2. 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.
3. Polioviruses
polioviruses are
nonenveloped, positive-
stranded 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
can retain infectivity for
4. Epidemiology
90–95% 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
6. Pathogenesis
Virus ingested
through mouth
Multiply in Peyer’s
patches of ileum
(M cells)
Go to blood
stream
Primary viremia
(2-3 days)
Multiply in
reticuloendothelial
system
Blood stream
2° viremia then
invade CNS
7. Clinical Manifestation
The incubation period of poliovirus from
contact to initial clinical symptoms is usually
considered to be 8–12 days, with a range of 5–
35 days.
Paralysis, if it occurs, appears 3–8 days after
the initial symptoms.
8. Abortive Poliomyelitis
o In about 5% of patients, a nonspecific influenza-like
syndrome occurs 1–2 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 2–3 days. Recovery is
complete, and no neurologic signs or sequel
develop.
Clinical Manifestation
9. Nonparalytic Poliomyelitis
o In about 1% of patient presents with the
manifestations of abortive type associated with
aseptic meningitis such as neck rigidity, +ve
Kernig’s sign and Brudzinski’s sign.
o CSF shows changes of aseptic meningitis.
o The manifestations disappear 1-2 days and leave
no paralytic manifestations.
Clinical Manifestation
10. Paralyitic Poliomyelitis
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. Spinal
2. Bulbar
3. Encephalitic
Clinical Manifestation
11. 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
12. 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:
1. 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
13. 3. Encephalitis poliomyelitis
Manifestation of encephalitis are evident.
o Disturbed consciousness (from drowsiness to
coma)
o Convulsions
o Localized manifestation as blindness, deafness and
paralysis (monoplegia or hemiplegia)
Diagnosis depend on:
a) Presence of epidemic of polio
b) Isolation of the virus from CSF
c) Increase antibody titre against polio
14. 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
hypoesthesia
Loss of
sensation in
lower limbs with
sensory level
Investigation ↑ lymphocyte
↑ proteins or
↑ protein but
normal cells
Normal Normal Normal
15. 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.
16. 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.
17. 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
18. (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