Infectious Disorders

Updated 09.14.2021
Released 01.08.2015
Expires For CME 09.14.2024

Poliomyelitis

Author: Douglas J Lanska MD FAAN MS MSPH

Introduction

Overview

Poliovirus is an acute enteroviral infection that is spread from person to person, primarily via the fecal-hand-oral routes. Although most patients who acquire the infection are asymptomatic, those afflicted may develop a variety of neurologic manifestations, including aseptic meningitis, polioencephalitis, bulbar poliomyelitis, and paralytic poliomyelitis. In paralytic poliomyelitis, muscle weakness is preceded by intense myalgias of the involved limbs and axial skeleton. Following recovery, as many as 20% to 30% of individuals who develop paralytic poliomyelitis may suffer from post-polio syndrome, which produces muscle weakness, pain, atrophy, and fatigue many years after acute illness.

There has been a large worldwide effort for poliomyelitis eradication. Polio cases have decreased by over 99% since 1988, from an estimated 350,000 cases in more than 125 endemic countries to 42 reported cases in 2016 (37 wild-type and 5 vaccine-derived) (32; 38; 83; 84; 89; 40; 53). Poliomyelitis due to wild type virus has now been eliminated from the Americas, Europe, and Western Pacific, and cases in Africa and Asia have markedly decreased. Although great strides have been made, poliomyelitis remains and is rising in regions, including Nigeria, Afghanistan, and Pakistan, and there is a risk for new outbreaks to occur.

Key points

	• Poliovirus is an acute enteroviral infection that is spread from person to person, primarily via the fecal-hand-oral route.
	• Neurologic manifestations of poliomyelitis include aseptic meningitis, polioencephalitis, bulbar poliomyelitis, and paralytic poliomyelitis.
	• As many as 20% to 30% of individuals who develop paralytic poliomyelitis may suffer from post-polio syndrome, which includes new muscle weakness, pain, atrophy, and fatigue many years after the acute illness.
	• There has been a large worldwide effort for poliomyelitis eradication, with a decrease of polio cases by over 99% since 1988. Though great strides have been made, there remains a high risk for new outbreaks.
	• On September 20, 2015, the Global Commission for the Certification of Poliomyelitis Eradication declared that poliovirus type 2 has been eradicated worldwide.

Historical note and terminology

Poliomyelitis has afflicted humans for centuries. The first recognized clinical description was by English physician and surgeon Michael Underwood (1736-1820) in the second edition of A Treatise on Diseases of Children, which was published in 1789 (116; 76; 98). Major contributions to the understanding of the disease were made by the German orthopedist Jacob Heine (1800-1879), who described the clinical features of acute poliomyelitis (47).

Jacob Heine (1800-1879)

Shown around 1870, Heine was the first to provide a clinical description of poliomyelitis in 1840. (Contributed by Dr. Douglas Lanska. Public domain.)

In 1870, French neurologist Jean-Martin Charcot (1825-1893) and his junior colleague Alix Joffroy (1844-1908) recognized that the flaccid paralysis of poliomyelitis was caused by spinal anterior horn cell damage (23).

Jean-Martin Charcot (1825-1893)

French neurologist Jean-Martin Charcot (1825-1893), who, with colleague Alix Jaffoy, recognized that the flaccid paralysis of poliomyelitis was caused by spinal anterior horn cell damage. (Contributed by Dr. Douglas Lanska. Courte...

In the mid- to late 19th century, the general belief was that polio was not infectious; in the late 19th century, when bacteriological explanations were in vogue for almost all conditions, polio was suspected to be another bacterial disease. Numerous attempts were made to identify the responsible microorganism, with many claims to have successfully done so, but none were reproducible.

Finally, in 1908, Austrian pathologist Karl Landsteiner (1868-1943) and his colleague Erwin Popper (1879-1955) showed that the etiological agent of poliomyelitis was a filterable virus (65). The existence of more than 1 type of poliovirus was first inferred by Australian virologist Frank Macfarlane Burnet (1899-1984) and his collaborator Dame Annie Jean Macnamara (1899-1968) in 1931, when they demonstrated that monkeys who had recovered from infection with a strain recovered in Melbourne subsequently developed disease when given a virulent mixed virus strain (18; 30).

Sir Frank Macfarlane Burnet (1899-1984)

Australian virologist Sir Frank Macfarlane Burnet (1899-1984) recognized the existence of more than 1 type of poliovirus in 1931. Burnet won the Nobel Prize in Physiology of Medicine in 1961 for predicting acquired immune toleranc...

In 1949, the 3 antigenic poliovirus types (poliovirus 1, poliovirus 2, poliovirus 3) were identified (13; 63).

The first recorded outbreaks of poliomyelitis occurred in the mid- and late nineteenth century in northern Europe and North America, followed by much larger epidemics in the early 20th century.

In August 1921, while vacationing with his family at their summer home on Campobello Island off the coast of Maine, politician Franklin Delano Roosevelt (FDR; 1882-1945) became ill, lost motor power in his legs, and was diagnosed with polio. Roosevelt later sought treatment at a resort in Warm Springs, Georgia. Because of his self-perceived improvement at the resort, in 1927, Roosevelt and his friend, American lawyer Basil OConnor, created the Georgia Warm Springs Foundation, in which O'Connor served first as treasurer and later as president.

The foundation was subsequently reconstituted as the National Foundation for Infantile Paralysis in 1938. A solicitation prior to Roosevelts birthday in 1938 resulted in a huge influx of small donations that swamped the White House mail room.

