Polio (Poliomyelitis): Causes, Symptoms, Treatment and Prevention

Poliomyelitis, or polio, is a highly infectious disease caused by the poliovirus. It mainly affects children under five, though anyone can catch it. In most cases, people recover without lasting problems, but in a small number of cases, the virus attacks the brain and spinal cord, causing permanent paralysis—usually in the legs. In the most severe cases, it can paralyze the muscles used for breathing, which can be fatal. Before vaccines became available in the mid-1900s, polio outbreaks caused widespread illness, disability, and death around the world.

Polio spreads mainly through the fecal–oral route, meaning people become infected by eating or drinking water or food contaminated with the feces of someone carrying the virus. It can also spread less commonly through close contact, such as coughing or sneezing. After entering the body, the virus first multiplies in the throat and intestines, then may enter the bloodstream and, in some cases, reach the nervous system.

The best way to prevent polio is through vaccination. There are two main types of vaccines: the inactivated poliovirus vaccine (IPV), given as an injection, and the oral poliovirus vaccine (OPV), taken by mouth. Large vaccination campaigns have greatly reduced polio cases worldwide. Since 1988, the Global Polio Eradication Initiative (GPEI) led by the World Health Organization (WHO), UNICEF, Rotary International, and other partners has worked to eliminate the disease.

Polio still exists in a few countries, and outbreaks can happen where vaccination rates are low. 

Types of Poliomyelitis

There are three clinical types of poliomyelitis: subclinical, nonparalytic, and paralytic.

1. Subclinical polio, also known as asymptomatic polio, accounts for the majority of infections. In this form, the infected person shows no noticeable symptoms and may be unaware of the infection. Despite the absence of symptoms, the individual can still shed the virus in their stool and potentially transmit it to others. Subclinical infections typically last a few days and do not cause lasting health effects.

2. Nonparalytic polio, sometimes referred to as abortive polio or aseptic meningitis caused by poliovirus, involves mild to moderate symptoms. These can include fever, sore throat, headache, fatigue, nausea, vomiting, and stiffness or pain in the neck, back, or muscles. In some cases, symptoms occur in two phases—initial flu-like signs followed by a brief improvement and then recurrence of more severe symptoms, such as muscle tenderness and meningitis-like stiffness. This form does not lead to permanent paralysis and usually resolves completely, although the illness can cause considerable discomfort.

3. Paralytic polio is the rarest and most severe form, occurring in less than 1% of poliovirus infections. It begins with symptoms similar to nonparalytic polio but progresses rapidly to irreversible muscle paralysis. The paralysis is typically asymmetric (affecting one side of the body more than the other) and more common in the legs than in the arms. There are subtypes of paralytic polio, including:

  • Spinal polio – affects motor neurons in the spinal cord, leading to limb weakness or paralysis.
  • Bulbar polio – affects the brainstem, impairing nerves that control swallowing, speaking, and breathing.
  • Bulbospinal polio – a combination of spinal and bulbar forms, often affecting both limbs and respiratory muscles.

If the diaphragm and intercostal muscles (muscles between the ribs) are paralyzed, the person may be unable to breathe without mechanical assistance. Before the development of modern respiratory support, such as portable ventilators, patients often required prolonged use of the “iron lung,” a large negative-pressure ventilator that could maintain breathing. Respiratory failure was a major cause of death in paralytic polio cases during pre-vaccine eras.

The paralytic form can lead to respiratory failure if it involves the diaphragm and chest muscles, which historically caused many fatalities prior to modern medical interventions.

Brief History of Polio

Although descriptions of illnesses resembling poliomyelitis appear in ancient Egyptian art and historical medical writings, widespread epidemics of polio did not emerge until the late 19th century. Before this period, cases were sporadic, often occurring in isolated communities. The first recognized outbreaks appeared in Northern Europe and North America in the 1880s and 1890s. Improvements in sanitation—ironically—are believed to have contributed to these epidemics by delaying first exposure to the virus from infancy (when maternal antibodies offered protection) to later childhood, when infection was more likely to cause paralysis.

