Continuing Education Activity

Poliomyelitis is a highly transmissible infection nearing global eradication. However, recent outbreaks and vaccine-derived cases highlight the ongoing risk. Most infections are asymptomatic, with 70% to 95% presenting as a self-limiting flu-like illness. However, up to 1 in 200 cases involve rapid-onset flaccid paralysis, with the potential for lifelong disability or death. Polio persists in areas with poor water, sanitation, and hygiene infrastructure, with sporadic cases reported globally.

Clinicians must remain vigilant for polio, especially in countries with low vaccination rates. Vaccine-derived strains, which cause paralytic disease indistinguishable from wild-type polio, complicate eradication efforts. Early recognition of symptoms, timely reporting to public health authorities, and reinforcing vaccination remain critical for patient outcomes and global eradication efforts. This activity provides healthcare providers with a comprehensive overview of polio identification, management, and control. Emphasizing the role of the interprofessional healthcare team and highlighting effective communication and collaboration strategies, the activity also discusses clinicians' ability to recognize polio and postpolio syndrome, report polio to public health authorities, and implement polio prevention measures, thereby improving patient outcomes and contribute to the global effort to eradicate polio.

Objectives:

• Compare clinical manifestations and apply diagnostic testing to differentiate poliomyelitis from similar infections as possible causes of acute flaccid paralysis.
• Improve polio vaccination rates as a primary prevention strategy against poliomyelitis infection.
• Identify early signs of post-polio syndrome in patients with a history of poliomyelitis.
• Implement effective communication as an interprofessional healthcare team member to ensure comprehensive care for patients with poliomyelitis and prevent future infections.

Introduction

Poliomyelitis, or polio, is an infection transmitted via the fecal-oral and oral-oral routes. Today, polio primarily affects children younger than 5 in countries with poor water, sanitation, and hygiene infrastructure.[1] While extremely rare outside these areas, polio presents a risk to populations with low vaccination rates, including in industrialized nations. The 2014 declaration deeming the global spread of polioviruses a public health emergency of international concern under the International Health Regulations remains in place.[WHO. Vaccine Position]

Previously one of the most feared diseases in the world, polio caused widespread morbidity and mortality in children during multiple epidemics between the 1900s and 1960s. The incidence of polio began to decline following the development of the injectable polio vaccine (IPV) and oral polio vaccine (OPV). Intensified worldwide vaccination efforts starting in the 1980s by the World Health Organization (WHO) and partners under the Global Polio Eradication Initiative (GPEI) have almost completely eradicated the disease.[1][2] Vaccination protocols worldwide now recommend administering at least 3 doses of IPV (IPV-only schedule) or at least 3 doses of bivalent OPV plus at least 2 doses of IPV (combined OPV-IPV schedule).[3] The latter is recommended in countries where poliovirus incidence rates remain unchanged or are at risk of increasing. See StatPearls' companion article "Polio Vaccine" for more information on polio vaccinations.

Healthcare providers must maintain a high index of suspicion to diagnose acute poliomyelitis in patients who present with new-onset paralysis following a viral prodrome and are living in an endemic region or under-vaccinated population. The presentation of polio is highly variable, ranging from asymptomatic to a transient flu-like viral illness to paralysis, quadriplegia, and even respiratory failure and death. Many polio survivors experience a poor quality of life.

Alternate diagnoses must be considered as polio is rare, and other more common diseases and conditions can present similarly. In particular, acute flaccid myelitis (AFM) presents with a polio-like syndrome. This condition is caused by epidemic enteroviral infections, most commonly enterovirus D68.[4][5]

As no antiviral treatment for acute poliomyelitis exists, prevention is critical. Paralytic deficits are often permanent, resulting in chronic pain, deformities, weakness, and eventual osteoporosis and fragility fracture. Between 25% and 40% of the estimated 12 to 20 million polio survivors worldwide will also develop postpolio syndrome (PPS).[6] A diagnosis of PPS requires new-onset, progressive muscle weakness or fatiguability, mental fatigue, or pain in a patient diagnosed with poliomyelitis up to 40 years prior. PPS is not contagious and is rarely life-threatening, but it often affects patients' independence and quality of life.

