AFP surveillance is critical for global polio eradication. All cases of acute flaccid paralysis in children under 15 are investigated to differentiate between polio and other causes like Guillain-Barre syndrome, transverse myelitis, traumatic neuritis, and post-diphtheritic polyneuropathy. Stool specimens are collected from AFP cases and tested to isolate poliovirus. If wild poliovirus is isolated, the case is confirmed as polio. Surveillance ensures rapid detection of wild poliovirus circulation.

1. AFP AND SURVEILLANCE

2. AFP
A clinical syndrome characterized by
 rapid onset of weakness of limbs
 accompanied by weakness of respiratory
muscles and difficulty in swallowing
 progressing to maximum severity within
1 to 10 days.

3.  AFP is defined as sudden
onset of weakness of a limb or
paralysis over a period of 15
days in a child less than 15
years.
GLOBAL POLIO ERADICATION INITIATIVE

4. CAUSES
Results from involvement at any point in the
motor unit.
Common causes include
GBS,poliomyelitis,transverse myelitis,traumatic
neuritis,nonpolio enteroviral illnesses,post
diphtheritic neuropathy.

5. D/D OF AFP

7. POLIOMYELITIS
 Highly infectious enteroviral disease.
 Virus transmitted through faeco-oral route 
multiplies in the intestine  invades the nervous
system  causes paralysis.
 Age at onset <5 years.
 Presents as acute febrile viral meningitis syndrome
with meningeal signs,headache,malaise,GI symptoms.

8.  Motor signs develop within 1 to 4 days
-start with severe myalgias.
-asymmetric.
-lumbar involvement > cervical.
-spinal cord involvement > brainstem.
-no sensory deficit.
-paralysis within 1 – 2 weeks.
-atrophy appears rapidly,
progresses over several weeks.

9. Diagnosis by isolation of pathogen from
stools.
CSF – neutrophilic pleocytosis
lymphocytes and monocytes
Protein content raises over time,becomes
normal by 6 weeks.

10. Electrophysiology studies to differentiate polio
from GBS (acute denervation,reduced compound
action potentials.)
MRI shows increased T2 weighted signal in
anterior horns and cord swelling.

11. Polio like illness due to non polio
viruses
Non-polio entero viruses like coxsackie
A7,enterovirus 71,japanese B virus,westnile
virus,tick borne encephalitis cause damage to
anterior horn cells resulting in AFP.

12. GUILLAIN-BARRE SYNDROME
 Immune attack (IgM,IgG,macrophages,complement
activation) directed at schwann cells,myelin
demyelination.
 Axonal injury is secondary to pathological events of
demyelination ( bystander injury )
 Synonymous with acute inflammatory
demyelinating polyneuropathy ( AIDP )

13. Two patterns of axonal involvement
- Involving both sensory and motor neurons
(acute motor-sensory axonal neuropathy)
- Involving only motor neurons
(acute motor axonal neuropathy)

14. Age at presentation - >3years .
M>F .
An antecedent infectious disease with
CMV,EBV,HIV,vaccinia virus,
campylobacter jejuni diarrhoea,
vaccinations precede AIDP.
(3days – 6 weeks before the onset of symptoms)

15. Motor + sensory symptoms
(hypo/hyperesthesia)+ ataxia.
Autonomic symptoms in 30%.
Present with pain in the back,thighs and legs
along with motor weakness starting in legs and
ascending upwards.
Maximal weakness within 2 weeks.
Areflexia/hyporeflexia.
Atonia/hypotonia.

17. CSF shows albumino-cytological dissociation.
Electrophysiology shows demyelination of
peripheral nerves.
Slow or block of Nerve conduction velocity.
MRI is normal.

18. Clinical variants
1–Polyneuritis cranialis
Cranial nerve involvement
2–Miller fisher syndrome
Ophthalmoplegia, ataxia, areflexia
3–Chronic progressive GBS
Symptoms persisting more than 6 weeks
4- Chronic relapsing GB

19. Differentiation from spinal cord
syndrome
Absence of sensory level
Lack of spinal tenderness
Normal bowel and bladder function

20. Treatment
 IVIG given (2g/kg/day over 2 days).
-As early as the diagnosis is made.
-A/E : mild flu like symptoms,nausea,headache,malaise.
 Plasmapheresis is equally effective.
- 5 exchanges of 50 ml plasma/ kg on alternate days (10
days course).
-Cannot be done in patients with cardiovascular
compromise.
 Trial of immunosuppressives,corticosteroids.
 Supportive treatment and treatment of complications.

22. Outcome
• Regressive : 90 % of patients make a good
recovery
Recovery begins 2 to 4 weeks after
progression stops starting from the last
muscles affected till lower limb ( descending
pattern .)
• Chronic Relapsing: Less than 5% of patients.
• Mortality: 3% die from complications.