By the early to mid-20th century, polio had become a major public health crisis in industrialized nations. Annual summer outbreaks in countries such as the United States, Canada, and Australia led to widespread fear. At its peak in the early 1950s, the United States alone recorded over 50,000 cases in a single year, with thousands left permanently disabled. Quarantine measures, public pool closures, and the use of “iron lungs” for patients with respiratory paralysis became symbols of the polio era.

The search for a vaccine began in the 1930s, but early attempts were unsuccessful. In 1955, American virologist Jonas Salk introduced the inactivated poliovirus vaccine (IPV), which used a killed version of the virus to trigger immunity. This was followed in the early 1960s by Albert Sabin’s oral poliovirus vaccine (OPV), which contained a weakened live virus and was easier to administer, especially in large-scale campaigns. The introduction of these vaccines revolutionized prevention and led to a sharp decline in cases in vaccinated populations.

In 1988, the Global Polio Eradication Initiative (GPEI) was launched by the World Health Organization (WHO), UNICEF, Rotary International, and the U.S. Centers for Disease Control and Prevention (CDC), with the goal of eliminating polio worldwide. At that time, polio was endemic in more than 125 countries, causing an estimated 350,000 cases annually. Mass immunization campaigns using OPV dramatically reduced the number of cases by over 99%.

By the early 21st century, wild poliovirus remained endemic in only a few countries—most notably Afghanistan and Pakistan—though sporadic outbreaks from vaccine-derived strains have continued to occur in areas with low immunization coverage.

Causes and Transmission

Poliomyelitis is caused by the poliovirus, a highly contagious pathogen that primarily targets the human nervous system. The virus is a member of the Enterovirus genus in the family Picornaviridae and contains RNA as its genetic material. There are three distinct serotypes—PV1, PV2, and PV3—each capable of causing paralysis. PV1 is the most widespread and most frequently associated with paralytic disease.

Once inside the body, the poliovirus first multiplies in the throat (oropharynx) and intestines. From there, it can enter the bloodstream (viremia) and, in some cases, invade the central nervous system (CNS). The virus has a particular affinity for motor neurons—nerve cells that control voluntary muscles—in the spinal cord, brainstem, and motor cortex. Destruction of these neurons results in acute flaccid paralysis, which may be permanent. However, the majority of infections are either asymptomatic or produce only mild, short-lived symptoms such as fever, fatigue, sore throat, or muscle stiffness.

Modes of Transmission

The poliovirus spreads mainly through the fecal–oral route, meaning it is contracted by ingesting food or water contaminated with the feces of an infected person. In areas with poor sanitation, the risk of transmission increases significantly. Less commonly, the virus can spread via oral–oral transmission, for example through direct contact with saliva or respiratory droplets. Overcrowded living conditions and inadequate sewage disposal systems create environments where the virus can spread rapidly.

Poliovirus can be excreted in feces for several weeks after infection, even in individuals without symptoms, making silent transmission a major challenge for eradication efforts. In some cases, the virus can also be present in the throat for a shorter period, contributing to its contagious nature.

Risk Factors for Infection

Children under the age of five are the most susceptible to poliovirus infection due to their less mature immune systems. Unvaccinated individuals—regardless of age—are at heightened risk. People living in crowded or unsanitary conditions face greater exposure, as do those in communities with low immunization coverage. Travelers to regions where polio remains endemic, or to areas experiencing outbreaks, are also at increased risk of infection.

Individuals with weakened immune systems such as those undergoing chemotherapy, living with HIV/AIDS, or taking immunosuppressive medications may experience more severe illness if infected. The absence of reliable sanitation infrastructure, safe drinking water, and effective waste management continues to play a key role in sustaining poliovirus transmission in some parts of the world.

Symptoms and Clinical Manifestations

Poliomyelitis presents with a range of symptoms that vary from mild to severe. These include early indicators, effects limited to non-paralytic forms, and symptoms associated with paralytic cases.

