Poliovirus poliomyelitis is an acute neurologic infection leading to acute flaccid paralysis caused by poliovirus (an enterovirus). Manifestations of poliovirus infection include a nonspecific minor illness, sometimes aseptic meningitis without paralysis, and, less often, flaccid weakness of various muscle groups (paralytic poliomyelitis). Diagnosis of acute flaccid paralysis is clinical, although laboratory diagnosis is necessary to confirm poliovirus, a nonpolio enterovirus, or other virus as the cause of disease. 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 transmissible via the fecal-oral, or less commonly respiratory, route. Asymptomatic and minor infections are more common than aseptic meningitis or paralytic poliomyelitis (< 1%) and are the main source of spread. (See also Overview of Enterovirus Infections.)
Extensive vaccination has almost eradicated the disease due to wild type poliovirus worldwide. Two of the three wild type polioviruses (types 2 and 3) have been eradicated. Efforts to eradicate poliovirus type 1 are ongoing, as it remains endemic in Pakistan and Afghanistan, and cases occurred in Malawi and Mozambique in 2023. In contrast, circulating vaccine-derived poliovirus, primarily Sabin OPV type 2, has been reported in an additional 31 countries, including the United States, the United Kingdom, and Israel. (See also the Polio Eradication Initiative.)
In the United States, a case of vaccine-derived paralytic poliomyelitis was identified in an unvaccinated person in New York (NY) state in July 2022 (1). Wastewater surveillance detected the virus in samples across several NY counties, indicating local transmission, but no additional cases were identified following this outbreak (2; see also New York State Department of Health: Wastewater Surveillance). The last case of wild type poliovirus acquired in the United States was in 1979.
References
1. Link-Gelles R, Lutterloh E, Schnabel Ruppert P, et al: Public Health Response to a Case of Paralytic Poliomyelitis in an Unvaccinated Person and Detection of Poliovirus in Wastewater - New York, June-August 2022. MMWR Morb Mortal Wkly Rep 71(33):1065-1068, 2022. Published 2022 Aug 19. doi:10.15585/mmwr.mm7133e2
2. Ryerson AB, Lang D, Alazawi MA, et al: Wastewater Testing and Detection of Poliovirus Type 2 Genetically Linked to Virus Isolated from a Paralytic Polio Case - New York, March 9-October 11, 2022. MMWR Morb Mortal Wkly Rep. 71(44):1418-1424, 2022. Published 2022 Nov 4. doi:10.15585/mmwr.mm7144e2
Pathophysiology of Poliomyelitis
Poliovirus is shed in feces and saliva, and is transmitted via the fecal-oral or respiratory route. It then replicates in oropharyngeal and lower gastrointestinal tract mucosa and enters the cervical and mesenteric lymph nodes. 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—either via secondary viremia or retrograde migration through peripheral nerves. Significant damage occurs in the spinal cord and brainstem, particularly in the areas controlling motor and autonomic function. Inflammation compounds the damage produced by primary viral invasion. Factors predisposing to serious neurologic damage include
Increasing age
Recent tonsillectomy or intramuscular injection
Pregnancy
Humoral immunodeficiency
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
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Symptoms and Signs of Poliomyelitis
Most (70 to 75%) poliovirus infections cause no symptoms (see Centers for Disease Control and Prevention: Epidemiology and Prevention of Vaccine-Preventable Diseases, Poliomyelitis). Symptomatic disease is classified as
Minor infection
Poliovirus aseptic meningitis without paralysis
Paralytic poliomyelitis
Minor poliovirus infection
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.
Poliovirus aseptic meningitis without paralysis
About 1 to 5% of patients with poliovirus infection develop nonparalytic central nervous system involvement with aseptic meningitis (see Centers for Disease Control and Prevention: Epidemiology and Prevention of Vaccine-Preventable Diseases, Poliomyelitis). Patients typically have a stiff neck and/or back and headache that appear after several days of prodrome similar to minor infections. Manifestations last 2 to 10 days.
Paralytic poliomyelitis
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 minor 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.
Dysphagia and dysphonia 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 of Poliomyelitis
MRI of spinal cord and brain
Lumbar puncture
Viral culture and testing (stool, throat, and cerebrospinal fluid)
Testing for other nonpolio enteroviruses and West Nile virus
When there are no central nervous system manifestations, mildly symptomatic polio resembles other systemic viral infections and is typically not considered or diagnosed except during an epidemic.
