Poliomyelitis (Child)

1. Clinical Overview

Poliomyelitis (polio) is an acute viral infection caused by poliovirus, a human enterovirus belonging to the Picornaviridae family. While the majority of poliovirus infections are asymptomatic or cause only minor illness, the virus has the capacity to invade the central nervous system and destroy motor neurons in the anterior horn of the spinal cord, resulting in acute flaccid paralysis (AFP). [1] This devastating complication occurs in less than 1% of infections but has historically caused widespread disability and death in children worldwide.

Poliovirus is transmitted primarily through the faecal-oral route in areas with poor sanitation, and via the oral-oral route (saliva and pharyngeal secretions) in regions with better hygiene. [2] The virus replicates in the oropharynx and gastrointestinal tract, causing viremia that occasionally leads to central nervous system invasion. The hallmark of paralytic poliomyelitis is asymmetric flaccid paralysis with absent or diminished deep tendon reflexes, but with preserved sensation—a critical distinguishing feature from other causes of acute flaccid paralysis. [3]

Three serotypes of wild poliovirus exist: types 1, 2, and 3. Thanks to the Global Polio Eradication Initiative (GPEI) launched in 1988, wild poliovirus type 2 was declared eradicated in 2015, and type 3 in 2019. [4] As of 2026, wild poliovirus type 1 remains endemic only in Afghanistan and Pakistan, representing one of the greatest public health achievements of the modern era. However, vaccine-derived poliovirus (VDPV)—arising from the live-attenuated oral polio vaccine (OPV)—continues to cause outbreaks in areas with low immunisation coverage, posing ongoing challenges to eradication efforts. [5]

The cornerstone of polio prevention is vaccination. Two types of vaccine are used: inactivated poliovirus vaccine (IPV), developed by Jonas Salk in 1955, and oral poliovirus vaccine (OPV), developed by Albert Sabin in 1961. IPV provides excellent individual protection without the risk of vaccine-associated paralytic poliomyelitis (VAPP) or VDPV, while OPV induces mucosal immunity and can interrupt transmission, making it the vaccine of choice in eradication campaigns despite its rare complications. [6] Most high-income countries, including the UK, have switched to IPV-only schedules.

There is no specific antiviral treatment for poliomyelitis. Management is entirely supportive, focusing on respiratory support, pain management, and prevention of complications during the acute phase, followed by comprehensive rehabilitation to maximise functional recovery. [7] Survivors of paralytic polio may develop post-polio syndrome (PPS) decades after the initial infection, characterised by new muscle weakness, fatigue, and pain affecting previously involved and uninvolved muscle groups. [8]

Key Facts

Clinical Pearls

"Asymmetric Flaccid Paralysis with Intact Sensation": The preservation of sensory function distinguishes polio from other causes of AFP such as Guillain-Barré syndrome (which is typically symmetric and ascending) or transverse myelitis (which affects both motor and sensory tracts).

"Peak Fever, Then Paralysis": Paralysis often begins as fever is resolving—a biphasic pattern where the initial febrile illness (minor illness) is followed 1–2 days later by aseptic meningitis or paralysis (major illness).

"Legs More Than Arms, Proximal More Than Distal": Paralytic polio preferentially affects lower limbs and proximal muscle groups, though the distribution is characteristically patchy and asymmetric.

"The Silent Reservoir": For every paralytic case, there are an estimated 100–200 asymptomatic infections shedding virus, sustaining transmission chains. [9]

"VDPV: The Vaccine Paradox": Oral polio vaccine (OPV) has been instrumental in near-eradication but can revert to neurovirulence in communities with low immunisation coverage, causing vaccine-derived poliovirus outbreaks.

"Post-Polio Syndrome is NOT Reactivation": PPS occurs decades after acute infection due to progressive dysfunction of surviving motor neurons, not viral reactivation. It affects 25–50% of paralytic polio survivors. [8]

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2. Epidemiology

Historical Context

Poliomyelitis was one of the most feared diseases of the 20th century. Epidemic polio emerged in Europe and North America in the late 19th and early 20th centuries, paradoxically as sanitation improved. Better hygiene delayed initial exposure, meaning children encountered the virus at older ages when paralysis risk is higher, rather than as infants when maternal antibodies and immune tolerance reduced severity. [10]

The worst epidemics occurred in the 1940s and 1950s. In 1952, the United States reported 57,628 polio cases, with 3,145 deaths and 21,269 cases of paralytic disease. [1] The introduction of the Salk inactivated poliovirus vaccine (IPV) in 1955 and the Sabin oral poliovirus vaccine (OPV) in 1961 transformed the epidemiology of the disease, leading to rapid declines in incidence in countries with high vaccine coverage.

The Global Polio Eradication Initiative (GPEI)

Launched in 1988 by the World Health Organization (WHO), UNICEF, Rotary International, and the US Centers for Disease Control and Prevention (CDC), the GPEI aimed to eradicate polio globally following the success of the smallpox eradication programme. [4]

This represents a > 99.9% reduction in global polio incidence since 1988. [4] However, final eradication has proven challenging due to conflict zones, vaccine hesitancy, population displacement, and the emergence of circulating vaccine-derived poliovirus (cVDPV).

Current Epidemiology (2026)

Wild Poliovirus Type 1 (WPV1)

• Endemic transmission: Afghanistan and Pakistan only
• Annual cases: Fluctuating, generally less than 100 cases globally
• Challenges: Insecurity, mobile populations, cross-border transmission, vaccine refusal

Vaccine-Derived Poliovirus (VDPV)

• Circulating VDPV (cVDPV): Predominantly type 2, occurring in populations with low OPV coverage
• Geographic distribution: Sub-Saharan Africa, Yemen, parts of Asia
• Mechanism: OPV contains live-attenuated virus that replicates in the gut; in under-immunised communities, the vaccine virus can circulate and revert to neurovirulence
• Novel OPV2 (nOPV2): A genetically modified OPV2 designed to be more stable and less likely to revert, introduced in 2021 to combat cVDPV2 outbreaks [5]

Demographics

Risk Factors for Paralytic Disease

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3. Aetiology & Pathophysiology

Virology

Poliovirus is a non-enveloped, single-stranded positive-sense RNA virus in the genus Enterovirus, family Picornaviridae. It is one of the most infectious human pathogens, with high attack rates in susceptible populations. [2]

Serotypes

• Type 1 (Brunhilde): Most commonly associated with paralytic disease and epidemics; the only wild serotype still circulating
• Type 2 (Lansing): Eradicated in the wild (1999), but cVDPV2 remains a problem
• Type 3 (Leon): Eradicated globally (2012)

There is no cross-protective immunity between serotypes, so vaccination must induce immunity to all three types.

