Polio

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Tarek Nafee, M.D. [2]

Poliomyelitis, often called polio or infantile paralysis, is an acute viral infectious disease spread from person to person, primarily via the fecal-oral route.^[1] The term derives from the Greek polio (πολίός), meaning “grey”, myelon (µυελός), referring to the “spinal cord“, and -itis, which denotes inflammation.^[2] Although around 90% of polio infections have no symptoms at all, effected individuals can exhibit a range of symptoms if the virus enters the blood stream.^[3] In fewer than 1% of cases the virus enters the central nervous system, preferentially infecting and destroying motor neurons, leading to muscle weakness and acute flaccid paralysis. Different types of paralysis may occur, depending on the nerves involved. Spinal polio is the most common form, characterized by asymmetric paralysis that most often involves the legs. Bulbar polio leads to weakness of muscles innervated by cranial nerves. Bulbospinal polio is a combination of bulbar and spinal paralysis.^[4]

Poliomyelitis was first recognized as a distinct condition by Jakob Heine in 1840.^[5] Its causative agent, poliovirus, was identified in 1908 by Karl Landsteiner.^[5] Although major polio epidemics were unknown before the 20th century, polio was one of the most dreaded childhood diseases of the 20th century in the United States. Polio epidemics have crippled thousands of people, mostly young children; the disease has caused paralysis and death for much of human history. Polio had existed for thousands of years quietly as an endemic pathogen until the 1880s, when major epidemics began to occur in Europe; soon after, widespread epidemics appeared in the United States. By 1910, much of the world experienced a dramatic increase in polio cases and frequent epidemics became regular events, primarily in cities during the summer months. These epidemics—which left thousands of children and adults paralyzed—provided the impetus for a “Great Race” towards the development of a vaccine. The polio vaccines developed by Jonas Salk in 1952 and Albert Sabin in 1962 are credited with reducing the annual number of polio cases from many hundreds of thousands to around a thousand.^[6] Enhanced vaccination efforts led by the World Health Organization, UNICEF and Rotary International could result in global eradication of the disease.^[7]

The term poliomyelitis is used to identify the disease caused by any of the three serotypes of poliovirus. Two basic patterns of polio infection are described: a minor illness which does not involve the central nervous system (CNS), sometimes called abortive poliomyelitis, and a major illness involving the CNS, which may be paralytic or non-paralytic.^[8]

The poliovirus is transmitted by the fecal-oral or oral route. Acute infection involves the oropharynx, gastrointestinal tract, and occasionally the central nervous system. Poliovirus divides within gastrointestinal cells for about one week before penetrating the intestinal lining. Once the virus enters the bloodstream it becomes a viremia and is widely-distributed throughout the body. Rarely, the major viremia progresses and the virus invades the central nervous system, causing a local inflammatory response.

Polio is a highly infectious disease caused by Poliovirus that invades the nervous system. Poliovirus are small (27–30 nm), nonenveloped viruses with capsids enclosing a single-stranded, positive-sense RNA genome about 7,500 nucleotides long. Person-to-person spread of poliovirus via the fecal-oral route is the most important route of transmission, although the oral-oral route may account for some cases.

Because of polio eradication efforts, the number of countries where travelers are at risk for polio has decreased dramatically. The last documented case of wild polio virus-associated paralysis in a US resident traveling abroad occurred in 1986 in a 29-year-old vaccinated adult who had been traveling in South and Southeast Asia. In 2005, an unvaccinated US adult traveling abroad acquired vaccine-associated paralytic poliomyelitis after contact with an infant recently vaccinated with oral polio vaccine.

Poliovirus is highly infectious, with seroconversion rates among susceptible household contacts of children nearly 100%, and greater than 90% among susceptible household contacts of adults. Persons infected with poliovirus are most infectious from 7 to 10 days before and after the onset of symptoms, but poliovirus may be present in the stool from 3 to 6 weeks.

Many cases of poliomyelitis result in only temporary paralysis. After an interval of 30–40 years, 25%–40% of persons who contracted paralytic poliomyelitis in childhood experience new muscle pain and exacerbation of existing weakness, or develop new weakness or paralysis. This disease entity is referred to as pos-tpolio syndrome. Patients with abortive polio infections recover completely. In those that develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery.

Clinical manifestations of poliovirus infection range from asymptomatic (most infections) to symptomatic, including acute flaccid paralysis of a single limb to quadriplegia, respiratory failure, and rarely, death.

