2. What is Poliomyelitis?
Greek word
• poliós – “grey”
• myelós - “spinal cord”
• suffix -itis – “inflammation”
• A crippling and potentially deadly infectious disease
caused by poliovirus.
3. History
Timeline Events
ANCIENT EGYPT
3.,700 B.C
An Egyptian stele portrays a
priest with a paralyzed leg
suggesting polio existence.
1,209 B.C Mummy Giptah with an
equinus foot.
Eighteenth century
1789
First known description by
underwood
Nineteenth century
1834
First epidemic of polio in
island of St. Helena
4. Timeline Events
1855 First description by
Duchenne of the
pathological process
Twentieth century
1908
Transmission of polio to
a monkey by Landsteiner
1949 Growth of virus on tissue
culture
1951 Three types of polio virus
isolated and identified
1953 First large scale trial of
Salk
1956 First general use of Sabin
6. Global Prevalence of Polio
1975 1980 1985 1988 1990 1993 1995 2000
0
10000
20000
30000
40000
50000
60000
Recorded cases
Recorded cases
49,293
7,035
10,487
23,484
35,251
38,637
52,552
719
7. Global Prevalence of Polio
0
500
1000
1500
2000
2500
2005 2010 2011 2012 2013 2014 2015 2016 2017 2018
Recorded cases
Recorded cases
1979
74
359
416
223
650
1352
37 22 1
8. Case Breakdown 2018
Countries
Year-to-date 2018 Year-to-date 2017 Total in 2017
Onset of paralysis of
most recent case
WPV cVDPV WPV cVDPV WPV cVDPV WPV cVDPV
Afghanista
n
1 0 0 0 14 0
1-Jan-
2018
NA
Democrati
c Republic
Of The
Congo
0 0 0 0 0 17 NA
25-Nov-
2017
Pakistan 0 0 0 0 8 0
15-Nov-
2017
NA
Syrian
Arab
Republic
0 0 0 0 0 74 NA
21-Sep-
2017
16. Transmission
Fecal oral route
Direct contact with
• Infected mucus
• Droplets or saliva from sneezing or cough.
• Infected feces (The virus can remain present in the stool from 3-6 weeks).
17.
18. Pathogenesis
o Fecal-oral
o Inhalational
o infects the pharynx and intestinal
mucosa.
o Gains entry by binding to an
immunoglobulin-like receptor,
known as the poliovirus receptor or
CD155, on the cell spinal
membrane
1
•Portal of Entry
•mouth
2
•Local Multiplication
3
•Minor/Primary viremia
4
•Major/Secondary Viremia
5
•To spinal and brain
6
•Multiplies in neurons
7
•Flaccid Paralysis
8
•Destroy THEM
19. o Epithelial cells of GIT
o Lymphatic tissue- from tonsils to
Payer's patches.
1
•Portal of Entry
•mouth
2
•Local Multiplication
3
•Minor/Primary viremia
4
•Major/Secondary Viremia
5
•To spinal and brain
6
•Multiplies in neurons
7
•Flaccid Paralysis
8
•Destroy THEM
20. o Spread to reticuloendothelial
tissue (connective tissues, spleen,
liver, lungs, bone marrow, and
lymph nodes)
o no symptoms
o Enter in blood
Primary Viremia
1
•Portal of Entry
•mouth
2
•Local Multiplication
3
•Minor/Primary viremia
4
•Major/Secondary Viremia
5
•To spinal and brain
6
•Multiplies in neurons
7
•Flaccid Paralysis
8
•Destroy THEM
21. o Multiplies in reticuloendothelial
tissues
o Enters again in blood
Secondary Viremia
o occurrence of viremia occurs in 4-
8% of individuals.
1
•Portal of Entry
•mouth
2
•Local Multiplication
3
•Minor/Primary viremia
4
•Major/Secondary viremia
5
•To spinal and brain
6
•Multiplies in neurons
7
•Flaccid Paralysis
8
•Destroy THEM
22. o Entry through blood brain barrier.
o It is thought that the virus may
travel on nerve fibers,
independent of its receptor.
1
•Portal of Entry
•mouth
2
•Local Multiplication
3
•Minor/Primary viremia
4
•Major/Secondary Viremia
5
•To spinal and brain
6
•Multiplies in neurons
7
•Flaccid Paralysis
8
•Destroy THEM
23. o Multiplies selectively in the
neurons destroys the anterior
horn cells of spinal cord.
o degeneration of Nissl’s bodies.
o When degeneration becomes
irreversible phagocytized
by macrophages or leucocytes.
