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date: 14 December 2018

Name and nature of organism

  • Poliomyelitis is caused by infection of the motor neurons of the CNS by poliovirus.

  • Poliovirus is a positive-strand RNA virus of the family Picornaviridae, now classified with many Coxsackie virus A types as a species C human enterovirus.

  • The virion consists of an icosahedral, non-enveloped protein capsid, composed of four capsid proteins (VP1, VP2, VP3, and VP4), which encapsulates the RNA genome.

  • Poliovirus has a rapid replication cycle, with ~8 hours elapsing between infection and the release of progeny virions upon host cell lysis.

  • There are three serotypes of the virus, designated types 1, 2, and 3. Infection gives immunity to the serotype, but immunity to one serotype does not protect adequately against the other two, so vaccines contain single strains of each serotype.


  • Humans are the only known natural host.

  • Poliovirus infection occurs predominantly in summer and autumn in temperate climates, but year-round in tropical regions.

  • Prior to the twentieth century, in a poor hygiene environment, exposure to infected faecal material will occur while the child is still protected by maternal antibody, and infection will be safely confined to the gut. Following the Industrial Revolution and improvements in hygiene and sanitation, children increasingly encountered poliovirus at older ages, without the benefit of passively conferred immunity, leading to epidemics of poliomyelitis. This gave rise to an alternative name of infantile paralysis of polio.

  • Attempts to control poliomyelitis through vaccination programmes in 1950 have led to a dramatic fall in the incidence of poliomyelitis. The Global Polio Eradication Initiative (GPEI) began in 1988; since then, wild poliovirus (WPV) transmission has decreased by 99%, and currently WPV transmission remains endemic only in Afghanistan, Nigeria, and Pakistan. During 2014, outbreaks caused by importation of WPV type 1 (WPV1) cases have been detected in previously polio-free countries such as the Horn of Africa and the Middle East (Syria to Iraq). WPV type 3 (WPV3) cases have not been detected in Pakistan since April 2012, and in Nigeria since November 2012; therefore, there is possible eradication of WPV3. No WPV type 2 (WPV2) cases have been detected anywhere in the world since 1999.

Transmission and incubation period

  • Transmission is primarily by the faecal–oral route.

  • The virus enters through the GI tract. The 1° site of replication is in the M cell lining the mucosa of the small intestine; then the virus spreads to deep local lymph nodes, and a 1° viraemia occurs after 2–3 days. From the blood, the virus gets to multiples sites, including skeletal muscle, fat, liver, reticuloendothelial system, and bone marrow until to the CNS. Gut infections are silent; the 2° infection sites correspond to the minor disease, and CNS infections cause the major (paralytic) disease.

  • The incubation period is generally between 7 and 14 days but can range from 3 to 35 days.

  • Typically, the minor disease occurs 7 days, and the major disease 30 days, after infection.

  • Patients are most infectious immediately before, and 1–2 weeks after, the onset of paralytic disease.

Clinical features and sequelae

  • The most serious result of poliovirus infection is paralysis, although 90–95% of infection are asymptomatic but induce protective immunity.

  • The minor disease occurs in about 5% of patients after 1–2 weeks after infection, also called ‘abortive poliomyelitis’. Fever, malaise, anorexia, and headache are prominent features; sore throat, and muscle and abdomen pain may be present. The illness is short-lived, lasting up to 2–3 days.

  • A small proportion of patients experiencing a major viraemia will manifest signs and symptoms of CNS invasion. These include:

    • Non-paralytic polio (1–2% of poliovirus infections) with specific features of aseptic meningitis. Patients experience the non-specific features of abortive poliomyelitis but, in addition, may complain of severe headache and neck, back, and lower limb pain. They may display nuchal rigidity and CSF lymphocytosis

    • Spinal poliomyelitis—characterized by acute flaccid paralysis 2° to the selective destruction of spinal motor neurons and subsequent denervation of the associated skeletal musculature. Children exhibit a biphasic illness, with 2–3 days of minor non-specific illness, followed by up to 5 days without symptoms. Abrupt onset of headache, fever, vomiting, neck stiffness, and intense muscle pain is followed, after 24–48 hours, by flaccid weakness and paralysis, which are usually asymmetrical. Multiple muscle groups and limbs may be involved, with proximal involvement usually more severe than distal. The lower limbs are involved more frequently than the upper limbs. Deep tendon reflexes may initially be hyperactive but are rapidly lost. Sensory loss has been described but is rare. Bladder paralysis and bowel ileus commonly occur but tend to improve over a few days

