poliomyelitis 12 04-2016

Rukhsar Khatoon

Elimination Vs Eradication

PoliomyelitisEpidemiology & control measures

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

Global Status 1988

Epidemiological determinants

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.


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.


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).

Cold Chain Vs Reverse Cold chain

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



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.

VACCINE VIAL MONITOR

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.

Thank You

poliomyelitis 12 04-2016

Healthcare