As a result, radio star Eddie Cantor dubbed it the March of Dimes -- a play on the contemporary radio and newsreel series, The March of Time. The March of Dimes ultimately became the official name of the organization, which served as the largest source of funding for research and clinical care for poliomyelitis at the time. Indeed, the organization supported the work of Jonas Salk and others that led to the development and testing of polio vaccines.

Prototype iron lung negative-pressure ventilators were developed in the late 1920s and early 1930s by industrial hygienist Philip A Drinker (1894-1972), physiology instructor Louis Agassiz Shaw Jr. (1886-1940), and inventor/medical-equipment manufacturer John Haven (Jack) Emerson (1908-1997). From around 1926 to 1928, Drinker and Shaw, both at Harvard Medical School in Boston, designed an electrically powered tank respirator. On October 13, 1928, Drinker and pediatrician Charles F McKhann demonstrated the potential of this device in an 8-year-old girl with poliomyelitis, respiratory failure, and coma who was treated at Boston Childrens Hospital and briefly survived before succumbing to pneumonia. A second trial on Friday, September 13, 1929, at Peter Bent Brigham Hospital in Boston, on a 21-year-old Harvard student, was unquestionably successful: Hoyt was weaned from the respirator in 4 weeks and was discharged from the hospital before Christmas. Emerson built a mechanically superior device in the summer of 1931; Emersons device was first used clinically to save the life of a priest with polio at the Providence City Hospital in Providence, Rhode Island.

Sister Elizabeth Kenny (1880-1952)

Sister Kenny demonstrating her therapy for polio patients to another nursing sister in a hospital in Queensland c1939. (Contributed by Dr. Douglas Lanska. Courtesy of the John Oxley Library, State Library of Queensland. Copyright ...

After this, the manufacture of "iron lungs" expanded markedly over the next 2 decades. At their peak use in the early 1950s, wards at some referral centers were crowded with dozens of these devices, all in use for affected patients, with a large compliment of attendant nursing and respiratory therapy staff.

Indeed, the iron lung required intensive nursing care and respiratory therapy and a supporting hospital infrastructure.

From the 1920s through at least the early 1940s, the orthodox treatment for poliomyelitis consisted largely of absolute and prolonged immobilization of affected limbs with splints or plaster casts, followed by often permanent orthopedic braces; in retrospect, this approach was less than ideal, and in many ways counterproductive as it caused or contributed to disuse atrophy, joint contractures, and lifelong disability. Beginning around 1911, in a sparsely populated area of Australia, Sister Elizabeth Kenny (1880-1952) developed an empiric approach to rehabilitation following poliomyelitis that combined physical and psychological techniques.

Iron-lung ward at Rancho Los Amigos Hospital

Iron-lung ward at Rancho Los Amigos Hospital, Downey (Los Angeles County), California, c1953. (Contributed by Dr. Douglas Lanska. Courtesy of the Rancho Los Amigos National Rehabilitation Center (Rancho Los Amigos) in Downey, Cali...

The physical methods she employed included the labor-intensive application of moist warm wraps for muscle spasms, passive range of motion, and massage. Kennys physical methods were combined with early mobilization, strong encouragement to achieve both functional independence and a prompt return to normal activities, and confident optimism for improvement. The Kenny methods were widely adopted in the United States and elsewhere in the 1940s (although not in Australia where she was strongly opposed by physicians and, particularly, orthopedic surgeons). Kennys approach represented a significant advance in the care of paralyzed patients and helped foster the growth of physical therapy and the medical discipline of physical medicine and rehabilitation.

It was not until the development of the first successful inactivated poliovirus vaccine in the 1950s by American virologist Jonas Salk that the severity of polio epidemics started to decrease.

Jonas Salk (1914-1995)

American virologist Jonas Salk (1914-1995) in 1988. Salk developed the first effective trivalent killed-virus poliovirus vaccine. (Contributed by Dr. Douglas Lanska. Courtesy of the U.S. Public Health Image Library.)

In 1954 and 1955, Salks inactivated poliovirus vaccine was successfully tested in a monumental controlled trial involving more than 1.8 million United States schoolchildren, all funded by the National Foundation for Infantile Paralysis (69).

Polish-American virologist Albert Sabin (1906-1993) developed the first effective trivalent live-attenuated (oral) poliovirus vaccine.

Clinical manifestations

Presentation and course

	• More than 90% of poliovirus infections are asymptomatic.
	• Approximately 4% to 8% of infected patients develop symptoms of acute poliomyelitis, which can be separated into 2 distinct clinical phases: the minor illness, with an incubation period of 3 to 7 days, and the major illness, with onset of symptoms generally 9 to 12 days after exposure.
	• During the major illness, patients may demonstrate signs of meningeal irritation, asymmetric flaccid weakness, muscle spasms, normal or accentuated muscle stretch reflexes, and hyperesthesias with preserved somatosensation.
	• Paralytic poliomyelitis accounts for only 0.1% to 2.0% of all poliovirus infections and can be divided into 3 types: spinal, bulbar, and bulbospinal.
	• Chronic poliomyelitis infections have occurred infrequently in children with immunodeficiencies who have received the live oral vaccine.

More than 90% of poliovirus infections are asymptomatic. Approximately 4% to 8% of infected patients develop symptoms of acute poliomyelitis, which can be separated into 2 distinct clinical phases: the minor illness, with an incubation period of 3 to 7 days, and the major illness, with onset of symptoms generally 9 to 12 days after exposure (51). During the minor illness, patients present with constitutional symptoms (eg, fever, headache, nausea and vomiting, coryza, and sore throat), which are typically self-limiting, lasting 1 to 2 days. Major illness is associated with CNS infection, which has been estimated to occur in 0.1% to 1.0% of all poliovirus infections (85; 93).