A laboratory diagnosis of poliomyelitis is usually made based on recovery of poliovirus from the stool or pharynx. Neutralizing antibodies to poliovirus can be diagnostic and are generally detected in the blood of infected patients early in the course of infection. Analysis of the patient’s cerebrospinal fluid (CSF), which is collected by a lumbar puncture (“spinal tap”) reveals an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level. Detection of virus from the CSF is diagnostic of paralytic polio, but rarely occurs.

Only treatment for symptoms is available, ranging from pain and fever relief to intubation and mechanical ventilation for patients with respiratory insufficiency.

Two polio vaccines are used throughout the world to combat polio. Both vaccines induce immunity to polio, efficiently blocking person-to-person transmission of wild poliovirus, thereby protecting both individual vaccine recipients and the wider community (so-called herd immunity).

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Poliomyelitis was first recognized as a distinct condition by Jakob Heine in 1840.^[1] Its causative agent, poliovirus, was identified in 1908 by Karl Landsteiner.^[1] Although major polio epidemics were unknown before the 20th century, polio was one of the most dreaded childhood diseases of the 20th century in the United States. Polio epidemics have crippled thousands of people, mostly young children; the disease has caused paralysis and death for much of human history. Polio had existed for thousands of years quietly as an endemic pathogen until the 1880s, when major epidemics began to occur in Europe; soon after, widespread epidemics appeared in the United States. By 1910, much of the world experienced a dramatic increase in polio cases and frequent epidemics became regular events, primarily in cities during the summer months. These epidemics—which left thousands of children and adults paralyzed—provided the impetus for a “Great Race” towards the development of a vaccine. The polio vaccines developed by Jonas Salk in 1952 and Albert Sabin in 1962 are credited with reducing the annual number of polio cases from many hundreds of thousands to around a thousand.^[2] Enhanced vaccination efforts led by the World Health Organization, UNICEF and Rotary International could result in global eradication of the disease.^[3]

The effects of polio have been known since prehistory; Ancient Egyptian paintings and carvings depict otherwise healthy people with withered limbs, and children walking with canes at a young age. The first clinical description was provided by the British physician Michael Underwood in 1789, where he refers to polio as “a debility of the lower extremities”.^[5] The work of physicians Jakob Heine in 1840 and Karl Oskar Medin in 1890 led to it being known as Heine-Medin disease.^[6] The disease was later called infantile paralysis, based on its propensity to affect children.

Before the 20th century, polio infections were rarely seen in infants before six months of age, most cases occurring in children six months to four years of age.^[7] Poorer sanitation of the time resulted in a constant exposure to the virus, which enhanced a natural immunity within the population. In developed countries during the late 19th and early 20th centuries, improvements were made in community sanitation, including better sewage disposal and clean water supplies. These changes drastically increased the proportion of children and adults at risk of paralytic polio infection, by reducing childhood exposure and immunity to the disease.

Small localized paralytic polio epidemics began to appear in Europe and the United States around 1900.^[8] Outbreaks reached pandemic proportions in Europe, North America, Australia, and New Zealand during the first half of the 20th century. By 1950 the peak age incidence of paralytic poliomyelitis in the United States had shifted from infants to children aged five to nine years, when the risk of paralysis is greater; about one-third of the cases were reported in persons over 15 years of age.^[9] Accordingly, the rate of paralysis and death due to polio infection also increased during this time.^[8] In the United States, the 1952 polio epidemic became the worst outbreak in the nation’s history. Of nearly 58,000 cases reported that year 3,145 died and 21,269 were left with mild to disabling paralysis.^[10]

The polio epidemics changed not only the lives of those who survived them, but also affected profound cultural changes; spurring grassroots fund-raising campaigns that would revolutionize medical philanthropy, and giving rise to the modern field of rehabilitation therapy. As one of the largest disabled groups in the world polio survivors also helped to advance the modern disability rights movement through campaigns for the social and civil rights of the disabled. The World Health Organization estimates that there are 10 to 20 million polio survivors worldwide.^[11] In 1977 there were 254,000 persons living in the United States who had been paralyzed by polio.^[12] According to doctors and local polio support groups, some 40,000 polio survivors with varying degrees of paralysis live in Germany, 30,000 in Japan, 24,000 in France, 16,000 in Australia, 12,000 in Canada and 12,000 in the United Kingdom.^[11] Many List of polio survivors|notable individuals have survived polio and often credit the prolonged immobility and residual paralysis associated with polio as a driving force in their lives and careers.^[13]

The disease was very well publicized during the polio epidemics of the 1950s, with extensive media coverage of any scientific advancements that might lead to a cure. Thus, the scientists working on polio became some of the most famous of the century. Fifteen scientists and two laymen who made important contributions to the knowledge and treatment of poliomyelitis are honored by the Polio Hall of Fame at the Roosevelt Warm Springs Institute for Rehabilitation in Warm Springs, Georgia, USA.

