Acute poliomyelitis

ACUTE POLIOMYELITIS DR. NATARAJ PL

CLINICAL DIAGNOSIS (WHO CASE DEFINITION)

“ A case of poliomyelitis is defined as any child under fifteen years of age with acute flaccid paralysis or any person with paralytic illness at any age when polio is suspected”

Cycle of infectionAgentPoliovirus : three serotypes (P1, P2, P3) with different

antigenicity The virus can live in water for three months and in the

faeces for six months.The poliovirus is rapidly inactivated by heat,

formaldehyde, chlorine and ultraviolet light.

Reservoir

Cases : clinical & subclinical plays a role in the spread of

infection

Carriers: faecal temporary. There is no chronic carrier.Source of infection:Faeces and pharyngeal secretions of the infected person

Person Age and sex: In developing countries Poliomyelitis is a

disease of young children and adolescents In developed countries adults were

affected more commonly than children with increased both the disease severity and deaths.

Sex difference have been noticed in the ratio of three male to one female

TimePoliovirus infection typically peaks in the

summer months.

Man is the only reservoir

TIME COURSE OF POLIOVIRUS INFECTION

Mode of transmission

1-Feaces (feco-oral): in areas with lack of personal hygiene

especially in young children in developing countries. It results in

infection not paralysis.

2-Droplet : in developed countries with high standard of

sanitation, droplet is common mode of transmission during the

acute phase of the disease when the virus is in the throat.

3-Direct contact with respiratory discharge

4- Common vehicle: ingestion of food or drink contaminated with

faeces

5- Indirect contact with articles contaminated with pharyngeal

discharge of infected person. Inlet The mouth and nose

PATHOGENESIS OF POLIO VIRUS INFECTION

IMMUNITY IN POLIO

Transplacentally acquired passive immunity

After natural infection After immunisation Local immunity

IMMUNITY TO POLIOVIRUS INFECTION Exposure to poliovirus initiates a complex

process that eventually results in both humoral (systemic) and mucosal (local) immunity.

Poliovirus infection provides lifelong immunity against the disease, but this protection is limited to the particular type of poliovirus involved (Type 1, 2, or 3)

Thus, infection with one type does not protect an individual against infection of the other two types. IgM and IgG antibodies are detected in the serum as early as 1-3 days following natural infection but disappears after 2-3 months.

POLIOMYELITIS: RISK FACTORS

Immune deficiency Pregnancy Poor sanitation and hygiene Poverty Unimmunized status, especially if <5 years Tonsillectomy: a risk factor for bulbar paralysis. Intramuscular injections or truama

Genetics: No genetic susceptibility has been identified.

RESPONSE TO INFECTION

ABORTIVE POLIOMYELITIS

5% cases Influenza like symptoms 1-2 weeks

later Lasts only for 2-3 days Clinical examination unremarkable Complete recovery

NON PARALYTIC POLIOMYELITIS

1% cases Initial minor illness-headache, nausea,

vomiting, soreness and stiffness of neck muscles, fleeting paralysis of bladder and constipation

Short symptom free interlude Major illness

NON PARALYTIC POLIOMYELITIS

Nuchal and spinal rigidity are hallmark Tripod sign, Kiss the knee Neck rigidity, Kernigs sign Head drop Reflexes usually normal Changes in reflex indicate impending

paralysis

PARALYTIC POLIOMYELITIS-SPINAL

2nd phase of the illness Spotty paralysis Asymmetric flaccid paralysis One leg most common followed by one

arm Absent DTRs


Absent DTRs No sensory deficits Full picture by 3 days. Usually no

further progression Bowel and bladder dysfunction Older age and provocation paralysis

the biphasic illness is not seen


Recovery is slow starting after several weeks of the disease, but usually within 6 months

If not then residual paralysis Recovery may continue for as long as

18 months Atrophy, deformity and failure to grow

PARALYTIC POLIOMYELITIS-BULBAR

Nasal twang to voice and nasal regurgitation of food

Inability to swallow and pooling of oral secretions

Palatal and tongue involvement Vocal cord palsy

PARALYTIC POLIOMYELITIS-BULBAR

Vital centers in medulla being involved Ascending paralysis Autonomic disturbances Recovery is variable