Viral Structure

• Genome: ~7,500 nucleotides encoding a polyprotein cleaved into structural (VP1-VP4) and non-structural proteins
• Capsid: Icosahedral, composed of 60 copies each of VP1, VP2, VP3, VP4
• Receptor: Human poliovirus receptor (PVR/CD155), expressed on motor neurons, intestinal epithelium, and pharyngeal cells [11]
• Stability: Resistant to gastric acid, bile, and detergents; survives weeks in water and sewage

Transmission Pathways

Faecal-Oral Route (Predominant)

In areas with poor sanitation:

• Contaminated water and food
• Person-to-person contact
• Faecal shedding for 3–6 weeks (up to 8–12 weeks in immunocompromised) [2]

Oral-Oral Route

In settings with better hygiene:

• Pharyngeal secretions
• Respiratory droplets (less efficient)
• Pharyngeal shedding for 1–2 weeks

Pathogenesis

The progression from infection to paralysis follows a series of steps, occurring in less than 1% of infected individuals:

Stage 1: Viral Entry and Replication (Days 0–3)

1. Ingestion of poliovirus
2. Primary replication in oropharyngeal lymphoid tissue (tonsils, Peyer's patches)
3. Secondary replication in gastrointestinal mucosa (small intestine)

At this stage, most infections are asymptomatic or cause minor febrile illness (abortive poliomyelitis).

Stage 2: Viremia (Days 3–7)

4. Virus enters the bloodstream (minor viremia)
5. Spreads to reticuloendothelial system (liver, spleen, lymph nodes, bone marrow)
6. Major viremia follows, with high-titer virus circulating

Most infections are controlled at this stage by humoral immunity (neutralising antibodies). Clinical manifestations may include fever, malaise, headache, nausea, vomiting, and sore throat.

Stage 3: Central Nervous System Invasion (Days 7–14)

7. In less than 1% of cases, virus crosses the blood-brain barrier or blood-CSF barrier
8. Mechanisms of CNS entry are incompletely understood but may involve:
   • Retrograde axonal transport from peripheral nerve endings
   • Direct invasion via the blood-brain barrier in areas of inflammation
   • Entry via circumventricular organs

Stage 4: Neuronal Infection and Destruction (Days 10–21)

9. Poliovirus binds to CD155 (PVR) on motor neurons in the anterior horn of the spinal cord and motor nuclei of the brainstem
10. Viral replication causes lysis and necrosis of motor neurons
11. Inflammation (perivascular cuffing, microglial activation) contributes to tissue damage
12. Sensory neurons are spared due to lack of CD155 expression

The characteristic lesions are found in:

• Spinal anterior horn cells: Lower motor neuron paralysis
• Brainstem motor nuclei: Bulbar poliomyelitis (cranial nerves VII, IX, X, XII)
• Reticular formation: Respiratory and cardiovascular control dysfunction
• Rarely: Motor cortex, cerebellum

Exam Detail: #### Molecular Pathophysiology

CD155 (Poliovirus Receptor):

• A member of the immunoglobulin superfamily, normally involved in cell adhesion and immune regulation
• Expressed on motor neurons, intestinal epithelial cells, and some immune cells
• Poliovirus binding to CD155 induces receptor-mediated endocytosis
• Conformational changes in the viral capsid release the RNA genome into the cytoplasm

Neurovirulence Determinants:

• Specific mutations in the 5' untranslated region (5'-UTR) and capsid proteins determine neurovirulence
• Sabin vaccine strains have attenuating mutations; reversion of these mutations can restore neurovirulence (VDPV)

Immune Evasion:

• Rapid viral replication outpaces innate immune responses
• Poliovirus 2A protease cleaves eIF4G, shutting down host cell protein synthesis
• Viral proteins inhibit type I interferon responses

Motor Neuron Destruction:

• Direct cytopathic effect: viral replication causes cell lysis
• Inflammatory damage: cytotoxic T cells and inflammatory cytokines exacerbate tissue injury
• ≥50% of motor neurons in a spinal segment must be destroyed before clinical weakness appears [12]

Post-Polio Syndrome (PPS) Pathophysiology:

• After acute infection, surviving motor neurons sprout new axonal branches to reinnervate orphaned muscle fibres
• This results in enlarged motor units (one motor neuron innervating many more muscle fibres than normal)
• Decades later, these overworked motor neurons undergo premature age-related degeneration
• PPS is NOT due to viral reactivation or persistent infection [8]

Why Anterior Horn Cells?

The selective tropism of poliovirus for motor neurons is due to:

1. CD155 expression on motor neurons
2. Blood supply: Anterior horn receives rich blood supply, facilitating viral delivery during viremia
3. Neuronal activity: Metabolically active neurons may be more susceptible
4. Retrograde axonal transport: Virus may enter motor neurons at neuromuscular junctions and travel retrogradely

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4. Clinical Presentation

Spectrum of Disease

The clinical manifestations of poliovirus infection exist on a spectrum:

1. Asymptomatic Infection (72%)

• No clinical symptoms
• Virus replicates in oropharynx and intestines
• Viral shedding in stool for weeks
• Induces protective immunity
• Public health significance: Represents the "silent reservoir" perpetuating transmission [9]

2. Abortive Poliomyelitis (24%)

A non-specific febrile illness indistinguishable from other viral infections:

• Symptoms: Fever, malaise, headache, sore throat, nausea, vomiting, abdominal pain
• Duration: 2–5 days
• Recovery: Complete, no sequelae
• No CNS involvement: Normal neurological examination

3. Non-Paralytic Poliomyelitis (Aseptic Meningitis, 1–5%)

Poliovirus invades the CNS but does not destroy motor neurons in sufficient numbers to cause paralysis.