Records from antiquity mention crippling diseases compatible with poliomyelitis. Michael Underwood first described a debility of the lower extremities in children that was recognizable as poliomyelitis in England in 1789. The first outbreaks in Europe were reported in the early 19th century, and outbreaks were first reported in the United States in 1843. For the next hundred years, epidemics of polio were reported from developed countries in the Northern Hemisphere each summer and fall. These epidemics became increasingly severe, and the average age of persons affected rose. The increasingly older age of persons with primary infection increased both the disease severity and number of deaths from polio. Polio reached a peak in the United States in 1952, with more than 21,000 paralytic cases. However, following introduction of effective vaccines, polio incidence declined rapidly. The last case of wild-virus polio acquired in the United States was in 1979, and global polio eradication may be achieved within the next decade.

Following the widespread use of poliovirus vaccine in the mid-1950s, the incidence of poliomyelitis declined rapidly in many industrialized countries. In the United States, the number of cases of paralytic poliomyelitis reported annually declined from more than 20,000 cases in 1952 to fewer than 100 cases in the mid-1960s. The last documented indigenous transmission of wild poliovirus in the United States was in 1979.

In 1985, the member countries of the Pan American Health Organization adopted the goal of eliminating poliomyelitis from the Western Hemisphere by 1990. The strategy to achieve this goal included increasing vaccination coverage; enhancing surveillance for suspected cases (i.e., surveillance for acute flaccid paralysis); and using supplemental immunization strategies such as national immunization days, house-to-house vaccination, and containment activities. Since 1991, when the last wild-virus–associated indigenous case was reported from Peru, no additional cases of liomyelitis have been confirmed despite intensive surveillance. In September 1994, an international commission certified the Western Hemisphere to be free of indigenous wild poliovirus. The commission based its judgment on detailed reports from national certification commissions that had been convened in every country in the region.

In 1988, the World Health Assembly (the governing body of the World Health Organization) adopted the goal of global eradication of poliovirus by the year 2000. Although this goal was not achieved, substantial progress has been made. One type of poliovirus appears to have already been eradicated. The last isolation of type 2 virus was in India in October 1999.

The Americas were declared polio-free in 1994.^[14] In 2000 polio was officially eradicated in 36 Western Pacific countries, including China and Australia.^[15][16] Europe was declared polio-free in 2002.^[17] In 2009, polio remained endemic in only four countries: Nigeria, India, Pakistan, and Afghanistan.^[18]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

The term poliomyelitis is used to identify the disease caused by any of the three serotypes of poliovirus (P1, P2 and P3). Most cases of poliovirus infection are asymptomatic. For symptomatic cases, two basic disease patterns are described: a minor form which does not involve the central nervous system (CNS), sometimes called abortive poliomyelitis, and a major form involving the CNS, which may be paralytic or non-paralytic.^[1] According to the ELCPPC classification, the paralytic form of the disease may be classified into: sporadic, epidemic; epidemiologically abnormal; or imported.^[2]

In most people with a normal immune system, poliovirus infection is asymptomatic. Patients with subclinical poliomyelitis often acquire active immunity against future infections, caused by the same viral strain.^[1]

Abortive poliomyelitis is a mild form of poliomyelitis, often presenting with symptoms of gastroenteritis, such as: fever, nausea, vomiting, diarrhea, or constipation; or symptoms of acute respiratory infection, such as: fever, headache, and sore throat.^[1]

Patients with this form of poliomyelitis often present with symptoms of non-paralytic meningitis, such as: fever; headache; vomiting; lethargy; irritability; neck, back, abdominal and upper or lower limb pain. Muscle spasm usually occurs in the neck, back and hamstring muscles.^[1]

Patients with paralytic poliomyelitis present with the same symptoms as those of the non-paralytic form. Additional symptoms in the paralytic form include: muscle weakness; asymmetrical paralysis; muscle atrophy; tremors; and skeletal deformities.^[3][1][4]

Paralytic poliomyelitis may be classified into 2 forms, that may coexist in the same patient:

This form of the disease affects the muscles supplied by spinal nerves.

This form of the disease affects the muscles supplied by cranial nerves. Encephalitis may also occur in this form.