During the major illness, patients may demonstrate signs of meningeal irritation, asymmetric flaccid weakness, muscle spasms, normal or accentuated muscle stretch reflexes, and hyperesthesias with preserved somatosensation. The major illness includes all forms of CNS disease caused by poliovirus, including aseptic meningitis, polioencephalitis, bulbar polio, and paralytic poliomyelitis. These manifestations may occur alone or in combination. About one third of young children who develop the major illness experience a biphasic illness with symptoms of the minor illness preceding onset of CNS disease (49; 119). The major illness often begins with an aseptic meningitis. One third of cases are limited to meningitis without detectable motor neuron impairment, which resolves within 5 to 10 days. Polioencephalitis can occur as well, manifesting as obtundation or agitation, autonomic dysfunction and upper motor neuron signs of spasticity, increased deep tendon reflexes, and Babinski signs. Muscle pains, muscle cramps, fasciculations, and radicular pain rarely occur without paralysis, which they precede by 24 to 48 hours.

Paralytic poliomyelitis accounts for only 0.1% to 2.0% of all poliovirus infections and can be divided into 3 types: spinal, bulbar, and bulbospinal (85; 50; 87). Muscle weakness is preceded by intense myalgias of the involved limbs and the axial skeleton, and it may be relieved by exercise. The hallmark of paralytic poliomyelitis is asymmetric motor paresis, which ranges from mild weakness of a single extremity to complete quadriplegia. Proximal limb muscles are more involved than distal, and legs are more commonly involved than arms. The reflexes are initially brisk and then become absent over time. The pace of development of the paresis ranges from several hours to several days. Rarely, a transverse myelitis with paraparesis, urinary retention, sensory complaints and signs, and autonomic dysfunction may be seen (100; 35). Bulbar poliomyelitis occurs in 5% to 35% of paralytic cases and most commonly affects the ninth and tenth cranial nerves.

Chronic poliomyelitis infections have occurred infrequently in children with immunodeficiencies who have received the live oral vaccine (105; 124; 122). Onset usually occurs several months after vaccination, and patients may present with a lower motor neuron paralysis or progressive cerebral dysfunction. As many as 20% to 30% of patients who recover from paralytic poliomyelitis experience new onset of slowly progressive muscle weakness, pain, atrophy, and fatigue many years after the acute illness, most commonly 3 to 4 decades after acute illness (62; 74; 75; 24). This is known as post-polio syndrome. Both muscle and joint pain are frequent. Patients with a history of bulbar poliomyelitis are particularly at risk of developing dysphagia as well as sleep-disordered breathing abnormalities.

Prognosis and complications

Morbidity and mortality in poliomyelitis vary depending on the severity of illness. Although a minor illness typically causes little or no sequelae, major illness can lead to muscle paralysis, respiratory arrest, and death. Case fatality is1.5% to 6.7%, assuming availability of optimal care (29). A study on a particularly virulent outbreak of wild poliovirus in the Republic of Congo found up to 92% of cases had residual paralysis 60 days after disease onset (97). Efficient surveillance and proactive case management may improve morbidity and mortality. Complications of poliomyelitis include respiratory distress often necessitating mechanical ventilation, dysphagia, and pneumonia (34; 37). Prolonged immobility may lead to decubitus ulcers and limb contractures (37). Provocative paralysis (which can occur following intramuscular injection) should also be anticipated when managing poliomyelitis.

Orthopedic issues include hip, back, and extremity pain; muscle strain; ligament sprain; spondylosis; kyphoscoliosis; exaggerated lumbar lordosis; genu recurvatum; and other deformities (25; 37; 115).

Child with gene recurvatum as a residua of polio

Gene recurvatum as a residua of polio generally results from persistent mechanical trauma from hyperextending the knee to provide adequate support when the quadriceps is severely weakened. (Contributed by Dr. Douglas Lanska. Cente...

In the past, poliomyelitis was probably the most common cause of an acquired quadrupedal human gait (as opposed to normal developmental or volitional quadrupedal gaits) (70; 71; 72).

Indeed, in a large series of patients hospitalized with poliomyelitis, 3 of 98 patients (3%) with disturbances of locomotion were noted to be hand walkers (among a total of 108 for whom function was recorded) (46). Note that the term hand walkers generally denoted those that walked with a quadrupedal gait but very rarely referred to individuals who learned to walk exclusively on their hands.

Postpoliomyelitis patients transitioning to adulthood have a high frequency of falls, osteoporosis, and fractures (110). Bone mineral density tends to be worse in the worst-affected leg (110). In a retrospective analysis of 204 postpoliomyelitis patients, recurrent falls were documented in 39% of patients and osteoporosis in 21%. Not surprisingly, osteoporosis was more frequent in women and patients with fractures. At least 1 fracture occurred in half (52%) of the patients and more than 1 fracture occurred in 40% of the patients. The median age for the first fracture was 58 years (range, 30 to 83 years) and most fractures occurred in the affected limb (73%).

Sleep disturbances also occur more frequently and are most commonly associated with the bulbar variant of poliomyelitis (25; 33; 06).

Physical disabilities experienced often lead to emotional symptoms (37). Psychotherapy, group rehabilitation, regular follow-ups, and patient education methods can be used to improve mental status and overall well-being (33).

Patients with post-polio syndrome develop generalized fatigue, muscle weakness, atrophy, pain, fasciculations, cramps, and cold intolerance occurring several years (usually more than 15 years) after the acute episode (44; 25; 62; 74; 75; 24).