23. TRANSVERSE MYELITIS
Caused by inflammation of the spinal cord.
In 60% unknown
In 40% , associated with autoimmune
disorders such as:
– multiple sclerosis
– neuromyelitis optica
– systemic lupus erythematous
– Sjogren’s syndrome
– sarcoidosis

25. In children <3 years and between 5-14 years.
H/O vaccination with OPV,MMR,Hep
A,DPT,influenza,varicella,Jap B,HiB in the
preceding month.
Earliest symptom is sensory loss or pain in the
back,thighs,legs.
Sudden onset of progressive weakness of legs.
Ascends leading to flaccid quadriplegia.
Bowel bladder involvement in 70% .

26.  Maximal weakness by 48hrs.
85% showed a sensory level.
Cranial nerves not involved.
Normal EMG,NCV.
MRI shows focal areas of >> T2 signals in the
cord.
Elevated wbc’s , high IgG index in CSF.

27. Diagnostic criteria

28. Treatment
Methyl prednisolone (1g/1.73 sq m) iv daily
for a period of 3-5days
Oral prednisolone tapered over 2-3 weeks.
IVIG,immunosuppressants in non responders.

29. Outcome
 Residual disabilities of
gait,numbness,bladder dysfunction persist in
40-75% of the cases even after many years.
 Better outcome if early time of diagnosis,
lower anatomic level,
involvement of only few spinal segments,
older age at onset,
lack of leucocytes in CSF.

30. TRAUMATIC NEURITIS
• Inflammation of a nerve following an injury.
• Sciatic nerve injury leading to paralysis of the
foot and permanent sequelae following
intramuscular injection in the gluteal region is
common.

31. POST DIPHTHERITIC POLYNEUROPATHY
 Vaccine preventable illness caused by
exotoxin producing strains of
Corynebacterium diphtheriae.
Initial symptoms of low grade fever,sore
throat,neck swelling,nasal twang,ipsilateral
palatal paralysis.
Polyneuropathy occurs as a complication in
20% of patients.
Due to higher release of exotoxin.

32. The time between initial symptoms and onset
of polyneuropathy is termed as latency
period.
Classic features include acute flaccid
paralysis,reduced/absent DTR,sensory
symptoms.
Onset of paralysis is 4 – 6 weeks after the
onset of bulbar signs and symptoms.

33. Low fatality rate.
Paralysis resolves with time.
Early administration of antitoxin(im/iv)
neutralizes the exotoxin.

34. AFP SURVEILLANCE
Poliomyelitis is targeted for eradication.
Highly sensitive surveillance including
immediate case investigation and specimen
collection are critical for the detection of wild
poliovirus circulation and for documenting the
absence of poliovirus circulation for polio-free
certification.

35.  All patients with acute flaccid paralysis should be reported to
Surveillance Medical Officer of World Health Organization.
 Every case of AFP within the last 6 months has to be reported.
 Additionally, other conditions which need notification are:
• Isolated facial palsy
• Isolated bulbar palsy
• Unproved hypokalemia
• Neck flop
• Floppy baby
• Flaccid hemiplegia
• Encephalitis
• Postictal weakness (Todd’s paralysis)
• Postdiphretic polyneuritis.

36. Cases are investigated
immediately, usually
within 48 hrs of
notification, by a trained
medical officer
-Detailed medical history,
examination & investigations are
done
- Collection & transportation of
stool specimens
- Search for additional cases &
outbreak response in affected
community
- 60 days follow up examination
- Analysis of laboratory results
- Case classification
AfterconfirmingthecasesasAFP

37. Stool Specimen Collection
For every cases of AFP,
2 stool specimens are collected (at least 24
hours apart)
Ideally within 14 days of onset of paralysis
(optimal time period for detection of polio virus)
Should also be collected in any late-reported AFP
case upto 60 days from the day of onset of
paralysis.

38. Voided stool sample is preferred.
 Each specimen should be 8 g each.
 Enema or purgatives are not recommended.
Collected in a clean, dry, screw-capped
container.
Labelled and transported in the ‘cold chain’

39. Poliovirus Isolation
2 types of cell lines are used:
– RD cell lines (derived from human rhabdomyosarcoma;
favour the growth of all enteroviruses)
– L20B cell lines (favour the growth of only poliovirus)
If cytopathic effects appears in L20B cell line,
the isolate then goes for neutralization test to
determine the serotype (type 1,2 or 3) of the
poliovirus by using appropriate antisera

40. Intratypic differentiation test is done to
determine whether the particular isolate is
wild poliovirus or vaccine poliovirus.
 All wild poliovirus isolates undergo genetic
sequencing.

41. A case is classified as polio if wild poliovirus is
isolated from the stool specimen.
Others undergo additional investigations & are
classified as compatible with polio or
discarded as nonpolio AFP.

42. THANK YOU !