While the near eradication of polio represents a tremendous achievement for global public health, multiple challenges and delays remain. Vaccine-derived polioviruses (VDPVs) revert or recombine to wild-type neurovirulence and transmissibility, causing outbreaks and distrust in vaccination programs. Poliovirus typically escapes early detection; most infections are asymptomatic, and the characteristic paralysis occurs in a small minority of those it infects.[CDC. Polio_HCP] Delays in detecting circulating wild poliovirus (WPV) and VDPVs pose a significant risk to eradication efforts. Political unrest or indecision and declining or competing interests threaten efforts to eradicate the disease. Recent polio cases and the discovery of poliovirus in wastewater in industrialized nations emphasize that, until completely eradicated, polio remains a global risk.[7][GPEI. Polio Eradication]

All suspected cases of poliomyelitis in the United States should be immediately reported to the United States Centers for Disease Control and Prevention (CDC). Clinicians should suspect polio in patients with acute-onset flaccid paralysis, decreased or absent tendon reflexes, and without sensory or cognitive deficits. Contact the CDC Emergency Operations Center within 4 hours of the suspected diagnosis to ensure appropriate diagnostic testing, surveillance, and public health follow-up at 770-488-7100.[CDC. Polio_Clinical]

Etiology

Poliovirus, Enterovirus subtype C, is a small, single positive-stranded RNA virus that is acid-resistant, non-enveloped, and encapsulated. This causative agent of acute polio and postpolio syndrome belongs to the family Picornaviridae and reproduces only in humans and some great apes. Poliovirus is extremely contagious, with seroconversion occurring in more than 90% of household contacts.[CDC. Pink Book_Polio][8]

Wild poliovirus (WPV) has 3 distinct serotypes (1, 2, and 3), each with a slightly different capsid protein (WPV1, WPV2, and WPV3). Surviving an infection confers complete and lifelong immunity, but only to the specific infecting serotype.[GPEI. Polio Eradication]

Vaccine-associated paralytic polio (VAPP) and circulating vaccine-derived polioviruses (cVDPVs) cause illness that is clinically indistinguishable from poliomyelitis caused by WPV.[WHO. Vaccine Position] VAPP results from the proliferation and mutation of polioviruses in OPV recipients or their contacts. Replicating viruses in the intestine revert to neurovirulent variants demonstrating close genetic similarity to the vaccine strain. VAPP is an adverse event triggered by immunization and is reportable under the Vaccine Adverse Event Reporting System.

VDPVs result from the naturally selective proliferation of OPV viruses in populations with low herd immunity (cVDPVs) or prolonged carriage in immunocompromised individuals (iVDVPs). Recombination with other enteroviruses or reversion of OPV strains allows the resulting cVDPVs to regain the neurovirulence and transmissibility of WPV.[9][WHO. Vaccine Position] Genetic divergence of cVDPVs from the attenuated OPV virus indicates prolonged replication and circulation. cVDPVs derived from OPV type 2 (cVDPV2) are the most common, although cVDVP types 1 and 3 also occur.

Epidemiology

Poliovirus primarily spreads via the fecal-oral route and less commonly via respiratory droplets or oral-oral contact with nasopharyngeal secretions.[CDC. Polio_HCP][9] In temperate climates, infections occur more commonly during the late summer and fall. Children younger than 5 face the highest infection risk, although unvaccinated individuals of any age can become infected.[8]

The infection is asymptomatic in 75% to 90% of patients.[WHO. About_Polio][CDC. About Polio] CNS invasion resulting in paralytic disease occurs in up to 1 in every 200 patients with a Poliovirus infection. The mortality rate of paralytic polio can be as high as 20%, although most references cite a rate closer to 10%.[CDC. Polio_HCP][CDC. VPD Manual_Polio] The risk and severity of paralysis increase with patient age and immune status.[WHO. Vaccine Position] The incubation period is usually 7 to 10 days but may range from 4 to 35 days.[WHO. About_Polio]

Polio has afflicted humans since ancient times, first exposing infants at an early age when maternal antibodies are present and then repeatedly over the lifetime, resulting in persistently high antibody levels. As such, paralytic polio was likely uncommon.[10][11] With the advent of modern sanitation, medical anthropologists believe early exposure to Poliovirus became less common, and maternal antibody levels decreased, leading to massive outbreaks with high rates of paralysis in the early 20th century.[11][GPEI. Polio History] By the mid-20th century, the virus killed or paralyzed about 500,000 people worldwide yearly. A US outbreak in 1916 killed more than 8,000 people; another in 1952 killed 3,000 and resulted in 20,000 cases of paralysis.[9][CDC. VPD Manual_Polio] Case rates in the United States dropped by 99% only 6 years after the first Poliovirus vaccine became available.[9] The most recent case of WPV acquired in the United States was in 1979. The most recent case in all of the Americas occurred in 1991.[CDC. Yellow_Book] WPV1 has been the primary cause of most of the world's paralytic polio cases throughout history and is the only circulating subtype; WPV1 remains endemic in Pakistan and Afghanistan.

In 1988, 350,000 cases of endemic poliomyelitis occurred across 125 countries. Based on success in the Americas, the World Health Assembly adopted a resolution to eradicate WPV worldwide by 2000 under the Global Polio Eradication Initiative.[12][GPEI. Polio Eradication][CDC. VPD Manual_Polio] While eradication remains elusive, establishing the polio vaccine in routine childhood immunization schedules has led to a greater than 99.9% worldwide reduction in WPV cases since 1988.[GPEI. Polio Eradication] The declaration of WPV2 eradication occurred in 2015, 6 years after the last case was reported in India. The WHO declared the eradication of WPV3 in October 2019, 7 years after the last reported case.[GPEI. Polio Eradication] The WHO declared Africa polio-free in 2020. A worldwide low of 6 cases of WPV1 was reported for 2021.

