Poliomyelitis and acute flaccid paralysis

• Poliomyelitis is infection with poliovirus, a small RNA enterovirus spread mainly by the faecal–oral route.
• Most infections cause no symptoms at all; about one in four people gets a mild feverish illness; fewer than 1% develop flaccid paralysis.^[2][3]
• Paralysis, when it happens, can be permanent. The disease mainly strikes young unvaccinated children, although anyone without immunity can be infected.^[1][3]
• There is no antiviral cure. Vaccination is the only protection, and two vaccines are used: oral polio vaccine (OPV) and inactivated polio vaccine (IPV).^[1]
• Wild poliovirus has been reduced by over 99% since 1988, and type 2 and type 3 wild poliovirus no longer exist in nature. Only two countries, Afghanistan and Pakistan, have never interrupted type 1 wild poliovirus.^[1][3]
• Because paralysis is rare, every unexplained acute flaccid paralysis (AFP) in a child is investigated as possible polio until laboratory testing and a national expert committee rule it out.^[2][5]

By the end of this page you should be able to:

1. Explain how poliovirus reaches the central nervous system and why it causes flaccid, not spastic, paralysis.
2. Describe the clinical spectrum from silent infection to paralytic polio, including spinal, bulbar and bulbospinal forms.
3. Work through the investigation of a child with acute flaccid paralysis and state the laboratory and follow-up requirements.
4. Explain the difference between wild poliovirus, vaccine-associated paralytic polio (VAPP) and vaccine-derived poliovirus, and why each matters.
5. Describe how IPV and OPV work, their schedules, efficacy and limitations.
6. Outline the global surveillance indicators for AFP and the remaining barriers to eradication.

Poliovirus is a small RNA virus that is transient in the gastrointestinal tract and stable in acid. It has three serotypes, PV1, PV2 and PV3, and immunity is type-specific: protection against one serotype gives little meaningful protection against the others.^[2][3]

Infection is classified by how far the virus travels along the neuraxis from the gut:

• Inapparent infection. No visible illness; the virus replicates in the oropharynx and gut and is shed in the stool. Roughly 70% of childhood infections are asymptomatic.^[3]
• Abortive poliomyelitis. A brief, non-specific feverish illness, usually under a week. About 24% of childhood infections.^[3]
• Nonparalytic (aseptic meningitic) poliomyelitis. Meningeal irritation with neck and back stiffness, headache and vomiting. Occurs in 1–5% of childhood infections.^[3]
• Paralytic poliomyelitis. Flaccid paralysis due to destruction of lower motor neurons. Less than 1% of infections.^[2][3]
• Bulbar and respiratory disease. Weakness of muscles supplied by cranial nerves, including those of swallowing and breathing.

A second, later problem is post-polio syndrome (PPS): new or worsening weakness, fatigue and pain appearing 15 to 40 years after an earlier paralytic infection. PPS is not an infection and the person does not shed poliovirus.^[2][3]

Finally, disease identical to wild-type polio can be caused by the vaccine itself: vaccine-associated paralytic polio (VAPP) from the live attenuated Sabin strains, and vaccine-derived poliovirus (VDPV), in which a Sabin strain has reverted and regained the neurovirulence and transmissibility of wild virus.^[3]

Polio once occurred worldwide. It mainly affects children under 5 years of age, although anyone of any age who is unvaccinated can be infected.^[1][3]

Global picture. In 1988, polio paralysed an estimated 350,000 people a year in over 125 countries. By 2019, only 125 cases caused by wild poliovirus were reported worldwide, a reduction of more than 99%, and wild polio remained endemic in only two countries.^[1][3] Type 2 wild poliovirus was declared eradicated in 2015, and type 3 in 2019.^[3] WHO also puts the scale of harm in plain terms: one in 200 infections leads to irreversible paralysis, and among those paralysed 5 to 10% die when their breathing muscles are immobilised.^[1]

Certified-free regions. The Americas were certified free of indigenous wild poliovirus in 1994, the Western Pacific in 2000, Europe in 2002, South-East Asia in 2014, and Africa in 2020.^[1][3]

United States. Wild poliovirus has not been acquired in the United States since 1979. In the immediate pre-vaccine era, improved sanitation shifted the age of first infection upward and turned polio into the feared summer epidemics of the early twentieth century; 1952 saw over 21,000 paralytic cases. IPV (1955) and then OPV (1961) collapsed incidence, from over 21,000 paralytic cases in 1952 to 2,525 in 1960 and 61 in 1965. A probable polio case remains a notifiable condition in the United States.