Symptoms

• Severe headache
• Fever (38–40°C)
• Neck stiffness, back pain
• Nausea and vomiting
• Irritability, photophobia

Signs

• Meningism: Neck rigidity, Kernig's sign, Brudzinski's sign
• Normal motor examination (by definition)
• Deep tendon reflexes: Preserved or hyperreflexic

CSF Findings (Aseptic Meningitis)

• Cell count: 10–500 cells/μL (initially polymorphs, then lymphocytes)
• Protein: Normal or mildly elevated (0.4–1.0 g/L)
• Glucose: Normal (CSF:serum ratio > 0.6)
• Gram stain and culture: Negative for bacteria

Course

• Duration: 3–10 days
• Recovery: Complete, no paralysis
• Prognosis: Excellent

4. Paralytic Poliomyelitis (less than 1%)

The feared complication of poliovirus infection, resulting from destruction of motor neurons.

Prodromal Phase (1–3 Days Before Paralysis)

• Biphasic illness: Minor illness (fever, malaise) followed by apparent recovery, then recurrence of fever with meningism
• Fever (38–40°C), severe headache, neck and back stiffness
• Muscle pain and tenderness (especially in limbs that will become paralysed)
• Deep muscle pain, fasciculations
• Hyperesthesia of skin

Paralytic Phase (Acute Onset, Over Hours to Days)

Classic Features:

• Asymmetric flaccid paralysis: Characteristic hallmark
• Rapid onset: Maximal weakness reached within 48–72 hours
• Proximal > Distal: Proximal muscles more affected
• Legs > Arms: Lower limbs more commonly involved
• Patchy distribution: Involvement of isolated muscle groups
• Deep tendon reflexes: Absent or markedly diminished (LMN lesion)
• Sensation: Completely preserved (critical diagnostic feature)
• Muscle tone: Flaccid (hypotonia)
• Muscle pain: Severe, especially early; improves as paralysis develops

Distribution Patterns (See Classification Below):

Spinal Poliomyelitis (79%)

Affects motor neurons in the spinal cord anterior horn.

Clinical Features:

• Lower limb paralysis: Most common (legs > arms)
• Asymmetric weakness: One leg or arm more affected than the other
• Patchy involvement: Individual muscles or muscle groups affected
• Proximal weakness: Hip flexors, quadriceps, shoulder muscles commonly affected
• Foot drop: Ankle dorsiflexion weakness
• Deep tendon reflexes: Absent in affected limbs
• Plantar responses: Flexor (LMN lesion)
• No sensory loss: Key differentiator
• Bladder and bowel: Usually spared (autonomic innervation preserved)

Respiratory Involvement:

• Diaphragm paralysis (C3-C5 anterior horn involvement)
• Intercostal muscle paralysis (thoracic anterior horn involvement)
• Leads to respiratory failure requiring mechanical ventilation

Bulbar Poliomyelitis (2%)

Affects motor nuclei in the brainstem (medulla and pons), involving cranial nerves IX, X, XI, XII primarily.

Clinical Features:

Key Clinical Signs:

• Dysphagia: Difficulty swallowing liquids and solids
• Nasal regurgitation of fluids
• Dysphonia: Nasal or hoarse voice
• Dysarthria: Difficulty articulating
• Pooling of secretions: Drooling, inability to manage saliva
• Loss of gag reflex
• Tongue fasciculations, weakness, deviation
• Respiratory dysfunction: Central respiratory drive impairment (medullary involvement)

Complications:

• Aspiration pneumonia: From inability to protect airway
• Respiratory failure: Central and/or from pharyngeal collapse
• Autonomic instability: Hypertension, hypotension, arrhythmias (from medullary cardiovascular centre involvement)
• Death: Historically 25–75% case fatality in bulbar polio [13]

Bulbospinal Poliomyelitis (19%)

Combined involvement of spinal and bulbar motor neurons. Clinically most severe form with highest mortality.

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5. Classification of Paralytic Poliomyelitis

Based on anatomical distribution:

Types

Severity Grading

Not universally standardised, but can be graded by:

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6. Clinical Examination Findings

General Inspection

• Posture: Abnormal posture of limbs; legs externally rotated, knees flexed
• Muscle wasting: Not present acutely (develops weeks later)
• Asymmetry: Obvious asymmetry of limb position or movement

Neurological Examination

Motor

Sensory

• Preserved: Light touch, pinprick, vibration, proprioception all NORMAL
• Critical distinguishing feature from Guillain-Barré syndrome, transverse myelitis

Cranial Nerves (If Bulbar Involvement)

Respiratory

• Respiratory rate: Tachypnoea (respiratory muscle weakness)
• Paradoxical breathing: Abdominal wall moves inward during inspiration (diaphragm paralysis)
• Accessory muscle use: Sternocleidomastoids, scalenes
• Weak cough: Inability to generate adequate expiratory force
• Oxygen saturation: May be reduced
• Auscultation: May reveal decreased breath sounds in lung bases

Later Examination Findings (Weeks to Months)

• Muscle atrophy: Visible wasting of affected muscles
• Contractures: Shortening of muscles and tendons from prolonged immobility
• Limb length discrepancy: Affected limb may be shorter (growth plate impact in children)
• Scoliosis: From trunk muscle weakness

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7. Differential Diagnosis

The key differential for paralytic poliomyelitis is acute flaccid paralysis (AFP) of any cause. WHO defines AFP as:

"Acute onset of flaccid paralysis in a child less than 15 years, or any paralysis with suspected polio at any age."

All AFP cases must be investigated for poliovirus to enable surveillance.

Differential Diagnoses of Acute Flaccid Paralysis

Key Clinical Clues to Distinguish Polio

Exam Detail: #### Acute Flaccid Myelitis (AFM)

AFM has emerged as an important differential since 2012, with outbreaks associated with enterovirus D68 and other enteroviruses. [14]

Similarities to polio:

• Acute onset flaccid paralysis
• Asymmetric weakness
• Anterior horn cell involvement
• Associated with enterovirus (different species)

Differences from polio:

• MRI findings: Gray matter lesions in spinal cord (hyperintensity on T2/FLAIR in anterior horn) are characteristic of AFM; polio rarely shows MRI changes acutely
• Age: AFM often affects school-age children (median 5–6 years); polio historically less than 5 years
• Geographic: AFM occurs in countries with no wild poliovirus circulation
• Seasonality: AFM peaks in late summer/autumn (enterovirus D68 season)

Diagnostic approach:

• Stool and throat swabs for poliovirus and non-polio enteroviruses
• Serology for West Nile virus, other arboviruses
• MRI spinal cord
• CSF analysis