Sporadic outbreaks continue to occur, including in countries previously declared polio-free. From late 2021 to early 2022, WPV1 caused paralytic polio in 9 patients in Malawi and Mozambique; this outbreak was traced to a transmission in Pakistan.[13] The total number of reported WPV1 cases was 22 in 2022 and 12 in 2023. The WHO reported 23 cases between 2023 and 2024, for which recent statistics are available.[GPEI. Polio Eradication] When polio is reintroduced into a country, transmission must be traced and halted within 12 months for that country to maintain polio-free status.[13]

VAPP is extremely rare, occurring an estimated 0.42 times per million doses of OPV [9][14][CDC. VPD Manual_Polio] or 3.8 times (range 2.9 to 4.7) per million births in countries that use trivalent OPV.[6][14][WHO. Vaccine Position] In high-resource countries, VAPP occurs most commonly after the first dose of OPV. In immunocompromised individuals, the risk of VAPP is approximately 3000 times higher than in healthy patients.[9] In low-resource countries, VAPP primarily affects children aged 1 to 4 receiving second or subsequent doses.[14][WHO. Vaccine Position] Providing IPV before OPV reduces or eliminates VAPP risk.[WHO. Vaccine Position]

First detected in an outbreak on the island of Hispaniola in 2001, cVDPVs are responsible for most cases of poliomyelitis today. cVDPV-associated paralysis occurs primarily in sub-Saharan Africa and Asia. A total of 345 people reported an onset of paralysis in the 12 months leading up to July 2024. Forty-nine cases of cVDPV type 1 were reported in Mozambique, DR Congo, and Madagascar, and 296 cases of cVDPV type 2 were reported in 20 other countries.[GPEI. Polio Eradication] This is a reduction from 881 total cases in 2022 and 524 in 2023. While the number of cases in 2023 was reduced compared to 2022, cVDPV cases were more widespread geographically in 2023.[3]

In 2022, an unvaccinated young adult from New York presented with acute flaccid paralysis. Stool testing revealed VDPV2. Environmental testing of samples taken before and after the patient's illness onset subsequently found VDPV2 in wastewater in surrounding counties. The virus was likely imported from a country that administers OPV but where the population remains under-vaccinated. In addition to this case, a case of polio in a young boy in Gaza, sporadic cases of WPV polio in Africa, and the discovery of cVDPV in wastewater across multiple countries, including the United Kingdom and Israel, emphasize the importance of maintaining high vaccination rates across all populations until polio is eradicated globally.

For further information on vaccination rates in the United States and globally, see StatPearls' companion article, "Polio Vaccine."

Pathophysiology

Following exposure, Poliovirus replicates in oropharynx and gastrointestinal tract tissues. Maternal antibodies or those acquired during a previous infection or oral vaccination often confine the virus to these tissues.[9] In the absence of antibodies, a typically transient and asymptomatic viremia occurs.[9]

However, in a small minority of viremic cases, the virus enters the CNS by crossing the blood-brain barrier or via peripheral nerve retrograde axonal transport.[9] Depending on the virus type and location of invasion, CNS invasion causes non-paralytic aseptic meningitis in up to 5% of symptomatic infections.[CDC. Polio_HCP] CNS invasion can also result in infection and destruction of alpha motor neurons in the anterior horns of the spinal cord, the cranial nerve nuclei of the medulla oblongata, and the pons and midbrain. Inflammatory infiltration of these motor neurons causes cell destruction and eventual glial cell scarring.

For patients who recover from acute polio, regeneration of reversibly damaged neurons, collateral axonal sprouting, and the development of other reparative and compensatory processes can result in the slow improvement of paralysis.[15] Human axons may be able to reinnervate as much as 5 times their original muscle fiber territory. In chronic cases, de-innervated muscles atrophy and cause functional disorders of the limbs, trunk, and respiratory muscles, including the diaphragm. In children, deformities progressively develop due to the influence of muscular imbalances or dysfunction on the growing skeleton. This can result in joint contractures, kyphosis, scoliosis, foot deformities, or leg-length discrepancies. Chronic overloading results in joint instabilities, degenerative changes, and pain.[15]

Following infection, immunocompetent patients develop complete immunity to poliovirus, which involves various mucosal and humoral immune responses. Mucosal immunity reduces viral replication and excretion, thereby reducing transmission risk.[WHO. Vaccine Position] Therefore, patients with B-cell immunodeficiency are at an increased risk of paralytic disease and prolonged shedding.