Clinical vignette

A 10-year-old boy living in Nigeria was brought to the pediatric emergency department for evaluation of a 2-day history of malaise and diarrhea, with both an increased frequency of stooling and the passage of watery, non-bloody stools. On examination, he was febrile with a temperature of 38.5 degrees Celsius. His abdomen was non-tender, and he had no palpable organomegaly. On neurologic examination, he was conscious and fully oriented but lethargic with mild neck stiffness. He had no cranial nerve palsy. Muscle tone was mildly reduced in the right leg compared to the left. Power was grade 4/5 on the Medical Research Council scale in the right ankle and 5/5 in all other muscle groups. Deep tendon reflexes were grade 1 at the right ankle and grade 2 at the other sites. Plantar response was flexor bilaterally. Sensory examination was unremarkable. Complete blood count, erythrocyte sedimentation rate, electrolytes, and stool (for microscopy, culture, and sensitivity) were ordered.

The following day, his motor strength was reduced to 3/5 in the right leg, and within 48 hours, it was 1/5 and 4/5 on the right and left legs, respectively. Blood count was unremarkable. CSF analysis revealed a mild increase in leukocytes (18 cells/µl) and protein (45 mg/dl). CSF glucose was normal (70 mg/dl). Stool was negative for pathogenic bacteria or blood. Stool samples were positive for wild-type poliovirus 1. He was maintained on bed rest, and specific instruction was given to be vigilant for respiratory distress and to avoid intramuscular injections.

Further interview with the mother revealed that the boy did not complete his polio immunizations as he had only the oral polio vaccine 1 at 6 weeks after birth but did not receive the second and third oral polio vaccine doses in the subsequent months. She could not remember if he had any booster doses at 18 months or later. Three weeks later, power was 2/5 on the right and 4/5 on the left legs.

Biological basis

	• Poliomyelitis is an infection caused by the polioviruses, which are human enteroviruses.
	• Poliovirus, as with other enteroviruses, is most commonly spread by fecal-hand-oral transmission.
	• Although the precise cause of post-polio syndrome is unknown, the cause is probably related to overstress or exhaustion of the residual surviving motor units following acute poliovirus infection.

Etiology and pathogenesis

Poliomyelitis is an infection caused by the polioviruses, which are human enteroviruses.

Single poliovirus virion

3-dimensional representation of a single poliovirus virion. Photograph by Meredith Boyter Newlove MS, James Archer MS. (Contributed by Dr. Douglas Lanska. Centers for Disease Control and Prevention. Public domain.)

Three poliovirus serotypes are distinguished from one another by type-specific antisera (04). Before the introduction of poliovirus vaccines, naturally occurring polioviruses circulated in temperate climates with a marked seasonal variation resulting in peak activity between July and October and low levels between December and May. Poliovirus type 1 was responsible for 80% to 90% of all epidemics of paralytic poliomyelitis in the United States (09; 93).

Poliovirus, as with other enteroviruses, is most commonly spread by fecal-hand-oral transmission. After ingestion, the poliovirus implants in the oropharynx and small bowel and penetrates the mucosa via specialized microfold cells and other epithelial cells overlying submucosal lymphoid tissues (50; 94). After replication in the submucosal lymphatic tissue, the virus spreads to the lymph nodes, and then to the bloodstream (11). In a minority of infections, further replication of virus in reticuloendothelial tissues leads to a major viremia. CNS invasion is much more likely to occur during secondary viremia, but can infrequently occur during primary viremia. As demonstrated in experimental studies in primates, tonsils, mesentery lymph nodes, and intestinal mucosa are major target sites of viral replication (109). Early in the infectious process, poliovirus replication occurs in both epithelial cells (which accounts for virus shedding in the gastrointestinal tract) and lymphoid/monocytic cells in tonsils and Peyer patches (which accounts for viremia) (109). Genetic variants in innate immune defenses and cell death pathways may contribute to the clinical presentation of poliovirus infection (05).

The exact route through which poliovirus enters the CNS is unclear (90; 91; 92). There is some suggestion based on animal models that viral replication in skeletal muscles precedes transport of poliovirus to the spinal cord via the peripheral nerve (15). The anterior horn cells and other motor neurons are selectively vulnerable to poliovirus infection (12; 61; 45; 27). Mitochondria are important in poliovirus-induced apoptosis and mitochondrial dysfunction results from an imbalance between pro- and anti-apoptotic pathways (10). Pathologic changes occur within 1 to 2 days after poliovirus infects the neuron, and an inflammatory response ensues with meningeal, perivascular, and parenchymal infiltrates (14; 13; 59; 121). Nevertheless, individuals who have had polio experience denervation with subsequent reinnervation for many years.

Although the precise cause of post-polio syndrome is unknown, the cause is probably related to overstress or exhaustion of the residual surviving motor units following acute poliovirus infection. Terminal elements of surviving alpha motor neurons that sprout to reinnervate adjacent myofibrils following initial infection are believed to become overstressed (42; 03; 95; 108). Muscle fatigue in post-polio syndrome may be due to impaired activation beyond the muscle membrane at the level of excitation-contraction coupling or may have a central origin. Other possible mechanisms have been considered, including immunologic events and other virus-host interactions (28).