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8. Investigations

Diagnostic Criteria (WHO)

A case of acute flaccid paralysis (AFP) requires investigation for polio if:

• Any child less than 15 years with AFP, OR
• Any person of any age with paralysis suspected to be polio

Virological Confirmation (Gold Standard)

Stool Specimens

Timing and collection:

• Collect two stool samples, ideally 24–48 hours apart
• Within 14 days of paralysis onset (virus shedding peaks early)
• Minimum 8–10 g of stool per sample

Laboratory testing:

1. Viral isolation: Stool cultured on cell lines (L20B, RD) to isolate poliovirus
2. Intratypic differentiation (ITD): PCR and sequencing to distinguish:
   • Wild poliovirus (types 1, 2, 3)
   • Vaccine-like poliovirus (Sabin strains)
   • Vaccine-derived poliovirus (VDPV): > 1% divergence from Sabin for type 1/3; > 0.6% for type 2

Interpretation:

• Isolation of wild poliovirus: Confirmed polio (notifiable, public health emergency)
• Isolation of VDPV: Confirmed vaccine-derived polio
• Isolation of Sabin-like virus: Recent OPV vaccination; clinical polio may be VAPP (vaccine-associated paralytic polio) if temporal relationship
• No virus isolated: Does not exclude polio (sensitivity ~85% if samples collected early and properly handled) [15]

Throat Swab

• Less sensitive than stool (virus shed for shorter period)
• Collect within 7 days of symptom onset
• Useful if stool collection delayed

Cerebrospinal Fluid (CSF) Analysis

Indications:

• All suspected cases of paralytic polio (to evaluate for aseptic meningitis and exclude bacterial causes)

Typical Findings in Polio:

Poliovirus isolation from CSF:

• Uncommon (less than 5% of cases)
• If isolated, confirms CNS invasion

Role of CSF:

• Supports diagnosis of aseptic meningitis
• Excludes bacterial meningitis
• Does NOT confirm poliovirus (requires stool/serology)

Serology

Acute and Convalescent Sera:

• Acute sample: As early as possible (less than 7 days from onset)
• Convalescent sample: 3–6 weeks later

Interpretation:

• Four-fold rise in neutralizing antibody titre: Suggests recent poliovirus infection
• Limitations:
  • Cannot distinguish wild from vaccine virus
  • Cannot determine serotype reliably if child recently vaccinated
  • Less useful than direct viral isolation
  • Not routinely used for diagnosis in endemic settings

Electromyography (EMG) and Nerve Conduction Studies (NCS)

Not required for diagnosis but may help differentiate polio from GBS or other neuropathies.

Typical Findings in Polio:

• EMG: Denervation potentials (fibrillations, positive sharp waves) in affected muscles after 2–3 weeks
• NCS:
  • "Motor: Reduced compound muscle action potential (CMAP) amplitudes; normal or mildly reduced conduction velocities"
  • "Sensory: Normal (key feature distinguishing from GBS)"

Comparison:

Magnetic Resonance Imaging (MRI)

Not diagnostic for polio, but may show:

• Acute phase: Often normal; occasionally anterior horn hyperintensity on T2/FLAIR (more typical of acute flaccid myelitis from other enteroviruses)
• Late phase: Spinal cord atrophy

Role of MRI:

• Exclude structural causes (spinal cord compression, transverse myelitis, ADEM)
• Differentiate from acute flaccid myelitis (AFM), which typically shows characteristic anterior horn lesions on MRI

Summary of Diagnostic Investigations

Exam Detail: #### Public Health Laboratory Response

Specimens from AFP cases are sent to WHO-accredited laboratories within the Global Polio Laboratory Network (GPLN):

1. Virus isolation and identification
2. Intratypic differentiation to classify isolate as wild-type, Sabin-like, or VDPV
3. Genomic sequencing for molecular epidemiology (tracking transmission chains)

Reporting timelines (WHO targets):

• Stool arrival at lab: Within 3 days of collection
• Preliminary results: Within 14 days of receipt
• Final results (ITD): Within 60 days

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9. Management

There is no specific antiviral therapy for poliomyelitis. Management is entirely supportive, focusing on:

1. Maintaining life during acute phase (respiratory support, nutrition)
2. Preventing complications (contractures, pressure sores, aspiration)
3. Maximising functional recovery through rehabilitation

Acute Phase Management (First Days to Weeks)

General Supportive Care

Respiratory Management

Monitoring:

• Respiratory rate, oxygen saturation
• Vital capacity (VC): Serial measurements; VC less than 50% predicted indicates high risk of respiratory failure
• Arterial blood gases: Monitor for hypoxia and hypercapnia
• Clinical signs: Use of accessory muscles, paradoxical breathing, weak cough

Indications for Mechanical Ventilation:

• Vital capacity less than 15–20 mL/kg
• Progressive hypoxia (SpO₂ less than 90% on oxygen)
• Hypercapnia (PaCO₂ > 50 mmHg) with respiratory acidosis
• Bulbar involvement with inability to protect airway
• Apnoea or irregular breathing

Ventilation Strategies:

Tracheostomy:

• Considered if prolonged ventilation anticipated (> 2 weeks)
• Facilitates secretion management, weaning, rehabilitation

Secretion Management:

• Chest physiotherapy
• Suctioning (especially if bulbar involvement)
• Postural drainage

Bulbar Poliomyelitis Specific Management

• Airway protection: Prevent aspiration; consider early intubation or tracheostomy
• Nasogastric or gastrostomy feeding: If dysphagia
• Monitor for autonomic instability: Blood pressure fluctuations, arrhythmias
• Avoid sedation: May worsen respiratory drive suppression

Bladder and Bowel Management

• Usually intact, but monitor for urinary retention (uncommon)
• Maintain bowel function with stool softeners, adequate fluids

Prevention of Complications

Rehabilitation Phase (Weeks to Months)

Physiotherapy

Goals:

• Prevent contractures and deformities
• Maintain range of motion
• Strengthen unaffected and recovering muscles
• Optimize functional independence

Techniques:

• Passive and active range-of-motion exercises
• Progressive strengthening exercises (caution: avoid overwork fatigue)
• Hydrotherapy (water-based exercise)
• Gait training, mobility aids (crutches, braces, wheelchairs)