Histopathology

Enlarged motor neurons are characteristic but not pathognomonic of infection with Poliovirus. In acute poliomyelitis, Poliovirus destroys the original innervating neurons in the muscle fibers. Neighboring neurons attempt to reinnervate the denervated tissue; this leaves the surrounding motor units innervating more muscle fibers than before. This extra workload enlarges the affected neuron and is suspected to be part of the fatigue associated with post-polio syndrome later in life.[16]

History and Physical

Until it is eradicated globally, clinicians must consider polio in the differential diagnosis of patients presenting with acute flaccid paralysis. The rapid onset of pure motor deficits without sensory or cognitive involvement following a flu-like prodrome is suggestive of paralytic polio. However, not all patients with acute polio report a prodrome. Various conditions can cause acute onset flaccid paralysis, and the clinician must differentiate between Poliovirus infection, other viral infections, and noninfectious causes. Disease caused by cVDPVs is clinically indistinguishable from that caused by WPVs.[CDC. VPD Manual_Polio] More information can be found in the Differential Diagnosis section.

Obtaining a thorough medical history and performing a comprehensive neurological exam are crucial. In addition to a complete review of systems, the history must include the patient's vaccination status, recent travel, ill contacts, recent attendance at large gatherings, socioeconomic status, and living situation. Clinicians should consider polio in patients with sudden-onset limb weakness and a history of fever or gastrointestinal symptoms. This suspicion should be heightened further for patients who are also incompletely vaccinated or unvaccinated and residing in or have recently traveled to regions with known polio transmission or in contact with someone who has traveled to such an area.[CDC. VPD Manual_Polio] The cranial nerves should be examined, and reflexes, tone, and strength in all limbs should be documented. Adequate hand hygiene and contact precautions must be observed during the physical examination of any patient with suspected polio.

The acute, prodromal, or pre-paralytic stage of Poliovirus infection is similar to many other viral illnesses; fever, malaise, headache, myalgia, fatigue, nausea, vomiting, abdominal pain, and sore throat are commonly observed.[WHO. About_Polio][CDC. VPD Manual_Polio] In almost all cases, the infection resolves in 2 to 10 days without further sequelae.[WHO. About_Polio] 

Meningitis develops within a few days after the prodrome resolves. While usually asymptomatic, recurrent fever, neck stiffness, back pain, and muscle spasms may be observed. These symptoms resolve within 2 to 10 days, typically resulting in a rapid and complete recovery.[WHO. Vaccine Position]

The return of the fever with severe muscle pain, fasciculations, spasms, and hyperreflexia occurring 1 to 3 days after apparent recovery heralds paralytic polio.[WHO. Vaccine Position] Weakness or flaccid paralysis ensues in an asymmetric distribution, with proximal to distal progression.[CDC. VPD Manual_Polio] Maximum paralysis is reached within 2 to 4 days, rarely progressing further after fever resolution.[CDC. Polio_HCP][CDC. Polio_HCP]

The clinical manifestations depend on the site of viral invasion and the extent of viral replication, resulting in paralysis with a variable distribution and severity, affecting whole or parts of muscles or entire muscle groups. In most cases, spinal paralysis results in paralysis of the muscles of the lower limbs and, less commonly, of the arms, trunk, or diaphragm.[WHO. About_Polio][8] Autonomic dysfunction occurs infrequently, resulting in bladder emptying problems, constipation, or sweat secretion abnormalities.

Poliovirus can invade the bulbar aspect of the brain, affecting the control of breathing and other vital functions, as well as the muscles for facial and eye movements and swallowing. Bulbar invasion can lead to respiratory insufficiency, vegetative crises, tachycardia, hypertension, and collapse. Fortunately, invasion of this severity rarely occurs.

Evaluation

Rapid investigation of acute flaccid paralysis is critical to identifying a possible polio infection and implementing control measures.

Poliovirus infection is assessed through viral cultures or detection of viral RNA in stool or throat irrigation or swabs.[CDC. Polio_HCP] The CDC recommends 2 specimens taken at least 24 hours apart during the first 14 days after the onset of paralysis. Specimens must be maintained at -20 ºC and shipped frozen.[CDC. Polio_HCP]

Clinical confirmation of polio requires the following:

• Poliovirus detected by sequencing of the capsid region of the genome by the CDC Poliovirus Laboratory;

or

• Poliovirus identified in an appropriate clinical specimen (eg, stool [preferred], cerebrospinal fluid, oropharyngeal secretions) using a validated assay, AND specimen is unavailable for sequencing by the CDC Poliovirus Laboratory.[CDC. Polio_HCP]

Confirmed cases of nonparalytic Poliovirus infections are those that meet laboratory but not clinical criteria.