Until 1976, paralytic poliomyelitis was classified according to the epidemiological data. The ECPPC, or Epidemiologic Classication of Paralytic Poliomyelitis Cases, distributed these cases into 1 of 4 categories:^[2]

• Epidemic
• Endemic
• Imported
• Immune deficient

In 1985, a new classification was proposed, in order to incorporate, not only epidemiological information but also viral isolation, and characterization of the viral strain. This new classification was named ELCPPC, or Epidemiologic and Laboratory Classification of Paralytic Poliomyelitis Cases, and it classifies paralytic poliomyelitis according to the following classes:^[2]

Any case of poliomyelitis that is not epidemiologically related to another, and that may be caused by either the wild form of the virus, or by the virus in the vaccine.

When a case of the disease is epidemiologically linked to a similar case. The virus may, or may not, be related to the virus in the vaccine.

Any presumed or confirmed case of poliomyelitis that may be caused by either the wild form of the virus, or by the virus in the vaccine, irrespectively to the origin of the host’s immunological deficiency.

Any new case of poliomyelitis in a person who has entered the US (either foreign or US resident), and that has been symptomatic for the previous 30 days of entrance, or that develops symptoms during the initial 30 days in the country.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]Gurmandeep Singh Sandhu,M.B.B.S.[3]

The word poliomyelitis is derived from the Greek, where polio means grey and the work myelin means the marrow referring to the spinal cord. Polio myelitis primarily affects the spinal cord in turn leading to the manifestations. Poliovirus is a member of the enterovirus subgroup, family Picornaviridae. Poliovirus is primarily spread from the stools of the infected person and enters the body orally through contaminated water or food (feco-oral transmission), infecting the cells of the gastrointestinal tract, from the mouth to the ileum and mesentrium. After replication, the virus may either be secreted in feces, contributing to the transmission of the disease, or reach the bloodstream, and be transported to other cells of the body, such as those of the reticuloendothelial system. Although the precise mechanism of infection of CNS is not fully understood, the most supported hypothesis is the retrograde axonal transport, according to which the virus enters the axoplasm of a motor neuron, travels to its cell body, where it replicates, and leads to neuron death. In the CNS, poliovirus shows tropism for cells of the anterior horn of the spinal cord, hypothalamus, thalamus, cerebellar vermis, vestibular and deep cerebral nuclei. Death of the motor neuron is responsible for the paralysis often seen in poliomyelitis.

CDC has given a case definition of paralytic poliomyelitis for surveillance purposes

• “Acute onset of flaccid paralysis of one or more limbs with decreased or absent tendon reflex in the affected limbs, without other apparent causes, and without sensory or cognitive loss.”.^[1]
• A confirmed case requires persistence of neurological deficit for 60 days after the onset of the initial symptoms, fatal illness, or unknown follow-up status.^[1]

WHO case definition for a suspected case of poliomyelitis is:

• A suspected case is defined as a child under 15 years of age presenting with acute flaccid paralysis (AFP), or as any person at any age with paralytic illness if poliomyelitis is suspected^[2]

Poliovirus is mostly transmitted through the fecal-oral route, by ingestion of contaminated food or water. In some instances, the oral-oral route may be relevant through pharyngeal secretions. ^[3][4] Poliomyelitis is highly contagious and spreads easily through human-to-human contact.^[5] In endemic areas, wild polioviruses can infect virtually the entire human population.^[6] Viral particles are excreted in the feces for several weeks, after initial infection. Although the virus can cross the placenta during pregnancy, the fetus does not appear to be affected by either maternal infection, or polio vaccination.^[7] Maternal antibodies can also cross the placenta, providing passive immunity that protects the infant from polio infection during the first few months of life.^[8]

Poliovirus enters the body orally and most often infects nearby cells, such as those of the mouth, nose, and throat. Poliovirus commonly targets specific tissues in the CNS such as:^[9]

• Anterior horn cells of the spinal cord (in severe cases of the disease, the intermediate, intermediolateral and posterior gray columns may also be affected)
• Hypothalamus
• Thalamus
• Vestibular nuclei
• Deep cerebral nuclei
• Reticular formation
• Cerebellar vermis

It infects cells by binding to an immunoglobulin-like receptor known as CD155 on the cell surface. The most common course of infection is the replication of poliovirus in cells of the gastrointestinal tract, followed by viral shedding in feces. The specific cells of the gastrointestinal tract, where poliovirus replicates, are not known, however, the virus was successfully isolated from lymphatic cells of the GI tract, including:^[9]. Viral particles have been seen in:

• Tonsillar cells
• Peyer’s patches of the ileum
• Lymph nodes of the mesenterium

The virus enters the bloodstream and migrates to the reticuloendothelial cells across the body. Poliovirus is able to reach the central nervous system in a small fraction of the symptomatic patients.^[9] Not only is the disease not a phase of the viral replication cycle, it also does not benefit the virus in any way. The molecular mechanism behind this disease process is not known.^[9]

Poliovirus replicates inside monocytes, which allows for secondary hematogenous spread. The pathological mechanism responsible for the clinical manifestations of CNS poliomyelitis is characterized by selective destruction of motor neurons. Depending of the involved site, motor neuron loss may lead to focal or generalized symptoms. Most commonly observed signs and symptoms include asymmetric limb paralysis in spinal polio and respiratory disturbance with cranial nerve defects in bulbar polio.