1
•Portal of Entry
•mouth
2
•Local Multiplication
3
•Minor/Primary viremia
4
•Major/Secondary Viremia
5
•To spinal and brain
6
•Multiplies in neurons
7
•Flaccid Paralysis
8
•Destroy THEM
24. o Lesions are in anterior horn of
spinal cord Flaccid
paralysis.
o Can cause encephalitis
Brainstem
Motor and premotor areas of
cerebral cortex
1
•Portal of Entry
•mouth
2
•Local Multiplication
3
•Minor/Primary viremia
4
•Major/Secondary Viremia
5
•To spinal and brain
6
•Multiplies in neurons
7
•Flaccid Paralysis
8
•Destroy THEM
25. 1
•Portal of Entry
•mouth
2
•Local Multiplication
3
•Minor/Primary viremia
4
•Major/Secondary Viremia
5
•To spinal and brain
6
•Multiplies in neurons
7
•Flaccid Paralysis
8
•Destroy THEM
27. Abortive Polio
• Occurrence
4-8% of infection
• Symptoms
Low grade fever
Sore throat
Vomiting
Abdominal pain
Loss of appetite
Malaise
• Recovery
Complete recovery within 2-3 days, no paralysis
28. Non-paralytic Aseptic meningitis
• Occurrence
1- 2 % of infections
• Symptoms
Headache, nausea, vomiting, pain and stiffness of back and legs.
• Signs
Tripod sign
Kiss the knee test
Head drop sign
Neck rigidity
• Recovery
within 2 – 10 days
31. Paralytic Poliomyelitis
• Occurrence
0.5 – 1% of infections
• Symptoms
2 PHASES
1. Minor- same as abortive polio
2. Major- muscle pain, spasm and return of fever followed by rapid
onset flaccid paralysis complete within 72hrs.
33. Spinal paralytic poliomyelitis
• Occurrence
Most common
80% of cases
• Symptoms
o Results from lower motor neuron
lesion of anterior horn cells of spinal cord.
o Affects muscles of legs, arms and/or trunk.
o Severe cases – quadriplegia , paralysis of trunk abdominal
and thoracic muscles.
34. Spinal paralytic poliomyelitis
• Paralysis – asymmetrical ( legs > arms),descending paralysis
• Muscles – floppy
• Reflexes diminished
• Sensation - normal
• Residual paralysis after 60 days
35. Bulbar polio
• Occurrence
Life threatening
2% of cases
• Symptoms
o Nasal twang and hoarseness of voice
o Nasal regurgitation
o Dyspnea
o Dysphagia
o Child refuses to feed
o Secretions accumulate in pharynx – aspiration
o Involvement of respiratory center - Shallow , irregular respiration
o Vasomotor center - BP rises then falls
o Pulse – rapid weak thready
o Skin – dusky red mottled
o Restless , confused and comatose
37. Polio Encephalitis
• Occurrence
Rare cases
• Symptoms
o Irritability
o Delirium
o Disorientation
o Tremors
o Convulsions
o Paralysis is of upper motor neuron type
MRI image of the brainstem of a paralyzed child,
showing brainstem encephalitis inflammation in white
(Source: Peter McMinn/Infectious
Diseases and Immunology, Sydney Medical School)
38. Residual paralysis
• Occurrence
Acute phase
Lasts for 0-4weeks
• Recovery –variable
o At 60 days mild to severe residual paralysis
o Maximum recovery – first 6 months
o Slow recovery upto 2 yrs.
o After 2 yrs. post polio residual paralysis persists throughout life
39. Diagnosis
• Based on clinical presentation
• CSF (leukocytosis, protein , normal glucose).
• Virus recovery from stool* , throat washing, & blood
samples.
• Serology for IgG (neutralizing Abs), IgM(Abs to C Ag),
Anti-D antibodies.
• Complement Fixation test( less often employed)
• PCR for viral RNA from CSF or serologically.
40. Differential Diagnosis
Most common
• GB syndrome
• Transverse myelitis
Others
• Traumatic neuritis
• Meningitis
• Encephalitis
• Toxin – diphtheria and botulism
41.
42.
43.
44. Early diagnosis and supportive treatments such as
• Bed rest
• Pain control
• Good nutrition
• Good Nursing
• Physical therapy to
prevent deformities.
52. Immunization
A Brief history of POLIO vaccine
1955 Inactivated vaccine
1961 Types 1 and 2 monovalent OPV
1962 Type 3 monovalent OPV
1963 Trivalent OPV
1987 Enhanced-potency IPV (eIPV)
1988 Global poliomyelitis eradication by WHO
56. Sabin vs. Salk
Feature Sabin’s Vaccine (live) Salk’s Vaccine (killed)
Strain Live attenuated virus Killed formalized vaccine
Administration Oral (preferred in mass campaigns) Injectable (adv. can be given with DPT)
Factors affecting efficacy Diarrheal disease preventing
colonization by vaccine virus
Not affected by these factors
Safety Safe But, cases of vaccine induced
paralysis reported
Safe
Economical More Less (because, virus content is 10,000
times more, hence costlier)
Nature of immunity Local and systemic Only systemic, no intestinal immunity -
No herd immunity
Duration Life long Periodic booster doses required
Use in epidemic Ideal Not very ideal- May promote
multiplication on 7 dissemination of
wild virus
57. Organizations working for POLIO
Eradication
Year Foundation
1985 The Pan American Health Organization
(PAHO)
1978 EPI (Extended Program of Immunization)
1988 World Health Organization, together
with Rotary International, UNICEF, and the
U.S. Centers for Disease Control and
Prevention passed the Global Polio
Eradication Initiative End Polio NOW.
1994 The Indian Government launched
the Pulse Polio Campaign.
1999 The CORE Group—with funding from
the USAID.
58. Why We Could Not Eradicate Polio From
Pakistan??
• Terrorism
• Lack of security
• Floods
• Political instability
• Bad economy