Epidemiology

	• There are now 3 countries with endemic poliomyelitisAfghanistan, Pakistan, and Papau New Guineaand there are major threats to increasing polio outbreaks due to lack of accessibility to polio vaccines in these regions and neighboring areas.
	• Among the 3 wild poliovirus serotypes, only type 1 has been reported in polio cases or detected from environmental surveillance globally since 2012.
	• Type 1 continues to be isolated regularly from environmental surveillance sites in Pakistan and Afghanistan, signifying persistent transmission.
	• Vaccine-derived polioviruses (VDPVs) are rare strains of poliovirus that have genetically mutated from the attenuated strains contained in the oral polio vaccine.
	• If a population is under-immunized, there may be sufficient susceptible children for the excreted VDPVs to begin circulating in the community; with sufficient time of uninterrupted recirculation, vaccine-derived poliovirus may reacquire neurovirulence and are then called circulating vaccine-derived polioviruses (cVDPV).
	• Prolonged replication of vaccine-derived polioviruses has also been observed in people with immune deficiency disorders; in the absence of an adequate immune response, such individuals may excrete immunodeficiency-related vaccine-derived polioviruses (or iVDPVs) for prolonged periods.
	• Ambiguous vaccine-derived poliovirus (aVDPV) are vaccine-derived polioviruses that are either isolated from people with no known immunodeficiency or isolated from sewage whose ultimate source is unknown.
	• As poliovirus serotypes are eliminated, it is necessary to continue to shift away from use of live attenuated vaccines to minimize the risk of vaccine-derived poliovirus cases.

Accurate prevalence figures estimating the number of survivors of poliomyelitis are not available (58).

Polio cases have decreased by over 99% since 1988, from an estimated 350,000 cases in more than 125 endemic countries to 42 reported cases in 2016 (37 wild-type and 5 vaccine-derived) (32; 38; 83; 84; 89; 40; 53). Due to the World Health Organization's polio eradication campaign, poliomyelitis due to wild-type virus has now been eliminated from the Americas, Europe, and the Western Pacific, whereas cases in Africa and Asia have markedly decreased (21; 22). In 1994, the WHO Region of the Americas was certified polio-free, followed by the WHO Western Pacific Region in 2000 and the WHO European Region in June 2002. In 2014, the WHO Southeast Asia Region was certified polio-free, meaning that transmission of wild poliovirus has been interrupted in 11 countries stretching from Indonesia to India.

There are now 3 countries with endemic poliomyelitisAfghanistan, Pakistan, and Papau New Guineaand there are major threats to increasing polio outbreaks due to lack of accessibility to polio vaccines in these regions and neighboring areas (31; 80; 81; 78; 17; 54; 43). Afghanistan and Pakistan are the only countries that continue to have ongoing wild poliovirus type 1 transmission (52; 55; 78).

The number of cases in Pakistan increased markedly from 2018 to 2019 (from 8 to 80 cases as of November 7 of each year, respectively) due to a breakdown of vaccinations resulting from vaccine refusals, chronically missed children, who remained unvaccinated, community campaign fatigue, and poor vaccination management and implementation (52). Pakistans polio eradication efforts suffered severe setbacks that began during 2018, with a sharp increase in wild poliovirus type 1 (WPV1) cases and positive environmental samples from systematic sewage sampling for WPV1 and circulating vaccine-derived poliovirus type (cVDPV2) in 2019 (55). The resurgence of WPV1 resulted from ongoing challenges reaching children in districts with endemic transmission and deterioration in the quality of supplementary immunization activities: supplementary immunization activities are mass national or subnational campaigns conducted for a brief period, from days to weeks, in which 1 dose of oral poliovirus vaccine is administered to all children aged less than 5 years, regardless of vaccination history. Efforts to halt transmission of WPV1 failed in 2019. During 2019, 147 WPV1 cases were reported in Pakistan, more than 12 times the 12 reported cases during 2018.

Poliomyelitis cases in Pakistan from January 2016 to July 2020

During 2019, 147 WPV1 cases were reported in Pakistan, more than 12 times the 12 reported cases during 2018. Since the detection of the first cVDPV2 case in July 2019 through September 15, 2020, 81 cases were reported. Abbrevia...

From January to September 2020, 72 WPV1 cases were reported among 33 districts in 4 provinces, compared with 72 from 22 districts in 4 provinces during the same period in 2019. Since the detection of the first cVDPV2 case in July 2019 through September 15, 2020, 81 cases affecting 30 districts in 6 provinces were reported. With the emergence of cVDPV2, spread of both poliovirus types was exacerbated in 2020 by the social, healthcare, and economic disruption associated with the COVID-19 pandemic. The COVID-19 pandemic placed significant demands on the health care system and disrupted surveillance and vaccination activities, in part because leaders, laboratory personnel, and frontline workers previously responsible for polio surveillance and vaccination activities were reassigned to combat the escalating COVID-19 epidemic. Consequently, the National Emergency Operations Center suspended all polio supplementary immunization activities from March to July 2020.

The number of cases in Afghanistan has increased since 2017 (81; 78). Insurgent groups banned house-to-house vaccination in effect from May to December 2018 in most southern and southeastern provinces, leaving approximately 1 million children inaccessible to oral poliovirus vaccine administration (81). From January to April 2019 vaccination was allowed at designated community sites, but since April 2019 vaccination campaigns were banned nationally in Afghanistan (81). During March through June 2020, all campaigns were paused because of the coronavirus disease 2019 (COVID-19) pandemic (78). The number of WPV1 cases reported in Afghanistan increased from 21 in 2018 to 29 in 2019. During January to July 2020, 41 wild poliovirus type 1 cases were reported as of August 29, 2020 (compared with 15 during the same period in 2019); in addition, 69 cases of circulating vaccine-derived poliovirus type 2 and 1 case of ambiguous vaccine-derived poliovirus type 2 (aVDPV2) (isolates with no evidence of person-to-person transmission or from persons with no known immunodeficiency) were detected (78).

