2. Introduction
Greek poliós= "grey", myelós= marrow, and the suffix -
itis= inflammation
First described by British physician Micheal Underwood in 1799
referring to it as "debility of the lower extremities.“
A viral infection most often recognized by acute onset of flaccid
paralysis.
Primarily an infection of human alimentary tract, but may infect
CNS in very small no. (i.e <1%)
Infection results in a spectrum of clinical manifestations……
3. Problem statement
World
A worldwide problem in pre vaccination era
With the wide use of polio vaccine from 1954 disease
being eliminated from most of the developed countries
In 1988 WHA resolved to eradicate the disease globally
Since than no. of endemic countries reduced from 125 in
1988 to 3 in 2012.
Reported cases worldwide decreased by 51% (1352 in
2010 to 650 in 2011)
4. Cont…
India
No reported cases since January 2011 (last
case reported in 13th Jan 2011, Howrah,
West Bengal)
Considered polio-free since February 2012
Attained the status of eradication in 13th
January 2014
6. Agent factors
Agent
Poliovirus: belongs to “Picorna” viruses which are
small RNA-containing viruses.
Three serotypes- 1, 2 & 3 giving no cross
immunity
Long survival in environment….lives upto 4hours
in water and 6 hours in faeces in cold
enviornment.
Readily destroyed by heat (e.g. pasteurization of
milk, and chlorination of water).
7. Reservoir of infection
Man is the only reservoir of infection of poliomyelitis.
Man: cases and carriers
Cases: all clinical forms of disease
Most of the infections are subclinical- dominant role in spread of
infection
Estimated subclinical infection ranges from 75 to 1000 per clinical case
No chronic cases or animal sources documented
Foci of infection
Pharynx: the virus is found in the oropharyngeal secretions.
Small intestine: the virus finds exit in stools.
8. Modes of transmission
Since foci of infection are the throat and small intestines,
poliomyelitis spreads by two routes:
Oral-oral infection: direct droplet infection
Faeco-oral infection:
– Through contaminated foods. Vehicles include milk, water, or any
others that may be contaminated by handling, flies, dust….
– Hand to mouth infection.
Polio virus has the ability to survive in cold environments.
Overcrowding and poor sanitation provide opportunities for
exposure to infection
9. Period of communicability
Estimated to about 2 weeks
Cases: 7 to 10 days before and after the onset of symptoms.
Virus is excreted commonly for 2 to 3 weeks, sometimes as
long as 3 to 4 months in faeces.
In polio cases, infectivity in the pharyngeal foci is around one
week, and in the intestinal foci 6-8 weeks.
Incubation Period: 7-14 days
10. Host factors
Age:
All age groups; children(6 MONTHS TO 3 YEARS most susceptible)
more than 95% reported in infancy and childhood with over 50% of them
in infancy.
Sex:
no sex ratio differences, but in some countries, males are infected more
frequently than females in a ratio 3:1.
Risk factors:
Fatigue, trauma,im injections, tonsillectomy, immunizing agents like alum
containing DPT vaccine and excessive muscular exercise…
Immunity:
Immunity by maternal antibodies till the age of 6months
Immunity conferred by natural infection fairly solid but doesn’t protects
against the reinfection by other strains
11. Environmental factors
Rainy season (june to september)
Environmental sources- food, flies and water
Overcrowding and poor sanitation-
oppourtinities
13. Inapparent infection
Occurs approximately in 91-96% of poliovirus infection.
Incidence is more than 75 to 1000 times the clinical
cases.
No clinical manifestations, but infection is associated
with acquired immunity.
Recognition only by virus isolation or rising antibody titre.
14. Clinical poliomyelitis
Abortive polio (minor illness):
Occurs approximately in 4-8% of the infection.
Causes only a mild or self limiting illness due to
viraemia.
Mild systemic manifestations for 1-2 days
Some abortive cases so mild to pass unnoticed.
Patient recovers quickly.
Manifestations:
Moderate fever
Upper respiratory manifestations: pharyngitis and sore throat
Gastrointestinal manifestations: vomiting, abdominal pain,
and diarrhea.
15. Cont…..
Involvement of the CNS (major illness):
Affects a small proportion of the clinical cases
Takes two forms: Non-paralytic and Paralytic polio.
Non paralytic polio:
Occurs approximately in one per cent of all infections.
Presenting features are stiffness and pain in neck and back.
Disease lasts for 2-10 days.
Recovery is rapid.
16. Cont…
Paralytic polio:
Occurs in less then one per cent of infections.
The virus enters the CNS and causes varying degree of disability
with destruction of the motor nerve cells, but not the sensory
nerve cells.
