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Poliomyelitis

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Poliomyelitis

  1. 1. PoliomyelitisPoliomyelitis
  2. 2. ObjectivesObjectives  EtiologyEtiology  EpidemiologyEpidemiology  PathogenesisPathogenesis  Clinical manifestationsClinical manifestations  DiagnosisDiagnosis  Differential diagnosisDifferential diagnosis  ManagementManagement  PreventionPrevention  PrognosisPrognosis
  3. 3. VotingVoting paralysis is the most commonparalysis is the most common Y/NY/N::presentation of poliomyelitispresentation of poliomyelitis
  4. 4. ETIOLOGYETIOLOGY  Poliomyelitis is an acutePoliomyelitis is an acute enteroviral illness caused by poliovirus.enteroviral illness caused by poliovirus.  3 serotypes are present: type 1, 2, 33 serotypes are present: type 1, 2, 3  The polioviruses are extremely hardy andThe polioviruses are extremely hardy and can retain infectivity for several days at roomcan retain infectivity for several days at room temperature.temperature.
  5. 5. EpidemiologyEpidemiology  The most devastating result of poliovirusThe most devastating result of poliovirus infection is paralysisinfection is paralysis  paralysis was more in adolescents in theparalysis was more in adolescents in the developed countries and more in infants in thedeveloped countries and more in infants in the developing countries (bad sanitation).developing countries (bad sanitation).  paralytic polio occurring in about 1/1,000paralytic polio occurring in about 1/1,000 infections among infants to about 1/100 infectionsinfections among infants to about 1/100 infections among adolescents.among adolescents.  Universal vaccination results in global eradicationUniversal vaccination results in global eradication by 2000 (99% decline) but continued transmissionby 2000 (99% decline) but continued transmission occurs in some poor countries in Asia and Africa.occurs in some poor countries in Asia and Africa.
  6. 6. The number of worldwide polio cases hasThe number of worldwide polio cases has fallen from an estimated 350,000 in 1988 tofallen from an estimated 350,000 in 1988 to fewer than 1300 in 2010—a decline of morefewer than 1300 in 2010—a decline of more than 99% in reported cases.than 99% in reported cases.
  7. 7. Successful Global PolioSuccessful Global Polio Eradication EffortsEradication Efforts  CDC and its international partners have madeCDC and its international partners have made significant progress over the past 22 years.significant progress over the past 22 years.  Three regions of the world are certified polio freeThree regions of the world are certified polio free —the Americas, Europe, and the Western Pacific.—the Americas, Europe, and the Western Pacific.  Only four polio-endemic countries (countries thatOnly four polio-endemic countries (countries that have never interrupted the transmission of wildhave never interrupted the transmission of wild poliovirus) remain—Afghanistan, India, Nigeria,poliovirus) remain—Afghanistan, India, Nigeria, and Pakistan.and Pakistan.
  8. 8. PathogenesisPathogenesis  Humans are the only known reservoir for theHumans are the only known reservoir for the polioviruses, which are spread by the fecal-oralpolioviruses, which are spread by the fecal-oral route.route.  Polioviruses spread from the intestinal tract to thePolioviruses spread from the intestinal tract to the CNS, where they cause aseptic meningitis andCNS, where they cause aseptic meningitis and poliomyelitis.poliomyelitis.  Poliovirus primarily infects AHC and medullaPoliovirus primarily infects AHC and medulla oblongata.oblongata.  However, poliovirus has almost never beenHowever, poliovirus has almost never been cultured from CSF in patients with paralyticcultured from CSF in patients with paralytic disease
  9. 9. Clinical manifestaionsClinical manifestaions  The incubation period is usually 8–12 days,The incubation period is usually 8–12 days, (5–35 days)(5–35 days)  Poliovirus infections with wild-type virusPoliovirus infections with wild-type virus may follow 1 of several courses:may follow 1 of several courses: 1.1. inapparent infection (90–95% of cases) andinapparent infection (90–95% of cases) and causes no disease and no sequelae;causes no disease and no sequelae; 2.2. abortive poliomyelitis (5%)abortive poliomyelitis (5%) 3.3. nonparalytic poliomyelitis (1%)nonparalytic poliomyelitis (1%) 4.4. paralytic poliomyelitis (0.1%)paralytic poliomyelitis (0.1%)
  10. 10. Abortive PoliomyelitisAbortive Poliomyelitis  nonspecific influenza-like syndrome occurs 1–2nonspecific influenza-like syndrome occurs 1–2 wk after infection.wk after infection.  Fever, malaise, anorexia, and headache areFever, malaise, anorexia, and headache are prominent features, and there may be sore throatprominent features, and there may be sore throat and abdominal or muscular pain and vomiting.and abdominal or muscular pain and vomiting.  The illness is short lived, up to 2–3 days.The illness is short lived, up to 2–3 days.  The physical examination may be normal or mayThe physical examination may be normal or may reveal nonspecific pharyngitis, abdominal orreveal nonspecific pharyngitis, abdominal or muscular tenderness, and weakness.muscular tenderness, and weakness.  Recovery is complete with no neurologic signs orRecovery is complete with no neurologic signs or sequelae develop.sequelae develop.