Poliomyelitis cases in Afghanistan from January 2016 to July 2020

A total of 91 cases of wild poliovirus type 1 (WPV1) and 71 cases of vaccine-derived poliovirus type 2 (VDPV2) were reported from January 2016 to July 2020, with a marked exacerbation in 2020 (data as of August 29, 2020). Abbre...

In August and September of 2021 there was marked social and economic disruption in the country associated with the withdrawal of U.S. troops and the sweeping victory of the Taliban. It is likely that there will be a marked exacerbation of poliomyelitis in Afghanistan but this may be difficult to ascertain immediately due to disruption of surveillance under the new regime.

Since June 2018 it was confirmed that poliovirus is again circulating in Papua New Guinea after that country was polio-free for 18 years (43); the current outbreak is caused by vaccine-derived poliovirus, an indicator of low polio vaccine coverage in the country.

Nigeria was also among the countries with endemic poliomyelitis. However, the last confirmed case due to wild poliovirus type 1 in Nigeria was in August 2016 (17; 02). However, since 2018 circulating vaccine-derived poliovirus type 2 has emerged and spread from Nigeria to Niger and Cameroon; outbreak responses so far have not interrupted transmission (02).

Among the 3 wild poliovirus serotypes, only type 1 has been reported in polio cases or detected from environmental surveillance globally since 2012 (54; 52; 79; 81). Type 1 continues to be isolated regularly from environmental surveillance sites in Pakistan and Afghanistan, signifying persistent transmission (54; 52; 79; 81).

On September 20, 2015, the Global Commission for the Certification of Eradication declared that poliovirus type 2 has been eradicated worldwide. With that declaration, it was necessary to develop a new immunization regimen that addresses solely serotypes 1 and 3 using oral polio vaccine (to minimize the risk of vaccine-derived cases of type 2) (89; 114).

Vaccine-derived polioviruses (VDPVs) are rare strains of poliovirus that have genetically mutated from the attenuated strains contained in the oral polio vaccine. Normally, when a child is vaccinated, the weakened vaccine strains replicate in the intestine and enter the bloodstream, triggering a protective immune response. Like infections with wild polioviruses, vaccinated children typically excrete the vaccine strains of poliovirus for 6 to 8 weeks. Some of the excreted vaccine strains of poliovirus may mutate during replication, forming vaccine-derived polioviruses. If a population is under-immunized, there may be sufficient susceptible children for the excreted VDPVs to begin circulating in the community; and, with sufficient time of uninterrupted recirculation, vaccine-derived poliovirus may reacquire neurovirulence and are then called circulating vaccine-derived polioviruses (cVDPV). Prolonged replication of vaccine-derived polioviruses has also been observed in people with immune deficiency disorders; in the absence of an adequate immune response, such individuals may excrete immunodeficiency-related vaccine-derived polioviruses (or iVDPVs) for prolonged periods. Most of patients with iVDPVs stop excretion within 6 months and/or die. Finally, ambiguous vaccine-derived poliovirus (aVDPV) are vaccine-derived polioviruses that are either isolated from people with no known immunodeficiency or isolated from sewage whose ultimate source is unknown. As poliovirus serotypes are eliminated, it is necessary to continue to shift away from use of live attenuated vaccines to minimize the risk of vaccine-derived poliovirus cases.

Prevention

	• Both the inactivated poliomyelitis vaccine (the Salk vaccine) and the live, attenuated oral poliovirus vaccine (the Sabin vaccine) have been effective in decreasing the incidence of poliomyelitis.
	• A person is considered fully immunized if he or she has received a primary series of at least 3 doses of inactivated poliovirus vaccine, live oral poliovirus vaccine, or 4 doses of any combination of inactivated poliovirus vaccine and oral poliovirus vaccine.
	• To eliminate the risk of vaccine-associated paralytic poliomyelitis, as of 2000, oral poliovirus vaccine was no longer recommended for routine immunization in the United States.
	• The World Health Organization plans to withdraw all oral polio vaccines and switch to the sole use of inactivated poliovirus vaccine. However, this will only occur after global eradication of wild poliovirus has been certified, which will be at least 3 years after the last case of wild poliovirus infection.
	• Because poliovirus type 2 has been eradicated worldwide, the type 2 component of the oral poliovirus vaccine is targeted for global withdrawal through a switch from the trivalent oral poliovirus vaccine to a bivalent oral poliovirus vaccine. This change is intended to prevent paralytic polio caused by circulating vaccine-derived poliovirus type 2.

Vaccination has been essential in the fight to eradicate polio because the virus can only be transmitted from person to person, and vaccination breaks this cycle of infection. Both the inactivated poliomyelitis vaccine (the Salk vaccine) and the live, attenuated oral poliovirus vaccine (the Sabin vaccine) have been effective in decreasing the incidence of poliomyelitis (98; 19). Today, a person is considered fully immunized if he or she has received a primary series of at least 3 doses of inactivated poliovirus vaccine, live oral poliovirus vaccine, or 4 doses of any combination of inactivated poliovirus vaccine and oral poliovirus vaccine.

Previously, the benefits of oral poliovirus vaccine use (ie, intestinal immunity, secondary spread) outweighed the risk for vaccine-associated paralytic poliomyelitis, which occurred in 1 child out of every 2.4 to 2.5 million oral poliovirus vaccine doses distributed (123).

To eliminate the risk of vaccine-associated paralytic poliomyelitis, as of 2000, oral poliovirus vaccine was no longer recommended for routine immunization in the United States. Russia used oral polio vaccine from 1998 to 2007 and inactivated polio vaccine followed by oral polio vaccine from 2008 to 2014 (56). China began introducing inactivated polio vaccine at the end of 2014, and so far, it has been successful (125). However, oral poliovirus vaccine continues to be used in the countries where polio is endemic or the risk of importation and transmission is high. Prevention can also occur by stopping the spread of infection using good personal, family, and public hygiene.

