Poliomyelitis is an infectious disease caused by the poliovirus. This virus is a member of the Picornaviridae family. It is a small, single-stranded, positive-sense RNA virus without a lipid envelope. Transmission occurs through the fecal–oral route and, occasionally, through respiratory aerosols. The majority of patients will be asymptomatic or have a mild, abortive presentation with flu-like symptoms. Those who develop nonparalytic poliomyelitis will develop signs and symptoms of aseptic meningitis. A very minor proportion of patients will progress to paralytic poliomyelitis, with neurologic progression (including asymmetric flaccid paralysis). The diagnosis is determined by the clinical presentation and can be supported by viral culture, PCR, and serology. Current antivirals are ineffective, and management is supportive. There are 2 vaccines available, which have almost eradicated this disease worldwide.

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RNA Viruses Flowchart Classification

RNA virus identification:
Viruses can be classified in many ways. Most viruses, however, will have a genome formed by either DNA or RNA. RNA genome viruses can be further characterized by either a single- or double-stranded RNA. “Enveloped” viruses are covered by a thin coat of cell membrane (usually taken from the host cell). If the coat is absent, the viruses are called “naked” viruses. Viruses with single-stranded genomes are “positive-sense” viruses if the genome is directly employed as messenger RNA (mRNA), which is translated into proteins. “Negative-sense,” single-stranded viruses employ RNA dependent RNA polymerase, a viral enzyme, to transcribe their genome into messenger RNA.

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General Characteristics and Epidemiology

General characteristics of poliovirus

  • Family: Picornaviridae
  • Genus: Enterovirus
  • Classified as a strain of Enterovirus C
  • RNA virus:
    • Linear
    • Single-stranded
    • Positive-sense
    • Functions as mRNA
  • Diameter: 25–30 nm
  • Icosahedral symmetry
  • Lacks a lipid envelope
  • Acid-stable

Clinically relevant species

Poliomyelitis is caused by 3 serotypes of poliovirus:

  • Wild type 1 (most common)
  • Wild types 2 and 3 (considered eradicated)


  • Poliovirus has been eradicated in most countries because of extensive vaccination efforts.
  • 150 cases were reported in 2019.
  • Endemic countries include: 
    • Pakistan
    • Afghanistan

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Humans are the only known reservoir.


This highly contagious virus is transmitted via:

  • Fecal–oral route
  • Respiratory aerosols


  • Oral entry of the virus → replication in the oropharyngeal and GI lymphatic tissues
  • Asymptomatic viremia → reticuloendothelial system
  • If the infection is not contained → secondary viremia occurs → viral symptoms
  • Virus enters the CNS (unclear process)
  • Viral replication occurs in neurons of the spine (particularly the anterior horn) and brain stem → damage and necrosis → neurologic signs and symptoms
pathogenesis of poliovirus

The pathogenesis of poliovirus:
The virus initially enters and infects lymphoid tissues. Viremia occurs, allowing eventual spread to the nervous system. Replication results in tissue damage and symptoms.

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Clinical Presentation and Diagnosis

Abortive poliomyelitis

The majority of patients are asymptomatic or develop a minor flu-like illness:

  • Fever
  • Malaise
  • Headache
  • Pharyngitis
  • Nausea and vomiting

Nonparalytic poliomyelitis

Approximately 4% of patients will develop nonparalytic poliomyelitis. These patients will present with aseptic meningitis after a prodrome similar to that of abortive poliomyelitis.

  • Fever
  • Headache
  • Nuchal rigidity

Paralytic poliomyelitis

A minority of patients with nonparalytic poliomyelitis will progress to the paralytic form of the disease, characterized by:

  • Muscle spasms
  • Myalgias
  • Profound, asymmetrical muscle weakness:
    • Legs most often affected
    • More severe in proximal muscles
  • Diminished or absent reflexes
  • Normal sensory exam
  • Urinary retention
  • Bulbar involvement:
    • Dysphagia
    • Dysphonia
    • Difficulty handling secretions
    • Respiratory compromise
    • Autonomic dysfunction
paralytic poliovirus infection

A young girl with a deformity of the right lower extremity as a consequence of paralysis from paralytic poliovirus infection

Image: “Paralytic poliovirus infection” by CDC. License: Public Domain

Postpoliomyelitis syndrome

Postpoliomyelitis syndrome manifests as worsening symptoms in poliomyelitis survivors. It can occur decades after the initial infection.

  • Fatigue
  • Progressive weakness and atrophy of affected muscles
  • Fasciculations
  • Pain
  • Restless leg syndrome
  • Respiratory insufficiency


Diagnosis is based on clinical presentation and supported by the diagnostic workup.