Poliovirus aseptic meningitis 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 can confirm infection with poliovirus.
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. MRI of the spinal cord and brain can confirm myelitis of the spinal cord gray matter and/or presence of brainstem lesions. However, nonpolio enteroviruses (D68, A71, and others) and West Nile virus may produce similar findings. Guillain-Barré syndrome causes flaccid paralysis but can be distinguished because Guillain-Barré syndrome does not usually cause fever but does cause
Symmetric muscle weakness
Sensory deficits in 70% of patients
Usually, elevated cerebrospinal fluid protein but normal cerebrospinal fluid cell count
Epidemiologic clues (eg, immunization history, recent travel, age, season) can help raise suspicion for poliovirus infection. Because identification of poliovirus or another enterovirus as the cause of acute flaccid paralysis is important for public health reasons, suspected cases should be reported to the local or state health department immediately to assist with diagnostic testing. Nasopharyngeal and oropharyngeal swabs, blood, and cerebrospinal fluid specimens should be collected. Two sets of stool specimens should be taken at least 24 hours apart to evaluate for poliovirus. Specific testing for polioviruses, other enteroviruses, and West Nile virus should be conducted on these specimens in conjunction with public health departments.
Treatment of Poliomyelitis
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 respiratory therapies.
Prognosis for Poliovirus infection
In aseptic meningitis without paralysis, 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 has been reported to be 2 to 5% among children, up to 15 to 30% in adolescents and adults, and increases to 25 to 75% in patients with bulbar disease (1). Mortality rates are improved with advancements in supportive care (2).
Prognosis references
1. Centers for Disease Control and Prevention: Epidemiology and Preventionof Vaccine-P reventable Diseases. Hall E., Wodi A.P., Hamborsky J., et al., eds: 14th ed.Washington, D.C. Public Health Foundation, 2021.
2. Murphy OC, Messacar K, Benson L, et al: Acute flaccid myelitis: cause, diagnosis, and management. Lancet. 2021;397(10271):334-346. doi:10.1016/S0140-6736(20)32723-9
Prevention of Poliomyelitis
All infants and children should be immunized with poliovirus vaccine. The American Academy of Pediatrics recommends vaccination with Salk inactivated poliovirus vaccine (IPV) at ages 2 months, 4 months, and 6 to 18 months and a booster dose at age 4 to 6 years (see Centers for Disease Control and Prevention: Routine Polio Vaccination). Childhood vaccination produces immunity in > 95% of recipients.
In the United Stated, Salk 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. These mutations usually occur in the type 2 poliovirus component of the vaccine. Because of this, OPV is no longer available in the United States. 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.
Due to the detection of circulating vaccine-derived poliovirus type 2 in the United States, the Advisory Committee on Immunization Practices (ACIP) updated adult poliovirus vaccination recommendations in 2023 (1). Nonimmunized or incompletely immunized adults 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. Immunized adults at increased risk for poliovirus exposure, such as those traveling to endemic or epidemic areas, may receive 1 lifetime booster dose of IPV. Immunocompromised patients and their household contacts should not be given OPV.
Prevention reference
1. Kidd S, Clark T, Routh J, Cineas S, Bahta L, Brooks O. Use of Inactivated Polio Vaccine Among U.S. Adults: Updated Recommendations of the Advisory Committee on Immunization Practices - United States, 2023. MMWR Morb Mortal Wkly Rep. 2023;72(49):1327-1330. Published 2023 Dec 8. doi:10.15585/mmwr.mm7249a3
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.
Local and state health departments should be notified immediately of suspected cases of poliovirus. Oropharyngeal and nasopharyngeal swabs, stools (2 samples separated by 24 hours), blood, and cerebrospinal fluid should be collected for testing in coordination with health departments.
In paralytic poliomyelitis, about two thirds of patients have residual permanent weakness.
All infants and children should be immunized. Adults who are not immunized or are incompletely immunized should be vaccinated.
More Information
The following English-language resource may be useful. Please note that THE MANUAL is not responsible for the content of this resource.
Polio Eradication Initiative: Information about The Global Polio Eradication Initiative, which intends to eradicate polio worldwide through a public-private partnership
