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Summary Table

Category	Details
Risk Factors	Unvaccinated or incompletely vaccinated children (< 5 years); immunocompromised individuals; travel to endemic areas (Afghanistan, Pakistan); poor sanitation and overcrowding; B-cell immunodeficiency (prolonged viral shedding)
Etiology	Poliovirus (genus Enterovirus, family Picornaviridae); three serotypes: type 1 (most paralytogenic, most epidemic), type 2 (eradicated in wild form since 2015), type 3 (eradicated in wild form since 2019); transmitted via the fecal-oral route (primary) and respiratory droplets (less common)
Patient Presentation	A young, unvaccinated child presenting with acute onset of asymmetric flaccid paralysis predominantly affecting the lower extremities, preceded by a febrile prodrome (fever, sore throat, headache, vomiting); sensation is intact
Classic Physical Exam	Asymmetric, descending flaccid paralysis; decreased or absent deep tendon reflexes in affected limbs; muscle atrophy in chronic cases; no sensory loss; nuchal rigidity if meningeal involvement is present; bulbar signs (dysphagia, dysphonia, respiratory failure) in bulbar polio
Key Diagnostic Results	CSF: lymphocytic pleocytosis (10-500 cells/mcL), mildly elevated protein, normal glucose; stool viral culture is the gold standard for virus isolation (highest yield); throat swab culture; viral PCR of CSF or stool
Management	No antiviral therapy exists; treatment is entirely supportive: antipyretics, IV fluids, respiratory support with mechanical ventilation if bulbar involvement is present; physical rehabilitation for residual paralysis; prevention through vaccination is the cornerstone
Keywords	"Asymmetric flaccid paralysis"; "intact sensation"; "anterior horn cell destruction"; "fecal-oral transmission"; "unvaccinated child"; "LMN signs without sensory deficit"; "acute flaccid paralysis (AFP)"; "post-polio syndrome"

1. Pathophysiology

Poliovirus is a small, non-enveloped, single-stranded positive-sense RNA virus belonging to the Enterovirus genus within the Picornaviridae family. It exists in three serotypes, of which type 1 is the most frequently associated with paralytic disease and was historically the predominant cause of epidemics.

The virus enters the body through the oropharynx, typically via the fecal-oral route in areas of poor sanitation, or less commonly through respiratory droplets. After ingestion, the virus replicates in the pharyngeal and intestinal mucosal lymphoid tissue (Peyer's patches and tonsils). This initial replication phase corresponds to the "minor illness" or prodromal phase, producing nonspecific symptoms such as fever, malaise, sore throat, nausea, and vomiting. During this phase, the virus is shed in the stool and pharyngeal secretions, making the individual highly contagious even before neurological symptoms appear.

From the gut-associated lymphoid tissue, the virus enters the bloodstream, causing a primary viremia. In the overwhelming majority of patients (approximately 95%), the immune response clears the virus at this stage, and the infection remains entirely asymptomatic. In a smaller proportion (1-5%), the virus causes non-paralytic aseptic meningitis, with headache, neck stiffness, and CSF pleocytosis, but without motor deficits.

In fewer than 1% of all infections, a secondary viremia allows the virus to cross the blood-brain barrier and invade the central nervous system. The key pathological target is the anterior horn motor neurons of the spinal cord. The virus selectively destroys these lower motor neurons (LMNs), which is why the clinical picture is that of a flaccid paralysis with hypotonia, hyporeflexia, and eventual muscle atrophy. Because the virus targets motor neurons exclusively and spares the dorsal horn (sensory neurons), sensation remains completely intact. This is a critical clinical feature that separates poliomyelitis from conditions like Guillain-Barre syndrome or transverse myelitis.