    • Bulbar poliomyelitis—characterized by paralysis of muscle groups innervated by cranial nerves. Patients present with dysphagia, nasal speech, and respiratory compromise 2° to involvement of the medullary respiratory centre

    • Bulbospinal poliomyelitis—where both the brainstem and spinal cord are affected, resulting in a mixed clinical picture

    • Paralytic poliomyelitis—occurs in 0.1–1% of all cases of poliovirus infections. Cranial nerve dysfunction is reported in 5–35% of paralytic polio cases. Respiratory compromise is an important complication, resulting from involvement of both the diaphragm and intercostal muscles, the medullary respiratory centre, and IXth, Xth, and XIIth cranial nerves affecting the pharyngeal, palatal, and vocal cord function. In the pre-vaccination era, mortality rates of up to 60% were reported, mainly due to respiratory compromise. With modern intensive care, mortality rates of 2–5% in children have been described

    • Most cases of paralytic disease will show clinical improvement, but ~60% of affected individuals will experience a residual deficit. Complete recovery is rare if the paralysis is severe or ventilatory support is required. Patients who survive bulbar involvement often recover quickly to normal function

    • Certain risk factors for paralysis have been identified. These include pregnancy, B-cell immunodeficiencies, strenuous exercise during the first days of the illness, and IM injections which seem to predispose to paralysis in the limb injected (provocation paralysis)

    • Complications of infection include respiratory compromise, myocarditis, GI haemorrhage, and ileus

    • Up to 30% of patients who have recovered from paralytic polio may experience new-onset weakness, pain, and atrophy in the previously affected muscle groups some 25–35 years after the 1° illness, referred to as the post-polio syndrome.


  • The virus may be cultured from throat and stool swabs.

  • After initial replication in the mucosal epithelium, poliovirus is shed in nasopharyngeal secretions and saliva for 1–2 weeks, and in faeces for 3–6 weeks. Immunocompromised individuals have been shown to excrete poliovirus for prolonged periods of time, occasionally 3 years or more, and, in some extreme situations, for as long as 20 years after mucosal infection.

  • WHO recommends the isolation and identification of poliovirus in the stool. Poliovirus concentrations are high in the first week after the onset of paralysis.

  • Poliovirus may be isolated from 80% to 90% of specimens from acutely ill patients, and 20% of specimens after 3–4 weeks after the onset of paralysis.

  • Isolation of virus from CSF is diagnostic but seldom achieved. CSF is often normal during minor illness, and, with CNS involvement, CSF may show raised cell count (10–200 leucocytes/mL) and mildly raised protein (40–50mg/dL).

  • Neutralizing antibody can be detected in serum as early as 1 week post-infection, and a greater increase after 3–4 weeks from the onset of paralysis. A 4-fold rise in acute and convalescent IgG titres demonstrates acute infection but cannot distinguish between vaccine and wild-type virus.

  • RT-PCR for poliovirus can be performed for stool, throat swabs, and CSF specimens.


  • There is no specific antiviral therapy.

  • Management is supportive:

    • Analgesia and bed rest in the acute phase to reduce extension of the paralysis

    • Decompression of the bladder, where indicated

    • Ventilatory assistance/tracheal intubation, where indicated

    • Avoid IM injections—risk of ‘provocation paralysis’ (see Polio Clinical features, p. [link][link])

    • Physiotherapy during the recovery phase.


  • Vaccination is the only effective method of preventing poliomyelitis, and, since its introduction in the 1950s, there was a dramatic effect on the incidence of polio. The two types of polio vaccines most widely use are the trivalent inactivated polio vaccine (IPV) and trivalent live attenuated OPV.

  • The first vaccine to be introduced was Salk’s IPV in 1955. This immunized against all three strains of poliovirus and reduced the incidence of paralytic poliomyelitis in the US from 13.9 cases per 100 000 in 1954 to 0.5 cases per 100 000 in 1961.