Occupational Therapy

• Activities of daily living (ADL) training
• Adaptive devices and home modifications
• Vocational training and school reintegration

Orthotics and Assistive Devices

Orthopaedic Surgery

Indications (delayed, after 12–18 months of stability):

• Correct deformities (equinus foot, flexion contractures)
• Tendon transfers to restore function
• Arthrodesis (joint fusion) for stability
• Limb lengthening for leg length discrepancy

Common Procedures:

• Achilles tendon lengthening (equinus deformity)
• Tibialis posterior transfer (foot drop)
• Hip stabilization procedures
• Scoliosis correction (spinal fusion if severe progressive curve)

Long-Term Follow-Up

• Annual review: Monitor for post-polio syndrome, progressive scoliosis, contractures
• Orthopedic surveillance: Growing children need monitoring for limb length discrepancy, joint degeneration
• Respiratory monitoring: If residual respiratory muscle weakness
• Psychological support: Address ongoing disability, social integration

Exam Detail: #### Post-Polio Syndrome (PPS)

Definition: New neuromuscular symptoms occurring ≥15 years after acute poliomyelitis, characterized by progressive muscle weakness, fatigue, and pain. [8]

Epidemiology:

• Affects 25–50% of paralytic polio survivors
• Onset typically 30–40 years after acute infection
• Not related to severity of initial paralysis

Pathophysiology:

• Following acute polio, surviving motor neurons sprout new axonal branches to reinnervate orphaned muscle fibers (post-polio motor units are 5–8 times normal size)
• Decades later, these overworked neurons undergo premature age-related degeneration
• NOT due to viral reactivation (no poliovirus detected in PPS patients)

Clinical Features:

• Weakness affects previously involved muscles (most common) but can also affect muscles thought to be unaffected
• Slow, progressive decline in function
• No upper motor neuron signs
• Bulbar symptoms (dysphagia, dysarthria) may develop or worsen

Diagnosis:

• Clinical diagnosis based on history and examination
• Exclusion of other causes: Thyroid disease, vitamin D deficiency, radiculopathy, myopathy
• EMG: Chronic denervation and reinnervation (large motor units); no active denervation
• Muscle biopsy: Fiber-type grouping (not routinely needed)

Management:

• Pacing: Energy conservation techniques; avoid overexertion
• Physiotherapy: Gentle, non-fatiguing exercises (avoid overwork)
• Assistive devices: Braces, mobility aids to reduce muscle strain
• Pain management: Analgesics, heat therapy
• Address sleep disorders: Screen for sleep apnea (common)
• Psychological support: Depression and anxiety are common

Prognosis:

• Slowly progressive (muscle strength declines ~1% per year)
• Does not lead to death (unlike ALS, which PPS is sometimes confused with)
• Quality of life significantly impacted

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10. Complications

Acute Complications (During Acute Illness)

Subacute/Chronic Complications (Weeks to Months)

Late Complications (Years to Decades)

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11. Prognosis

Natural History by Presentation

Paralytic Poliomyelitis Outcomes

Mortality

Modern ICU care has dramatically reduced mortality, even in bulbar and respiratory polio.

Functional Recovery

Recovery of muscle strength follows a predictable pattern:

Factors Predicting Better Recovery:

• Younger age
• Less extensive initial paralysis
• Early and intensive physiotherapy
• Absence of bulbar or respiratory involvement

Long-Term Functional Outcomes (among survivors):

• Complete recovery: 15–20% (mainly those with mild initial paralysis)
• Mild residual weakness: 30–40% (can walk independently, may need brace)
• Moderate disability: 20–30% (require assistive devices, crutches, wheelchair for long distances)
• Severe disability: 10–20% (wheelchair-dependent, ventilator-dependent)

Prognostic Factors

Post-Polio Syndrome

• Affects 25–50% of paralytic polio survivors [8]
• Slow progressive decline in muscle strength (~1% per year)
• Does not reduce life expectancy (unlike motor neuron diseases)
• Significant impact on quality of life and independence

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12. Prevention & Vaccination

Poliovirus Vaccines

Two types of polio vaccine are in use globally:

Inactivated Poliovirus Vaccine (IPV) — Salk Vaccine

Composition:

• Contains inactivated (killed) poliovirus types 1, 2, and 3
• Virus grown in cell culture, then inactivated with formaldehyde
• Cannot replicate

Administration:

• Intramuscular or subcutaneous injection

Advantages:

• No risk of vaccine-associated paralytic poliomyelitis (VAPP)
• No risk of vaccine-derived poliovirus (VDPV)
• Safe in immunocompromised individuals
• Induces strong systemic (humoral) immunity

Disadvantages:

• Does not induce robust mucosal (intestinal) immunity
• Cannot interrupt wild poliovirus transmission as effectively as OPV
• Requires trained personnel for injection
• More expensive than OPV
• Requires cold chain

Efficacy:

• Three doses: > 99% seroconversion for all three serotypes [6]

Use:

• Standard vaccine in most high-income countries (USA, UK, most of Europe)
• WHO recommends at least one dose of IPV in all countries to maintain population immunity

Oral Poliovirus Vaccine (OPV) — Sabin Vaccine

Composition:

• Contains live-attenuated poliovirus (Sabin strains) types 1, 2, and/or 3
• Virus is weakened by passage through cell culture; retains ability to replicate but has reduced neurovirulence

Types of OPV:

Administration:

• Oral drops (two drops)

Advantages:

• Induces strong intestinal mucosal immunity (secretory IgA)
• Interrupts transmission: Vaccinated children shed vaccine virus, passively immunizing unvaccinated contacts
• Easy to administer (no needles, less training required)
• Inexpensive (~$0.15 per dose)
• Does not require cold chain as stringently as IPV

Disadvantages:

• Risk of vaccine-associated paralytic poliomyelitis (VAPP): ~1 per 2.7 million first doses [16]
• Risk of vaccine-derived poliovirus (VDPV): In areas with low immunisation coverage, vaccine virus can circulate, mutate, and revert to neurovirulence
• Contraindicated in immunocompromised individuals (risk of prolonged shedding and VAPP)
• Less effective in children with diarrhea or enteric infections

Efficacy:

• Three doses: > 95% seroconversion [6]

Use:

• Mass vaccination campaigns in endemic and high-risk countries
• Outbreak response (rapid, large-scale immunization)
• Not used in routine schedules in countries that have eliminated polio (switched to IPV)