Although the mechanism of viral spread to the CNS is not fully understood, two main hypotheses have been proposed:^[9]

1. Poliovirus diffuses directly through the blood brain barrier from the bloodstream to the CNS, regardless of cellular receptors.
2. Poliovirus is transported from the peripheral muscles to the brain and spinal cord, through retrograde axonal transport. This hypothesis has been experimentally proven in mice, after CD155 transformation.

Several recent findings supporting the retrograde axonal transport hypothesis have been reported:^[9].

• • Detection of axonal poliovirus in patients with poliomyelitis.
  • Interruption of a nerve connection between a site of multiple intramuscular injections and the spinal cord in mice with poliovirus viremia led to improved clinical course of infection. This supports the provocation poliomyelitis hypothesis which states that muscle injury in patients with poliovirus viremia triggers retrograde axonal transport of the virus. This phenomenon is seen in children receiving intramuscular vaccines in areas endemic for poliovirus.^[10]
  • In mice genetically transformed to express CD155, injection of poliovirus in the left limb led to viral detection in the left anterior horn of the spinal cord only. When the sciatic nerve was promptly sectioned after injection of the virus, the risk of paralysis in the injected limb was greatly reduced.
  • Bulbar poliomyelitis following tonsillectomy may possibly be explained by the previously described mechanisms.
  • Overexpression of CD155 in the muscle fibers of patients with paralytic poliomyelitis. To note, CD155 directly interacts with the dynein retrograde complex through Tctex-1.^[9]

The main explanation for increased susceptibility to retrograde axonal transport of poliovirus in areas of injured muscle has been explained. In a neuronal synapse, the rate of endocytosis is related to the level of neuron activity. Correspondingly, for a motor neuron, the level of neuron activity and rate of endocytosis at the neuromuscular junction is related to the extent of muscle contraction. This explains the connection between extreme exercise or muscle injury and development of poliomyelitis in patients with viremia. Also, since most of CD155 receptors are transported back to the cell body, the virus is carried along, supporting the retrograde transport hypothesis.^[9]

Once at the cell body of the neuron, the change from axoplasm to cytoplasm is thought to interfere with the stability of the viral coat, leading to the exposure of the viral RNA. Viral replication interferes with neuron stability, killing the motor neuron. Death of a motor neuron paralyzes the respective muscle fiber.

The pre- paralytic or non-paralytic course of the disease includes:-^[11]

• Headache
• Pharyngitis
• Myalgia
• Anorexia
• Nausea
• Vomiting

In non- paralytic illness, the symptoms go away within one or two weeks.

Paralytic Poliomyelitis: ^[11] After the meningitis phase, the spinal form of poliomyelitis occurs which consists of:

• Muscle pain
• Muscle spasms
• Fasciculations

Weakness is asymmetrical affecting the lower limbs more than the upper limbs. The weakness usually becomes maximum within 48hrs, especially in children. In some, the weakness may further increase after a period of stability but no further weakness occurs once the fever subsides. Muscle tone is flaccid and the reflexes are absent along with paraesthesia. Any cranial nerve may be involved but most frequently leads to dysphasia, dysphasia, and respiratory failure^[12]. Vasomotor involvement such as hypertension, hypotension, and circulatory collapse lead to mortality in patients.

Bulbar form:^[13] Seen more in children in which tonsils and adenoids have been removed.

Oral polio vaccine (OPV) is one of the safest and most effective vaccination programs that prevented millions of cases of polio not only through direct immunization but also through herd immunity. In rare occasions, the vaccine is associated with paralytic polio. There are two subtypes of paralytic polio related to OPV vaccine: vaccine associated paralytic polio and vaccine derived paralytic polio.

• Vaccine associated paralytic polio (VAPP) occurs when the attenuated strain used in the vaccine reverts inside the intestine into more virulent form.^[2][14][15]
• The more virulent form is capable of causing the disease only in the vaccinated child or a close susceptible contact. Therfore, no outbreaks are associated with VAPP.
• The prevalence of (VAPP) is 1 in 2.7 million doses of the vaccine.
• In developed countries, the risk of VAPP is increased with the first dose of the vaccine while in developed countries, It’s increased with subsequent doses.

