Infection of a susceptible individual with poliovirus type 1, 2 or 3, which can lead to a mild meningitic illness with acute paralysis and subsequently postpolio syndrome.
Mainly a disease of childhood.
No sexual preponderance.
Acute poliomyelitis has been eradicated in developed countries, apart from rare cases due to the live, attenuated oral polio vaccine. Serotype 2 has been completely eradicated worldwide (announced by WHO in 1999).
Poliovirus is a ssRNA, non-encapsulated, icosahedral virus 25–30 nm in size. It is an enterovirus, i.e. it spreads by the faeco–oral route.
The virus is neurotropic, with propensity for the anterior horn cells of the spinal cord and cranial nerve motor neurones. The virus enters via the gastrointestinal tract, then migrates up peripheral nerves.
The incubation period is 7–14 days, a number of patterns occur:
· Subclinical infection occurs in 95% of infected individuals.
· Acute polio presents with a mild self-limiting fever with or without meningism.
· Paralytic poliomyelitis occurs in about 0.1% of individuals. This form is predisposed to by male sex; exercise early in the illness; trauma, surgery, or intra-muscular injection which localises the paralysis, recent tonsillectomy (bulbar poliomyelitis).
i. After an initial febrile illness, symptoms subside for 4–5 days.
ii. Symptoms then reoccur with greater severity and signs of meningeal irritation and muscle pain, followed by paralysis typically affecting one arm and the opposite leg.
iii. Bulbar poliomyelitis is characterised by cranial nerve involvement commonly with palsies of the soft palate, pharyngeal and laryngeal muscles. Dysphagia and dysarthria result, with the risk of aspiration pneumonia.
iv. Respiratory involvement may lead to the need for ventilatory support.
Postpolio syndrome – this is progressive, often painful weakness in the territories originally affected by the acute illness which can occur many years later (usually 20–40 years) in about a quarter of patients. More suffer from pain, but without progressive weakness. It appears to be a failure of the compensatory mechanisms which occur to bring about the original recovery – those with a greater original recovery tend to have the greatest decline, and those who were younger at the age of acute polio appear to be relatively protected.
Diagnosis is clinical but laboratory confirmation is by viral culture. In post-polio syndrome, polio virus is not found in the CNS, but muscle EMG and biopsy show evidence of motor unit loss.
Acute treatment is supportive with bed rest, respiratory support where indicated.
i. Occupational and physical therapy should be used to maximise function.
ii. Splinting and even tendon transfer or arthrodesis may be required for weakness or joint deformity.
Shortening: Leg length inequality of up to 3 cm may be treated by built up shoes, larger differences may require leg lengthening (or shortening of the opposite leg) procedures.
Post-polio syndrome management is non-specific, with the treatment of limb and joint deformities, management of pain, and maximisation of function and strength by not overworking muscles. Sleep disorders, including nocturnal hypoventilation, need to be treated with non-invasive ventilation.
Prophylaxis: Live attenuated (Sabin) or killed (Salk) polio vaccine.