Maximum viral excretion in the stool and nasopharyngeal fluids begins 2 to 3 days before (and lasts for a week after) symptom onset.[17] However, the virus may be present in the nasopharyngeal secretions for up to 2 weeks and 3 to 6 weeks in the stool, even in asymptomatic patients.[CDC. Polio][CDC. Yellow_Book] Finding Poliovirus in cerebral spinal fluid is uncommon. A CSF test result negative for poliovirus does not exclude polio.

Polioviruses undergo RT-PCR testing following culture to differentiate between WPV and VDPVs. Serology is not helpful due to the high seroprevalence of anti-polio antibodies due to vaccination or previous asymptomatic infection. Researchers continue to seek direct molecular methods to diagnose polio, replacing culture-dependent methods.[WHO. Vaccine Position]

Magnetic resonance imaging of the brain and spinal cord may identify typical patterns of poliomyelitis and rule out other pathologies, such as spinal cord infarction. Characteristic electromyographic findings develop later in the course of illness.

Treatment / Management

Supportive care is the mainstay of treatment for acute poliomyelitis, as no effective antiviral therapy exists. Therapy may include medication for fever and irritation, preventing respiratory tract infections, and managing respiratory paralysis via mechanical ventilation if required. Physiotherapists use splints to relieve pain and spasms; splints also play an imperative role in preventing the development of deformities.

Following the acute stage, rehabilitation, exercise, counseling, and education help patients achieve their best functional status. Orthopedic surgery may be warranted to help patients walk and correct factors potentially leading to deformity as the patient grows and ages. Surgery may include joint contracture release, correction of muscle imbalances around the joint to prevent deformities, or correction of deformities.[18]

Following phase 1 trials, the capsid inhibitor pocapavir is available for compassionate use in patients who cannot clear the virus due to primary immunodeficiency disorder.[WHO. Vaccine Position]

Differential Diagnosis

Globally, acute flaccid paralysis occurs at a rate of about 1 of every 100,000 children under the age of 15 per year. These are due to a wide variety of infectious and noninfectious causes.

Other enteroviruses cause acute flaccid paralysis with greater frequency than poliovirus, including enteroviruses A71 and D68, coxsackievirus A, and rarely enteroviruses such as C105 and C109.[4] Like polio, enterovirus infections are frequently asymptomatic or present with a mild viral prodrome.[8] While paralytic polio predominantly affects the lower limbs, most other enterovirus-related acute flaccid paralysis have an upper extremity predilection.[19]

Other infections that may present similarly include adeno-associated virus, West Nile virus, varicella-zoster virus, Japanese encephalitis virus, rabies virus, and Clostridium botulinum.[20][21] A careful history and physical exam usually differentiate these infections from polio.[8]

Noninfectious considerations include spinal cord infarctions, transverse myelitis, acquired axonal neuropathies, myasthenia gravis, and Lambert-Eaton myasthenic syndrome. Guillain-Barré syndrome is a common cause of acute flaccid paralysis, clinically differentiated from polio by ascending, symmetrical onset, sensory defects, and the absence of preceding meningeal symptoms.[8]

See StatPearls' companion article "Acute Flaccid Myelitis" for more information on acute flaccid paralysis associated with other viruses.

Prognosis

Most poliovirus infections are asymptomatic or self-limiting. For those with poliomyelitis (ie, symptomatic Poliovirus infection), 10% to 15% will die due to bulbar involvement, with respiratory and cardiovascular collapse.

For those who survive, recovery and residual paralysis stages follow. Convalescence or recovery begins when the acute, flu-like illness resolves and no further paralysis occurs. Neighboring nerves or axonal regeneration reinnervates paralyzed muscles. Recovery can last up to 2 years, with maximal improvement occurring in the first 6 months. Approximately 60% of polio survivors have permanent deficits. The more severe the acute phase of the disease, the greater the likelihood of residual deficits and the development of postpolio syndrome in the future.[22]

Complications

Morbidity following paralytic polio commonly results from biomechanical alterations due to muscle weakness, imbalances of muscle power, deformities, and complications of polio-related surgeries.[15] Pain, easy fatiguability, limited function, and reduced quality of life are common. Osteoporosis develops due to lack of function and other factors, with frequent fractures.[15]

Approximately 25% to 40% of patients with previous paralytic polio also develop PPS over their lifetime.[CDC. Polio_HCP] The diagnosis of PPS requires at least 1 year of new and progressive muscle weakness or fatiguability following decades of stable paralysis after the acute infection. Other symptoms include generalized fatigue, muscle or joint pain, worsening respiratory function, and dysphagia.[23] The true prevalence of PPS is not known, partly due to a lack of established biomarkers to diagnose postpolio syndrome.[24] While the prevalence of PPS is decreasing in industrialized nations due to the elimination of the virus, it remains highly prevalent in developing nations.