• Vaccine derived paralytic polio (VDPP) is caused by very rare mutation of the original strain of polio in the vaccine.^[2][16]
• VDPP has the ability to cause the disease in any non immune person whether the vaccinated person or a contact, therefore it has the ability to cause outbreaks or even epidemics especially in communities that are not properly covered with the vaccination program.
• When it causes outbreaks, VDPP is called circulating vaccine derived paralytic polio (cVDPP).
• In the last 10 years, 24 VDPP reported outbreaks happened in 21 countries causing 750 cases of paralytic polio.
• The management of VDPP is conducting extensive vaccination campaigns in the affected community aiming for vaccinating every child and thus preventing the spread of the infection.

• 
  A photomicrograph of skeletal muscle tissue revealing myotonic dystrophic changes as a result of Polio Type III.Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]
• 
  A photomicrograph of the lumbar spinal cord depicting an infarct due to Polio Type III surrounding the anterior spinal artery.Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]
• 
  A photomicrograph of the lumbar spinal cord depicting an infarct due to Polio Type III surrounding the anterior spinal artery.Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]
• 
  A photomicrograph of the lumbar spinal cord depicting degenerative changes due to an infarct caused by Polio Type III.Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]
• 
  A photomicrograph of the thoracic spinal cord depicting degenerative changes due to Polio Type III.Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]
• 
  A photomicrograph of the thoracic spinal cord depicting degenerative changes due to Polio Type III.Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]
• 
  A photomicrograph of the cervical spinal cord in the region of the anterior horn revealing Polio Type III degenerative changes.Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]
• 
  A photomicrograph of the cervical spinal cord in the region of the anterior horn revealing Polio Type III degenerative changes.Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]
• 
  A photomicrograph of the cervical spinal cord in the region of the anterior horn revealing Polio Type III degenerative changes.Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]
• 
  Under a low magnification, this photomicrograph of pontine tissue at the level of abducens nucleus reveals histopathologic changes in a poliomyelitis patient.Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]
• 
  Photomicrograph of the Cervical Spinal Cord Affected by Polio Type III VirusAdapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.^[17]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Abortive poliomyelitis must be differentiated from other diseases that cause fever, nausea, vomiting, diarrhea, headache, and sore throat, such as gastroenteritis or acute respiratory infection.^[1][2]

Paralytic poliomyelitis must be differentiated from other diseases that cause headache, muscle pain, lethargy, muscle weakness, spams, and tremors, such as Guillain-Barré syndrome, traumatic neuritis of the sciatic nervev transverse myelitisv and West Nile Virus.^{[2][1][3][4][5][6]}

The table below summarizes the findings that differentiate poliomyelitis from other conditions that cause headache, fever, muscle pain; nausea and vomiting:^{[2][1][3][4][5][6][7]}

The table below summarizes the findings that differentiate poliomyelitis from other conditions that cause headache, muscle pain; lethargy, muscle weakness, spams and tremors:^{[2][1][3][4][5][6][7]}

The following table differentiates poliomyelitis from other diseases that cause muscle weakness, hypotonia, and flaccid paralysis:^{[8][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Tarek Nafee, M.D. [3]

Following the poliomyelitis eradication efforts, started by the GPEI (Global Polio Eradication Initiative) in 1988, the number of reported cases has fallen by over 99%, to the point that in 2015 only 74 cases were reported. In 2016 only 3 countries remain polio-endemic: Nigeria, Pakistan, and Afghanistan. The incidence of poliomyelitis is higher in children under 5 years of age, however, the death-to-case ratio for paralytic poliomyelitis is higher among adults. Incidence and prevalence of poliomyelitis do not vary by gender. The last case of wild-virus poliomyelitis acquired in the United States was in 1979. Of the 3 strains of wild poliovirus worldwide, wild poliovirus type 2 was eradicated in 1999, and case numbers of wild poliovirus type 3 are down to the all-time lowest levels. The last reported case of type 3 was in Nigeria in November 2012.

• In the immediate prevaccine era, improved sanitation led to less frequent exposure and increased the age of primary infection. Boost of immunity from natural exposure became less frequent, and the number of susceptible persons accumulated, ultimately resulting in the occurrence of epidemics, with 13,000 to 20,000 paralytic cases reported annually.^[1]

• Since the GPEI, launched in 1988, the number of cases has fallen by over 99%.

