POLIOMYELI

TIS
Name:Nurzawani Binti Shamsudin
Matric No: 0918424

Definition
Acute enteroviral illness with

prodorme
vomiting
and
fever associated with an
aseptic meningitis picture
during which the patient
experiences the evolution of
an asymmetrical flaccid
weakness without sensory
loss as groups of anterior
horn cells become infected.

Polioviruses
polioviruses are

nonenveloped, positivestranded RNA viruses

belonging to the genus
Enterovirus, in the
Picornaviridae family
3 antigenically distinct
serotypes (types 1, 2,
and 3)
spread from the
intestinal tract to the
central nervous system
(CNS), where they cause
aseptic meningitis and
poliomyelitis, or polio

Epidemiology
9095% of infections are in apparent but induce

protective immunity
out of 5%, paralytic polio occurring in about
1/1,000 infections among infants to about 1/100
infections among adolescents
in
developed countries prior to universal
vaccination, epidemics of paralytic poliomyelitis
occurred primarily in adolescents
conversely, in developing countries with poor
sanitation, infection early in life results in
infantile paralysis
poor sanitation and crowding have permitted
the continued transmission of poliovirus in
certain poor countries in Africa and Asia

Epidemiology

Pathogenesis
Virus
ingested
through
mouth

Multiply in
Peyers
patches of
ileum (M
cells)

Go to blood
stream

Blood stream

Multiply in
reticuloendot
helial system

Primary
viremia (2-3
days)

2 viremia
then invade
CNS

Clinical Manifestation

The incubation period of poliovirus

from contact to initial clinical

symptoms is usually considered to be
812 days, with a range of 535 days.
Paralysis, if it occurs, appears 38
days after the initial symptoms.

Abortive Poliomyelitis
Clinical Manifestation

o In

about 5% of patients, a nonspecific

influenza-like syndrome occurs 12 wk after
infection,
which
is
termed
abortive
poliomyelitis.
o Fever, malaise, anorexia, and headache are
prominent features, and there may be sore
throat and abdominal or muscular pain.
Vomiting occurs irregularly.
o The illness is short lived, up to 23 days.
Recovery is complete, and no neurologic signs
or sequel develop.

Nonparalytic Poliomyelitis
Clinical Manifestation

o In about 1% of patient presents with the

manifestations of abortive type associated

with aseptic meningitis such as neck
rigidity, +ve Kernigs sign and Brudzinskis
sign.
o CSF shows changes of aseptic meningitis.
o The manifestations disappear 1-2 days and
leave no paralytic manifestations.

Paralyitic Poliomyelitis
Clinical Manifestation

o Occur in 0.5-1% of all cases, usually

begins with manifestations of abortive

or non paralytic poliomyelitis.
o Then after 3-8 days paralytic
manifest
o The major symptoms, however, are
due to invasion of the motor nerves,
which are responsible for movement
of the muscles.
o This viral invasion causes
inflammation, and then destruction of
these nerves.
o Divided into 3 types:
1.
2.
3.

Spinal
Bulbar
Encephalitic

1. Spinal Poliomyelitis
o The muscle affected are: lower limbs

(quadriceps, harmstrings, anterior tibial and

peroneal muscle) and upper limbs (deltiod
muscle).
o The muscle limbs are the most common
affected ones but muscles of chest wall,
diaphragm, abdominal wall, urinary bladder and
bowel may affected.
o The paralysis is characterized by being:
Asymmetrical
Patchy
Non Progressive
Purely motor
Lower motor neuron lesion: associated with hypotonia,

loss of deep reflexes and muscle wasting

2. Bulbar poliomyelitis
o Bulb of brain mid brain, pons and medulla

contain following centers: respiratory, heat

regulating centre and motor nuclei of cranial
nerves.
o Clinically patient will get:
Bradycardia
2. Irregular respiration with apnoea, cyanosis
and respiratory failure
3. Cranial nerve palsy; squint, pin point pupils,
dysphagia, nasal tone and nasal
regurgitation of fluids
4. Hypo or Hyperthermia
1.

3. Encephalitis poliomyelitis

Manifestation of encephalitis are evident.

o Disturbed consciousness (from drowsiness to

coma)
o Convulsions
o Localized
manifestation
deafness and paralysis
hemiplegia)

as
blindness,
(monoplegia or

Diagnosis depend on:

a) Presence of epidemic of polio
b) Isolation of the virus from CSF
c) Increase antibody titre against polio

Poliomyelitis

Gullain Barre
syndrome

Botulism

Peripheral
neuritis

Transverse
myelitis

Etiology

Poliovirus

Post infectious
(immunologic)

Clostridium
botulinum in
contaminated
food

Post
diphtheritic
Vit. B
deficiency,
lead posoning,
DM

Post infectious

Onset of
paralysis

Acute

Insidious

Acute

Acute

Acute

Fever at
onset of
paralysis

Present

Absent

Absent

Absent

Absent

Sign of
meningeal
irritation

Present

Absent

Absent

Absent

Absent

Character
of paralysis

LMNL (reduce
tone, diminished
reflex, wasting
muscle,
asymmetry
patchy, pure
motor)

LMNL
(bilateral and
symmetric,
predominantly
motor)

LMNL
(bilateral and
symmetric,
pure motor)

LMNL
(bilateral and
symmetric,
motor and
sensory)

In lower limb
Early: flaccid
paralysis
Late: spastic

Progressive
of paralysis

Non Progressive

Progressive
in the 1st 2
weeks in an
ascending
manner

Non
Progressive

Non
Progressive

Non
Progressive

Sensory
changes

No sensory
changes

Paraesthesia

No sensory
changes

Gloves and
stockings

Loss of
sensation in

Investigation
1. Isolation of the virus from throat

swabs, faeces and rectal swabs. It is

rarely isolated from CSF. Can be readily
grown and identified in cell culture.
Require molecular technique.
2. Rise in antibodies in paired samples,
one in acute stage and another one 2-3
weeks later.
3. CSF: Show normal or increased pressure,
clear or turbid with increase cells (mainly
lymphocytes), proteins (30-60mg % and
later may rise to 100-600mg%) and
normal glucose level.

Treatment
Prevent disease by immunization with inactivated

polio vaccine
Supportive treatment aimed at limiting
progression of disease
Intubation/tracheostomy, bladder catheter, tube
feeding may be required
Post polio paralysis is mild in 30%, permanent in
15%. Physical therapy may be required
Immunodeficiency and underimmunization are the
major causes of paralytic polio in the worldwide
today. Vaccine-associated paralytic polio has been
nearly eliminated by the use of inactivated vaccine.

Vaccine
Oral Poliovirus Vaccine
(OPV)
Consists of live attenuated
virus of all 3 serotypes
Produce local immunity
through induction of an
IgA response as well as
systemic immunity
Rarely cause paralytic
poliomyelitis, around 1 in 3
million doses
Much cheaper than IPV
Known as Sabin vaccine

(Intramuscular) Inactivated Poliovirus

Vaccine (IPV)
Consists of formalin inactivated virus of all
3 poliovirus serotypes
Produce serum Ab only; does not induce
local gut immunity. Thus , do not prevent
local infection of gut.
It will prevent paralytic poliomyelitis since
viremia is essential cause pathogenesis of
the disease.
Known as Salk vaccine