  11. 11. Nonparalytic PoliomyelitisNonparalytic Poliomyelitis  more intense headache, nausea, and vomiting, asmore intense headache, nausea, and vomiting, as well as soreness and stiffness of the posteriorwell as soreness and stiffness of the posterior muscles of the neck, trunk, and limbs.muscles of the neck, trunk, and limbs.  Fleeting paralysis of the bladder and constipationFleeting paralysis of the bladder and constipation are frequent.are frequent.  Approximately of these children have a short⅔Approximately of these children have a short⅔ symptom-free interlude between the 1st phasesymptom-free interlude between the 1st phase (minor illness) and the 2nd phase (CNS disease or(minor illness) and the 2nd phase (CNS disease or major illness).major illness).
  12. 12.  Nuchal and spinal rigidity are the basis forNuchal and spinal rigidity are the basis for the diagnosis of nonparalytic poliomyelitisthe diagnosis of nonparalytic poliomyelitis during the 2nd phase.during the 2nd phase.  Reflexes are absent with onset of flaccidReflexes are absent with onset of flaccid paralysis.paralysis.  Sensory changes don’t occur.Sensory changes don’t occur.  Patients with aseptic meningitis never havePatients with aseptic meningitis never have paralysis.paralysis.
  13. 13. Paralytic poliomyelitisParalytic poliomyelitis  3 clinically recognizable syndromes that3 clinically recognizable syndromes that represent a continuum of infectionrepresent a continuum of infection differentiated only by the portions of thedifferentiated only by the portions of the CNS most severely affected.CNS most severely affected. (1)(1) spinal paralytic poliomyelitisspinal paralytic poliomyelitis (2)(2)bulbar poliomyelitis, andbulbar poliomyelitis, and (3)(3)polioencephalitis.polioencephalitis.
  14. 14. Spinal paralytic polioSpinal paralytic polio  11stst phase corresponds to the abotive poliophase corresponds to the abotive polio  This may be followed by 2-5 days of apparentThis may be followed by 2-5 days of apparent normalcy then the 2normalcy then the 2ndnd phase which is characterizedphase which is characterized by:by:  Severe headache and feverSevere headache and fever  Motor and sensory changes: parasthesia,Motor and sensory changes: parasthesia, hypersthesia, fasiculations, spasmhypersthesia, fasiculations, spasm  Paralysis that is characteristically spotty andParalysis that is characteristically spotty and commonly involves one leg or one arm with morecommonly involves one leg or one arm with more proximal that distal weaknessproximal that distal weakness  Bowel and bladder dysfunction are commonBowel and bladder dysfunction are common  Sensation is intactSensation is intact
  15. 15. Bulbar paralytic polioBulbar paralytic polio  Dysfunction of the cranial nerves andDysfunction of the cranial nerves and medullary centers are the dominant featuresmedullary centers are the dominant features  Hypertension and autonomic disturbancesHypertension and autonomic disturbances are commonare common  Associated paralysis may occur.Associated paralysis may occur.
  16. 16. PolioencephalitisPolioencephalitis  Higher brain centers are involvedHigher brain centers are involved  Seizures, coma and spastic paralysis maySeizures, coma and spastic paralysis may occur.occur.  Irritability, disorientation, drowsiness, andIrritability, disorientation, drowsiness, and coarse tremors are often present withcoarse tremors are often present with peripheral or cranial nerve paralysis thatperipheral or cranial nerve paralysis that coexists or ensues.coexists or ensues.  Hypoxia and hypercapnia due to respiratoryHypoxia and hypercapnia due to respiratory insufficiency may produce disorientationinsufficiency may produce disorientation without true encephalitis.without true encephalitis.
