1. POLIOMYELITIS
DR (MRS) M.B. FETUGA

2. POLIOMYELITIS
Poliomyelitis is an infective disease caused by an enterovirus called Poliovirus.
Other enteroviruses are echoviruses and coxsachie viruses.
There are 3 antigenically distinct types of the virus known as Types 1, 2 and 3 with no cross immunity.
DR (MRS) M.B. FETUGA

3. EPIDEMIOLOGY
Polio has been largely eliminated from the developed world with vaccination. Presently, Nigeria is one of the 5 major countries in the developing world where Polio wild virus is still widely seen.
More than 90% of the world polio cases are found in Nigeria, particularly, the northern states.
Infants and young children are predominantly affected: more than 90% of victims are less than 3 years of age at the onset of paralysis.
DR (MRS) M.B. FETUGA

4. PATHOGENESIS 1
The neuropathy of poliomyelitis is due to direct cellular destruction. Secondary immunologic damage may also occur.
In poliomyelitis, neuronal lesions occur mostly in the (1) spinal cord (chiefly in the anterior horn cells) (2) medulla (vestibular nuclei, cranial nerve nuclei, and the reticular formation, which contains the vital centers controlling respiration and circulation) (3) motor part of the cerebellum.
The cerebral cortex is usually spared.
DR (MRS) M.B. FETUGA

5. PATHOGENESIS 2
The polio virus, like other enteroviruses, is acquired through the gastrointestinal tract. From the epithelial tract, the virus invades the lymphoid tissue from where viraemia occurs.
Infants acquire immunity from their mothers transplacentally but this wanes after 6 months.
Active immunity develops after natural infection and it persists for life.
DR (MRS) M.B. FETUGA

6. NATURAL HISTORY OF POLIO
Poliovirus infections may follow one of several courses:
subclinical inapparent infection, which occurs in 90–95% of cases and causes no disease and no sequelae.
abortive poliomyelitis.
nonparalytic poliomyelitis.
paralytic poliomyelitis.
DR (MRS) M.B. FETUGA

7. CLINICAL PRESENTATION 1
Subclinical- About % of infections.
No symptoms but viral replication in the GIT and lymphoid tissues are going on.
Abortive Polio occurs in about 4 – 8% of cases. It is a brief non-specific febrile illness characterised by features of URT and GIT infections like anorexia, cough, diarrhoea, nausea, vomiting, malaise, sore throat, constipation and abdominal pain (unlocalized). Pharynx often appears normal despite complaints of sore throat. No CNS involvement. It may progress to the non-paralytic form after a transient recovery of 2 – 5 days.
DR (MRS) M.B. FETUGA

8. CLINICAL PRESENTATION 2
Non-paralytic Polio (aseptic meningitis):
-The symptoms are exactly as described under Abortive Polio but the headache, nausea and vomiting are more severe. In addition the patient has features of meningeal irritation (vomiting, headache, nuchal rigidity, positive kernig and brudzinski signs). Constipation-frequent, fleeting paralysis of the bladder-not uncommon.
-This meningitic illness is followed by complete recovery within 2 weeks of onset. No paralysis occurs.
DR (MRS) M.B. FETUGA

9. CLINICAL PRESENTATION 3
Paralytic Polio: This is the least common (less than 1%). Initial symptoms are same as for non- paralytic plus weakness of one or more muscle groups – skeletal or cranial with or without bladder paralysis. Bowel atony is common
DR (MRS) M.B. FETUGA

10. CLINICAL PRESENTATION 4
Sudden flaccid paralysis follows fever and pain or tenderness over the affected muscle occurs within 3 to 4 days.
No sensory loss but muscle atrophy-(due to denervation + atrophy of disuse), hypotonia and loss of tendon reflexes also occur. Paralysis is usually precipitated by trauma and exertion of the affected muscles.
DR (MRS) M.B. FETUGA

11. CLINICAL PRESENTATION 5
Paralysis may be Spinal (muscles supplied by spinal nerves), Bulbar (muscles supplied by cranial nerves) and Bulbospinal (combination of the two groups of nerves).
Spinal paralysis-
-weakness of some of the muscles of the neck, trunk, diaphragm, thorax or extremities.
- usually affects one lower limb (49.6% at -Ibadan).
- both lower limbs (26.9% at Ibadan).
-Usually asymmetrical.
DR (MRS) M.B. FETUGA

12. CLINICAL PRESENTATION 6
Bulbar paralysis- (weakness in the motor distribution of one or more Cranial nerves with or without dysfunction of the vital centres of respiration & circulation) characterised by drooling of saliva, dysphonia, dysphagia, stridor and respiratory and cardiac arrhythmias is rare.
DR (MRS) M.B. FETUGA

13. CLINICAL PRESENTATION 7
Encephalitic form- characterized by irritability, disorientation, drowsiness.
Hypoxia & hypercapnia may produce disorientation without true encephalitis
DR (MRS) M.B. FETUGA

14. DIAGNOSIS
Polio should be suspected in any un-immunized or incompletely immunized child with a febrile illness associated with sudden flaccid paralysis without sensory loss.
Viral culture from stool and nasopharyngeal secretions.
CSF shows raised pressure, cell count 50 – 250 /mm3 , initial polymorphonuclear pleocytosis followed after about a week by lymphocytosis, minimally raised protein and normal glucose levels.
Serology – four-fold rise in antibody titre.
DR (MRS) M.B. FETUGA

15. MANAGEMENT This is mainly symptomatic.
Antibiotics are useless since it is viral.
Bed rest till fever has abated OR over the ensuing 2 weeks may reduce the chances of paralysis.
Acetaminophen for pain.
Use of warm moist packs may relax muscles.
Skin care to prevent bed sores.
Physiotherapy to prevent contractures (proper body positioning, active motion, use of assistive devices).
DR (MRS) M.B. FETUGA

16. PROGNOSIS
Mortality data is not readily available in the developing world.
Most deaths occur within the first 2wk after onset.
In general, the more extensive the paralysis in the first 10 days of illness, the more severe is the ultimate disability.
Unexpected improvement may appear soon after defervescence and again about 6wk after onset, a time that corresponds to functional restoration of temporarily inactive neurons.
The degree of functional recovery also depends upon the adequacy and promptness of supportive therapy.
DR (MRS) M.B. FETUGA

17. PREVENTION
Oral Polio vaccine (Sabin) is a live attenuated vaccine. It still widely used in Nigeria like most other developing countries. Its main advantage is the tendency to increase herd immunity from GIT losses to the environment but paralytic disease may follow its use.
Four doses of OPV are given between birth and 14 weeks. Multiple pulsatile doses are also administered on all Under-5s during Polio eradication campaign known as NID.
The injectable vaccine (Salk) is routinely used in the developed world because it does not cause paralytic disease and the disease has been largely eliminated in those countries.
DR (MRS) M.B. FETUGA