PARALYTIC POLIOMYELITIS-ENCEPHALITIS

Involvement of higher centers Seizures,coma,spastic paralysis Peripheral & cranial nerve palsies Respiratory paralysis-due to variety of

possibilities

CLINICAL EVOLUTION

POLIOMYELITIS: COMPLICATIONS

Urinary tract infection Skin ulcers Traumatic injuries to affected limb(s) Atelectasis & Pneumonia Myocarditis Postpoliomyelitis progressive muscular atrophy. Postpoliomyelitis motor neuron disease. Respiratory muscle involvement and death

POLIOMYELITIS: DIAGNOSIS Based on the clinical presentation. Cerebrospinal Fluid: Leukocytosis, Increased protein, Normal glucose.

Virus recovery from stool, throat washing, blood. Virus recovery from stool is essential to diagnosis. Obtain stool, blood and throat samples for viral serology,

demonstrating a four fold rise in IgG is helpful but not always easy.

Positive IgM is diagnostic. Polymerase chain reaction amplification of poliovirus

RNA from CSF or serologically, by comparing viral titers in acute and convalescent sera.

DIAGNOSIS…CONT

Electrodiagnostic investigations reveal normal sensory nerve studies.

Motor nerve studies: show normal to mildly slowed conduction

velocities and low to normal amplitudes. MRI may be helpful to evaluate involvement of

anterior horn of the spinal cord or other findings.

DIFFERENTIAL DIAGNOSIS

Guillain-Barre syndrome Diphtheric paralysis Botulism Myasthenia Gravis Polymyositis & Viral myositis Transverse Myelitis Spinal cord compression Hypokalemic periodic paralysis

Polio GBS TN TM

Etiology Polio type 1,2,3 viruses Immunologic Trauma Unknown-multiple viruses

Onset of paralysis 24-48hrs Few hrs -10 days Few hrs -4 days Few hrs -4 days

Fever at onset High at onset of paralysis Not common Before during or after paralysis

Rarely present

Flaccid paralysis Acute asymmetric,proximal Acute,symmetrical,distal

Acute asymmetrical ,only onelimb

Acute symmetrical involving LL

CNS involvement Only Bulbar involvement In MF syndrome Absent Absent

Respiratory insufficiency

Only Bulbar involvement In severe cases Absent Absent

Autonomic nervous system

Plus Rare May be present May be present

CSF High WBC’s; Normal to Slightly elevated protein

< 10 WBC’s; High Protein

Normal Normal Count; Normal to Slightly elevated protein

Bladder Involvement Absent Transient Never Present

EMG (@ 3 weeks) Abnormal Normal Normal Normal

Nerve Conduction(@ 3 weeks)

AHC disease Abnormal demyelination

Abnormal (Axonil damage)

Normal or Abnormal

Scquelae (3 months – 1 year)

Severe asymmetrical atrophy Symmetrical atrophy of distal muscles

Moderate atrophy (affected limbs)

Flaccid diplegia

TREATMENT-ABORTIVE

Analgesics & sedatives Bed rest Nutrition Avoid exertion & IM injections

TREATMENT-NON PARALYTIC

Above mentioned methods Hot packs & hot tub baths Firm bed Foot board or splint Gentle physical therapy

TREATMENT-PARALYTIC

Care of bowel & bladder Increased fluid intake Care of airway & secretions Monitor vital signs Ventilation Tracheostomy

OUTCOME

Complete recovery in abortive & non paralytic polio

60% mortality in bulbar polio & 5% in spinal polio

Recovery beyond 6 months is unlikely

Four different oral polio vaccines are available to stop polio transmission. From left to right: mOPV3, mOPV1, bOPV and OPV

ORAL POLIO VACCINE

Contains 3 serotypes of vaccine virus Grown on monkey kidney (Vero) cells Contains magnesium sulfate,

phenolphthalein Heat sensitive – to be stored at –200 c Stored at 2-80 c during administration VVM on the vial