  17. 17. DIAGNOSISDIAGNOSIS  Poliomyelitis should be considered in anyPoliomyelitis should be considered in any unimmunized or incompletely immunized childunimmunized or incompletely immunized child with paralytic disease.with paralytic disease.  (WHO) recommends that the laboratory diagnosis(WHO) recommends that the laboratory diagnosis of poliomyelitis be confirmed by isolation andof poliomyelitis be confirmed by isolation and identification of poliovirus in the stool.identification of poliovirus in the stool.  2 stool specimens should be collected 24–48 hr2 stool specimens should be collected 24–48 hr apart, as soon as possible after the diagnosis ofapart, as soon as possible after the diagnosis of poliomyelitis is suspected (the optimal time forpoliomyelitis is suspected (the optimal time for collection of stool specimens is the 1st week aftercollection of stool specimens is the 1st week after the onset of paralysis)the onset of paralysis)
  18. 18.  The CSF, while often normal during theThe CSF, while often normal during the minor illness, with CNS involvementminor illness, with CNS involvement demonstrates a pleocytosis of 20–300demonstrates a pleocytosis of 20–300 cells/mmcells/mm33 with normal or slightly elevatedwith normal or slightly elevated protein during 1protein during 1stst week. However, during 2week. However, during 2ndnd week, cells fall to normal and proteinweek, cells fall to normal and protein elevates up to 50-100 mg/dl.elevates up to 50-100 mg/dl.  Serologic testing demonstratesSerologic testing demonstrates seroconversion or a 4-fold or greaterseroconversion or a 4-fold or greater increase in antibody titers, when measuredincrease in antibody titers, when measured during the acute phase of illness and 3–6 wkduring the acute phase of illness and 3–6 wk later.later.
  19. 19. Differential diagnosisDifferential diagnosis Poliomyelitis should be considered in thePoliomyelitis should be considered in the differential diagnosis of any case of acutedifferential diagnosis of any case of acute flaccid paralysisflaccid paralysis (?)(?)  Guillian-Barre syndromeGuillian-Barre syndrome  Infectious : non-polio enteroviruses, west-Infectious : non-polio enteroviruses, west- nile virus, rabies, varicella, botulism..nile virus, rabies, varicella, botulism..  Acute transverse myelitisAcute transverse myelitis  Tick bite paralysisTick bite paralysis  PolymyositisPolymyositis
  20. 20. Poliomyelitis GBS Prodrome Fever, headache, meningeal signs Preceeding infection with less notable prodrome Progression of paralysis within 24-48 hs Within hours- 10 days Distribution of paralysis asymmetric symmetric Sensory changes absent common Pyramidal signs absent common DTR Reduced/absent Reduced/absent Residual paralysis yes -/+ CSF Pleocytosis with normal or slightly elevated protein Few cells with high protein
  21. 21. TreatmentTreatment  There is no specific antiviral treatment forThere is no specific antiviral treatment for poliomyelitis.poliomyelitis.  The management is supportive and aimed atThe management is supportive and aimed at limiting progression of disease, preventionlimiting progression of disease, prevention of ensuing skeletal deformities, andof ensuing skeletal deformities, and preparation of the child and family forpreparation of the child and family for prolonged treatment required and forprolonged treatment required and for permanent disability if this seems likely.permanent disability if this seems likely.
  22. 22. Abotive and nonparalytic polioAbotive and nonparalytic polio  Supportive management: analgesics,Supportive management: analgesics, sedatives, diet, and bed rest till feversedatives, diet, and bed rest till fever disappears.disappears.  All intramuscular injections and surgicalAll intramuscular injections and surgical procedures are contraindicated during theprocedures are contraindicated during the acute phase of the illness, because theseacute phase of the illness, because these may result in progression of disease.may result in progression of disease.  Careful neurologic and musculoskeletalCareful neurologic and musculoskeletal examination 2 months after recovery toexamination 2 months after recovery to detect minor defects.detect minor defects.
