poliomyelitis 12 04-2016
TRANSCRIPT
Introduction
Highly infectious disease caused by three serotypes
of poliovirus.
Primarily an infection of GIT, & about 1% get CNS
infection.
Spectrum of clinical manifestations:
Inapparent infection - non-specific febrile illness -
aseptic meningitis - paralytic disease - death.
Infection most often recognized by acute onset of
flaccid paralysis.
Problem
Pre-vaccination era – worldwide.
Since introduction of vaccine in 1954 – eliminated in
developed countries.
1988 – world health assembly resolved to eradicate
polio globally.
In 1988 it was endemic 125 countries, by 2008 in 4
countries (India Pakistan, Afghanistan & Nigeria)
Since February 2012 – India polio free
EPIDEMIOLOGICAL TRIAD
ENVIRONMENT
(Rainy season, Poor sanitation)
AGENT HOST
(Poliovirus- 3 Serotypes) (Children, male)
Agent factors:
1.Agent:
Family – Picorna
Genus: Enterovirus
Species: Poliovirus
Genome – RNA
Capsid symmetry – Icosahedral with no
envelop
Serotypes - Three (no cross immunity)
1.Type 1 - 90% (Weakest, only 1% causes
neuroparalysis)
2.Type 2 - 9% (Eliminated)
3.Type 3 - 1% (Greater temperature
stability)
Agent factors:
2. Reservoir of infection:
Man only (clinical or sub-clinical (mostly))
For every clinical cases – 1000 sub-clinical cases in
children & 75 in adults.
No chronic carriers.
3. Infectious material:
Faeces & oropharyngeal secretion of infected
persons.
4. Period of communicability:
7 to 10 days before & after onset of symptoms.
In faeces virus may be excreted as long as 3 to 4
months.
Host factors
1. Age:
All age groups
Children more susceptible (more vulnerable in 6 months
to 3 years)
2. Sex:
M/F ratio, 3 : 1
3. Risk factors:
Fatigue, trauma, IM injection, Operation during
epidemics, DPT vaccine.
4. Immunity:
Maternal antibody protect up to first 6 months.
No cross immunity with other sero-types.
Type 2 PV – most effective antigen.
Environmental factors
• Common in rainy season (June to
September)
• Over-crowiding & poor sanitation
favors
Sewage Drinking water
Sewage
MODE OF TRANSMISSION:
A. Faeco-oral route (mainly in developing con.):
Directly – by contaminated fingers,
Indirectly – by contaminated water, milk, food,
flies, fomites.
B. Droplet infection:
In acute phase of dis.(virus in throat)
INCUBATION PERIOD: 7 to 14 days( 3 - 35 days)
Pathology
Polio virus
Infect intestinal
epithelium
Replication of virus
in epithelial cells
Infect Peyr's patches &
secondary multiplication
Viremia
Antibody production
CNS infection
IgA secretory antibodies
Sequelae of polio infection
Polio infection
In apparent infection(91 to 96%)
Clinical poliomyelitis
Abortive polio (minor illness)
(4 to 8%)
Involvement of CNS(major illness)
Paralytic polio (<1%) Non-paralyticpolio (2 to 10%)
Spinal polio
Bulbar polio
Bulbospinal polio
Clinical poliomyelitis
1. Inapparent (subclinical) infection
No clinical manifestations, but infection is associated
with acquired immunity, & carrier state.
2. Abortive polio (minor illness):
Mild systemic manifestations for 1or 2 days only,
then clears up, giving immunity.
Manifestations:
Moderate fever
Pharyngitis & sore throat
Vomiting, abdominal pain, & diarrhea.
Clinical poliomyelitis (cont.)
3. Involvement of the CNS (major illness):
A. Nonparalytic polio:
Manifested by:
Fever, headache, nausea, vomiting, & abdominal pain.
Pain & stiffness in the neck back & limbs may also
occur.
The case either recovers or passes to the paralytic
stage.
Clinical poliomyelitis (cont.)
B. Paralytic poliomyelitis:
Paralysis usually appears around 7-10 days from
onset of disease.