ORAL POLIO VACCINE

Shed in stool for up to 6 weeks following vaccination – Herd immunity

Seroconversion rates of 73%, 90% and 70% for 1, 2, 3 serotypes after 3 doses

4 doses in the first year of life and boosters-IAP recommendation

Type 2 serotype disappears first with immunisation

Used in pulse polio programme

ORAL POLIO VACCINE-ADVERSE REACTIONS

Vaccine associated paralytic poliomyelitis(VAPP)-250 to 800 cases annually-1/5 million doses

Most common by type2 (type 3 as per Nelson and Park)

Circulating vaccine derived polio viruses (cVDPV)-out breaks of paralytic polio

Differences between IPV and OPV

Killed formalised virus Live attenuated

SC/IM Oral

Circulating AB +, NO INTESTINAL IMMUNITY

HUMORAL+ INTESTINAL

Prevents paralysis but not re-infection

Prevents paralysis and intestinal re-infection

No use epidemics Useful

Can be given in HIV, no VAPP VAPP +,not in immunocompromised

No stringent storage conditions, longer shelf –life

Stored and transported at sub-zero

No herd immunity Herd immunity +

VACCINE VIAL MONITOR

3 = bad:Don’t Utilize

4 = bad:Don’t Utilize

The central square is equal to, or darker than the surrounding circle

X

X

1 = good:Utilize

2 = good:Utilize

The central square is lighter than the surrounding circle

POLIO IS SUITABLE TO BE ERADICATED FOR THE FOLLOWING REASONS

Polio only affects humans, there are no known animal reservoirs

An effective, inexpensive vaccine is available: Oral Polio Vaccine (OPV)

Immunity is life long There are no chronic carriers Half life of excreted virus in the sewage is

48hrs ( spread occurs only during this period)

AFP SURVEILLANCE

AFP is defined as sudden onset of weakness and floppiness in any part of body in a child <15 years or paralysis in a person of any age in whom polio is suspected

Background rate of AFP 1/1,00,000 children is minimum

AFP SURVEILLANCE

Case notification and investigation –within 48 hours

2 stool samples 24 hours apart within 2 weeks (upto 60 days)

Outbreak response immunization Active case searching Hot cases identification

AFP SURVEILLANCE

Collection of stool samples Transportation Eight national laboratories 60 day follow up

AFP SURVEILLANCE – STRATEGIES

High coverage of routine immunization Supplemental doses of OPV Surveillance of AFP cases Conducting mop-up vaccination

campaigns

AFP SURVEILLANCE – VIROLOGICAL CLASSIFICATION

BEFORE A WHO REGION CAN BE CERTIFIED POLIO-FREE, THREE CONDITIONS MUST BE SATISFIED:

There are at least three years of zero polio cases due to wild poliovirus;

Disease surveillance efforts in countries meet international standards; and

Each country must illustrate the capacity to detect, report and respond to “imported” polio cases

WHAT IS POST POLIO SYNDROME ? It is the late manifestation of acute paralytic polio. 25-40% of people who had paralytic polio15-40yr previously. They show symptoms of muscle and joint pain, general

fatigue and weakness. Three indications of PPS: A. Previous diagnoses of polio B. Long interval following recovery: people usually live long but effect can occur during 30-35 years after the diagnoses.

C. Gradual onset: weakness that tends to be perceptible until it interferes with daily activities.

CRITERIA FOR DIAGNOSIS OF POST POLIO SYNDROME

A prior episode of paralytic poliomyelitis.

EMG evidence of longstanding denervation.

A period of neurologic recovery and functional stability preceding the onset of new problems (Usually >20 years).

STRATEGIES OF POLIO ERADICATION

There are four core strategies to stop transmission of the wild poliovirus

A-Routine immunization of infants B-Supplementary immunization

National immunization days ( EPI)Mopping up immunization ( EPI)

C- Surveillance Acute flaccid paralysis and mop-up vaccination campaigns.

D-An effective virological laboratory

REVERSE COLD CHAIN Sister kennys treatment Why PPI during nov-feb Brunhilde, lansing and lean WPV2 is not reported since 1999 Mc -1,VAPP-3

Thank you

Health & Medicine

Acute poliomyelitis