Transmission. Virus enters through the mouth and multiplies in the oropharynx and gut. It appears in nasopharyngeal secretions for 1 to 2 weeks and may be shed in stools for several weeks, even in people with minor or no symptoms.^[2][3] Seroconversion rates among susceptible household contacts approach 100% for contacts of children, and over 90% for contacts of adults, so polio is highly transmissible.^[3] The faecal–oral route dominates where sanitation is poor; oral–oral spread also occurs. In temperate climates infections peak in summer and autumn; in the tropics there is no clear season.^[2][3]

Burden prevented. Over 20 million people are walking today who would otherwise have been paralysed, and about 1.5 million childhood deaths have been prevented by giving vitamin A alongside polio immunisation activities.^[1]

The agent is poliovirus itself, a human enterovirus with no animal reservoir. Risk rises with:

• Lack of immunity from incomplete or absent vaccination.^[2][3]
• Poor water, sanitation and hygiene, which drives early infection and transmission.^[1]
• Age: infection is more common in infants and young children, but severity and death rise with age.^[2][3]
• Immunodeficiency, which permits prolonged shedding, provokes VDPV and raises the risk of VAPP enormously.^[3]
• Travel or contact with travellers from areas where polio still circulates, and populations with low vaccine coverage.^[2][4]
• A person fully vaccinated is at very low risk; IPV is the only vaccine used in the United States and has been since 2000, because OPV can rarely cause VAPP.^[3][4]

Poliovirus is swallowed, replicates in the oropharynx and intestinal mucosa, and invades local lymphoid tissue. From there it can enter the bloodstream and infect cells of the central nervous system.^[2][3] When it destroys the motor neurons of the anterior horn of the spinal cord and of the brainstem, the result is the distinctive flaccid paralysis: a lower motor neuron lesion. Sensation and cognition are preserved.

Key points about the paralysis:

• It is flaccid, not spastic, because the lesion is in the lower motor neuron. Reflexes are decreased or absent.^[2]
• It is usually asymmetrical, worse proximally than distally, and progresses over 2 to 3 days.^[3]
• Paralysis may follow a biphasic illness: a minor febrile illness, a day or two of wellness, then major illness with fever, muscle pain and weakness. In adolescents and adults the minor phase is often absent and pain and paralysis are worse.^[3]
• The virus is most infectious in the days immediately before and after symptom onset, and stool shedding can continue for up to 6 weeks.^[3]
• About two-thirds of patients with paralysis still have weakness or paralysis at 12 months, and that deficit is usually permanent.^[3]

Most infected people have no visible illness. The common presentations are summarised below.^[2][3]

The incubation period for nonparalytic symptoms is 3 to 6 days. The onset of paralysis usually occurs 7 to 21 days after infection.^[2] Paralysis is often permanent, although partial or total recovery can occur through compensation by unaffected muscles. Weakness present at 12 months is usually permanent.^[3]

Paralytic polio is classified by the level of involvement:

• Spinal polio (about 79% of paralytic cases in 1969–1979): asymmetric paralysis, most often of the legs, with absent or diminished reflexes.^[3]
• Bulbar polio (about 2%): weakness of muscles innervated by cranial nerves, including swallowing and breathing.
• Bulbospinal polio (about 19%): a combination of both.^[3]

Case fatality for paralytic polio is generally 2–5% in children and up to 15–30% in adolescents and adults, rising to 25–75% with bulbar involvement.^[3]

Adults who had paralytic polio in childhood may develop PPS 15 to 40 years later, with slow, progressive worsening of muscle strength, new weakness, general fatigue and muscle or joint pain, usually in the muscle groups affected during the original illness.^[2][3] PPS is not infectious and the person does not shed virus.^[3] Studies estimate that 25–40% of polio survivors suffer from it, though prevalence is uncertain and diagnostic criteria differ, so estimates range widely.^[2]

AFP is a syndrome, not a diagnosis: acute onset of flaccid weakness affecting one or more limbs, with decreased or absent tendon reflexes, without sensory or cognitive loss.^[2] It occurs in children worldwide and, even without poliovirus, is expected to happen at a rate of at least 1 per 100,000 children a year.^[2] Because polio can only be recognised reliably by laboratory testing, every child with compatible AFP is investigated for poliovirus until it is excluded.

The aim is to decide whether a paralysed child has poliovirus infection or another cause of a lower motor neuron picture. Poliovirus paralysis is asymmetric, descending and flaccid, with preserved sensation and cognition. Other important causes include:

Wherever polio remains possible, the investigation proceeds in parallel with treatment of the patient.

Rapidly investigating suspected cases is essential, because missed importation allows further transmission.

• Stool specimens. The highest yield comes from two stool specimens collected at least 24 hours apart, within 14 days of onset; specimens must reach a WHO-accredited laboratory by reverse cold chain in good condition. Poliovirus can be detected in stools for weeks even after mild illness, and the highest concentration is in the first two weeks.^[3][5]
• Oropharyngeal specimens. Virus may be found 3 to 10 days after paralysis onset, but stool is preferred.^[3]
• Laboratory analysis. Viral culture, RT-PCR and genomic sequencing identify the serotype and whether the isolate is wild, Sabin (vaccine) or VDPV.^[3]
• Cerebrospinal fluid. Poliovirus is only rarely recovered from CSF, and a negative CSF test does not exclude polio.^[2][3]
• Lumbar puncture and imaging are often done to exclude other causes of flaccid paralysis.

