Poliomyelitis is an acute infection caused by a poliovirus. Manifestations include a nonspecific minor illness (abortive poliomyelitis), sometimes aseptic meningitis without paralysis (nonparalytic poliomyelitis), and, less often, flaccid weakness of various muscle groups (paralytic poliomyelitis). Diagnosis is clinical, although laboratory diagnosis is possible. Treatment is supportive.
Polioviruses have 3 serotypes. Type 1 is the most paralytogenic and used to be the most common cause of epidemics. Humans are the only natural host. Infection is highly transmittable via direct contact. Asymptomatic and minor infections (abortive poliomyelitis) are more common than nonparalytic or paralytic infections by ≥ 60:1 and are the main source of spread. Extensive vaccination has almost eradicated the disease in developed countries. However, cases still occur in regions with incomplete immunization, such as sub-Saharan Africa and southern Asia.
The virus enters via the fecal-oral or respiratory route, then enters the lymphoid tissues of the GI tract. A primary (minor) viremia follows with spread of virus to the reticuloendothelial system. Infection may be contained at this point, or the virus may further multiply and cause several days of secondary viremia, culminating in the development of symptoms and antibodies.
In paralytic infections, poliovirus enters the CNS—whether via secondary viremia or via migration up peripheral nerves is unclear. Significant damage occurs in only the spinal cord and brain, particularly in the nerves controlling motor and autonomic function. Inflammation compounds the damage produced by primary viral invasion. Factors predisposing to serious neurologic damage include increasing age (throughout life), recent tonsillectomy or intramuscular injection, pregnancy, impairment of B-cell function, and physical exertion concurrent with onset of the CNS phase.
Poliovirus is present in the throat and feces during incubation and, after symptom onset, persists 1 to 2 wk in the throat and ≥ 3 to 6 wk in feces; the fecal-oral and respiratory routes are the usual method of transmission.
Symptoms and Signs
Most (70 to 75%) infections cause no symptoms. Symptomatic disease is classified as abortive poliomyelitis or as paralytic or nonparalytic poliomyelitis.
Most symptomatic infections, particularly in young children, are minor, with 1 to 3 days of slight fever, malaise, headache, sore throat, and vomiting, which develop 3 to 5 days after exposure. There are no neurologic symptoms or signs, and physical examination is unremarkable except for the presence of fever.
Paralytic and nonparalytic:
Paralytic poliomyelitis occurs in < 1% of all infections. It may develop without a preceding minor illness, particularly in older children and adults. Incubation is usually 7 to 21 days.
Common manifestations include aseptic meningitis, deep muscle pain, hyperesthesias, paresthesias, and, during active myelitis, urinary retention and muscle spasms. Asymmetric flaccid paralysis may develop and progress over 2 to 3 days. Encephalitic signs occasionally predominate.
Dysphagia, nasal regurgitation, and nasal voice are usually the earliest signs of bulbar involvement, but some patients have pharyngeal paralysis and cannot control oral secretions. As with skeletal muscle paralysis, bulbar involvement may worsen over 2 to 3 days and, in some patients, affects the respiratory and circulatory centers of the brain stem, leading to respiratory compromise. Infrequently, respiratory failure develops when the diaphragm or intercostal muscles are affected.
Some patients develop postpoliomyelitis syndrome (see below).
When there are no CNS manifestations, symptomatic polio resembles other systemic viral infections and is typically not considered or diagnosed except during an epidemic.
Nonparalytic poliomyelitis resembles other viral meningitides. In such patients, lumbar puncture is usually done; typical CSF findings are normal glucose, mildly elevated protein, and a cell count of 10 to 500/μL (predominantly lymphocytes). Detection of the virus in a throat swab, feces, or CSF or demonstration of a rise in specific antibody titer confirms infection with poliovirus but is usually not needed in patients with uncomplicated aseptic meningitis.
Asymmetric flaccid limb paralysis or bulbar palsies without sensory loss during an acute febrile illness in a nonimmunized child or young adult almost always indicates paralytic poliomyelitis. However, certain group A and B coxsackieviruses (especially A7), several echoviruses, and enterovirus type 71 may produce similar findings. West Nile virus infection can also cause an acute flaccid paralysis that is clinically indistinguishable from paralytic poliomyelitis due to polioviruses. Guillain-Barré syndrome (see Guillain-Barré Syndrome (GBS)) causes flaccid paralysis but can be distinguished because it usually causes no fever, muscle weakness is symmetric, sensory deficits occur in 70% of patients, and CSF protein is usually elevated and CSF cell count is normal.
Epidemiologic clues (eg, immunization history, recent travel, age, season) can help suggest the cause. Because identification of poliovirus or another enterovirus as the cause of acute flaccid paralysis is important for public health reasons, viral culture of throat swabs, stool, and CSF and reverse transcriptase–PCR of CSF and blood should be done in all cases. Specific serologic testing for polioviruses, other enteroviruses, and West Nile virus should also be done.
In nonparalytic forms, recovery is complete.
In paralytic forms, about two thirds of patients have residual permanent weakness. Bulbar paralysis is more likely to resolve than peripheral paralysis. Mortality is 4 to 6% but increases to 10 to 20% in adults and in patients with bulbar disease.
Muscle fatigue and decreased endurance, often accompanied by weakness, fasciculations, and atrophy, may develop years or decades after paralytic poliomyelitis, particularly in older patients and in patients who are severely affected initially. Damage usually occurs in previously affected muscle groups. The cause may be related to further loss of anterior horn cells due to aging in a population of neurons already depleted by earlier poliovirus infection. However, it rarely substantially increases disability.
Standard treatment is supportive and includes rest, analgesics, and antipyretics as needed. Specific antiviral therapy is not available.
During active myelitis, precautions to avoid complications of bed rest (eg, deep venous thrombosis, atelectasis, UTI) and prolonged immobility (eg, contractures) may be necessary. Respiratory failure may require mechanical ventilation. Mechanical ventilation or bulbar paralysis requires intensive pulmonary toilet measures.
Treatment of postpoliomyelitis syndrome is supportive.
All infants and children should be immunized. The American Academy of Pediatrics recommends vaccination at ages 2 mo, 4 mo, and 6 to 18 mo and a booster dose at age 4 to 6 yr (see also Poliomyelitis Vaccine and Table 2: Recommended Immunization Schedule for Ages 0–6 yr). Childhood vaccination produces immunity in > 95% of recipients.
Salk inactivated poliovirus vaccine (IPV) is preferred to Sabin live-attenuated oral polio vaccine (OPV), which causes paralytic poliomyelitis in about 1 case per 2,400,000 doses and is thus no longer available in the US. Serious adverse effects have not been associated with IPV.
Adults are not routinely vaccinated. Nonimmunized adults traveling to endemic or epidemic areas should receive primary vaccination with IPV, including 2 doses given 4 to 8 wk apart and a 3rd dose given 6 to 12 mo later. At least 1 dose is given before travel. Immunized adults traveling to endemic or epidemic areas should be given 1 dose of IPV. Immunocompromised hosts and their household contacts should not be given OPV.
Last full review/revision June 2013 by Mary T. Caserta, MD
Content last modified September 2013