Early Signs of Polio

Initial symptoms typically appear 3 to 7 days after exposure. Patients commonly experience fever, fatigue, headache, and sore throat.

Muscle pain and stiffness, particularly in the neck and back, often occur. These signs may resemble a common viral infection, making early diagnosis difficult without laboratory tests.

Gastrointestinal symptoms such as nausea, vomiting, and abdominal discomfort can also be present. These early manifestations usually resolve within a week, but they herald possible progression to more severe forms.

Non-Paralytic Polio Symptoms

In non-paralytic polio, symptoms progress beyond early signs but do not involve muscle weakness. Patients may develop meningitis-like symptoms such as neck stiffness and sensitivity to light.

Fever remains moderate and muscle spasms or twitching may be reported. The condition often includes increased irritability and discomfort in the back and limbs without paralysis.

Neurological examination typically shows no muscle weakness or loss of reflexes. Recovery from this form is generally complete, although symptoms can last up to two weeks.

Paralytic Polio Features

Paralytic polio occurs when the virus invades motor neurons in the spinal cord. This leads to flaccid paralysis, often asymmetrical, affecting the limbs or respiratory muscles.

Muscle weakness starts suddenly following the initial febrile phase. The paralysis may progress rapidly, impairing movements and reflexes.

Respiratory muscle involvement can cause breathing difficulties, necessitating mechanical support. Long-term outcomes vary, with some patients experiencing permanent disability.

Diagnosis

Diagnosis of poliomyelitis relies on a combination of physical examination, laboratory testing, and established diagnostic criteria. Accurate identification is critical for appropriate management and prevention of outbreaks.

Clinical Assessment

Initial diagnosis is based on clinical presentation, with particular attention to signs and symptoms characteristic of poliomyelitis. A hallmark feature is the sudden onset of asymmetric flaccid paralysis, meaning muscle weakness that is not equal on both sides of the body and without spasticity. Paralysis most commonly affects the legs but can also involve the arms or, in more severe cases, respiratory muscles.

The illness often begins with nonspecific symptoms such as fever, fatigue, headache, sore throat, and muscle pain. This prodromal phase may be followed within days by rapidly progressive muscle weakness. Neurological examination typically reveals reduced or absent deep tendon reflexes, decreased muscle tone (hypotonia), and preserved sensory function, distinguishing poliomyelitis from conditions that cause both motor and sensory deficits.

A detailed patient history including recent travel to endemic regions, exposure to suspected cases, and vaccination status is important for guiding suspicion. In children, sudden leg weakness during or after a febrile illness is a common trigger for urgent evaluation.

Laboratory Testing

Definitive diagnosis requires laboratory confirmation of poliovirus infection. The gold standard for detection is virus isolation from stool samples, as poliovirus is shed in high concentrations in feces for several weeks after infection. Two separate stool specimens, collected at least 24 hours apart and within 14 days of symptom onset, increase diagnostic yield.

Additional specimen types include throat swabs, which are more useful early in infection, and cerebrospinal fluid (CSF), although poliovirus is rarely detected in CSF. Polymerase chain reaction (PCR) testing allows for rapid and highly sensitive detection of poliovirus RNA, enabling differentiation between wild-type virus and vaccine-derived strains. Serologic testing for poliovirus-specific antibodies can provide supporting evidence but is less reliable for confirming acute infection.

Diagnostic Criteria

The World Health Organization (WHO) defines a confirmed case of poliomyelitis as an instance of acute flaccid paralysis (AFP) in which poliovirus is identified in stool, throat swab, or CSF, or in which there is an epidemiological link to a laboratory-confirmed case. Exclusion of other causes of AFP such as Guillain–Barré syndrome, transverse myelitis, or traumatic neuritis is critical for diagnostic accuracy.

