The incubation period is usually 3-6 days in a person with no symptoms or for a person to develop non-specific symptoms. The incubation period between exposure and development of paralytic disease is usually 7-21 days but could be as short as 3 days or as long as 35 days.
After infection the poliovirus initially incubates in the gastrointestinal tract. Polio has four possible presentations:
1. The majority of poliovirus infections (about 95%) are subclinical, inapparent infection without symptoms.
2. About 4-8% of cases only develop a minor non-specific illness. Symptoms may include low grade fever, fatigue, malaise, drowsiness, headache, vomiting, constipation, neck stiffness, sore throat and/or muscle pain.
3. About 1-5% of cases are nonparalytic poliomyelitis. Initial symptoms are non-specific (fever, malaise, vomiting, sore throat). One to two days later symptoms of meningeal irritation from aseptic meningitis develop. Recovery is usually complete however nonparalytic poliomyelitis can progress to the paralytic form of the disease.
4. Between 0.1-2% of cases are paralytic poliomyelitis. The paralytic form of the disease occurs when the poliovirus spreads to the motor neurons of the anterior horn cells in the spinal cord (spinal poliomyelitis) and/or brain stem (bulbar paralysis). The cranial nerves may also be affected by polioviruses. The area paralysed depends on the anatomic location of the motor neuron damage. Although the motor neurons do not recover and are not replaced it is possible for other muscles to compensate for the paralysis, resulting in partial or complete recovery from paralytic poliomyelitis for some people.
In polio-free countries with pockets of non-immune/unimmunised communities adults are more likely to present with paralytic poliomyelitis. In countries with endemic polio children less than 3 years are more likely to develop paralytic polio.
The person initially experiences symptoms of a minor non-specific illness, becomes symptom free, then one to three day later develops fever with a rapid onset of descending acute flaccid paralysis. Adolescents and adults may not experience the minor illness symptoms but develop more severe pain in the affected extremities. The progression of paralysis usually stops once the fever abates. Paralysis is usually asymmetrical with reduced or absent deep tendon reflexes. The sensory nerves are not affected.
The diagnosis of paralytic poliomyelitis is based on the clinical course, isolation of poliovirus in two stool samples and the presence of a neurologic deficit 60 days after symptom onset. Neurologic deficit may be complete or partial flaccid paralysis or weakness.
The two stool samples must be taken at least 24 hours apart in the first 14 days after the onset of paralysis are required to diagnose paralytic poliomyelitis. The laboratory must be notified before sending the specimen. Isolation of the virus in stool samples is important to determine if the virus is wild-type or vaccine related.
The differential diagnoses for acute flaccid paralysis include infection by other enteroviruses, other viruses (e.g., Epstein-Barr virus, human immunodeficiency virus, mumps virus), campylobacter jejuni, hypokalaemia, antibiotic reaction (aminoglycosides, tetracyclines, polymixin B), chemical poisoning, cephalic tetanus, fungal-mycotoxins, wasp venom, Guillain-Barre Syndrome, Bell’s Palsy, transverse myelitis.
The complications from polio depend on the anatomic location of the motor neuron damage. People may experience permanent muscle weakness or paralysis, difficulty passing urine and urinary tract infections, uneven limb growth (the affected leg does not grow and the unaffected leg continues to grow normally), bone deformities, heart problems, breathing problems, cranial nerve damage, brain damage and death.
The fatality rate from poliomyelitis varies depending on the presentation. For paralytic spinal poliomyelitis 2-5% of child cases and 15-30% of adult cases may result in death. Up to 75% of cases with bulbar poliomyelitis will die.
People who are immunocompromised are more likely to experience complications and a fatal outcome from poliomyelitis.
Post-polio syndrome occurs 15-40 years after a person has recovered from paralytic poliomyelitis. It is characterised by exacerbation of existing weakness, development of new weakness or paralysis and/or increased muscle pain. Increasing length of time since the acute infection, presence of residual impairment form the acute illness and being female are risk factors for post-polio syndrome. The pathogenesis of post-polio syndrome does not involve ongoing or recurrent poliovirus infection. It is thought to be related to the aging of muscles and nerves that are compensating for the original damage.