acute flaccid paralysis and surveillance

AFP AND SURVEILLANCE

AFPA 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.

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

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.

D/D OF AFP

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.

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.

Diagnosis by isolation of pathogen from stools.CSF – neutrophilic pleocytosis

lymphocytes and monocytes

Protein content raises over time,becomes normal by 6 weeks.

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.

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.

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 )

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

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)

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.

CSF shows albumino-cytological dissociation.

Electrophysiology shows demyelination of peripheral nerves.

Slow or block of Nerve conduction velocity.

MRI is normal.

Clinical variants

1–Polyneuritis cranialis Cranial nerve involvement2–Miller fisher syndrome Ophthalmoplegia, ataxia, areflexia3–Chronic progressive GBS Symptoms persisting more than 6 weeks4- Chronic relapsing GB

Differentiation from spinal cord syndrome

Absence of sensory level

Lack of spinal tenderness

Normal bowel and bladder function

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.

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.

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

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% .

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.

Diagnostic criteria

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.

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.

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.

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.

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.

Low fatality rate.Paralysis resolves with time.Early administration of antitoxin(im/iv)

neutralizes the exotoxin.

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.

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.

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

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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.

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’

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

Intratypic differentiation test is done to determine whether the particular isolate is wild poliovirus or vaccine poliovirus.

All wild poliovirus isolates undergo genetic sequencing.

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.

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