Global Switch from tOPV to bOPV (April 2016)

Following the eradication of wild poliovirus type 2 in 1999 and its formal declaration in 2015, continued use of OPV type 2 posed a risk of cVDPV2 outbreaks. In a globally synchronized switch in April 2016, all countries using OPV replaced trivalent OPV (types 1, 2, 3) with bivalent OPV (types 1, 3). [17]

However, cVDPV2 outbreaks have continued, especially in Africa, due to low immunisation coverage and waning type 2 immunity. Novel OPV2 (nOPV2), genetically stabilized to reduce reversion risk, was introduced in 2021 for outbreak response. [5]

Vaccination Schedules

United Kingdom (IPV-Only Schedule)

Polio vaccine (IPV) is part of the 6-in-1 vaccine (DTaP/IPV/Hib/HepB) and later booster vaccines:

Total doses: 5 doses of IPV provide lifelong protection

WHO-Recommended Schedule (OPV or IPV)

Vaccine-Associated Paralytic Poliomyelitis (VAPP)

Definition: Acute flaccid paralysis caused by vaccine-strain poliovirus (Sabin strains) occurring within 4–40 days of OPV administration (or in close contacts of OPV recipients).

Incidence:

• ~1 case per 2.7 million first doses of OPV [16]
• Higher risk in immunocompromised individuals

Clinical Features:

• Identical to wild poliovirus poliomyelitis
• Asymmetric flaccid paralysis
• Stool isolate: Sabin strain poliovirus

Risk Factors:

• First dose of OPV (highest risk)
• Immunodeficiency (e.g., SCID, HIV, congenital immunodeficiency)

Prevention:

• Use IPV instead of OPV in countries with no wild poliovirus circulation
• Screen for immunodeficiency before OPV administration
• Do not give OPV to immunocompromised children or household contacts of immunocompromised individuals

Vaccine-Derived Poliovirus (VDPV)

Definition: Poliovirus that has genetically diverged from the original Sabin vaccine strain:

• > 1% nucleotide divergence for types 1 and 3
• > 0.6% divergence for type 2

Types:

Mechanism:

• OPV contains live-attenuated virus
• Vaccine virus replicates in the gut of vaccinees
• In communities with low immunisation coverage, vaccine virus circulates person-to-person
• Genetic reversion mutations restore neurovirulence over time (~1 year of circulation)

Epidemiology:

• cVDPV2 is the most common (accounts for > 90% of cVDPV cases globally)
• Predominantly in sub-Saharan Africa, Yemen, Afghanistan, Pakistan
• Risk increases in areas with less than 80% OPV coverage

Prevention:

• High immunisation coverage (> 95%) prevents circulation
• Use of novel OPV2 (nOPV2) instead of mOPV2 for outbreak response
• Transition to IPV-only schedules in polio-free countries

Public Health Response:

• cVDPV outbreaks are treated like wild poliovirus outbreaks: mass OPV campaigns, surveillance intensification

Exam Detail: #### Immunodeficiency-Associated VDPV (iVDPV)

Children with primary immunodeficiency disorders (e.g., SCID, common variable immunodeficiency) who receive OPV may shed vaccine virus for years or even decades, with progressive genetic divergence and reversion to neurovirulence.

Risks:

• Chronic shedding (months to years)
• Paralytic disease in the immunocompromised individual
• Transmission to community (potential outbreak if virus reverts)

Management:

• Antiviral therapy: Pocapavir (investigational capsid inhibitor) has shown promise in reducing viral shedding [18]
• Immunoglobulin therapy: May reduce viral load
• Isolation precautions: Prevent transmission
• Surveillance: Environmental monitoring in regions where iVDPV cases identified

Screening:

• Contraindicate OPV in children with known or suspected immunodeficiency
• Use IPV instead

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13. Public Health & Global Eradication Efforts

The Global Polio Eradication Initiative (GPEI)

Launched in 1988, the GPEI is a public-private partnership led by WHO, UNICEF, Rotary International, CDC, and the Bill & Melinda Gates Foundation. [4]

Goals:

1. Interrupt wild poliovirus transmission globally
2. Certify polio eradication (no wild poliovirus cases for 3 consecutive years in all WHO regions)
3. Contain poliovirus in laboratories and vaccine production facilities
4. Plan for the post-eradication era (OPV cessation, IPV-based immunity maintenance)

Strategies:

Challenges to Eradication

Environmental Surveillance

Rationale: Poliovirus is shed in stool for weeks; sewage testing can detect circulation before paralytic cases appear.

Method:

• Collect sewage samples from wastewater treatment plants or open drains
• Concentrate and test for poliovirus
• Sequence isolates to determine type (wild, VDPV, Sabin-like)

Utility:

• Early warning system for silent circulation
• Monitoring immunity gaps
• Verification of eradication

Post-Eradication Strategy

Once wild poliovirus is eradicated globally and cVDPV is controlled:

1. OPV cessation: Withdraw all OPV globally (already done for type 2 in routine schedules)
2. IPV continuation: Maintain at least one dose of IPV to sustain population immunity and prevent re-emergence
3. Containment: Destroy or securely contain all poliovirus stocks (laboratories, vaccine production facilities)
4. Surveillance: Continue AFP and environmental surveillance to rapidly detect any re-emergence

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14. Examination Focus

High-Yield Facts for MRCPCH / Paediatric Infectious Diseases Exams

1. Paralytic polio occurs in less than 1% of poliovirus infections; 72% are asymptomatic.
2. Asymmetric flaccid paralysis with preserved sensation is the hallmark.
3. Anterior horn motor neurons are selectively destroyed; sensory neurons spared.
4. Three serotypes: Wild types 2 and 3 are eradicated; only type 1 remains endemic (Afghanistan, Pakistan).
5. Stool culture (two samples, 24–48 hours apart, within 14 days) is the gold standard diagnostic test.
6. CSF: Lymphocytic pleocytosis, normal glucose, mildly elevated protein (aseptic meningitis pattern).
7. No specific treatment: Management is entirely supportive (respiratory support, physiotherapy, pain management).
8. Two vaccines: IPV (no VAPP/VDPV risk, used in UK) and OPV (mucosal immunity, used in eradication campaigns, risk of VAPP/VDPV).
9. VAPP risk: ~1 per 2.7 million first doses of OPV.
10. cVDPV: Occurs in under-vaccinated populations where OPV virus circulates and reverts to neurovirulence.
11. Post-polio syndrome: Affects 25–50% of survivors, 15–40 years after acute infection; progressive weakness, fatigue, pain.
12. Bulbar polio: Cranial nerve IX, X, XII involvement; dysphagia, dysphonia, respiratory failure; historically 25–75% mortality.
13. Differential diagnosis: Guillain-Barré syndrome (symmetric, ascending, sensory symptoms, albumin-cytological dissociation), acute flaccid myelitis (MRI shows anterior horn lesions, enterovirus D68).
14. Notifiable disease: All AFP cases in children less than 15 years must be reported and investigated for polio.
15. Global eradication: > 99.9% reduction since 1988; wild type 1 endemic in two countries only.

