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Name:Nurzawani Binti Shamsudin
Matric No: 0918424
POLIOMYELITIS
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, 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
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
Epidemiology
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
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.
 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
 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
 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
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:
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
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
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
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
Poliomyelitis

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Poliomyelitis

  • 1. Name:Nurzawani Binti Shamsudin Matric No: 0918424 POLIOMYELITIS
  • 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