Forms: spinal, bulbar, and bulbospinal.
Paralysis usually appears within 4 days (around 7-10 days from
onset of disease).
History of fever at the time of paralysis- suggestive of polio.
Progression of paralysis reaches maximum by 4th day (4-7 days)
17. Cont….
Other symptoms- malaise, anorexia, vommiting, headache, sore
throat, constipation and headache.
Signs of meningeal irritation
Tripod sign may be present
Assymetrical, patchy flaccid paralysis, of descending type
affecting the proximal group of muscle the most
Deep tendon reflexes (DTR) deminished before the the onset of
paralysis.
Cranial nerve involvement seen in bulbar and bulbospinal
paralytic poliomyelitis
Facial assymetry, difficulty in swallowing weakness of voice;
respiratory insuffiency may lead to death
18.
19. Spinal polio
Different spinal nerves are involved
Injury of the anterior horn cells of the spinal cord
causing tenderness, weakness, and flaccid
paralysis of the corresponding striated muscles.
The lower limbs are the most commonly affected.
20. Bulbar polio
Nuclei of the cranial nerves are involved, causing
weakness of the supplied muscles, and maybe
encephalitis.
Bulbar manifestations include dysphagia, nasal voice,
fluid regurgitation from the nose, difficult chewing, facial
weakness and diplopia
Paralysis of the muscles of respiration is the most
serious life-threatening manifestation.
Bulbospinal polio
Combination of both spinal and bulbar forms
22. Complications and case fatality
Respiratory complications: pneumonia, pulmonary edema
Cardiovascular complications: myocarditis, cor pulmonale.
Late complications: soft tissue and bone deformities,
osteoporosis, and chronic distension of the colon.
Case fatality: varies from 1% to 10% according to the form
of disease (higher in bulbar), complications and age (
fatality increases with age).
23. Diagnosis and laboratory testing
Laboratory studies critical to rule out or confirm the
diagnosis of paralytic poliomyelitis.
Virus isolation
The likelihood of poliovirus isolation is highest from stool
specimens,
Intermediate from pharyngeal swabs, and very low from blood
or spinal fluid.
Serologic testing
A four-fold titer rise between the acute and convalescent
specimens suggests poliovirus infection.
25. Cont….
Seroprophylaxis by immunoglobulins:
Not a practical way of giving protection
because it must be given either or before or
very shortly after exposure to infection.
Dose-(0.25-0.3 ml/kg of body weight).
Immunized status after a few weeks
26. Active immunization
Inactivated (Salk) vaccine
Contains 3 serotypes of vaccine virus
Route of administration-intramuscular/ Subcutaneous.
Schedule
First dose given at the age of 6 weeks
Next 2 doses 1-2 months apart
4th dose after 6-12 month of 3rd dose
Additional doses prior to school entry
Repeated doses every 5 year after that till age of 18
Highly effective in producing immunity to poliovirus
>90% immune after 2 doses
>99% immune after 3 doses
Duration of immunity not known with certainty
27. Cont…
Oral (Sabin) Polio Vaccine
Contains 3 serotypes of vaccine virus
Route of administration-intramuscular/ Subcutaneous.
Schedule
Zero dose vaccination recommended in hospital delivery
First dose given at the age of 6 weeks
Next 2 doses 1-2 months apart
One booster dose 12-18 months later recommended
Highly effective in producing immunity to poliovirus
50% immune after 1 dose
>95% immune after 3 doses
Immunity probably lifelong
Shed in stool for up to 6 weeks following vaccination
28. Salk versus Sabin vaccine
IPV (Salk) OPV (Sabin)
killed formolised virus
Given SC or IM
Induces circulating antibodies, but
not local (intestinal immunity)
Prevents paralysis but does not
prevent reinfection
Not useful in controlling epidemics
More difficult to manufacture and is
relatively costly
Does not require stringent conditions
during storage and transportation. Has
a longer shelf life.
live attenuated virus
given orally
immunity is both humoral and
intestinal. induces antibody quickly
Prevents paralysis and prevents
reinfection
Can be effectively used in controlling
epidemics.
Easy to manufacture and is cheaper
Requires to be stored and
transported at subzero temperatures,
and is damaged easily.
29. Epidemiological Investigations
Epidemic
Occurrence of 2 or more local cases caused by the same virus in any
4-weeks period
Sample of faeces to be collected from all the cases and suspected
cases and subjected to lab testing
If possible, paired sera to be tested
– First specimen at the clinical suspicion
– Second at the period of convalescence
An increase in antibody titre provides confirmatory evidence
OPV should be provided to all persons over 6 weeks age who are not
completely immunize de or immune status unknown in the epidemic
area