The asymmetry of the paralysis results from the uneven, patchy destruction of anterior horn cells along the spinal cord. The lower extremities are affected more frequently than the upper extremities. In bulbar poliomyelitis, the virus destroys motor nuclei of cranial nerves in the brainstem (CN IX, X, XII), leading to pharyngeal and laryngeal paralysis, inability to swallow, and potentially fatal respiratory center failure. In bulbospinal polio, both spinal and brainstem motor neurons are involved simultaneously, carrying the highest mortality.

The destruction of anterior horn cells is irreversible. During recovery, surviving motor neurons undergo collateral sprouting, extending new axonal branches to reinnervate orphaned muscle fibers. This compensatory mechanism explains partial recovery of motor function over months. However, decades later, these overworked surviving neurons may begin to fail, giving rise to post-polio syndrome (new muscle weakness, fatigue, and pain appearing 15 to 40 years after the initial infection).

2. Classification and Clinical Manifestation

Clinical Form	Frequency	Key Features	Prognosis
Asymptomatic (Inapparent) Infection	~95% of all infections	No symptoms; virus replicates in gut and pharynx; individual is still infectious	Complete recovery; important reservoir for transmission
Abortive Poliomyelitis (Minor Illness)	~4-8%	Nonspecific: low-grade fever, malaise, sore throat, headache, nausea, vomiting; lasts 2-3 days; no CNS involvement	Complete recovery
Non-Paralytic Poliomyelitis (Aseptic Meningitis)	~1-5%	All symptoms of minor illness PLUS signs of meningeal irritation: neck and back stiffness, headache; CSF shows lymphocytic pleocytosis; no paralysis	Complete recovery within 1-2 weeks
Paralytic Poliomyelitis	< 1%	Follows a biphasic course (minor illness then brief improvement then paralysis); acute onset of asymmetric flaccid paralysis; see subtypes below	Two-thirds of patients with paralysis have permanent residual weakness at 12 months

Subtypes of Paralytic Poliomyelitis

Subtype	Proportion of Paralytic Cases	Features	Mortality
Spinal	~79%	Asymmetric flaccid paralysis of limbs (legs > arms); absent DTRs; intact sensation; maximum paralysis within 48 hours of onset	2-5% (children); 15-30% (adults)
Bulbar	~2%	Cranial nerve motor nuclei involvement; dysphagia, dysphonia, nasal regurgitation; respiratory center paralysis; inability to handle secretions	25-75%
Bulbospinal	~19%	Combined spinal and bulbar features; highest risk of respiratory failure from both diaphragmatic and central respiratory failure	25-75%

The Biphasic ("Dromedary") Pattern

Paralytic poliomyelitis classically follows a biphasic illness pattern: the initial minor illness (fever, GI symptoms) improves for 1-3 days, then the patient deteriorates abruptly with the onset of high fever, severe myalgias, nuchal rigidity, and rapidly progressive asymmetric flaccid paralysis reaching maximum severity within 48 hours in children. This biphasic course is a commonly tested feature in exam vignettes.

3. Diagnostic Workup

Test	Role	Expected Findings
Stool viral culture	Gold standard for poliovirus isolation	Highest yield; virus detectable for up to 3-6 weeks after symptom onset; distinguishes wild-type vs. vaccine-derived strains
Throat swab viral culture	Supportive early diagnosis	Virus recoverable within first 5 days of illness; lower yield than stool
CSF analysis (lumbar puncture)	Evaluate for CNS involvement	Lymphocytic pleocytosis (10-500 cells/mcL); mildly elevated protein (40-50 mg/dL); normal glucose; early neutrophilic predominance may shift to lymphocytic within days
Viral PCR (RT-PCR)	Rapid confirmation	Detects poliovirus RNA in stool or CSF; can differentiate serotype and wild vs. vaccine-derived virus
Serology (neutralizing antibodies)	Supplementary evidence	Fourfold rise in antibody titer between acute and convalescent sera; less useful in vaccinated populations
Nerve conduction studies / EMG	Characterize the paralysis	Findings consistent with anterior horn cell disease (LMN pattern): reduced motor amplitudes, fibrillation potentials, fasciculations; normal sensory nerve conduction
MRI of the spinal cord	Rule out structural causes	May show T2 hyperintensity in the anterior horns of the spinal cord; helps exclude cord compression or transverse myelitis

When a child presents with acute flaccid paralysis (AFP), the clinical evaluation begins with a thorough history and neurological examination. The presence of asymmetric flaccid weakness with absent reflexes and intact sensation in an unvaccinated or incompletely vaccinated child should raise immediate concern for paralytic poliomyelitis.

