Epidemiology & Prevention of

Poliomyelitis

04/18/2024
 Introduction
• Acute viral infection
• Caused by RNA virus (Picronaviruses)
• Human is natural reservoir of Infection
• Primary infection of alimentary tract
• May infect the CNS (Paralysis and possibly
death)
• Origin came from Greek word “Polio”
meaning “grey matter”

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 Epidemiology
AGENT FACTORS:
• Agent: Poliovirus – picronavirus
• 3 serotypes: WPV1, WPV2 & WPV3
• WPV2 not detected since 1999 & declared
eradicated in September 2015
• WPV3 not detected since November 2012
• WPV1 is the sole serotype remaining in circulation
• Can Survive in cold environment in water for 4
months and in faeces for 6 months
• Inactivated by Pasteurization, heat, formaldehyde,
chlorine, UV light
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Left: Picture of
poliovirus. The
poliovirus is extremely Right: Cross-section of the
small, about 50 nm poliovirus showing the RNA,
(nanometer = one- capsid, and nerve cell
billionth of a meter) receptors Illustration courtesy
Courtesy of David of Link Studio
Belnap and James
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Reservoir of Infection:
• Man only known reservoir
• Most of infection are Subclinical
• It is estimated every clinical case there may be
1000 subclinical cases
• No chronic carriers
• No animal source of infection

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Infectious material:
• Faeces
• Oropharyngeal secretion

Period of communicability:
• 7-10 days before and after onset of symptom
• Virus excreted 2-3 weeks sometimes 3-4
months

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HOST FACTORS:
Age:
• All age
• Children are more susceptible
• Most cases (50%) reported in infancy (Vulnerable
age: 6 months to 3 years)
Sex:
• 3 male to 1 female
Risk factors:
• Fatigue, trauma, IM injection, operative procedure
like tonsillectomy during polio outbreaks and
immunization with DPT containing Alum
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Immunity
• Maternal antibodies disappear in first 6
months of life
• Immunity against one type doesn’t protect
against the other two types of virus (No cross
immunity)

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ENVIRONMENTAL FACTORS:
 More likely to occur during rainy season
 60 % cases recorded during June to September
 Contaminated water, food and flies- Sanitation
barrier
 Overcrowding and poor sanitation

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 Mode of transmission
• Faecal-oral route:
 Main route of spread in developing countries
 Infection spreads either directly through contaminated
fingers or indirectly through contaminated water, milk,
foods and articles of daily use
• Droplet infection:
 This may occur in the acute phase of disease when
virus occurs in throat
 Close personal contact with infected person facilitates
droplet spread
 More important in developed countries
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INCUBATION PERIOD:
• 7-14 days (Range 3-35 days)
CLINICAL SPECTRUM:
• When exposed to infection one of the
following response may occurs:
1. Inapparent (subclinical) infection
2. Abortive polio (minor illness)
3. Non-paralytic polio
4. Paralytic polio
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• Inapparent (Subclinical) Infection:
91-96 % of infection
No presenting symptoms
Virus isolation or rising antibody titer

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• Abortive polio or Minor illness:
4-8% of infection
Mild or self-limiting illness
Recover quickly
Virus isolation or rising antibody titer

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• Non-Paralytic Polio:
1 % of all infection
Stiffness and pain in neck and back
Last for 2-10 days – rapid recovery

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 Outcome of polio virus infection

