Pediatric Poliomyelitis

Poliovirus is an RNA virus that is transmitted through the oral-fecal route or by ingestion of contaminated water. Three serotypes are able to cause human infection. The incubation period for poliovirus is 5-35 days. The viral particles initially replicate in the nasopharynx and GI tract and then invade lymphoid tissues, with subsequent hematologic spread. After a period of viremia, the virus becomes neurotropic and produces destruction of the motor neurons in the anterior horn and brainstem. The destruction of motor neurons leads to the development of flaccid paralysis, which may be bulbar or spinal in distribution.

Polioviruses are enteroviruses within the Picornaviridae family. These viruses are resistant to ether and chloroform but can be inactivated by formaldehyde. They multiply in the GI tract but are particularly neurotropic.

Documentation suggests that infections with polioviruses can be potentiated by factors such as exercise and tonsillectomy. Additionally, patients who are immunocompromised, such as those with human immunodeficiency virus (HIV) infection, B-cell disfunction, immunoglobulin A (IgA) deficiency, or severe combined immunodeficiency, are particularly at high risk of developing poliomyelitis when exposed to both wild-type polioviruses and vaccine-attenuated viruses present in the oral poliovirus vaccine.

United States statistics

No cases of wild-type poliovirus infection have been reported in the United States since 1979. Until 1998, an average of 8-10 cases associated with the vaccine virus were reported every year. Since the institution of an all-inactivated poliovirus vaccine (IPV) policy in the routine immunization schedule, the number of vaccine-associated cases has significantly decreased. Four cases of vaccine-derived poliovirus were identified in 2005 among unvaccinated children in an Amish community in Minnesota.[3, 4]

In 2022, vaccine-derived poliovirus type 2 infection was confirmed in an unvaccinated immunocompetent adult in New York State, who had been hospitalized with flaccid lower limb weakness. Related type 2 polioviruses were also detected in wastewater samples in two neighboring New York counties.[5]

International statistics

The global incidence of poliovirus infection has decreased by more than 99% since 1988. Although no outbreaks had been reported in the western hemisphere since 1991, the Pan American Health Organization reported an outbreak in Haiti and the Dominican Republic in 2001. Since 2001, no additional outbreaks of disease caused by wild poliovirus have been reported in the Americas. Clusters of wild-type disease are still found in some areas in Africa and Southeast Asia.

Significant progress has been made towards poliomyelitis eradication in India, which is considered a nonendemic area.[6, 7] Pakistan, Afghanistan, and Nigeria are 4 countries in which indigenous transmission of wild poliovirus still occurs. However, importation of wild poliovirus into countries previously considered free of poliomyelitis continues to be a problem, especially in Africa.[8, 9] In addition, there have been confirmed cases of poliomyelitis in Syria and Iraq caused by wild poliovirus type 1 (WPV1).[10]

Concern for importation of cases from Afghanistan and Pakistan into Israel has resulted in a change in their routine polio immunization to include at least one dose of oral vaccine. In 2014, India began requiring a dose of oral polio vaccine for anyone coming from countries where polio is still seen, particularly Afghanistan and Pakistan.[11]

Wild poliovirus type 2 (WPV2) was officially eradicated in 2015, which prompted the replacement of trivalent oral poliovirus vaccine with OPV containing only types 1 and 3.[12]

 In 2017, the WHO confirmed two separate outbreaks of polio in the Democratic Republic of Congo as well as an outbreak in Syria.[13, 14]

In 2022, a case of wild poliovirus type 1 infection was confirmed in a 3-year-old girl in Lilongwe, Malawi. According to the WHO, it was the first case in Africa in 5 years.[15]  The strain of poliovirus that infected the child was closely related to a strain detected in a sewage sample from Pakistan.[16]

Sex- and age-related demographics

Males and females of pediatric age are affected with equal frequency.

Poliovirus affects mainly children. However, individuals of any age (especially those who are immunocompromised) may also develop the disease.

Bulbar paralytic poliomyelitis has been associated with the highest rate of complications and a mortality rate as high as 60%; spinal poliomyelitis follows. Patients with inapparent or abortive poliomyelitis recover without significant sequelae.

Morbidity/mortality

Mortality is more frequently observed in cases of paralytic poliomyelitis and is associated with complications such as respiratory failure. No deaths due to wild-type poliovirus have been reported in the United States since 1979.

Although most cases of poliomyelitis (90-95%) are inapparent, 5-10% of patients who acquire this infection develop symptoms.

Most patients infected with poliovirus develop inapparent infections and are frequently asymptomatic.

In cases of abortive poliomyelitis (5-10%), a history of the following is found with normal neurologic examination findings:

• Anorexia

• Vomiting

• Abdominal pain

• Duration of illness usually less than 5 days

When nonparalytic poliomyelitis develops, symptoms are usually those observed in abortive disease in addition to meningeal irritation.

Paralytic poliomyelitis involves systemic manifestation, such as respiratory failure, in addition to symptoms observed in nonparalytic poliomyelitis.

Patients who have recovered from poliomyelitis occasionally develop a post-poliomyelitis syndrome, in which recurrences of weakness or fatigue are observed and which usually involve groups of muscles that were initially affected. This postpolio syndrome may develop 20-40 years after infection with poliovirus and constitutes a persistent healthcare problem, even in countries in which poliomyelitis has been eradicated.[17, 7, 18]

The spectrum of disease varies from inapparent infection to paralytic disease.