The best initial step in the workup is to collect two stool specimens taken 24-48 hours apart. Stool specimens have the highest likelihood of poliovirus isolation and remain the gold standard. The virus can be recovered from stool for 3-6 weeks after symptom onset, making this the most reliable sample even if the patient presents late. A throat swab can also be obtained but is useful only in the first 5 days of illness.

Lumbar puncture should be performed to evaluate the CSF. Typical cerebrospinal fluid findings include normal glucose, mildly elevated protein, and a cell count of 10 to 500 per microliter with predominantly lymphocytes. It is important to note that in the very early phase (first few days), the pleocytosis may show a neutrophilic predominance before shifting to lymphocytes. Isolation of virus from the CSF is diagnostic but is rarely accomplished.

RT-PCR testing of stool or CSF provides rapid and type-able confirmation and can distinguish between wild-type poliovirus and vaccine-derived poliovirus (VDPV), which is critical for public health response. Intratypic differentiation through genomic sequencing further classifies the isolate.

EMG and nerve conduction studies are not required for diagnosis but may be performed to support the clinical picture, showing an anterior horn cell (LMN) pattern. Characteristically, motor amplitudes are reduced while sensory nerve conduction is normal, reinforcing the purely motor nature of the disease.

MRI of the spinal cord may show signal abnormality in the anterior horns, but its primary role is to exclude other causes of AFP such as spinal cord compression, transverse myelitis, or infarction.

4. Management and Treatment

Phase	Intervention	Details
Acute Stabilization	Supportive care	Bed rest; antipyretics (acetaminophen or ibuprofen) for fever and pain; IV fluid resuscitation; monitoring for respiratory compromise
Respiratory Failure	Mechanical ventilation	Required in bulbar or bulbospinal polio with loss of airway protective reflexes or diaphragmatic paralysis; may need tracheostomy for prolonged ventilatory support
Pain Management	Analgesics, warm compresses	Moist heat to affected muscles; positioning with supportive devices to relieve muscle spasm
Acute Rehabilitation	Physical therapy	Gentle passive range-of-motion exercises during acute phase; active strengthening exercises once pain resolves; prevention of contractures
Long-Term Rehabilitation	Orthopedic and rehabilitative care	Braces, orthoses, and assistive devices; corrective surgery for skeletal deformities (e.g., scoliosis, limb-length discrepancy); vocational rehabilitation
Post-Polio Syndrome	Supportive; no disease-modifying therapy	Energy conservation strategies; moderate low-impact exercise; weight management; monitoring for new respiratory insufficiency; IVIG has been studied but remains investigational
Prevention	Vaccination	The single most important intervention (see immunization schedule below)

No treatment for acute poliomyelitis exists except supportive care, which may help to ensure survival, modify the disability, and improve the outcome. This is a foundational fact. The emphasis on any exam question about polio treatment will center on supportive care and prevention.

During the acute phase, the patient should be placed on bed rest. Fever is managed with standard antipyretics such as acetaminophen. Adequate hydration with intravenous fluids is maintained. Pain and muscle spasm are addressed with analgesics and application of moist heat or warm packs to the affected muscles. Positioning and supportive splinting help prevent contractures in paralyzed limbs.