In the context of surveillance, all AFP cases in children under 15 years of age are investigated for poliovirus as part of the Global Polio Eradication Initiative (GPEI). Even in the absence of laboratory confirmation, cases may be classified as polio-compatible if clinical and epidemiological findings strongly suggest poliovirus infection.

Treatment of Polio

There is no specific antiviral cure for poliomyelitis; treatment focuses on supportive care to relieve symptoms, prevent complications, and aid recovery. Management strategies vary depending on the severity of the illness, ranging from basic outpatient care for mild cases to intensive hospital-based management for severe or paralytic forms. It requires careful monitoring to manage breathing, pain, and muscle function.

Supportive Care

In most cases, treatment aims to keep the patient comfortable while the body’s immune system fights the virus. Bed rest is often recommended to reduce strain on affected muscles and limit fatigue. Pain and fever are typically managed with analgesics such as acetaminophen or ibuprofen; aspirin is generally avoided in children to prevent the risk of Reye’s syndrome.

Physical therapy plays a key role in recovery, both during the acute illness and in the rehabilitation phase. Gentle exercises help maintain muscle strength, preserve joint range of motion, and prevent contractures (permanent tightening of muscles or tendons). Long-term physiotherapy may be required for patients with lasting weakness or deformities.

Nutritional support ensures adequate hydration and energy intake, especially for patients experiencing difficulty swallowing (dysphagia). In some cases, feeding assistance—such as a soft diet or, if necessary, feeding tubes—may be used to prevent malnutrition and aspiration.

Regular respiratory function monitoring is critical in patients with weakness of the chest or diaphragm muscles. Measuring vital capacity and oxygen saturation can detect early breathing problems, allowing for timely intervention.

Severe Case Management

In paralytic polio, muscle weakness may involve the respiratory muscles, leading to life-threatening respiratory failure. Mechanical ventilation historically provided by the “iron lung” and now by modern positive-pressure ventilators may be required, sometimes for prolonged periods. In cases where swallowing is impaired, airway protection and suctioning are used to prevent aspiration pneumonia.

Patients with severe paralysis often need orthopedic interventions to prevent or correct skeletal deformities such as scoliosis, hip dislocation, or foot drop. Assistive devices, including leg braces, crutches, or wheelchairs, can improve mobility and independence.

Close medical supervision in an intensive care unit (ICU) is sometimes necessary, especially for patients with combined respiratory and cardiovascular instability. Management may also include antibiotics to treat or prevent secondary bacterial infections, particularly in immobilized patients.

Because severe polio can cause significant physical disability, psychological support and counseling are recommended to help patients and families cope with emotional distress and lifestyle changes. Long-term follow-up is important to address post-polio syndrome, a late complication characterized by new muscle weakness and fatigue decades after the initial infection.

Complications and Long-Term Effects

Polio can cause lasting damage that affects the nervous and muscular systems. These effects may appear soon after infection or decades later, impacting mobility and overall health.

Post-Polio Syndrome

Post-polio syndrome is a late complication that typically appears 15–40 years after recovery from acute poliomyelitis. It is characterized by the gradual onset of new muscle weakness, fatigue, and sometimes pain in muscles and joints. The condition is believed to result from the slow deterioration of motor neurons that were partially damaged during the initial infection and compensated over time by nerve sprouting. Eventually, these overworked neurons lose function, leading to renewed muscle weakness.

Symptoms of PPS can vary but commonly include muscle atrophy (wasting), joint stiffness, decreased endurance, and in some cases, breathing difficulties if respiratory muscles are affected. PPS does not represent a new viral infection, nor is it contagious; rather, it is a progressive neurological disorder linked to the original poliovirus damage.

Diagnosis of PPS relies on a confirmed history of prior polio, the emergence of new neuromuscular symptoms, and exclusion of other causes such as arthritis, neuropathies, or myopathies. Treatment is focused on symptom management—including energy conservation strategies, tailored physical therapy, orthotic support, pain control, and, when necessary, respiratory assistance.

