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Poliomyelitis

(Infantile Paralysis; Acute Anterior Poliomyelitis; Polio)

By

Brenda L. Tesini

, MD, University of Rochester School of Medicine and Dentistry

Last full review/revision Sep 2019| Content last modified Sep 2019
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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. (See also Overview of Enterovirus Infections.)

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. In 2018, there were 33 reported cases of wild-type poliovirus type 1 (Afghanistan, 21 cases; Pakistan, 12 cases) and 104 cases of circulating vaccine-derived poliovirus (Democratic Republic of the Congo, 20 cases; Niger, 10 cases; Nigeria, 34 cases; Papua New Guinea, 26 cases; Somalia, 12 cases; and 1 cases each in Indonesia and Mozambique). (See also the Polio Eradication Initiative.)

Pathophysiology

The virus enters via the fecal-oral or respiratory route, then enters the lymphoid tissues of the gastrointestinal 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 central nervous system—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

  • Physical exertion concurrent with onset of the central nervous system phase

Poliovirus is present in the throat and feces during incubation and, after symptom onset, persists 1 to 2 weeks in the throat and 3 to 6 weeks in feces.

Pearls & Pitfalls

  • Most poliovirus infections do not involve the central nervous system or cause paralysis.

Symptoms and Signs

Most (70 to 75%) infections cause no symptoms. Symptomatic disease is classified as

  • Abortive poliomyelitis

  • Paralytic or nonparalytic poliomyelitis

Abortive 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 poliomyelitis and nonparalytic poliomyelitis

About 4% of patients with poliovirus infection develop nonparalytic central nervous system involvement with aseptic meningitis. Patients typically have a stiff neck and/or back and headache that appear after several days of prodrome similar to abortive poliomyelitis. Manifestations last 2 to 10 days.

Paralytic poliomyelitis occurs in < 1% of all poliovirus infections. It can manifest as a biphasic illness in infants and young children with a paralytic phase occurring several days after resolution of abortive poliomyelitis symptoms. Incubation is usually 7 to 21 days.

Common manifestations of paralytic poliomyelitis in addition to aseptic meningitis include 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.

Diagnosis

  • Lumbar puncture

  • Viral culture (stool, throat, and cerebrospinal fluid)

  • Reverse transcriptase–polymerase chain reaction of blood or cerebrospinal fluid

  • Serologic testing for poliovirus serotypes, enteroviruses, and West Nile virus

When there are no central nervous system manifestations, symptomatic polio (abortive poliomyelitis) 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 cerebrospinal fluid findings are normal glucose, mildly elevated protein, and a cell count of 10 to 500/mcL (predominantly lymphocytes). Detection of the virus in a throat swab, feces, or cerebrospinal fluid 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 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:

  • It usually causes no fever.

  • Muscle weakness is symmetric.

  • Sensory deficits occur in 70% of patients

  • Cerebrospinal fluid protein is usually elevated and cerebrospinal fluid 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 cerebrospinal fluid and reverse transcriptase–polymerase chain reaction of cerebrospinal fluid and blood should be done in all cases. Specific serologic testing for polioviruses, other enteroviruses, and West Nile virus should also be done.

Prognosis

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.

Treatment

  • Supportive care

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, urinary tract infection) and prolonged immobility (eg, contractures) may be necessary. Respiratory failure may require mechanical ventilation. Mechanical ventilation or bulbar paralysis requires intensive pulmonary toilet measures.

Prevention

All infants and children should be immunized with poliomyelitis vaccine. The American Academy of Pediatrics recommends vaccination at ages 2 months, 4 months, and 6 to 18 months and a booster dose at age 4 to 6 years (see table Recommended Immunization Schedule for Ages 0–6 years). Childhood vaccination produces immunity in > 95% of recipients.

Salk inactivated poliovirus vaccine (IPV) is preferred to Sabin live-attenuated oral polio vaccine (OPV). The attenuated virus in OPV replicates in the intestines of recipients and is transiently excreted in feces and thus is capable of fecal-oral spread to other individuals, potentially immunizing some who had not directly received the vaccine. However, such passage through multiple individuals can lead to mutations of the vaccine virus, very rarely to a strain (vaccine-derived poliovirus) that can cause paralytic poliomyelitis, which results in about 1 case per 2,400,000 OPV doses. This mutation usually occurs in the type 2 poliovirus component of the vaccine. Because of this, OPV is no longer available in the US. Also, poliovirus type 2 was removed from OPV in 2016 because of outbreaks resulting from genetically divergent circulating vaccine-derived virus despite official eradication of wild-type poliovirus type 2. 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 weeks apart and a 3rd dose given 6 to 12 months 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.

Key Points

  • 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 cerebrospinal fluid and reverse transcriptase–polymerase chain reaction of cerebrospinal fluid 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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NOTE: This is the Professional Version. CONSUMERS: Click here for the Consumer Version
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