The pathogenic mechanisms resulting in PPS are incompletely understood. The most common theory involves degeneration of the enlarged motor units formed following the initial infection. Longitudinal research demonstrates a parallel between a decreasing size and number of active motor units and a gradual strength decline in PPS.[15] The precise etiology of this decline is unclear; it likely results from the overuse of remaining motor units, stress-induced aging of motor units, deteriorating neuromuscular junctions, weight gain, deconditioning, and other factors.[18][25] Although some authors suggest subgroups of patients may have a predominantly neuroinflammatory pathogenesis of their PPS, recent evidence does not support the role of humoral or cellular pro-inflammatory processes.[25][6] Normal age-related sarcopenia contributes significantly and independently to decreasing muscle mass and strength; however, PPS may accelerate the decline in some patients, with an annual loss of up to 8% of muscle strength.[6]

PPS is a clinical diagnosis using Halstead, March of Dimes, or other criteria. Neither electromyography nor muscle biopsy reliably differentiates patients with or without PPS.[15] Clinicians must carefully exclude other treatable medical and orthopedic conditions that may cause or contribute to the condition.[24][25][15] Depending on the presenting symptomatology, the differential includes a wide variety of disorders, including the following:

• Metabolic: iron deficiency, hypothyroidism, type 2 diabetes
• Sleep: apnea, restless leg syndrome
• Inflammatory: rheumatoid arthritis, polymyalgia rheumatica
• Chronic pain: fibromyalgia

The severity and speed of progression are variable and are influenced by factors such as the severity of acute paralysis, age of onset, and socioeconomic status.[22][26][15] Complications include respiratory failure, fractures, decreased function, and worsening quality of life. Tailored muscle strengthening, aquatic conditioning, and pain control are the mainstays of treatment.[6]

Postoperative and Rehabilitation Care

Rehabilitation, exercise, counseling, and education are crucial for patients with polio or PPS to maintain function, prevent further morbidity, and achieve the best possible health. Of patients previously diagnosed with polio, 60% to 80% reported falling at least once in the past year.[15] One-third of falls result in a fragility fracture of the polio-affected limb.

Based on experience and extrapolated from studies in other conditions, physiatrists recommend energy conservation techniques, pacing strategies, and lifestyle and activity modification to prevent premature fatigue, weight gain, and other factors that can worsen symptoms.[6] Assistive equipment (eg, grab bars, raised toilet seats, modified utensils) can maximize functioning and decrease energy use. Patients often require mobility aids such as canes, walkers, wheelchairs, or scooters.

Fitted ankle-foot or knee-ankle foot orthoses can mitigate gait disturbances. Orthoses made with lightweight carbon fiber are about 30% lighter and can increase comfort and function but are more expensive than those made with thermoplastics and metal.[6] An interdisciplinary approach to fitting orthotics is vital due to the difficulty of assessing and mitigating individual gait patterns and parameters.

Research shows that non-fatiguing strengthening exercises increase muscle strength and prevent further decline in patients with moderate weakness due to PPS. Muscle training lessens muscle pain and fatigue and improves functional activity levels and quality of life.[6] Physiatrists recommend intermittent (eg, alternate days) submaximal exercise be interspersed with short rest periods to avoid fatigue and overuse. Studies suggest individualized exercise programs within a comprehensive rehabilitation program provide long-term positive effects on physical, functional, and psychological outcomes.[6]

Studies of aerobic exercise in patients with PPS have yielded mixed results.[6] In some patients, muscles may already be maximally adapted for daily life activities, limiting the potential for improvement. However, whole-body aerobic exercise, such as non-swimming aquatic exercises in heated water, recruits more muscles and benefits patient well-being, cardiovascular conditioning, and pain relief.

Medications and supplements, such as creatine and intravenous immunoglobulin (IVIG), may improve strength and lessen pain and fatigue in some patients with polio or PPS. However, more research is needed to determine which subgroups of patients may respond to which medication.[6]

Deterrence and Patient Education

Infection Prevention and Control

Hand hygiene and contact precautions are imperative for clinicians or household members interacting with patients. As household members may be exposed to poliovirus before the patient becomes ill, household members must watch for symptoms and maintain excellent hygiene to avoid potentially infecting others.

Chlorine, heat, UV light, and formaldehyde rapidly inactivate poliovirus.[CDC. VPD Manual_Polio] The virus resists inactivation by lipid solvents and common detergents.[WHO. Vaccine Position]

Depending on conditions, poliovirus can remain stable outside, with sunlight and repeated freeze-thaw cycles decreasing its activity. The virus retains infectivity for months at 4 ºC but only days at 30 ºC.[WHO. Vaccine Position]

Routine Childhood Polio Vaccinations

Polio vaccination programs worldwide use IPV with or without live-attenuated OPV. The first polio vaccine, licensed by Jonas Salk in 1955, consisted of inactivated (killed) viruses of all 3 WPV types. This first IPV protected children against severe polio but could not prevent human-to-human transmission due to its inability to induce a robust mucosal immune response in the gut.

