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1. PoliomyelitisPoliomyelitis

2. ObjectivesObjectives
 EtiologyEtiology
 EpidemiologyEpidemiology
 PathogenesisPathogenesis
 Clinical manifestationsClinical manifestations
 DiagnosisDiagnosis
 Differential diagnosisDifferential diagnosis
 ManagementManagement
 PreventionPrevention
 PrognosisPrognosis

3. VotingVoting
paralysis is the most commonparalysis is the most common
Y/NY/N::presentation of poliomyelitispresentation of poliomyelitis

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. 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. 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. 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. 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. 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. 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. 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.  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. 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. 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. 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. 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. 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.  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. 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. 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. 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. 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. 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

25. 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.

26. PREVENTIONPREVENTION

27. ImmunizationImmunization

28. 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.

29. 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.

30. 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.

32. 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

34. 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.

35. Thank youThank you