Asymptomatic Minor non-CNS illness

Aseptic menigitis Paralytic

0 20 40 60 80 100
Percent

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 Paralytic polio
 In < 1 % of infection
 Invade CNS - flaccid paralysis
 Fever with onset of paralysis
 Progression of paralysis reaches maximum in <4 days
 Paralysis is descending i.e. starting at hip and then
moving down to distal parts of the extremities
 Asymmetrical patchy paralysis- Muscle strength varies
in different groups of different limbs
 Other associated symptom like malaise, anorexia, nausea,
vomiting, headache, sore throat, constipation and abdominal
pain
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Tripod sign may be present
 Paralytic polio
 Deep tendon reflexes are diminished
 No sensory loss in the affected area
 Cranial nerve involved in bulbar and bulbo-spinal
form of paralytic polio
 Facial asymmetry, difficulty in swallowing,
weakness or loss of voice may be present
 Respiratory insufficiency is usually the cause of
death
 After acute phase – atrophy of affected muscle lead to
residual paralysis
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 Treatment and Prevention
TREATMENT:
• No specific treatment
• Good nursing care can minimize crippling
• Physiotherapy is of vital importance
PREVENTION:
• Immunization is sole effective means of
prevention
• Two types of vaccines available:
 Inactivated (Salk)polio vaccine
 Oral (Sabin) polio vaccine
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 Inactivated (Salk) polio vaccine
• IPV may contain trace amounts of formaldehyde,
streptomycin, neomycin or polymyxin B or
phenoxyethanol
• Available as a stand alone vaccine or in combination
with DPT, Hep B or H influenza B components
• Given intramuscular or intra-dermal as a fractional
dose
• Induces humoral antibodies (IgM,G and A) but
doesn’t induce local (intestinal) immunity
• Thus antibodies circulate in blood but cannot prevent
re-infection of the gut
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Merits:
 Safe to administer
 Can be given to individuals with immune deficiency
diseases
 Can be given to individuals taking corticosteroid and
radiation therapy
 Can be given to those aged >50 yrs
 Can be given during pregnancy
 No reported occurrence of VAPP or VDPV

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 Dose schedule of IPV (stand-alone)

Dose Time of vaccination

1st Dose 6 weeks
2nd Dose 10 weeks
3rd Dose 14 weeks
4th Dose After 9 and half months
Booster doses At school entry and
thereafter every 5 years
till 18 yrs of age

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• Currently a part of Universal Immunization
programme
• Given at 6 and 14 weeks
• Fractional IPV given intra-dermal
• Along with Bivalent OPV

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De merits:
 Doesn’t provide Gut immunity
 Cannot be administered during outbreaks
 Needs expertise from the vaccinator

Associated Risks:
 No serious AEFI reported
 Minor erythema, induration and tenderness

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 Oral (Sabin) polio vaccine
• OPV described by Sabin in 1957
• Contains Live attenuated virus grown in monkey
kidney or HDC
• Currently used as Bivalent OPV containing P1 and P3
Dose- schedule:
• According to UIP 2 drops by Oral route
• At Birth ( 0-polio)
• 3 doses 6, 10 and 14 weeks
• Booster at 1 and ½ year (along with DPT booster and
Measles 2nd dose)
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 OPV and VACCINE VIAL MONITOR
(VVM)
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 Development of Immunity
• Live vaccine strains infect intestinal epithelial cells
• After replication virus transported to Peyer’s patches
where secondary multiplication occurs
• The virus spreads now to other parts of the body
resulting in circulating antibodies
• Intestinal infection stimulates IgA antibodies which
prevent subsequent infection with wild strains
• Produces local and systemic immunity
• Vaccine virus gets transmitted to other close contacts
as it is shed off in faeces- Protects unimmunized
contacts leading to “Herd Immunity”
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Advantages:
• Easy to administered – not required highly trained
person
• Provide local and systemic immunity
• Quick antibody production
• Provide herd immunity
• Inexpensive and useful in control of epidemic
Complication:
• Free from complication
• VAPP about 1 per million vaccinees
• VDPV and rarely cVDPV outbreaks
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Contraindications:
• Immunocompromised individuals, those
suffering from leukemias, HIV positive and
malignancy shouldn’t receive live vaccine

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Differences between IPV & OPV
IPV OPV

Killed virus Live attenuated virus

ID or IM Orally

Circulating antibody but no Immunity is both humoral and

local immunity local
Prevents paralysis but doesn’t Prevents both
prevent reinfection
Not useful for epidemics Effective in epidemics

Difficult to manufacture Easy to manufacture

Virus content is 10,000 times Cheaper

more than OPV-Costlier
Non stringent storage Stringent storage
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