Poliovirus/Poliomyelitis

Classification

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)

Epidemiology

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

Pathogenesis

Reservoir

Humans are the only known reservoir.

Transmission

This highly contagious virus is transmitted via:

• Fecal–oral route
• Respiratory aerosols

Pathophysiology

• 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

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

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

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

Management

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

Prognosis

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

Prevention

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

Comparison of Enteroviruses

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.