Physical Disabilities

In cases of paralytic polio, irreversible muscle paralysis can occur within days of symptom onset. This paralysis may be partial (affecting only certain muscle groups) or complete, often more pronounced in the legs than the arms. Paralysis of the respiratory muscles can cause acute breathing failure, necessitating mechanical ventilation.

Long-term muscle weakness can alter gait and posture, leading to secondary musculoskeletal deformities such as scoliosis, foot drop, joint contractures, and limb-length discrepancies. These changes may require orthopedic interventions, leg braces, or wheelchairs to maintain mobility and independence.

Other Chronic Consequences

Many polio survivors experience chronic musculoskeletal pain, often resulting from abnormal joint loading and muscle imbalances. Persistent fatigue—unrelated to PPS—is also common and can limit daily activities.

If cranial nerves were involved in the original infection, long-term difficulties with swallowing (dysphagia) or speech (dysarthria) may persist. Damage to respiratory control centers or muscles increases susceptibility to respiratory infections, sometimes requiring ongoing ventilatory support.

The psychological impact of polio and its complications can be considerable. Survivors may experience depression, anxiety, and reduced social participation due to chronic disability.

Prevention and Vaccination

Prevention of polio is almost entirely dependent on vaccination, which has proven to be the most effective public health intervention against the disease. Through extensive immunization programs, global cases of poliomyelitis have been reduced by over 99% since the late 20th century.

Polio Vaccines Overview

There are two main vaccines used to protect against poliovirus:

  • Inactivated Polio Vaccine (IPV): Developed by Dr. Jonas Salk and introduced in 1955, IPV contains inactivated (killed) poliovirus. It is administered by injection and induces strong systemic immunity without the risk of causing the disease. IPV is widely used in countries where wild poliovirus transmission has been interrupted, as it eliminates the risk of vaccine-associated paralytic poliomyelitis (VAPP).
  • Oral Polio Vaccine (OPV): Developed by Dr. Albert Sabin and licensed in the early 1960s, OPV contains a live, attenuated (weakened) virus. Administered orally, it stimulates both systemic immunity and local intestinal immunity, preventing virus replication in the gut—the primary site of poliovirus multiplication and shedding. OPV is particularly effective for stopping person-to-person transmission and is used extensively in outbreak control and mass immunization campaigns.

While OPV remains critical in areas where wild poliovirus still circulates, it carries a small risk of evolving into vaccine-derived polioviruses (VDPVs) in under-immunized populations. As eradication nears, the global strategy aims to transition fully to IPV.

IPV is considered safer in countries free of wild poliovirus, as it carries no risk of vaccine-derived poliovirus. OPV is more effective in stopping virus transmission and is often used in mass immunization campaigns due to its ease of administration.

Immunization Schedules

The immunization schedule may vary by national guidelines, but the World Health Organization (WHO) recommends:

  • At least three primary doses of IPV or OPV, starting at 6 weeks of age.
  • Subsequent booster doses in the second year of life or during school entry to maintain long-term immunity.
  • In some regions, a mixed schedule of both IPV and OPV is used to maximize protection and reduce transmission risk.

Combination vaccines (such as DTP–IPV–Hib) are often used in routine programs to improve coverage, reduce the number of injections, and streamline logistics.

Global Vaccination Campaigns

The Global Polio Eradication Initiative (GPEI), launched in 1988 by WHO, UNICEF, Rotary International, and the U.S. Centers for Disease Control and Prevention (CDC), has been the cornerstone of worldwide polio prevention. Since its inception, GPEI has vaccinated more than 2.5 billion children in over 200 countries.

Key strategies in these campaigns include:

  • National Immunization Days (NIDs): Large-scale events where millions of children are vaccinated in a short period.
  • House-to-House Outreach: Health workers visit homes directly to ensure no child under five is missed, particularly in remote or conflict-affected areas.
  • Environmental Surveillance: Testing sewage and wastewater for poliovirus to detect silent circulation in communities.
  • Rapid Outbreak Response: Swift mass vaccination in areas where new cases are detected to contain spread