Polio virus is one of the highly infectious enterovirus & responsible for endemic infection in many parts of the world. Man appears to be the only reservoir. Poliomyelitis has been eradicated in the western hemisphere & many industrialized countries. Incidence is highest in developing countries specially where immunisation coverage is low & sanitation is poor. India, Pakistan & Bangladesh have accounted for 70% of reported polio cases world wide. The disease is seasonal, occurring more frequently in summer & early autumn, in temperate climates & during the rainy season in tropical climates.
AETIOLOGY
lThere are 3 antigenically distinct serotypes-Type1, 2, 3. All 3 types cause paralysis. But type 1 has been associated with most of the major epidemics & shows the greatest propensity to cause paralytic forms of the disease.
lThe disease is spread by direct contact with the infected person through pharyngeal secretions & faeces. Infectivity is more on the early period of the disease transmission, is usually wide spread by the time of paralysis onset.
lThe virus is excreted intermittently for 2 months or more after infection, with heaviest excreation occurring just before paralysis & during 1st two weeks of onset. Faecal-oral spread is more common; oral-oral spread is also common. Rarely it may occur from oral vaccine. The most frequent cause of vaccine associated paralytic polio is type 3.
PATHOGENESIS & PATHOLOGY
lPolio viruses enter in body via oral route & multiply in the tonsillopharyngeal tissue & in the intestinal wall. From there they pass to regional lymph node & infectivity of the pharyngeal secretions disappears rapidly, from the latter viruses also pass to the appropriate regional lymph nodes but in this case there is continued excretion into the bowel. As a result polio viruses can be isolated from faeces for weeks & sometimes months.
In poliomyelitis neuronal lesions occur in the following-
lSpinal cord (anterior horn cells chiefly)
lMedulla
lCerebellum
lMid brain
lThalamus & hypothalamus
lPalladium & cerebral cortex (motor cortex)
The following areas are speared-
lCerebral cortex (except motor cortex)
lCerebellum (except vermis & deep mid line nuclei)
lWhite matter of spinal cord.
Infants acquire immunity transplacentally from
their mother. Thus immunity is usually complete
during the first 4-6 months of the life & disappears
at variable rate. Active immunity after natural
infection probably lasts for life.
CLINICAL MANIFESTATIONS
lIP: - 1-3 weeks
lTime between infection & onset of paralysis is 10-12 days. Paralytic disease occurs virtually in unimmunised children or adults. Polio virus infection may follow one of several courses-
1. Inapparent infection : -90-95% of cases
-No disease & no sequelae
2. Abortive poliomyelitis : -4-8% of cases
-Minor illness with low grade fever
-Sore throat
-Vomiting
-Abdominal pain
-Loss of appetite
-Malaise
Recovery is rapid & complete. There is no paralysis. It can not be distinguished from other mild viral infections.
3. Non-paralytic aseptic meningitis :- 1-2 % of cases.
It is manifested by headache & neck, back & or leg stiffness several days after a prodromal stage similar to abortive poliomyelitis. Cases recover within 3-10 days. It can not be distinguished from other causes of aseptic meningitis.
4. Paralytic poliomyelitis :- 0.5-1% cases.
Symptoms often occur in 2 phases-Minor & major. And are often separated by several days without symptoms.
vMinor phase: - Similar to abortive poliomyelitis.
vMajor phase: - Begins with muscle pain, spasm & return of fever. This is followed by rapid onset of flaccid paralysis which is usually completed within 72 hours (hence the term acute flaccid paralysis-AFP).
There are 3 types of paralytic form:-
i. Spinal paralytic poliomyelitis-About 79% cases of paralytic cases. Residual flaccid is usally present after 60 days.
ii. Bulbar polio-2% of cases. Cranial nerve lesions.
iii. Bulbo-spinal polio-19% of cases.
lCase fatality rate (CFR)-
- Spinal : 2.5%
- Bulbar : 25-75%
Clinical findings associate with involvement of the respiratory muscles include:-
lAnxious looking.
lInability to speak without frequent causes.
lIncreased respiratory rate.
lMovement of alae nasi & of the of the accessory muscles of the respiration.
lInability to cough & sniff with full depth.
lParadoxical abdominal movements.
lRelative immobility of Intercostal muscle.
When the arms are weak & especially when deltoid
paralysis occurs, there may be impending respiratory
paralysis, because the phrenic nerve nuclei are in adjacent
areas of spinal cord.
Clinical findings of bulbar poliomyelitis with respiratory difficulty:-
1. Nasal twang.
2. Inability to swallow smoothly.
3. Accumulation of pharyngeal secretion.
4. Absence of effective coughing.
5. Nasal regurgitation.
6. Deviation of palate, uvula or tongue.
7. Involvement of respiratory centres of medulla.
8. Paralysis of one or both vocal cords.
9. Rope sign.
INVESTIGATIONS
1. Isolation of virus
- Two stool specimens collected 24-48 hours apart & within 14 days of paralysis onset.
- Send to National Polio Laboratory at IPH, Mohakhali, Dhaka
2. CSF study-Pleocytosis (20-300 cells per mm)
3. Specific antibody
TREATMENT
lPrinciples-
1. To allay fear.
2. To minimize ensuing skeletal deformities.
3. To anticipate & meet complication.
4. To prepare the child & family for prolong treatment.
5. Others-
q Bed rest.
q Muscle pain, spasm & tenderness-Heat pack & analgesic.
q Neutral position of patient.
q Active & passive motions are indicated as soon as the pain disappears.
q Bowel & bladder care.
q Cardiovascular complication should be treated.
q Long term management of paralysis, muscle wasting & skeletal deformities
may require specific orthopaedic procedures & physiotherapy.
q Fluid & electrolyte balance should be maintained.