• In 2016, only 3 countries in the world remain polio-endemic: Nigeria, Pakistan, and Afghanistan.^[2]

• On Thursday June 8th, WHO announced a vaccine related polio outbreak in Syria.^[4]
• In Deir El-zor governorate, 2 children were paralyzed by a virus strain related to the used vaccine and the virus was also isolated from other child who was not paralyzed.
• Syria witnessed an outbreak in 2013 and 2014  but this outbreak was related to wild poliovirus not the vaccine strains.
• Emergency vaccination of 200,000 children is planned in an effort to contain the outbreak.

• Poliomyelitis cases have decreased by over 99% since 1988, from an estimated 350 000 cases in more than 125 endemic countries then, to 406 reported cases in 2013. These included only 160 cases in endemic countries; international spread of the virus from endemic areas, into poliomyelitis-free areas accounted for the remainder.

• In 2015, only 74 cases were reported worldwide.^[5]

• The year-to-date incidence of polio in 2016 shows a 59.5% reduction from 2015. The precise figures are demonstrated in the table below:

• Poliomyelitis affects mainly children under 5 years of age ^[3]. However, the death-to-case ratio for paralytic poliomyelitis is generally 2-5% among children and up to 15-30% for adults (depending on age).^[6]

• The prevalence and incidence of poliomyelitis do not vary by gender.^[1]
• Female gender carries a higher risk of developing “postpolio syndrome”.^[1]

• In 2016, only parts of 3 countries in the world remain endemic for the disease – the smallest geographic area in history. Of the 3 strains of wild poliovirus (type 1, type 2, and type 3), wild poliovirus type 2 was eradicated in 1999, and case numbers of wild poliovirus type 3 are down to the lowest-ever levels with the last case reported in November 2012 from Nigeria.^[2]
• Polio remains endemic in three countries – Afghanistan, Nigeria and Pakistan.
• As of 2016, the following countries are considered outbreak regions (those affected by either re-infection due to an imported poliovirus, or the emergence of a circulating vaccine-derived poliovirus)^[7]:
  • Guinea
  • Lao People’s Democratic Republic,
  • Madagascar
  • Myanmar

• Poliomyelitis reached a peak in the United States in 1952, with more than 21,000 paralytic cases. However, following introduction of effective vaccines, poliomyelitis incidence declined rapidly. A poliomyelitis eradication program conducted by the Pan American Health Organization led to elimination of polio in the Western Hemisphere in 1991.
• The Global Polio Eradication Program has dramatically reduced poliovirus transmission throughout the world. The last case of wild-virus poliomyelitis acquired in the United States was in 1979, and global polio eradication may be achieved within the next decade.^[1][6]
• Since 1991, when the last wild-virus-associated indigenous case was reported from Peru, no additional cases of poliomyelitis have been confirmed despite intensive surveillance. In September 1994, an international commission certified the Western Hemisphere to be free of indigenous wild poliovirus. ^[6]
• From 1980 through 1999, a total of 152 confirmed cases of paralytic poliomyelitis were reported, an average of 8 cases per year. Six cases were acquired outside the United States and imported. The last imported case was reported in 1993. Of the total, 144 (95%) cases were vaccine-associated paralytic polio (VAPP) caused by live oral polio vaccine.^[1]
• In order to eliminate VAPP from the United States, ACIP recommended in 2000 that IPV to be used exclusively in the United States. The last case of VAPP acquired in the United States was reported in 1999. In 2005, an unvaccinated U.S. resident was infected with polio vaccine virus in Costa Rica and subsequently developed VAPP. Also in 2005, several asymptomatic infections with a vaccine-derived poliovirus were detected in unvaccinated children in Minnesota. The source of the vaccine virus has not been determined, but it appeared to have been circulating among humans for at least 2 years based on genetic changes in the virus.^[1][6]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Risk factors for infection with poliovirus include not receiving the vaccine, traveling to countries endemic for the virus, immunodeficiency, and malnutrition. Once infected with the virus, risks for developing poliomyelitis and severe forms of the disease include muscle trauma, excessive exercise, pregnancy, B-cell immunodeficiency, and tonsillectomy.

Risk factors for the development of poliomyelitis include:^[1][2]

• Unvaccinated status
• Traveling to endemic countries or regions
• Immunodeficiency^[3]
• Malnutrition^[4]

Factors that increase the risk of developing poliomyelitis, after infection with poliovirus include:^[5]

• Muscle trauma (provocation poliomyelitis)
• Excessive exercise (provocation poliomyelitis)^[6]
• Injections (provocation poliomyelitis)^[7]
• Pregnancy^[8]
• B-cell immunodeficiency
• Tonsilectomy^[9]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Poliovirus initially colonizes the cells of the gastrointestinal tract. When symptoms occur, these usually follow an incubation period of 7 to 14 days. The disease may manifest as abortive poliomyelitis, lasting for 2-3 days with nonspecific symptoms of fatigue, nausea, and sore throat, non-paralytic poliomyelitis, lasting about 2-10 days which with signs of meningeal irritation, and paralytic poliomyelitis with symptoms such as hyperesthesia, paresthesia, and paralysis. Complications of poliomyelitis may include respiratory compromise, gastrointestinal symptoms, musculoskeletal deformities, and post-poliomyelitis syndrome. The prognosis of poliomyelitis depends on the form of the disease: patients with abortive poliomyelitis often have a full recovery; while patients with severe form of disease have poorer outcome. Paralysis of the respiratory muscles is a sign of bad prognosis and these patients have higher mortality.