In mild cases, the following nonspecific signs and symptoms are observed and usually resolve within a few days:

• Fever

• Headache

• Nausea

• Vomiting

• Abdominal pain

• Oropharyngeal hyperemia

Nonparalytic poliomyelitis is characterized by the symptoms described above in addition to the following:

• Nuchal rigidity

• More severe headache

• Back and lower extremity pain

• Meningitis with lymphocytic pleocytosis (usually)

Paralytic poliomyelitis occurs in fewer than 5% of affected patients and is characterized by the following:

• Compromise of the motor neurons may be localized or widespread.

• More frequently, asymmetric loss of muscle function is observed with involvement of major muscle groups.

• Muscle atrophy is generally observed several weeks after the beginning of symptoms.

• Recovery may be complete, partial, or absent.

Obtain specimens from the cerebrospinal fluid (CSF), stool, and throat for viral cultures in patients with suspected poliomyelitis infection.

Obtain acute and convalescent serum for antibody concentrations against the 3 polioviruses.

A 4-fold increase in the immunoglobulin G (IgG) antibody titers or a positive anti-immunoglobulin M (IgM) titer during the acute stage is diagnostic.

Ferraz-Filho et al observed that magnetic resonance imaging (MRI) is useful in differentiating between vaccine-associated paralytic poliomyelitis and other conditions and in assessing the extent of lesions.[19] Choudhary et al studied poliomyelitis in India and concluded that MRI revealed signal changes in bilateral substantia nigra and anterior horns of the spinal cord that could be of diagnostic significance in a child with poliomyelitis.[20]

Medical care

No antivirals are effective against polioviruses. The treatment of poliomyelitis is mainly supportive.

Analgesia is indicated in cases of myalgias or headache.

Mechanical ventilation is often needed in patients with bulbar paralysis.

Tracheostomy care is often needed in patients who require long-term ventilatory support.

Physical therapy is indicated in cases of paralytic disease. In paralytic disease, provide frequent mobilization to avoid development of chronic decubitus ulcerations. Active and passive motion exercises are indicated during the convalescent stage.

Fecal impaction is frequent in cases of paralytic disease and can be treated with laxatives as soon as it develops.

Because patients with poliomyelitis are prone to develop constipation, a diet rich in fiber is usually indicated.

Surgical care

Total hip arthroplasty is a surgical therapeutic options for patients with paralytic sequelae of poliomyelitis who develop of hip dysplasia and degenerative disease.[21]

Further care

Patients who suffer from long-term complications of poliomyelitis should be included in rehabilitation programs that focus on individual needs.[22]

Patients with poliomyelitis may develop bladder dysfunction for which catheterization is frequently required.

Consultations include the following:

• Physical therapist and rehabilitation therapist

• Pulmonologist

• Neurologist

• Immunologist

• Infectious diseases specialist

Two types of vaccines used in the prevention of poliomyelitis are inactivated poliovirus vaccine (IPV) administered parenterally and oral attenuated poliovirus vaccine (OPV).

Inactivated poliovirus vaccine

IPV was the first polio vaccine available on the market, and its widespread administration began in the 1950s. An enhanced inactivated poliovirus vaccine (eIPV) formulation is now available. Nonenhanced early formulations had the disadvantages of not being as immunogenic as OPV, not being able to induce mucosal immunity, and having to be administered parenterally, which increased costs and decreased compliance.[23]

One of the major advantages of IPV is that it contains an inactivated virus; for that reason, IPV is not associated with the development of vaccine-associated poliomyelitis. Although they do not induce mucosal immunity, new eIPV formulations have been proven to be as immunogenic as OPV. For that reason, countries in which no cases of wild-type disease have been reported during the last several years (eg, the United States) have now adopted eIPV immunization schedules. This new prophylactic approach has the advantage of eliminating vaccine-associated cases.

This vaccine is administered when individuals are aged 2 months, 4 months, and 6-12 months and before school entry, which is usually at age 4 years.[24, 25]

IPV is now included in different combination vaccine products available in the United States.[26]

Oral attenuated poliovirus vaccine

Trivalent OPV has been used since the early 1960s. Immunization with this formulation was responsible for the significant decrease in the prevalence of disease throughout the world. This formulation has the advantages of inducing mucosal immunity, providing appropriate herd immunity, and increasing vaccine uptake because of oral administration. Additionally, it is cost-effective, especially in countries in the developing world.

The major disadvantage of trivalent OPV is its association with vaccine-associated paralytic poliomyelitis (VAPP). Although the virus contained in this formulation is attenuated, it may occasionally become neurotropic and be able to produce disease similar to wild-type virus.

Trivalent OPV was administered in developing countries when individuals at ages 2 months, 4 months, and 6 months and with a booster at age 4 years. VAPP occurs most frequently after the first dose of OPV but may also occur after administration of the second or third doses. Since the global eradication of WPV2 in 2015, bivalent OPV containing types 1 and 3 is being utilized.[12]

A high-potency monovalent oral poliovirus type 1 vaccine (mOPV1) was introduced in India in April 2005. This vaccine is targeted to eliminate some of the last poliovirus reservoirs. This product constitutes part of an international effort to eradicate wild poliovirus. Studies have revealed that mOPV1 is 3 times more effective against type 1 poliomyelitis than trivalent OPV. In addition, it has been demonstrated to be particularly efficacious in areas in which the efficacy of trivalent OPV may be compromised by the high prevalence of diarrhea and other infectious processes. mOPV1 may be the preferred option to control a poliovirus outbreak in areas that have already been declared free of wild poliovirus transmission.[27, 28]

According to a study by Sutter et al, a combination of four dose bivalent oral polio vaccine and single inactivated polio vaccine has a superior immunogenicity to the conventional trivalent OPV, especially against poliovirus type 3.[29]

No antiviral agents are effective against poliovirus.