Lumbar puncture:

  • Often done in the setting of aseptic meningitis
  • Findings:
    • Moderate pleocytosis
    • ↑ Protein
    • Normal glucose

Specific testing:

  • Viral culture
  • PCR
  • Serology

Management and Prevention


There is no effective antiviral therapy for poliomyelitis. Management is supportive.

  • Close hemodynamic monitoring for patients with bulbar involvement
  • Mechanical ventilation for respiratory failure or airway protection
  • Analgesics for pain
  • Splints to prevent deformities


Patients with nonparalytic poliomyelitis make complete recoveries. For those with paralytic poliomyelitis:

  • 2 out of 3 patients will not regain full strength.
  • 30%–40% will develop postpoliomyelitis syndrome.
  • Mortality: 
    • 4%–6%
    • 10%–20% in adults or bulbar disease


There are 2 vaccines used:

  • Salk (inactivated poliovirus vaccine):
    • Given parenterally
    • Forms only IgG antibodies, not IgA
  • Sabin (oral poliovirus vaccine):
    • Live attenuated
    • Creates IgG and IgA
    • Not used in the United States
    • Patients shed the virus → may be able to mutate and circulate
Poliodrops vaccine poliovirus

A young girl receiving the oral poliovirus vaccine

Image: “A child receiving an oral polio vaccine” by USAID. License: Public Domain

Comparison of Enteroviruses

Table: Comparison of enteroviruses
  • ssRNA virus
  • Icosahedral
  • Nonenveloped
  • Approximately 30 nm
  • ssRNA virus
  • Icosahedral
  • Nonenveloped
  • 25–30 nm
  • ssRNA virus
  • Icosahedral
  • Nonenveloped
  • 20–30 nm
  • Fecal–oral route
  • Respiratory aerosols
  • Fecal–oral route
  • Respiratory aerosols
  • Fecal–oral route
  • Respiratory aerosols
  • URI
  • Herpangina
  • HFMD
  • Aseptic meningitis
  • Myopericarditis
  • Epidemic pleurodynia
  • Neonatal infection
  • Flu-like illness
  • Aseptic meningitis
  • Asymmetric flaccid paralysis
  • Bulbar involvement
  • URI
  • Exanthem
  • Aseptic meningitis
  • Encephalitis
  • Myopericarditis
  • Neonatal infection
  • Clinical
  • PCR
  • Viral culture
  • Clinical
  • PCR
  • Serology
  • Viral culture
  • Clinical
  • PCR
  • Viral culture
HFMD: hand, foot, and mouth disease
URI: upper respiratory tract infection

Differential Diagnosis

  • Guillain–Barré syndrome (GBS): acute, rapidly progressive, acquired inflammatory neuropathy that can be triggered by infectious pathogens. Unlike poliomyelitis, the progressive muscle weakness in GBS is symmetric, there is sensory loss, and fever is rare. The diagnosis is clinical. A lumbar puncture will show a normal cell count and elevated protein. Management requires intensive care support, IV immune globulin, and plasma exchange.
  • West Nile virus infection: infection by a flavivirus. The majority of patients with West Nile virus will be asymptomatic or have headache, myalgias and arthralgias, vomiting, diarrhea, or a rash. A small proportion develop encephalitis, meningitis, or flaccid paralysis. The diagnosis can be made with serology, PCR, and viral cultures. This will differentiate West Nile virus from poliomyelitis. Management is supportive.
  • Acute intermittent porphyria: rare, autosomal dominant disease that results in a deficiency of hydroxymethylbilane synthase. This deficiency leads to accumulation of heme precursors. Patients may experience abdominal pain, psychiatric symptoms, and peripheral neuropathies that can mimic GBS. Progression to quadriplegia and respiratory failure can occur. The diagnosis is based on elevated porphyrin precursors in the urine. Management includes IV heme, dextrose, and trigger avoidance.
  • Muscular dystrophy: group of noninflammatory muscle disorders caused by a mutation in the DMD gene. This mutation leads to muscle fiber destruction and replacement with fatty or fibrous tissue. Patients present with progressive proximal muscle weakness, which leads to the eventual loss of ambulation, as well as contractures, scoliosis, cardiomyopathy, and respiratory failure. Unlike poliomyelitis, a marked elevation in CK may be observed. Genetic testing confirms the diagnosis. Management is supportive.   
  • Multiple sclerosis (MS): chronic inflammatory autoimmune disease leading to demyelination of the CNS. The clinical presentation of MS varies depending on the site of lesions, but it may include neurologic symptoms affecting vision, motor functions, sensation, and autonomic function. Diagnosis is made with MRI of the brain and spine, as well as CSF examination. Management involves corticosteroids for acute exacerbations and disease-modifying agents to slow progression of the disease.


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