The original Salk IPV was replaced globally in 1961 by a trivalent OPV developed by Albert Sabin. Consisting of live, attenuated viruses of all 3 WPV types (OPV1, OPV2, and OPV3), this vaccine was cheap, easy to administer, and could stop transmission by inducing mucosal antibodies that prevented infection. While immensely successful in eliminating the wild-type poliovirus, the high virus mutability of OPV viruses also leads to VAPP and the emergence of cVDPVs.

Healthcare workers can administer the polio vaccine via the intramuscular or intradermal route. The vaccines are highly effective, providing greater than 99% protection after receiving all recommended doses.[GPEI. Polio Eradication] Their safety profile is excellent, with no systemic severe adverse reactions reported. No risk of VAPP exists with IPV use.

OPV is similar to IPV in effectiveness. The WHO recommends OPV in endemic countries and those at higher risk for WPV reintroduction primarily because of cost, ease of administration, and ability to stop transmission. Countries at higher risk of reintroduction include those with poor water, sanitation, and hygiene infrastructure and connections with endemic countries.

As of 2022, the WHO recommends one of the following primary immunization regimes for all children worldwide: at least 3 doses of IPV or at least 3 doses of bivalent OPV plus 2 doses of IPV.[3] A booster dose is given with a minimum interval of 6 months following the initial dose.

The United States was declared WPV-free in 1994 and switched solely to IPV in 2000.[9][CDC. About Polio] The CDC recommends children receive 4 doses of IPV at 2, 4, and 6 to 18 months, followed by a booster between 4 and 6 years of age. This vaccine schedule confers total immunity in more than 95% of patients.

Adults at Increased Risk of Exposure 

The CDC recommends a single lifetime IPV booster for adults who have fully completed the childhood series but are at an increased risk for exposure.[19][27] All travelers to countries that are endemic for polio or have an actively circulating virus are at risk, as are travelers working in high-risk settings (eg, humanitarian or healthcare) in countries adjacent to and with strong social connections to countries with an actively circulating virus.

Others at increased risk include workers with potential occupational exposure to poliovirus, such as poliovirus laboratory workers and healthcare workers in close contact with patients during a polio outbreak. Other situations may also increase risk, such as an outbreak or a low vaccination community with strong social ties to a country with a circulating virus.

See StatPearls' companion article "Polio Vaccine" for further information on polio vaccine use.

Enhancing Healthcare Team Outcomes

With effective vaccines, poliomyelitis is an oft-forgotten disease. However, continued polio endemicity in Pakistan and Afghanistan and cVDPVs elsewhere pose an ongoing global threat, made worse by political unrest, growing opposition to vaccination in developed countries, and other factors.[28] The interprofessional healthcare team plays a vital role in polio eradication efforts across multiple levels of intervention.

Polio Eradication Strategy 2022-2026

The GPEI, a public-private partnership under the WHO of national governments, the CDC, Rotary International, the United Nations Children's Fund, and the Bill & Melinda Gates Foundation, coordinates and leads global polio eradication efforts. The GPEI's Polio Eradication Strategy 2022 to 2026 has only 2 high-level goals:[GPEI. Polio Eradication]

1. Permanently interrupt all poliovirus transmission in endemic countries.
2. Stop cVDPV transmission and prevent outbreaks in non-endemic countries.

As expected, polio eradication is proving more challenging than smallpox eradication. Firstly, the poliovirus does not have optimal characteristics for eradication.[9] Unlike smallpox, poliovirus has a high rate of asymptomatic illness, facilitating undetected viral spread. Many other diseases have clinically similar presentations to poliomyelitis, resulting in diagnostic delays. The natural genetic instability of the poliovirus results in cVDPVs, requiring the eventual coordinated stoppage of OPV.[29]

Multiple sociopolitical challenges also exist in the polio endgame.[GPEI. Polio Eradication] These include the following:

• Poor access to healthcare in remote areas and for transient population
• Difficulty delivering vaccinations in countries with poorly resourced healthcare systems
• Competing governmental priorities, such as the COVID-19 pandemic
• Inadequate development and maintenance of water, sanitation, and hygiene infrastructure
• Ongoing political conflict and uncertainty
• Political indecision, reduced financial resources, and decreased public awareness as polio cases dwindle

The GPEI works with governments at all levels, civil society partners, and local healthcare providers to build, maintain, and improve systems in areas with or at high risk for polio transmission to increase polio vaccination, detect cases of acute flaccid paralysis, and ensure adequate reporting and surveillance systems for rapid detection of poliovirus transmission. These depend highly on solid relationships with communities and seasonally migrant populations for trust building, capacity building, increasing local government ownership and control, using a gender lens, and ensuring accountability.[GPEI. Polio Eradication] Supporting national governments to have maximum control over polio prevention, surveillance, and outbreak responses is a key strategy to improve global polio eradication efforts.[GPEI. Polio Eradication]