The most critical component of acute management is monitoring for respiratory failure. In bulbar and bulbospinal forms, paralysis of the pharyngeal muscles, diaphragm, or brainstem respiratory centers can cause life-threatening respiratory compromise. Therapy may include providing medication for fever and irritation, preventing respiratory tract infections, and managing respiratory paralysis via mechanical ventilation if required. Inability to swallow or handle oral secretions may necessitate nasogastric feeding and suctioning. Tracheostomy may be required for prolonged ventilatory support.

During recovery, physical therapy is initiated early with gentle passive range-of-motion exercises to prevent joint contractures and muscle shortening. Once the acute pain subsides, active rehabilitation is introduced to maximize the function of surviving motor units. Orthopedic interventions such as braces, crutches, or corrective surgery are used for long-term management of residual deformity.

Post-polio syndrome (PPS) affects approximately 25-40% of persons with paralytic poliomyelitis during childhood, developing approximately 15 to 40 years later, with new onset of muscle pain, weakness, or paralysis. The mechanism involves progressive failure of the compensatory collateral motor neuron sprouts established during initial recovery. Currently, there is no treatment for PPS. It is recommended that polio survivors follow a healthy diet, exercise in moderation, and visit a physician regularly. IVIG has been studied in clinical trials for PPS but is not part of standard therapy.

Prevention: The Kemenkes RI Polio Immunization Schedule

Prevention through vaccination is the single most important concept tested in association with poliomyelitis. The combination totals 6 doses: 4 doses of oral polio vaccine (bOPV) and 2 doses of inactivated polio vaccine (IPV), which is in line with WHO and ITAGI recommendations.

Age	Vaccine	Route	Notes
< 1 month (at birth or with BCG)	bOPV dose 1	Oral (drops)	Given at earliest contact
2 months	bOPV dose 2	Oral (drops)	Given with DPT-HB-Hib 1, PCV 1, RV 1
3 months	bOPV dose 3	Oral (drops)	Given with DPT-HB-Hib 2, PCV 2, RV 2
4 months	bOPV dose 4 + IPV dose 1	Oral + IM injection	Given with DPT-HB-Hib 3, RV 3
9 months	IPV dose 2	IM injection	Given with Campak-Rubella dose 1
18 months	IPV booster (optional/recommended)	IM injection	Given with DPT-HB-Hib booster, Campak-Rubella dose 2

OPV (bivalent oral polio vaccine / bOPV): A live-attenuated vaccine covering types 1 and 3. It induces mucosal (intestinal) immunity, which is critical for interrupting fecal-oral transmission. The drawback is the extremely rare risk of vaccine-associated paralytic poliomyelitis (VAPP), estimated at approximately 1 case per 2.4 million doses. There is also the risk of circulating vaccine-derived poliovirus (cVDPV) in under-immunized communities where the attenuated virus can mutate back toward neurovirulence.

IPV (inactivated polio vaccine): A killed whole-virus vaccine administered by injection that covers all three serotypes. It provides excellent humoral (systemic) immunity but does not induce significant mucosal immunity. No risk of VAPP exists with IPV use. The second dose of IPV was introduced to strengthen protection against all poliovirus types, including type 2, which is no longer contained in bOPV, as part of Indonesia's commitment to achieving global polio eradication by 2026.