Presented with:
Fever, anorexia, nausea, vomiting, headache, sore
throat, constipation, abdominal pain.
May be sign of meningeal irritation.
Tripod sign (difficulties in sitting & sits by supporting
hands at back & by partially flexing the hip & knees.
Clinical poliomyelitis (cont.)
Different paralytic manifestations according to
the part of the CNS involved, with destruction
of the motor nerve cells, but not the sensory
nerve cells (i. e. no sensory loss).
Paralysis reach maximum in less than 4 days
in majority of cases (4 – 7 days).
Forms: 1. Spinal, 2. Bulbar, 3. Bulbospinal.
1. Spinal polio
Different spinal nerves are involved, due to injury
of the anterior horn cells of the spinal cord,
causing tenderness, weakness, & flaccid paralysis
of the corresponding striated muscles
The lower limbs are the most commonly affected.
Paralysis:
o Characterized as descending i.e. start at hip &
then moving down to the distal parts of the
extremity.
o Asymmetrical patchy,
o Muscle strength varies in different muscle groups of
different limbs.
o Proximal muscle groups are more involved than
distal one.
2. Bulbar polio
Nuclei of the cranial nerves are involved, causing
weakness of the supplied muscles, & maybe
encephalitis.
Bulbar manifestations include dysphagia, nasal voice,
fluid regurgitation from the nose, difficult chewing,
facial weakness & diplopia
Paralysis of the muscles of respiration is the most serious
life-threatening manifestation.
3. Bulbospinal polio
Combination of both spinal & bulbar forms
Among children who are paralyzed by
polio:
30% make a full recovery
30% are left with mild paralysis
30% have medium to severe
paralysis
10% die
Complications & case fatality
Respiratory complications: pneumonia, pulmonary
edema
Cardiovascular complications: myocarditis, cor-
pulmonale.
Late complications: soft tissue & bone deformities,
osteoporosis, chronic distension of the colon.
Case fatality: varies from 1% to 10% according to the
form of disease (higher in bulbar), complications &
age (fatality increases with age).
Diagnosis & laboratory testingTo rule out or confirm the diagnosis of paralytic poliomyelitis.
1. Virus isolation
The likelihood of poliovirus isolation is highest from stool specimens,
intermediate from pharyngeal swabs, & very low from blood or spinal fluid.
2. Serologic testing
A four-fold titer rise between the acute & convalescent specimens suggests poliovirus infection.
3. Cerebrospinal fluid (CSF) analysis
The cerebrospinal fluid usually contains an increased number of leukocytes—from 10 to 200 cells/mm3 (primarily lymphocytes) & a mildly elevated protein, from 40 to 50 mg/100 ml.
Treatment
No specific t/t
Good nursing care – minimise or prevent
crippling.
Physiotherapy – can be initiated immediately
in affected limb.
Prevention
A. General prevention:
Health promotion through environmental sanitation.
Health education (modes of spread, protective value of
vaccination).
B. Specific protection
1. Passive immunization by human immunoglobulins:
Dose: (0.25 - 0.3 ml/kg of body weight).
Schedule: given either or before or very shortly after
exposure to infection (not practical).
2. Active immunization:
Salk vaccine (intramuscular, trivalent killed vacc.)
Sabin vaccine (oral polio trivalent live attenuated va.)
Inactivated Polio Vaccine
Contains 3 serotypes & inactivated with formaldehyde
Contains 2-phenoxyethanol, neomycin, streptomycin, polymyxin B
A. Classical IPV:
Contain 20, 2 & 4D antigen unit of type 1, 2 & 3 serotype respectively.
Dose: Primary 4 doses at interval of 1 - 2 months & Booster – every 5 years
B. Improved IPV:
Contain 40, 8 & 32D antigen unit of type 1, 2 & 3 serotype respectively
100% effective after 2nd dose.
Can be combined with DPT.