Poliovirus enters the body through the oral cavity, infecting nearby cells, such as those of the oral mucosa, nose and throat. The incubation period often ranges from 7 to 14 days, however, it may vary from 5 to 35 days.^[1][2]

Typical manifestations of poliomyelitis may range from asymptomatic disease, to death. 95% of infections with poliovirus are asymptomatic. 4 to 8% of the cases present as abortive poliomyelitis. In about 1 to 2% of infections, the disease manifests as non-paralytic poliomyelitis. Less than 1% of infected patients develop paralytic disease.

Abortive poliomyelitis often presents with 2 to 3 days of fever. Neurological exam is normal in this form of the disease, and common symptoms may include sore throat, headache, anorexia, nausea, vomiting, and abdominal pain.^[2]

This form of the disease presents with symptoms of abortive poliomyelitis; however, these are often more severe, and signs of meningeal irritation are present.^[2] Typically symptoms in non-paralytic polio last for 2 to 10 days, and patients are expected to achieve complete recovery.^[3]

Paralytic symptoms generally begin 1 to 10 days after prodromal symptoms, and evolve during 2 to 3 days. The prodrome may be biphasic, especially in children, with initial minor symptoms separated from major symptoms, by 1 to 7 days. Adults commonly present with a single phase of symptoms, with prolongation of the prodrome until onset of paralysis.^[3][2][4]

Severe paralysis occurs in about 0.1% of the cases. Initial minor symptoms are similar to those of abortive poliomyelitis, lasting 1 to 3 days. After this initial period, the patient recovers over 2 to 5 days, until severe symptoms develop. The severe phase of this form of poliomyelitis is characterized by signs and symptoms of aseptic meningitis. These include fever, chills, nausea, vomiting, photophobia, and neck stiffness.^[2]

The more severe phase begins with hyperesthesia, paresthesia, myalgia, and muscle spasms. Meningeal symptoms start 2 days before the onset of paralysis. Muscular symptoms are often asymmetrical and may vary from mild weakness to quadriplegia. Lower limbs tend to be more affected than the upper limbs, and symptoms may occur in different combinations of limbs. Paralysis usually lasts 2 to 3 days, and its progression stops when fever decreases. Twenty five percent of adults also experience bladder muscle paralysis.^[2]

Patients with bulbar paralytic poliomyelitis often experience difficulty swallowing and breathing. This form occurs in about 5-35% of the cases where paralysis occurs. The most common sign is accumulation of pharyngeal secretions.^[5]

Occurrence of encephalitis in a patient with poliomyelitis is uncommon and occurs more frequently in infants. Confusion is commonly the first symptom of polioencephalitis. It may also be accompanied by spastic paralysis and seizures.^[2]

Potential complications of poliomyelitis may include:^{[2][6][7][8][9][10][11][12]}

• The mortality rate from acute paralytic poliomyelitis during its epidemic stage was approximately 5-10% of symptomatic individuals; higher mortality was noted in cases of bulbar poliomyelitis.^[13]
• Patients with abortive poliomyelitis often have a full recovery.^[2]
• Patients who develop aseptic meningitis can have symptoms for 2-10 days and often recover fully.^[14]
• In paralytic poliomyelitis, muscle paralysis usually lasts 1-3 days, and in some cases up to 1 week.^[15] Persistent weakness occurs in two thirds of patients.
• Patients with severe form of paralytic poliomyelitis, and those who require mechanical ventilation have lower probability of achieving recovery.^[2]
• 5- 10% of patients with paralytic poliomyelitis die ofrespiratory muscles paralysis. The mortality rate varies with age: 2-5% in children, 15-30% in adults.
• In the absence of support, bulbar poliomyelitis has a mortality rate of 25-75%, depending on the patient’s age.^[16] With adequate positive pressure ventilation, the mortality can be reduced to 15%.^[17]
• Permanent sequelae are uncommon in patients who have survived bulbar poliomyelitis.^[2]

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