not affected by theseefficacy colonisation by vaccine virus factorsSafety Safe Safe But, cases of vaccine induced paralysis reported

Sabin Vs SalkFeature Sabin’s Vaccine (live) Salk’s Vaccine (killed)Economical More Less (because, virus content is 10,000 times more, hence costlier)Nature of Local and systemic Only systemic, noimmunity intestinal immunity  No herd immunityDuration Life long Periodic booster doses requiredUse in epidemic Ideal Not very ideal- May promote multiplication on 7 dissemination of wild virus.

Pulse Polio Immunization Largest public health campaign ever conducted in a single country• Occurs as two rounds 4-6 wks apart during low transmission season of polio- Nov to Feb• First round- 9th Dec ‘95 and 20th Jan ‘96• Sudden, simultaneous, mass administration of OPV on a single day• To all children 0-5 years• Regardless of previous immunization• Extra doses which supplement• Do not replace the doses during routine immunization• Children/infants should receive all their schedules OPV doses.

WE NEED JUST ONEMORE THING TO END POLIO FOREVER “YOU”

Acute Flaccid Paralysis

Introduction Case definition• Child less than 15 yrs with acute onset flaccid paralysis for which no obvious cause is found• Acute - onset paralysis < 4 wks• Flaccid - floppy or limp paralysis• Background rate of AFP• One case of AFP per year for every one lakh population of children less than 15 years

Conditions causing AFP Site ConditionsMuscle Myoglobinuric myopathy Hypokalemic paralysis Toxic paralysis Myopathy of intensive careNeuromuscular junction Myasthenia gravis Botulism HypermagnesemiaPeripheral nerve Guillian barre syndrome Diphtheric neuropathy Porphyria Lead neuropathy Hypophosphatemia Cobalamin deficiencyAnterior horn cells Poliomyelitis Other enteroviruses

Differential Diagnosis of AFPFeature Poliomyelitis G.B. Syndrome Transverse Traumatic myelitis neuritisHistoryProgression to 24-48 hrs Hours to days Hours to 4 days Hours to 4 daysfull paralysisFever onset High always No Present before No present at onset paralysis of paralysisBladder Absent Transient Present Neverdysfunction

Feature Poliomyelitis G.B. Syndrome Transverse Traumatic myelitis neuritis Differential Diagnosis of AFP ExaminationFlaccidity Acute, Acute, Acute, Acute, assymetric assymetrical, symmetrical, symmetrical, proximal distal, ascending lower limbMuscle tone Diminished Diminished Diminished in Diminished lower limbsDeep tendon Decrease or Absent Absent early, Decreased orreflexes absent hyperreflexia late absentSensation Severe myalgia Cramps, tingling, Anesthesia of Pain in gluteal and backache, no hypo anesthesia lower limb with region sensory changes of palms and sensory level solesCranial nerves Only when Often present Absent Absent bulbar and affecting nerves bulbo-spinal VII,IX,X,XI,XIIRespiratory Only when bulbo In severe cases Sometimes Absentinsufficiency and bulbo-spinal

Feature Poliomyelitis G.B. Syndrome Transverse Traumatic myelitis neuritis Differential Diagnosis of AFP InvestigationsCSF examination High Less than 10 Cellular or Normal leucocytosis; leucocytes: high acellular; normal normal or slightly protein or slighly increased protein increased proteinEMG at three Abnormal Normal Normal May showweeks abnormalityNerve Normal Abnormal, Normal Abnormalconduction demylination orvelocity at 3 axonal damageweeks Sequlae at 3 months Severe, Symmetrical Diplegia, atrophy Moderate assymetrical atrophy of distal after years, atrophy in the atrophy; skeletal muscles recovery recovery in affected limb deformity appear in milder cases milder cases late

AFP Surveillance• All cases to be reported• All reported cases classified as polio non polio• High sensitivity of reporting will ensure detection of all cases resulting in control measures to interrupt transmission• Two critical indicators of quality of surveillance are -a. rate of non polio AFPb. proportion of AFP cases with two adequate stools collected within 14 days of onset of paralysis

Case investigation• Stool sample collection• Stool sample result• 60 days follow up• Special investigations if indicated• Final classification

Stool examination Collection of sample Two samples 24 hr apart Within 14 days of onset of paralysis 8-10 grams or thumb size Collected in a clean wide mouth bottle – plastic or glass with screw cap Sample stored below 8 C No dessication or leakage till received at WHO Accredited Lab If paralysis detected after 2 wks sample taken upto 60 days from onset

Stool examination Contact sampling Done when child has died without adequate stool sampling 5 children in close contact with the child are taken Single stool sample collected

Virological AFP Compatible Wild polio Confirm virus expert Residual review weakness, died lost to follow up discardAFP Inadequate or No no specimen residual discard No wild virus weakness 2 adequate stool specimen discard

Clinical AFP Lost follow confirm up Residual paralysis confirmAFP Follow-up at 60 days Positive for confirm wild polio virus No residual paralysis discard

Sequence of action to be taken after detecting a case of AFP Acute onset of paralysis Within 48 hrs Investigate the suspected case Discard the case of traumatic / electrolyte imbalance Within 3 days 2 adequate stool specimen National lab to collected report within 28 daysOutbreak response immunization and active surveillance Intratyping 60 days follow up (before 70 Final classification of days) case within 90 days

BibliographyTextbooks1. M.D RMK, Stanton BF, Geme JS, Schor N, Behrman RE. Nelson Textbook of Pediatrics: Expert Consult Premium Edition - Enhanced Online Features and Print. Elsevier - Health Sciences Division; 2011.2. Parthasarathy et al. Textbook of Pediatrics IAP. Jaypee Brothers Publishers; 2005.3. O.P. Ghai et al. Essential Pediatrics. CBS Publishers & Distributors; 2009.4. Park JE. Textbook of preventive and social medicine: a treatise on community health. Banarsidas Bhanot; 1972.5. Fauci AS, Eugene B, M.D SLH, M.D DLL, J J, Joseph L. Harrison’s principles of internal medicine. McGraw-Hill; 2008.

Bibliography• Online Resources• AFP Statistics: i. National Polio Surveillance Project http://www.npspindia.org/• Image Courtesy: i. Rotary International Foundation http://www.rotary.org ii. Bill and Melinda Gates foundation http://www.gatesfoundation.org/ iii. Global Polio Eradication Initiative http://www.polioeradication.org/

Contact• For distribution and discussion: Dr. Ankush Goa Medical College, Goa drankush1989@gmail.com

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Polio final presentation

by Ankush Kapil on Jul 07, 2012

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Polio final presentation Presentation Transcript