Oral Polio Vaccine by Sabin in 1957
Contains 3 serotypes of vaccine virus
Live attenuated virus grown on monkey kidney (Vero) cells
Contain:
1. Over 3LakhTCDI 50 of type 1PV
2. Over 1LakhTCDI 50 of type 2PV
3. Over 3LakhTCDI 50 of type 3PV
Contains neomycin & streptomycin
Vaccine virus shed in stool for up to 6 weeks following
vaccination
Dose: 2 drops/dose
1. Primary 4 doses (at 0, 6, 10 & 14 weeks)
2. Booster – at age of 16 to 24 months.
Salk versus Sabin vaccine
IPV (Salk)1. Killed formolised virus
2. Given SC or IM
3. Induces circulating antibodies, but not local (intestinal immunity)
4. Prevents paralysis but does not prevent re-infection.
5. Not useful in controlling epidemics
6. More difficult to manufacture & is relatively costly
7. Does not require stringent conditions during storage & transportation. Has a longer shelf life.
OPV (Sabin1. Live attenuated virus
2. Given orally
3. Immunity is both humoral and intestinal. induces antibody quickly
4. Prevents paralysis and prevents re-infection
5. Can be effectively used in controlling epidemics.
6. Easy to manufacture and is cheaper
7. Requires to be stored & transported at subzero temperatures, & is damaged easily.
Polio Vaccination of Adults
A. Previously Unvaccinated:
IPV
Use standard IPV schedule if possible 3 doses (0,
1-2 months, 12 months)
May separate doses by 4 weeks if accelerated
schedule needed
B. Previously Vaccinated:
@ Previously complete series:
administer one dose of IPV
@ Incomplete series:
Administer remaining doses in series
No need to restart series
Polio Vaccine Adverse Reactions
• Rare local reactions (IPV)
• No serious reactions to IPV have been
documented
• Paralytic poliomyelitis (OPV)
Vaccine-Associated Paralytic Polio
Increased risk in persons
Age >18 years
with immunodeficiency
5-10 cases/ year with exclusive use of OPV
Most cases in healthy children & their household
contacts
Polio Vaccine
Contraindications & Precautions
Severe allergic reaction to a vaccine
component or following a prior dose of
vaccine
Moderate or severe acute illness
POLIO ERADICATION PROGRAMME- Strategies in India
1. Conduct pulse polio immunization for 2 days every year
for 3 to 4 years or until polio is eradicated.
2. Sustain high level of routine immunization.
3. Monitor OPV coverage at district levels and below.
4. Improve surveillance capable of detecting all cases of
polio.
5. Ensure rapid case investigation, including the collection
of stool samples.
6. Arrange follow-up of all cases of paralytic polio at 60
days to check for residual paralysis.
7. Conduct outbreak control for cases confirmed or
suspected to stop transmission.
GOAL:
Immunize every child against polio until polio
transmission has stopped, so that the world can be
certified polio-free.
Objective:
Replacement of wild PV with Vaccine virus in the
community
Strategy:
Intensified pulse polio immunization (From 1996-97
to all children under the age of 5 years were
covered).
AFP Surveillance
Acute flaccid paralysis is defined as:
Any case of AFP in a child aged <15 years, or any
case of paralytic illness in a person of any age when
polio is suspected.
Acute: rapid progression of paralysis from onset to
maximum paralysis
Flaccid: loss of muscle tone, “floppy” – as opposed
to spastic or rigid
Paralysis: weakness, loss of voluntary movement
Any case meeting this definition undergoes a thorough
investigation to determine if the paralysis is caused by
polio.
COMPONENTS OF AFP SURVEILANCE
1. The AFP surveillance network & case notification
2. Case & laboratory investigation
3. Outbreak response & active case search in the
community
4. 60-day follow-up, cross-notification & tracking of
cases
5. Data management & case classification
6. Virologic case classification scheme
7. Surveillance performance indicators
Sample collectionA
Collection of 2 adequate stool samples from all
cases.
1. Collected within 14 days of paralysis onset & at
least 24 hours apart;
2. Adequate volume (8-10g)
3. Arrives at a WHO-accredited laboratory in good
condition (ie, no desiccation, no leakage), with
adequate documentation & evidence of cold-chain
maintenance.