Pediatric Poliomyelitis

Author: Benjamin Estrada, Russell W Steele, Leonard R Krilov

Background
Poliomyelitis is an enteroviral infection that can manifest in 4 different forms: inapparent
infection, abortive disease, nonparalytic poliomyelitis, and paralytic disease. Before the 19th
century, poliomyelitis occurred sporadically. During the 19th and 20th centuries, epidemic
poliomyelitis was more frequently observed, reaching its peak in the mid 1950s. The worldwide
prevalence of this infection has decreased significantly since then because of aggressive
immunization programs. Eradication of this disease during the present decade is a top priority for
the World Health Organization (WHO).[1] See the image below.

The typical contractures of postpolio residual paralysis.

Epidemiology
International
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.
As of 2014, significant progress has been made towards poliomyelitis eradication in India, which
is now considered a nonendemic area.[4, 5] 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.[6, 7] In addition, there have been recently confirmed cases of poliomyelitis in
Syria and Iraq caused by wild poliovirus type 1 (WPV1).[8]
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.[9

Causes
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.

Pathophysiology
Acute poliomyelitis is caused by small ribonucleic acid (RNA) viruses of the enterovirus group
of the picornavirus family. The single-stranded RNA core is surrounded by a protein capsid
without a lipid envelope, which makes poliovirus resistant to lipid solvents and stable at low pH.
Three antigenically distinct strains are known, with type I accounting for 85% of cases of
paralytic illnesses. Infection with one type does not protect from the other types; however,
immunity to each of the 3 strains is lifelong.
The enteroviruses of poliomyelitis infect the human intestinal tract mainly through the fecal-oral
route (hand to mouth). The viruses multiply in oropharyngeal and lower gastrointestinal tract
mucosa during the first 1-3 weeks of the incubation period. Virus may be secreted in saliva and
feces during this period, causing most host-to-host transmission. After the initial alimentary
phase, the virus drains into the cervical and mesenteric lymph nodes and then into the blood
stream. Only 5% of infected patients have selective nervous system involvement after viremia. It
is believed that replication in extraneural sites maintains the viremia and increases the likelihood
that the virus will enter the nervous system.
The poliovirus enters the nervous system by either crossing the blood-brain barrier or by axonal
transportation from a peripheral nerve. It can cause nervous system infection by involving the
precentral gyrus, thalamus, hypothalamus, motor nuclei of the brainstem and surrounding
reticular formation, vestibular and cerebellar nuclei, and neurons of the anterior and intermediate
 columns of the spinal cord. The nerve cells undergo central chromatolysis along with an
inflammatory reaction while multiplication of the virus precedes onset of paralysis. As the
chromatolysis process goes on further, muscle paralysis or even atrophy appears when fewer
than 10% of neurons survive in the corresponding cord segments. Gliosis develops when the
inflammatory infiltrate has subsided, but most surviving neurons show full recovery.[4, 5]

DIAGNOSIS
History
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.[10, 5]

Physical
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.

Laboratory Studies
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.

TREATMENT

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.
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.[13]
 Consultations
See the list below:
 Physical therapist and rehabilitation therapist
 Pulmonologist
 Neurologist
 Immunologist
 Infectious diseases specialist

Diet
Because patients with poliomyelitis are prone to develop constipation, a diet rich in fiber is
usually indicated.
Further Inpatient Care
Patients with poliomyelitis may develop bladder dysfunction for which catheterization is
frequently required.

PREVENTION
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.[15]
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.[16, 17]
IPV is now included in different combination vaccine products available in the United States.[18]
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 is being administered in developing countries when individuals are aged 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.
A new 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.[19, 20]
Prognosis
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.

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