The World Health Organization plans to withdraw all oral polio vaccines and switch to the sole use of inactivated poliovirus vaccine (99). However, this will only occur after global eradication of wild poliovirus has been certified, which will be at least 3 years after the last case of wild poliovirus infection (99). Given the most recent cases of polio, which occurred in February 2018 in Afghanistan, oral polio vaccine will not be withdrawn until at least 2022 (99).

Because poliovirus type 2 has been eradicated worldwide, the type 2 component of the oral poliovirus vaccine is targeted for global withdrawal through a switch from the trivalent oral poliovirus vaccine to a bivalent oral poliovirus vaccine (102). This change is intended to prevent paralytic polio caused by circulating vaccine-derived poliovirus type 2.

Differential diagnosis

A clinical diagnosis of paralytic poliomyelitis is usually straightforward in countries where polio has not been eradicated. A physician should have a high index of suspicion of polio in any patient presenting with acute-onset fever, nuchal rigidity, and asymmetrical flaccid muscle paresis with hyperesthesia and relative preservation of somatosensation. Absent or poor immunization history against poliomyelitis will also strengthen the clinical suspicion. Identification of poliovirus in stool or CSF confirms the diagnosis.

Other causes of acute flaccid paralysis include Guillain-Barre syndrome and acute transverse myelitis. Although polio is not as common as Guillain-Barre syndrome or acute transverse myelitis, the importance of correct diagnosis cannot be overemphasized due to its high risk of transmission (36).

Guillain-Barre syndrome is a leading cause of acute flaccid paralysis and presents as a rapidly progressive, symmetric flaccid paralysis; there may also be a distal paresthesia with CSF cytoalbuminologic dissociation early in the disease. Although myalgias and fever at onset of paralysis are prominent features in paralytic polio, they are not as common during Guillain-Barre syndrome (36).

Flaccid paralysis may also occur in the early phase of acute transverse myelitis; however, accompanying sensory symptoms (eg, anesthesia, paresthesia with a sensory level) and neurogenic bowel and bladder dysfunction differentiates it from polio (36).

In recent years, West Nile virus has increased in geographical spread. Although the neurologic manifestations of West Nile virus typically include meningitis and encephalitis, an acute flaccid paralysis may also occur, ranging from monoparesis to quadriparesis, with or without bulbar symptoms. Acute flaccid paralysis due to West Nile virus can be clinically difficult to differentiate from poliomyelitis. A history of mosquito bites, a summer flu, and acute flaccid paralysis may suggest West Nile virus in endemic areas.

Diphtheric polyneuropathy is a vaccine-preventable bacterial infection that can also produce fever and acute flaccid paralysis (commonly symmetric) and should be considered in the differential diagnosis of patients presenting with acute flaccid paralysis in countries where poliomyelitis and diphtheria have not been eradicated (82).

Other viral respiratory or gastrointestinal illnesses can present with features similar to the minor nonparalytic poliomyelitis (36). In addition, other non-polio enteroviruses (NPEV) have been found to be associated with acute flaccid paralysis (48). An acute flaccid paralysis surveillance report in India found Coxsackie and Echovirus the most common NPEV isolates implicated (73). In 2014, the United States experienced a nationwide outbreak of enterovirus D68 (EV-D68) in which a total of 1152 people, particularly children, in 49 states and the District of Columbia, were confirmed with respiratory illness.

During the outbreak, the Centers for Disease Control and Prevention was notified by the Colorado Department of Public Health and Environment of a cluster of 9 children evaluated at Children's Hospital Colorado with acute neurologic illness characterized by extremity weakness, cranial nerve dysfunction (eg, diplopia, facial droop, dysphagia, or dysarthria), or both (96). Enterovirus D68 has since been recognized as a cause of polio-like illness (07; 20; 66; 77; 86; 26; 107; 120). Isolated cases of poliomyelitis-like illness have been reported elsewhere since the 2014 United States outbreak (113).

The paralytic presentation of rabies virus infection (so-called dumb rabies) may also be confused with poliomyelitis. A history of an animal bite should warrant consideration of rabies (41). Outbreaks of dumb rabies have occurred in humans as a result of bites from vampire bats (67; 68).

Other conditions that may give a polio-like picture include spinal cord compression; tick, snake, or spider bite; botulism; and toxic substances such as arsenic (39; 07).

Diagnostic workup

	• Viral isolation, serology, and polymerase chain reaction assays can be used to confirm the laboratory diagnosis of poliomyelitis.
	• A laboratory diagnosis of poliomyelitis is made by isolation of the virus from stool or pharynx. Virus isolation is highest in stool, lower in the pharynx, and lowest in blood and CSF.
	• The use of serological tests in the diagnosis of polio depends on the rise in antibody titer between the acute and convalescent phases; a serum specimen should be obtained as early as possible during the acute phase as well as 4 weeks later (convalescent phase). A 4-fold rise in titer between the acute and convalescent phase specimens suggests infection.
	• CSF abnormalities are present in up to 90% of poliomyelitis cases.
	• Post-polio syndrome is a diagnosis of exclusion that is made based on evidence of new muscle weakness and/or muscle fatigability that is persistent for at least 1 year.
	• Electromyographic and muscle biopsy findings, including evidence of ongoing denervation, cannot reliably distinguish between patients with or without post-polio syndrome.

