Epidemiology

Etiology

Caused by Poliovirus, a single-stranded RNA virus from the Picornavirus family (an enterovirus).
Transmitted via the fecal-oral route.
Virus replicates in the oropharynx and GI tract, then spreads via viremia to the CNS.
Specifically targets and destroys anterior horn cells (motor neurons) of the spinal cord, leading to lower motor neuron (LMN) signs.

~70-95% Asymptomatic or mild, nonspecific illness (fever, malaise, headache, sore throat).
Abortive Poliomyelitis (~5%): Minor, flu-like symptoms lasting 2-3 days.
Nonparalytic Poliomyelitis (1-5%): Presents as aseptic meningitis with meningeal signs (nuchal rigidity, headache) without paralysis.
Paralytic Poliomyelitis (<1%): The most severe form.
- Characterized by an asymmetric flaccid paralysis, typically affecting the lower limbs more than the upper limbs.
- Associated with muscle atrophy, areflexia/hyporeflexia, and coarse fasciculations.
- Sensation is usually intact.
- Bulbar poliomyelitis involves cranial nerves (IX, X) and can lead to respiratory failure.

Confirmatory test: PCR of CSF, stool, or oropharyngeal samples to test for poliovirus RNA
CSF will show:
- High protein levels
- Pleocytosis with either neutrophils (early infection) or lymphocytes (late infection)

Guillain-Barré syndrome: Paralysis is typically symmetrical in Guillain-Barré syndrome. In addition, it would not manifest with CSF pleocytosis.
Acute intermittent porphyria: may also present with muscle weakness and bulbar paralysis
Spinal muscular atrophy: Paralysis is typically symmetrical.

Post-polio syndrome (PPS)
- Most frequent complication observed following poliovirus infection (up to 40% of survivors)
- Occurs decades after infection
- Manifests with progressive muscle weakness and pain