Contact the responsible public health authority early: in the United States, all suspected cases must be reported and investigated under the surveillance manual.^[2]

The widely used clinical definition of a probable polio case is an acute onset of flaccid paralysis of one or more limbs, with decreased or absent tendon reflexes in the affected limbs, without other apparent cause, and without sensory or cognitive loss. Paralysis usually begins in an arm or leg on one side (asymmetric) and moves distally, a descending pattern.^[2]

Final classification into confirmed, compatible or discarded poliomyelitis is made by a national expert review committee using the investigation, follow-up and laboratory results. When a case is investigated fully and poliovirus is not isolated from stool or recognised contacts, and there is no residual weakness, it is discarded. Where follow-up or sampling is incomplete, it may be classified as compatible.

AFP case investigation and laboratory standards are published in the surveillance manuals of WHO and CDC; the CDC manual guides state and local surveillance staff in the United States.

There is no specific antiviral treatment for polio. Care is supportive and rehabilitative.

Acute phase. Ensure airway, breathing and circulation. Watch for respiratory and bulbar failure, which is what kills after paralysis; provide ventilatory support where needed. Manage hydration and pain, maintain limb positioning and begin gentle passive movement to prevent deformity. Avoid excessive exertion in acute denervated muscle.

Rehabilitation. Physiotherapy, orthoses, assistive devices and later corrective surgery help recovery through compensation by muscles that were not affected. Pacing is important because fatigue and overuse can worsen outcome.

Post-polio syndrome. Management is supportive: energy conservation, pacing, appropriate exercise within tolerance, orthoses, pain management and respiratory support if needed. No drug has been shown to reverse established PPS, and reassurance and long-term follow-up matter.

• Permanent paralysis and deformity; about two-thirds of patients with paralysis still have weakness at 12 months, usually permanent.^[3]
• Respiratory failure, which accounts for most deaths. Case fatality is 2–5% in paralysed children, 15–30% in older patients and 25–75% with bulbar involvement.^[3]
• Paralysis from VAPP and from VDPV, which are clinically identical to wild-type disease.^[3]
• Enormous economic and personal burden in survivors; lifelong disability.
• Post-polio syndrome decades later in 25–40% of paralytic cases.^[2][3]

Prognosis depends on the site and severity of the anterior horn cell destruction. Recovery occurs when neighbouring cells compensate and muscles that escaped infection take over. Permanent weakness is likely if it remains at 12 months. Younger patients generally fare better, and bulbar or respiratory involvement carries the highest mortality. With modern respiratory and rehabilitation support, most patients survive, but impairment is usually lifelong. The absence of poliovirus in survivors means PPS is not contagious and not caused by lingering infection in any proven sense.

Two effective and safe vaccines are used worldwide, in different combinations depending on local epidemiology.^[1]

• Inactivated polio vaccine (IPV). A killed vaccine given by injection. It contains all three serotypes and protects against paralytic disease by inducing serum antibody; it is highly effective, with at least 90% of recipients immune after 2 doses and at least 99% after 3.^[3][4] It does not replicate and cannot cause VAPP or VDPV. Duration of protection is uncertain but is most likely many years after a complete series, and possibly lifelong.^[3][4]
• Oral polio vaccine (OPV). A live attenuated vaccine taken by mouth. It induces both serum immunity and local intestinal immunity, reducing shedding and onward transmission. It can therefore provide indirect protection to unvaccinated people. One dose of trivalent OPV gives immunity to all three types in about 50% of recipients because of interference between serotypes; later doses raise this to over 95% in industrialised countries. Immunity is probably lifelong.^[3]
• Risks of live vaccine. VAPP occurs extremely rarely, about 1 case per 2 to 3 million doses of trivalent OPV, and more often with the first dose, in adults and in immunodeficient people. VDPVs arise when OPV Sabin virus circulates for long periods in under-immunised communities or in immunodeficient individuals and reverts.^[3] VDPV outbreaks exceeded the wild poliovirus case count after 2017.^[3]

United States practice. IPV is the only vaccine used, and has been since 2000. Children receive 4 doses, at 2 months, 4 months, 6 through 18 months, and 4 through 6 years. Routine adult vaccination is not needed; unvaccinated adults who need protection receive 3 doses of IPV at 0, 1 to 2 months and 6 to 12 months.^[4] In the United States, 90% or more of recipients are immune after 2 doses and at least 99% after 3.^[4] For children travelling to risk areas, an accelerated schedule can be used.^[4] At-risk adults who have completed a series may receive one lifetime IPV booster.^[4] IPV is contraindicated after anaphylaxis to a vaccine component; pregnancy is a precaution unless immediate protection is needed.^[3][4]

International changeover. In April 2016 all OPV-using countries stopped trivalent OPV and switched to bivalent OPV (types 1 and 3), to remove the risk of circulation of type 2 VDPV, because type 2 wild poliovirus had been eradicated. All countries now use one or more doses of IPV, either exclusively or combined with bivalent OPV. Outbreak response with monovalent OPV type 2 is reserved for type 2 events.