Common Viva Questions

Q1: "What is poliomyelitis and what causes it?"

Model Answer: "Poliomyelitis is an acute viral infection caused by poliovirus, a human enterovirus in the Picornaviridae family. There are three serotypes: types 1, 2, and 3, though wild types 2 and 3 have been eradicated. The virus is transmitted via the faecal-oral route and replicates in the gastrointestinal tract. While most infections are asymptomatic, in less than 1% of cases, the virus invades the central nervous system and destroys motor neurons in the anterior horn of the spinal cord, causing acute flaccid paralysis. This is characterised by asymmetric weakness, absent reflexes, but importantly, preserved sensation."

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Q2: "How do you differentiate polio from Guillain-Barré syndrome?"

Model Answer:

"The key distinguishing features are the asymmetric pattern of paralysis in polio, the presence of fever at onset, and the preservation of sensation. GBS is typically symmetric, ascending, with prominent sensory symptoms and albumin-cytological dissociation on CSF analysis."

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Q3: "What is the difference between IPV and OPV vaccines?"

Model Answer:

"IPV is safer, with no risk of vaccine-associated paralysis or vaccine-derived poliovirus, making it ideal for routine immunisation in polio-free countries. OPV induces mucosal immunity and can interrupt transmission, which is critical for eradication efforts in endemic regions, but carries the risk of VAPP and emergence of circulating vaccine-derived poliovirus in areas with low vaccine coverage."

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Q4: "What is vaccine-derived poliovirus (VDPV) and why is it a concern?"

Model Answer: "Vaccine-derived poliovirus occurs when the live-attenuated virus in oral polio vaccine circulates in a community with low immunisation coverage. Over time, as the vaccine virus replicates and is transmitted person-to-person, it undergoes genetic mutations that can restore neurovirulence. When the vaccine virus has diverged by more than 1% (for types 1 and 3) or 0.6% (for type 2) from the original Sabin strain, it is classified as VDPV. Circulating VDPV (cVDPV) can cause outbreaks of paralytic polio, particularly cVDPV type 2, which is the most common. This is a major challenge to global eradication efforts. The solution is to achieve high OPV coverage (> 95%) to prevent prolonged circulation, use novel OPV2 which is genetically more stable, and transition polio-free countries to IPV-only schedules."

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Q5: "What is post-polio syndrome?"

Model Answer: "Post-polio syndrome is a condition affecting 25–50% of paralytic polio survivors, typically 15 to 40 years after the acute infection. It is characterised by new progressive muscle weakness, fatigue, and pain in muscles that were previously affected or thought to be unaffected. The pathophysiology involves the premature degeneration of motor neurons that survived the initial infection. After acute polio, surviving motor neurons sprouted new axonal branches to reinnervate orphaned muscle fibres, resulting in enlarged motor units. Decades later, these overworked neurons fail due to metabolic stress and aging. Importantly, post-polio syndrome is NOT due to viral reactivation—no poliovirus is detected in these patients. Management is supportive, focusing on pacing activities, energy conservation, gentle physiotherapy, assistive devices, and pain management. It is a slowly progressive condition that does not reduce life expectancy."

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Q6: "A 3-year-old unvaccinated child from Pakistan presents with acute onset of left leg weakness over 24 hours, preceded by fever and vomiting. On examination, there is flaccid paralysis of the left leg, absent knee and ankle reflexes, but sensation is intact. What is your approach?"

Model Answer: "This presentation is highly suggestive of paralytic poliomyelitis, given the acute asymmetric flaccid paralysis with preserved sensation in an unvaccinated child from an endemic country. My immediate priorities are:

1. Assess for life-threatening complications:

• Respiratory assessment: Check for bulbar or respiratory muscle involvement (respiratory rate, oxygen saturation, vital capacity, ability to cough)
• If any signs of respiratory compromise, arrange ICU admission and prepare for mechanical ventilation

2. Supportive management:

• Bed rest, analgesia for muscle pain (paracetamol, NSAIDs)
• Maintain nutrition and hydration
• Prevent contractures: position limbs in neutral alignment, start passive range-of-motion exercises

3. Diagnostic investigations:

• Stool samples: Two samples, 24–48 hours apart, sent urgently for poliovirus isolation and typing
• Throat swab: For viral isolation
• CSF analysis: Expect lymphocytic pleocytosis with normal glucose (aseptic meningitis pattern)
• Bloods: FBC, CRP, U&E, consider other causes

4. Public health notification:

• This is a notifiable disease. Inform local public health authorities immediately
• Isolate the child using contact precautions (faecal-oral transmission)

5. Differential diagnosis:

• Consider Guillain-Barré syndrome (but more typically symmetric), acute flaccid myelitis (associated with enterovirus D68, West Nile virus), transverse myelitis (would have sensory level and sphincter involvement)

6. Rehabilitation:

• Involve physiotherapy early to prevent contractures and optimize functional recovery

7. Family counselling:

• Explain diagnosis, prognosis, importance of vaccination for other children in the family and community."

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Common Exam Mistakes

❌ Mistake 1: Stating that polio causes sensory loss (it does not; sensation is preserved).

✅ Correction: Poliovirus selectively destroys anterior horn motor neurons; sensory pathways are unaffected.

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❌ Mistake 2: Confusing VAPP with VDPV.

✅ Correction:

• VAPP (Vaccine-Associated Paralytic Polio): Paralysis caused by the vaccine strain virus in a vaccinee or close contact, typically within 4–40 days of OPV administration.
• VDPV (Vaccine-Derived Poliovirus): Vaccine virus that has circulated in under-immunised communities and genetically reverted to neurovirulence (> 1% divergence from Sabin strain).

