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Poliomyelitis
is an acute infection caused by a poliovirus. Manifestations include
a nonspecific minor illness, 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 the most common cause of epidemics. Humans are the only natural host. Infection is highly transmittable via direct contact. Asymptomatic or minor infections exceed 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.
Virus enters the mouth via the fecal-oral route, multiplies in lymphoid tissues resulting in primary viremia and later, several days of secondary viremia, culminating in development of antibodies and development of symptoms. Virus reaches the CNS via secondary viremia or migration up peripheral nerves. Virus 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.
Significant damage occurs in only the spinal cord and brain. Inflammation compounds 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-lymphocyte function, and physical exertion concurrent with onset of the CNS phase.
Symptoms and Signs
Symptomatic disease may be major (paralytic or nonparalytic) or minor. 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.
Major poliomyelitis usually develops without a preceding minor illness, particularly in older children and adults. Incubation is usually 7 to 14 days. Common manifestations may include aseptic meningitis, deep muscle pain, hyperesthesias, paresthesias, and, during active myelitis, urinary retention and muscle spasms. Asymmetric flaccid paralysis may develop. Dysphagia, nasal regurgitation, and nasal voice are early signs of bulbar involvement. Encephalitic signs occasionally predominate. Infrequently, respiratory failure develops.
Some patients develop postpoliomyelitis syndrome (see below).
Diagnosis
Nonparalytic poliomyelitis may resemble other viral meningitides, with CSF usually revealing normal glucose, mildly elevated protein, and a cell count of 10 to 500/μL (predominantly lymphocytes). Isolation of the virus from the throat or feces or demonstration of a rise in specific antibody titer confirms poliomyelitis.
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. Rarely, 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 polio viruses. Epidemiologic clues as well as specific serologic testing for West Nile virus can differentiate these disorders. Guillain-Barré syndrome (see Peripheral Nervous System and Motor Unit Disorders: Guillain-Barré Syndrome (GBS)) produces flaccid paralysis, but usually it produces no fever, muscle weakness is symmetric, sensory deficits occur in 70% of cases, and CSF protein is usually elevated with a normal cell count.
Prognosis
In nonparalytic forms, recovery is complete. In paralytic forms, about 2⁄3 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 those with bulbar disease.
Postpoliomyelitis
syndrome—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 those more 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. It rarely produces severe increases in disability.
Treatment
Standard treatment is supportive, including rest, analgesics, and antipyretics as needed. Specific antiviral therapy is still investigational.
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.
Prevention
All infants and children should be immunized. The American Academy of Pediatrics recommends vaccination at 2 mo, 4 mo, and 6 to 18 mo and a booster dose at 4 to 6 yr (see also Immunization: Poliomyelitis; see Approach to the Care of Normal Infants and Children:Health Supervision of the Well Child for and Fig. Fig. 3: Approach to the Care of Normal Infants and Children: Recommended childhood and adolescence immunization schedule.). 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 given 6 to 12 mo later. At least 1 dose is given before travel. Immunized adults traveling to endemic or epidemic areas should receive 1 dose of IPV. Immunocompromised hosts and their household contacts should not receive OPV.
Last full review/revision November 2005
Content last modified November 2005
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