Eradication uses four pillars: routine immunisation; supplementary immunisation (campaigns and mop-up); AFP surveillance; and, where needed, targeted outbreak response. Environmental surveillance of sewage adds sensitivity by detecting circulation before a paralysed case occurs, because paralysis is under 1% of infections.^[2][3]

Vitamin A given during immunisation campaigns is credited with preventing about 1.5 million childhood deaths.^[1]

The biggest remaining risks are low vaccine coverage, conflict and inaccessible populations, importation into polio-free countries and the emergence of cVDPV where coverage slips. Since 2017, circulating VDPV has caused more paralytic cases than wild poliovirus.^[3]

• Pregnancy. Pregnancy is a precaution to IPV, because only theoretical concerns exist; if a pregnant woman is at increased risk and needs immediate protection, IPV should be given on the standard adult schedule.^[3][4]
• Immunocompromised people. They should not receive OPV; VAPP risk is almost 7,000 times higher in certain antibody-deficiency disorders. IPV is used instead.^[3]
• Travellers. Unvaccinated travellers to endemic or epidemic areas should complete IPV; accelerated schedules are available.^[4]
• Older adults. Most US-born adults are already immune from childhood vaccination; true infection risk in older adults mainly applies to the unvaccinated.^[3][4]

• Report every case of flaccid paralysis in a child under 15 years of age, ideally within 48 hours, even if polio seems unlikely clinically. A single confirmed silent infection can signal widespread transmission.^[5]
• Collect two stool specimens 24 to 48 hours apart, keep them at 4–8 °C, get them to a WHO-accredited laboratory within 72 hours or freeze them for transport.^[5]
• In areas with no laboratory, AFP surveillance still has value and clinical criteria remain the entry point.
• Follow up at least 80% of AFP cases at 60 days to look for residual paralysis.^[5]
• Rehabilitation resources are limited in many settings; simple positioning, passive movement and low-cost orthoses prevent deformity.

Even in polio-free countries, sensitive AFP surveillance is required to detect importation. The key indicators, drawn from international surveillance standards, enable quality to be measured.^[5][6]

The Global Polio Laboratory Network (GPLN) consists of 145 quality-assured poliovirus laboratories in all six WHO regions; it tested about 147,582 stool specimens in 2020 and 170,881 in 2021.^[6] Environmental surveillance is complementary because it detects silent circulation, including cVDPV before any paralysed case occurs.^[6]

No direct prerequisites were identified for this topic. Related reading includes meningitis, Guillain–Barré syndrome, botulism, other enterovirus infections, travel medicine and lifelong polio vaccination, all referenced in this page as plain text because none is linked as a verified topic here.

• Poliomyelitis is a lower motor neuron infection caused by poliovirus, an enterovirus with three serotypes and type-specific immunity.
• Roughly 70% of infected children are asymptomatic, about 24% have a minor feverish illness, 1–5% have aseptic meningitis, and under 1% develop flaccid paralysis.
• Paralysis is asymmetric and descending, with preserved sensation and cognition, and usually remains permanent if present at 12 months.
• Case fatality is 2–5% in children, rising to 15–30% in older patients and 25–75% with bulbar involvement.
• Post-polio syndrome affects 25–40% of paralytic survivors 15 to 40 years later and is not an infection.
• Humans are the only reservoir; transmission is faecal–oral, and virus is shed for weeks after infection.
• AFP is a syndrome with many causes; every case in a child under 15 must be investigated for poliovirus until excluded.
• Background AFP occurs in children at a rate of at least 1 per 100,000 per year; a target non-polio AFP rate of 2 per 100,000 is used in endemic regions.
• Two stool specimens, 24 hours apart and within 14 days of onset, plus follow-up at 60 days, are the minimum standard.
• IPV protects at least 90% after two doses and at least 99% after three, without risk of VAPP; OPV adds intestinal immunity but carries a tiny VAPP risk and the risk of VDPV where coverage is poor.
• Wild poliovirus has fallen by over 99% since 1988; type 2 and type 3 are eradicated; only two countries remain endemic for type 1.
• Eradication relies on high routine coverage, campaigns, strict AFP surveillance and environmental monitoring.