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(Infantile Paralysis; Acute Anterior Poliomyelitis; Polio)
Poliomyelitis is an acute infection caused by a poliovirus (an enterovirus). 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 worldwide. 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
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.
Most (70 to 75%) infections cause no symptoms. Symptomatic disease is classified as
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 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 years or decades after paralytic poliomyelitis. This syndrome is characterized by muscle fatigue and decreased endurance, often with weakness, fasciculations, and atrophy.
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.
Paralytic poliomyelitis may be suspected in nonimmunized children or young adults who have asymmetric flaccid limb paralysis or bulbar palsies without sensory loss during an acute febrile illness. However, certain group A and B coxsackieviruses (especially A7), several echoviruses, and enterovirus type 71 may produce similar findings. Also, cases of focal limb weakness or paralysis have been identified after infection with enterovirus D68. West Nile virus infection can also cause an acute flaccid paralysis that is clinically indistinguishable from paralytic poliomyelitis due to polioviruses. Guillain-Barré syndrome causes flaccid paralysis but can be distinguished because of the following:
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 poliomyelitis, recovery is complete.
In paralytic poliomyelitis, 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.
Standard treatment of poliomyelitis 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.
All infants and children should be immunized with poliomyelitis vaccine. 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 Table: 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. As part of the Global Polio Eradication Initiative, all countries are to implement routine IPV vaccination programs by the end of 2016.
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 patients and their household contacts should not be given OPV.
Most poliovirus infections are asymptomatic or cause nonspecific minor illness or aseptic meningitis without paralysis; < 1% of patients develop the classic syndrome of flaccid weakness (paralytic poliomyelitis).
Asymmetric flaccid limb paralysis or bulbar palsies without sensory loss during an acute febrile illness in a nonimmunized child or young adult may indicate paralytic poliomyelitis.
Viral culture of throat swabs, stool, and CSF and reverse transcriptase–PCR of CSF and blood should be done.
In paralytic poliomyelitis, about two thirds of patients have residual permanent weakness.
All infants and children should be immunized, but adults are not routinely vaccinated unless they are at increased risk (eg, because of travel or occupation).
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