  23. 23. Paralytic polioParalytic polio  Complete bed rest in a calm atmosphere forComplete bed rest in a calm atmosphere for the 1the 1stst 2-3 weeks2-3 weeks  Suppotive management is neededSuppotive management is needed  Ventilatory support is usually needed forVentilatory support is usually needed for respiratory failurerespiratory failure
  24. 24. ComplicationsComplications  Acute gastric dilatation may occur abruptly.Acute gastric dilatation may occur abruptly.  Melena from superficial intestinal erosions;Melena from superficial intestinal erosions; perforation is rare.perforation is rare.  Mild hypertension for days or weeks is commonMild hypertension for days or weeks is common in the acute stage.in the acute stage.  In the later stages, because of immobilization,In the later stages, because of immobilization, hypertension may occur along withhypertension may occur along with hypercalcemia, nephrocalcinosis, and vascularhypercalcemia, nephrocalcinosis, and vascular lesions.lesions.  ECG abnormalities suggesting myocarditis areECG abnormalities suggesting myocarditis are not rare.not rare.
  25. 25. PREVENTIONPREVENTION
  26. 26. ImmunizationImmunization
  27. 27. Polio vaccinesPolio vaccines  OPV and IPV protect against the 3 strains ofOPV and IPV protect against the 3 strains of poliopolio  IPV induces higher serum IgG antibodies whileIPV induces higher serum IgG antibodies while OPV induce greater mucosal IgA in the GIT.OPV induce greater mucosal IgA in the GIT.  All children should receive 4 doses of IPV atAll children should receive 4 doses of IPV at 2,4,6- 18 months and at 4-6 years.2,4,6- 18 months and at 4-6 years.  In our country:In our country:  IPV is given at 1 ,2 monthsIPV is given at 1 ,2 months  OPV is given at 2, 4, 6, 18 months and at 6 years.OPV is given at 2, 4, 6, 18 months and at 6 years.
  28. 28. VAPPVAPP  Very rare ( 1/6.2 million ) but the risk for paralysis in theVery rare ( 1/6.2 million ) but the risk for paralysis in the immunodeficient recipient may be as much as 6,800immunodeficient recipient may be as much as 6,800 times that in normal subjects.times that in normal subjects.  OPV is safe ( vaccine strains don’t replicate in the CNS ).OPV is safe ( vaccine strains don’t replicate in the CNS ). However, reversion in the small intestine occursHowever, reversion in the small intestine occurs occasionally with access the CNS via peripheral nervesoccasionally with access the CNS via peripheral nerves causing VAPP.causing VAPP.  VAPP should be considered in any child with paralyticVAPP should be considered in any child with paralytic disease occurring 7–14 days or at later times afterdisease occurring 7–14 days or at later times after receiving OPV in countries or regions where wild-typereceiving OPV in countries or regions where wild-type poliovirus has been eradicated and the OPV has beenpoliovirus has been eradicated and the OPV has been administered to the child or a contact.administered to the child or a contact.
  29. 29. PROGNOSISPROGNOSIS  Inapparent, abortive polio and asepticInapparent, abortive polio and aseptic meningitis have good prognosis with nomeningitis have good prognosis with no long-term sequel.long-term sequel.  Mortality rate in severe bulbar polio is asMortality rate in severe bulbar polio is as high as 60 % and is 5- 10% in less severehigh as 60 % and is 5- 10% in less severe disease.disease.  Recovery from paralysis is usually up to 6Recovery from paralysis is usually up to 6 months after which paralysis is permanent.months after which paralysis is permanent.
  30. 30. Postpolio syndromePostpolio syndrome  30-40 % of of patients who survived30-40 % of of patients who survived paralytic polio may develop exacerbation orparalytic polio may develop exacerbation or new weakness and muscle pain 30-40 yearsnew weakness and muscle pain 30-40 years after infectionafter infection
  31. 31. ConclusionConclusion  poliomyelitis is acute enteroviral illness.poliomyelitis is acute enteroviral illness.  The most devastating result of poliovirusThe most devastating result of poliovirus infection is paralysisinfection is paralysis  Poliomyelitis should be considered in thePoliomyelitis should be considered in the differential diagnosis of any case ofdifferential diagnosis of any case of paralysis.paralysis.  Vaccination is the only effective method ofVaccination is the only effective method of prevention.prevention.
  32. 32. Thank youThank you

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