Following a clinical suspicion of polio, it is imperative to confirm the diagnosis and report the case to the local and national public health department. Early detection will allow timely measures, such as successful vaccination, to limit the spread and promote eradication of poliomyelitis. Viral isolation, serology, and polymerase chain reaction assays can be used to confirm the laboratory diagnosis of poliomyelitis.

A laboratory diagnosis of poliomyelitis is made by isolation of the virus from stool or pharynx. Virus isolation is highest in stool, lower in the pharynx, and lowest in blood and CSF. CSF viral isolation, though rare, is diagnostic (118). It is recommended that at least 2 stool specimens and 2 throat swabs be obtained 24 hours apart from suspected poliomyelitis patients as early as possible (118). The frequency of obtaining samples increases the likelihood of viral isolation as there is intermittent shedding of the virus from the mucous membranes. Although poliovirus has been the most common enterovirus isolated in the stool in cases of acute flaccid paralysis, a small proportion of non-poliovirus infections can also be isolated (01).

The use of serological tests in the diagnosis of polio depends on the rise in antibody titer between the acute and convalescent phases; a serum specimen should be obtained as early as possible during the acute phase as well as 4 weeks later (convalescent phase). A 4-fold rise in titer between the acute and convalescent phase specimens suggests infection (118). False negatives can occur in the immunocompromised. Serology cannot differentiate wild virus from antibodies generated from vaccination. Serology is used to detect the degree of protection conferred by polio vaccination (112). Polymerase chain reaction can be used to differentiate between wild and vaccine types of poliovirus as well as the various strains of poliovirus (01).

CSF abnormalities are present in up to 90% of poliomyelitis cases. Typically, the CSF white blood cell count ranges from 10 to 200 cells/µl. A polymorphonuclear leukocytosis is followed by a mononuclear response. CSF protein is typically normal or mildly elevated (36).

Post-polio syndrome is a diagnosis of exclusion that is made based on evidence of new muscle weakness and/or muscle fatigability that is persistent for at least 1 year (74). Electromyographic and muscle biopsy findings, including evidence of ongoing denervation, cannot reliably distinguish between patients with or without post-polio syndrome (74).

Management

	• Initial treatment of paralytic poliomyelitis relies on supportive care, followed by passive, and then active, physical therapy and orthopedic measures. During the preparalytic stage, which would only be suspected during epidemics, bed rest is recommended because physical exercise can increase the severity of paralysis.
	• Paralytic disease in the acute stage should be treated in a similar fashion as the preparalytic stage with the following additions: (1) hospitalization is required; (2) respiratory support on a ventilator may be required; and (3) appropriate positioning such as splints to prevent contractures, foot boards to prevent foot-drop, and frequent turning to prevent decubiti should be provided.

Initial treatment of paralytic poliomyelitis relies on supportive care, followed by passive, and then active, physical therapy and orthopedic measures. During the preparalytic stage, which would only be suspected during epidemics, bed rest is recommended because physical exercise can increase the severity of paralysis (60). In addition, sore muscles can be treated with hot packs, fever with acetaminophen, and anxiety with anxiolytics. Paralytic disease in the acute stage should be treated in a similar fashion as the pre-paralytic stage with the following additions: (1) hospitalization is required; (2) respiratory support on a ventilator may be required; and (3) appropriate positioning such as splints to prevent contractures, foot boards to prevent foot-drop, and frequent turning to prevent decubiti should be provided (101). Patients with bulbar involvement may require fluid and electrolyte support and additional support if cardiovascular, respiratory, or autonomic dysfunction occurs (117). Physical therapy is deferred until the convalescent stage, except for gentle passive range of motion to prevent contractures. During the convalescent period, active physical therapy with non-fatiguing muscle-strengthening exercises and hydrotherapy can be instituted. Patients with late and new effects of polio may need individualized multidisciplinary intervention and physiotherapy (08; 74; 75). Interventions may include adaptive equipment, orthotic equipment, gait/mobility aids, and a variety of therapeutic exercises (75). A metaanalysis of 21 studies showed that muscle strengthening and cardiovascular interventions among polio survivors are helpful in improving outcomes according to the International Classification of Functioning, Disability, and Health (103).

Orthopedic surgical intervention (eg, arthrodesis, tendon transfers, leg-shortening measures) should be deferred for 1.5 to 2 years, after maximum recovery has been obtained (104; 57). For patients with residual effects of poliomyelitis, surgeons should optimize the position, choice, approach, and soft tissue tensioning because stability of prosthesis may be difficult to ensure and maintain (64).

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Poliomyelitis

Associated Disorders

Aseptic meningitis
Bulbar polio
Bulbospinal polio
Infantile paralysis
Nonparalytic polio
- Paralytic polio
- Polioencephalitis
- Post-polio progressive muscular atrophy
- Post-polio syndrome
- Spinal paralytic polio

Differential Diagnosis

Guillain-Barre syndrome
acute transverse myelitis
West Nile virus
diphtheric polyneuropathy
non-polio enteroviruses
- Coxsackie
- Echovirus
- enterovirus D68 (EV-D68)
- rabies
- spinal cord compression
- tick, snake, or spider bite
- botulism
- toxic substances

Poliomyelitis …

Poliomyelitis

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Special considerations

Pregnancy

Media

References

Contributors

Author

Former Authors

Patient Profile

ICD & OMIM codes

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Poliomyelitis

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Special considerations

Pregnancy

Media

References

Contributors

Author

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Headache associated with HIV and AIDS

Measles: neurologic complications

Scoliosis and kyphoscoliosis

HTLV-1 associated myelopathy

Disorders of lipid metabolism

X-linked myotubular myopathy

Prion diseases

Creutzfeldt-Jakob disease

This is an article preview.
Start a Free Account
to access the full version.