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❌ Mistake 3: Believing that post-polio syndrome is due to viral reactivation.

✅ Correction: PPS is due to age-related degeneration of surviving motor neurons that were overworked after reinnervating orphaned muscle fibres. No poliovirus is detected in PPS patients.

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❌ Mistake 4: Saying that OPV is no longer used anywhere.

✅ Correction: OPV is still used in mass vaccination campaigns in endemic and high-risk countries (Afghanistan, Pakistan, parts of Africa) because it provides mucosal immunity and can interrupt transmission. However, most polio-free countries have switched to IPV-only schedules.

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❌ Mistake 5: Failing to recognize that polio is a notifiable disease and that all AFP cases in children less than 15 years must be investigated.

✅ Correction: Acute flaccid paralysis (AFP) surveillance is the cornerstone of polio eradication. Every AFP case must be reported, and stool samples sent for poliovirus testing.

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15. Patient/Layperson Explanation

What is Polio?

Polio (short for poliomyelitis) is a viral infection that can attack the nerves and cause paralysis, usually in the legs. It mainly affects young children, though anyone who is unvaccinated can catch it.

How Do You Catch Polio?

The polio virus spreads through contaminated food and water, or from close contact with someone who is infected. It is more common in places with poor sanitation.

What Are the Symptoms?

Most people who get infected with polio (about 7 out of 10) have no symptoms at all. Some people (about 1 in 4) get a mild flu-like illness with fever, tiredness, headache, and sore throat, and recover completely.

In rare cases (less than 1 in 100), the virus attacks the nerves in the spinal cord or brain, causing:

• Sudden weakness or paralysis (usually in one or both legs)
• The weakness is "floppy" (the muscles are limp, not stiff)
• Sensation (feeling) is normal—you can still feel touch and pain
• In severe cases, the muscles that control breathing can be affected, leading to breathing difficulties

Is There a Cure?

No, there is no cure for polio. Treatment focuses on:

• Helping the person breathe if the breathing muscles are weak (using a ventilator)
• Managing pain (with pain relief medicines)
• Physiotherapy to prevent stiffness and help recovery
• Using braces or other supports to help with movement

Can Polio Be Prevented?

Yes! Polio can be prevented with a vaccine. The polio vaccine is very safe and effective. In the UK, the polio vaccine is given as part of the routine childhood vaccines (the "6-in-1" vaccine). Children receive it at 8 weeks, 12 weeks, and 16 weeks of age, with booster doses later.

Is Polio Still Around?

Thanks to global vaccination efforts, polio has been eliminated from most of the world. Wild polio now only exists in two countries: Afghanistan and Pakistan. However, outbreaks can still occur in areas where not enough children are vaccinated.

What is Post-Polio Syndrome?

Some people who had polio as children develop new muscle weakness, tiredness, and pain many years later (usually 20 to 40 years after the original infection). This is called post-polio syndrome. It is not caused by the virus coming back, but by the surviving nerves wearing out over time. Treatment focuses on managing symptoms and maintaining quality of life.

Key Takeaway

Polio is a serious disease, but it can be prevented with vaccination. Make sure your child is up to date with their immunisations.

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16. References

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2. Pallansch MA, Sandhu HS. The eradication of polio—progress and challenges. N Engl J Med. 2006;355(24):2508-2511. doi:10.1056/NEJMp068200

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5. Macklin GR, O'Reilly KM, Grassly NC, et al. Evolving epidemiology of poliovirus serotype 2 following withdrawal of the serotype 2 oral poliovirus vaccine. Science. 2020;368(6489):401-405. doi:10.1126/science.aba1238

6. Plotkin SA, Orenstein WA, Offit PA, Edwards KM. Plotkin's Vaccines. 7th ed. Philadelphia: Elsevier; 2018.

7. Halstead LS, Rossi CD. Post-polio syndrome: clinical experience with 132 consecutive outpatients. Birth Defects Orig Artic Ser. 1987;23(4):13-26. PMID: 3620612

8. Gonzalez H, Olsson T, Borg K. Management of postpolio syndrome. Lancet Neurol. 2010;9(6):634-642. doi:10.1016/S1474-4422(10)70095-8

9. Morales M, Tangermann RH, Wassilak SG. Progress toward polio eradication — worldwide, 2015–2016. MMWR Morb Mortal Wkly Rep. 2016;65(18):470-473. doi:10.15585/mmwr.mm6518a4

10. Paul JR. A History of Poliomyelitis. New Haven: Yale University Press; 1971.

11. Racaniello VR. One hundred years of poliovirus pathogenesis. Virology. 2006;344(1):9-16. doi:10.1016/j.virol.2005.09.015

12. Bodian D. Histopathologic basis of clinical findings in poliomyelitis. Am J Med. 1949;6(5):563-578. doi:10.1016/0002-9343(49)90044-8

13. Howard RS. Poliomyelitis and the postpolio syndrome. BMJ. 2005;330(7503):1314-1318. doi:10.1136/bmj.330.7503.1314

14. Messacar K, Schreiner TL, Maloney JA, et al. A cluster of acute flaccid paralysis and cranial nerve dysfunction temporally associated with an outbreak of enterovirus D68 in children in Colorado, USA. Lancet. 2015;385(9978):1662-1671. doi:10.1016/S0140-6736(14)62457-0

15. World Health Organization. Polio Laboratory Manual. 4th ed. Geneva: WHO; 2004.

16. Alexander JP, Ehresmann K, Seward J, et al. Transmission of imported vaccine-derived poliovirus in an undervaccinated community in Minnesota. J Infect Dis. 2009;199(3):391-397. doi:10.1086/596052

17. Hampton LM, Farrell M, Ramirez-Gonzalez A, et al. Cessation of trivalent oral poliovirus vaccine and introduction of inactivated poliovirus vaccine — worldwide, 2016. MMWR Morb Mortal Wkly Rep. 2016;65(35):934-938. doi:10.15585/mmwr.mm6535a3

18. Collett MS, Hincks JR, Benschop K, et al. Antiviral activity of pocapavir in a randomized, blinded, placebo-controlled human oral poliovirus vaccine challenge model. J Infect Dis. 2017;215(3):335-343. doi:10.1093/infdis/jiw542

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