Improving Access to Quality Healthcare

A comprehensive, coordinated interprofessional approach to polio diagnosis, management, and vaccination is essential to ensure quality care for individuals and populations. Clinicians must consider polio infection in the differential of acute flaccid paralysis and be familiar with diagnosing and managing poliovirus infections and PPS. Reporting suspected acute flaccid paralysis cases to public health authorities ensures appropriate testing, surveillance, and public health follow-up. Physiatrists, neurologists, orthotists, and occupational and physiotherapists are critical to polio and PPS rehabilitation. Clinicians, advanced practitioners, nurses, pharmacists, community workers, and public health teams working collaboratively to develop community partnerships and deliver consistent, culturally appropriate messages to patients can increase trust and improve vaccination rates. In countries with or at risk of WPV or cVDPVs, interprofessional teams can further stress the importance of hygiene and reinforce the best practices for treating the disease when it occurs.

Surveillance and Reporting

Delays in the detection and reporting of circulating WPV1 and VDPVs pose one of the most significant risks to polio eradication efforts. While global surveillance systems perform well overall, barriers to adequate surveillance continue, particularly in hard-to-reach areas and people with inadequate connections to the formal healthcare system.[WHO. Polio Surv] Surveillance activities declined in the first months of the COVID-19 pandemic, followed in 2020 by increased cases due to pandemic-related setbacks in surveillance and control activities.

The GPEI uses the following 3 types of surveillance for poliovirus detection:[WHO. Polio Surv]

• Reporting of acute flaccid paralysis cases
• Environmental surveillance
• Monitoring of immunodeficiency-associated vaccine-derived poliovirus

The WHO requires all countries to urgently report (within 24 hours) all cases of acute flaccid paralysis in patients younger than 15 and anyone with suspected polio. All other poliovirus detection from environmental samples, contacts of patients with polio, or surveillance in patients with primary immune disorders must also be reported to the WHO, although timelines are less stringent.[WHO. Polio Surv]

Epidemiologists assess AFP surveillance-system performance by the number of nonpolio AFP cases (target: ≥2 per 100,000 children younger than 15) and the percent of adequately collected stool specimens from AFP patients (target: ≥80% with ≥2 samples collected ≥24 hours apart within 14 days of paralysis onset, with the cool chain maintained throughout transit).[WHO. Polio Surv] Of the more than 100,000 samples tested by the Global Polio Laboratory Network each year, few are positive, indicating other diagnoses.[GPEI. Polio Eradication]

Environmental surveillance significantly increases the poliovirus surveillance system sensitivity. This surveillance form is increasingly used to monitor the virus and implement public health measures before cases of AFP arise, such as community awareness campaigns, targeted increases in vaccination coverage, and active surveillance for AFP. Environmental surveillance is focused on priority countries (ie, patients with medium-high to very high risk of poliovirus transmission and with persistent surveillance gaps).[WHO. Polio Surv]

As the world reaches polio eradication and cases decrease, the polio surveillance systems must continue to become increasingly sensitive. Detection of poliovirus excretion among people with primary immunodeficiency disorders is a new addition to the standard surveillance methods.[WHO. Polio Surv] While no iVDPV outbreaks have yet been detected, patients with primary immunodeficiency disorders have the risk of developing paralysis or seeding a cVDPV outbreak. Several high-risk countries are piloting iVDPV surveillance, with plans to expand and continue through the post-eradication period. All patients identified with VDPV are provided treatment.

Research and Development

Research increases the effectiveness of eradication activities, documents and verifies achievements, and identifies policy needs for the post-eradication era. Research priorities identified by the GPEI include the following:[GPEI. Polio Eradication]

• Basic immunology: To better understand patient responses to polio vaccines, we need an improved understanding of humoral and mucosal immunity, duration of immunity, and the effects of malnutrition and other variables on vaccination response.
• Antiviral therapy development: With early evidence of pocapavir resistance developing in polioviruses, researchers are investigating combinations and other therapies, such as polio monoclonal antibodies, for patients with prolonged excretion.
• Monitoring and evaluation: Policy developers and program providers require optimal surveillance methodologies and VAPP and VDPV seroprevalence studies to develop local strategies and improve program delivery.
• Genetics: A better understanding of virus mutation and phylogenetic links can help understand the evolution of VDPVs.

For further information on vaccine research, optimal vaccination schedules, and improved vaccination program delivery, see StatPearls' companion article, "Polio Vaccines."

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Disclosure: Jonathan Wolbert declares no relevant financial relationships with ineligible companies.

Disclosure: Michael Rajnik declares no relevant financial relationships with ineligible companies.

Disclosure: Helena Swinkels declares no relevant financial relationships with ineligible companies.

Disclosure: Karla Higginbotham declares no relevant financial relationships with ineligible companies.