Contraindication to OPV: OPV must never be given to immunocompromised patients (e.g., severe combined immunodeficiency, HIV with severe immunosuppression, patients on immunosuppressive therapy) due to the risk of VAPP. These patients must receive IPV only. For catch-up vaccination, children above 7 years of age should receive IPV only.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Guillain-Barre Syndrome (GBS)	Acute flaccid paralysis; hyporeflexia or areflexia; can follow a viral prodrome	GBS produces symmetric, ascending paralysis with sensory involvement (paresthesias, pain); CSF shows albuminocytologic dissociation (elevated protein, normal cell count), NOT pleocytosis; NCS shows demyelinating pattern
Transverse Myelitis	Acute onset of limb weakness with UMN or LMN features depending on the level	Transverse myelitis causes a sensory level (band-like sensory loss); bladder dysfunction is prominent; MRI shows a T2 hyperintense lesion extending over multiple segments; symmetric weakness
Acute Flaccid Myelitis (AFM)	Acute flaccid limb weakness in a child, often preceded by viral illness (enterovirus D68); anterior horn cell involvement on MRI	AFM is clinically very similar but caused by non-polio enteroviruses (EV-D68 or EV-A71); stool culture is negative for poliovirus; MRI similarly shows anterior horn involvement; epidemiologically distinct (occurs in clusters in temperate climates)
Spinal Cord Compression	Acute weakness of limbs; can present with hyporeflexia at the level of the lesion	Produces upper motor neuron signs below the level of compression (hyperreflexia, Babinski sign); sensory level and bladder/bowel dysfunction; MRI shows compressive pathology (tumor, abscess, hematoma)
Botulism (Infant)	Flaccid paralysis in an infant; hypotonia ("floppy baby"); areflexia	Botulism produces symmetric, descending paralysis starting with cranial nerves (ptosis, weak cry, poor feeding); constipation is a classic early feature; no fever; EMG shows incremental response to repetitive stimulation
Myasthenia Gravis	Weakness; may involve bulbar muscles (dysphagia, dysphonia)	Produces fatigable weakness that worsens with use; reflexes are preserved; positive edrophonium (Tensilon) test; AChR or MuSK antibodies present; no CSF pleocytosis
Diphtheric Neuropathy	Pharyngeal weakness with dysphagia, followed by limb weakness; occurs in children	History of pharyngeal membrane (gray pseudomembrane); paralysis is delayed (weeks after pharyngitis); palatal palsy occurs first; caused by diphtheria toxin affecting peripheral nerves

6. Traps and High-Yield Pearls

The single most common way students get poliomyelitis questions wrong is by confusing it with Guillain-Barre syndrome. Both present with acute flaccid paralysis and hyporeflexia, and both may follow a prodromal illness. The discriminating features that the test-writer will embed in the vignette are: poliomyelitis produces asymmetric paralysis with intact sensation and a CSF pleocytosis, while GBS produces symmetric ascending paralysis with sensory symptoms and a classic albuminocytologic dissociation (high protein, no cells). If you see "ascending, symmetric, areflexia, paresthesias" in the stem, think GBS. If you see "asymmetric, flaccid, lower limbs, no sensory loss, unvaccinated child," think polio.

A second trap involves the CSF findings. Students may confuse the early neutrophilic predominance in the CSF for a bacterial process. Remember that poliomyelitis CSF will transition to a lymphocytic predominance within days, and glucose is always normal. Bacterial meningitis will show a low glucose and very high protein.

A third high-yield pearl: always connect the discussion of poliomyelitis to vaccination and public health prevention. Many vignettes will test your understanding of OPV vs. IPV, particularly the contraindication of OPV in immunodeficient patients and the concept of VAPP. If a vignette describes an immunocompromised infant developing flaccid paralysis after receiving oral polio drops, the answer is VAPP and the teaching point is that this child should have received IPV only.

A fourth trap concerns post-polio syndrome. A vignette may present a 50- or 60-year-old patient with a childhood history of polio who develops new muscle weakness and fatigue. Students may be tempted to select recurrent poliomyelitis or a new neurological diagnosis. The correct answer is post-polio syndrome, which results from progressive degeneration of the compensatory motor neuron sprouts established during the initial recovery decades earlier. There is no curative treatment.

Finally, remember the anterior horn cell localization. Poliomyelitis is the prototypical lower motor neuron disease of the anterior horn. The tested competency is your ability to recognize LMN signs (flaccid paralysis, muscle atrophy, fasciculations, hyporeflexia) and distinguish them from UMN signs (spasticity, hyperreflexia, Babinski). The presence of preserved sensation is the clinical feature that points to the anterior horn rather than the peripheral nerve.

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