поліомієліт

(дитячий параліч; гострий передній поліомієліт; поліомієліт)

ЗаBrenda L. Tesini, MD, University of Rochester School of Medicine and Dentistry
Переглянуто/перевірено черв. 2023

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 transmissible 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. In 2022, wild-type poliovirus type 1 was circulating in only 2 countries (Afghanistan, 2 paralytic cases; Pakistan, 20 cases). In contrast, vaccine-derived poliovirus outbreaks were reported in an additional 31 countries, including the United States, the United Kingdom, Israel, Malawi, Chad, the Democratic Republic of the Congo, and Yemen. (See also the Polio Eradication Initiative.)

In the United States, a case of vaccine-derived paralytic polio was identified in an unvaccinated person who acquired it in New York State in July 2022 (1). No additional cases have been identified in the United States, but wastewater surveillance has detected the virus in samples across several NY counties, indicating local transmission (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.

Довідкові матеріали

  1. 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. 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

The virus enters via the fecal-oral or respiratory route, then multiplies in oropharyngeal and lower gastrointestinal tract mucosa. The virus is secreted into saliva and feces, from which it can be transmitted to others. The virus then 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—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.

Цінні поради та підводні камені

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

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

  • Abortive poliomyelitis

  • Paralytic or nonparalytic poliomyelitis

Абортний поліомієліт

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.

Паралітичний поліомієліт і непаралітичний поліомієліт

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 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 of Poliomyelitis

  • Lumbar puncture

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

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

  • Serologic testing for poliovirus serotypes, other 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, suspected cases should be reported to the local or state health department immediately to assist with diagnostic testing. Two sets of throat swabs and whole stool specimens should be taken at least 24 hours apart for viral culture and reverse transcriptase–polymerase chain reaction. Cerebrospinal fluid and blood specimens will likely also be requested. Specific serologic testing for polioviruses, other enteroviruses, and West Nile virus should also be done.

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 pulmonary toilet measures.

Prognosis for Poliomyelitis

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.

Prevention of Poliomyelitis

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 Centers for Disease Control and Prevention: Routine Polio Vaccination). 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 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.

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. New York residents in areas with repeated poliovirus detection may be at higher risk of infection and should follow updated vaccination recommendations from the New York State Department of Health (see New York State Department of Health: Polio Vaccine). Immunocompromised patients and their household contacts should not be given OPV.

Ключові моменти

  • 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 of suspected cases immediately. Viral culture of throat swabs, stool, and cerebrospinal fluid and reverse transcriptase–polymerase chain reaction of cerebrospinal fluid and blood should be done in coordination with health departments.

  • 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, occupation, or local outbreak).

Додаткова інформація

The following English-language resource may be useful. Please note that THE MANUAL is not responsible for the content of this resource.

  1. Polio Eradication Initiative: Information about The Global Polio Eradication Initiative, which intends to eradicate polio worldwide through a public-private partnership