  • In 1961, Sabin developed monovalent live OPVs which were replaced by a trivalent OPV in 1963. These were seen to offer the advantage of superior immunogenicity, ease of oral administration, induction of local mucosal immunity, and the potential public health benefit of the spread of live vaccine (attenuated) viruses from immunized to unimmunized contacts. However, the genetic instability of the Sabin vaccine strains, combined with the potential for recombination with other viruses, allows reversion of attenuated strains to neurovirulence, leading to rare cases of vaccine-associated paralytic poliomyelitis (VAPP).

  • VAPP is defined by WHO as poliomyelitis that occurs in a vaccinee between 7 and 30 days after a dose or in a close contact of a vaccinee between 7 and 60 days after receipt of the dose. VAPP is commonest after the first vaccine dose. Hypogammaglobulinaemic individuals have a 3000-fold higher risk of developing VAPP than healthy vaccinees. OPV is contraindicated in patients with immunodeficiency or household contacts of immunodeficient individuals.

  • In addition to VAPP, a further consequence of OPV is the development of vaccine-derived polioviruses (VDPVs). A VDPV is defined as a Sabin poliovirus with ≥1% of genetic variation, compared to the prototype sequence (reflecting sustained viral replication over at least 1 year in one or more persons). These viruses can be further subdivided into two subtypes: circulating VDPV (cVDPV) when the reversion to neurovirulence is associated with person-to-person transmission, and immunodeficiency-related VDPV (iVDPV) caused by prolonged virus replication in an immunodeficient individual. Individuals with deficient B-cell immunity may fail to clear the virus after OPV vaccination and may continue to excrete the virus for prolonged periods (months to decades).

  • Outbreaks of cVDPV, with sustained transmission in affected communities, have occurred primarily in areas where poor vaccine coverage has led to diminished herd immunity and have involved all three serotypes (including serotype 2 which has been eradicated in its wild form). These outbreaks have been interrupted with widespread targeted vaccination programmes using OPV.

  • IPV does not run the risk of VAPP or VDPV but, in its current form, may be prohibitively expensive in the developing world.

  • The reasons for failure, to date, of the global initiative to achieve its goal are multiple. Interruption of vaccination programmes due to military conflicts, local cultural or political misconceptions regarding the vaccine, and fears of VAPP impact on herd immunity all predispose to local outbreaks. Reintroduction of the virus into previously polio-free countries has occurred through travel. Low OPV vaccine efficacy has been reported in certain states in India, with children requiring multiple doses to achieve levels of population immunity to stop poliovirus transmission.

  • The GPEI Strategic Plan for 2013–2018 is to: (1) interrupt all poliovirus transmission, (2) progressively withdraw OPV and introduce IPV, (3) certify polio eradication, and (4) transition assets and infrastructure to routine immunization programmes as part of the GPEI legacy.

  • To obtain a progressive withdrawal of OPV, WHO has recommended that all 124 countries currently using only OPV introduce at least one dose of IPV before the global withdrawal of serotype 2 OPV in 2016. A 1- or 2-dose schedule, potentially administered intradermally with a reduced antigen content, may make this affordable.

Further reading

Aylward B, Tangermann R. The global polio eradication initiative: lessons learned and prospects for success. Vaccine 2011;29:D80–5.Find this resource:

Gonzalez H, Olsson T, Borg K. Management of postpolio syndrome. Lancet Neurol 2010;9:634–42.Find this resource:

Grassly NC. Immunogenicity and effectiveness of routine immunization with 1 or 2 doses of inactivated poliovirus vaccine: systematic review and meta-analysis. J Infect Dis 2014;210 Suppl 1:S439–46.Find this resource:

Hawken J, Troy BS. Adjuvants and inactivated polio vaccine: a systematic review. Vaccine 2012;30:6971–9.Find this resource:

Minot P. The polio-eradication programme and issues of the end game. J Gen Virol 2012;93:457–74.Find this resource:

Moturi EK, Porter KA, Wassilak SG, et al. Progress toward polio eradication—worldwide, 2013–2014. MMWR Morb Mortal Wkly Rep 2014;63:468–72.Find this resource:

Okayasua H, Suttera RW, Czerkinskyb C, Ograc PL. Mucosal immunity and poliovirus vaccines: impact on wild poliovirus infection and transmission. Vaccine 2011;29:8205–14.Find this resource:

The Global Polio Eradication Initiative. Available at: Polio <>.