Polio no longer poses a public health threat in the United States. No cases of wild-type PV infection have been reported since 1979. From 1980 to 1999, an average of 8 cases per year were reported in the United States, 95% of which were due to vaccine-associated paralytic polio (VAPP) caused by live oral polio vaccine (OPV) (with the remaining cases imported or indeterminant). Starting in 2000, the Advisory Committee on Immunization Practices recommended the exclusive use of inactivated PV vaccine (IPV) in routine immunizations in the United States to eliminate VAPP.
Areas of endemic wild-type PV still exist in other areas of the world such as Pakistan, Nigeria, and Afghanistan. Moreover, several countries are considered to have active transmission of imported PV, including Equatorial Guinea, Iraq, Cameroon, Syria, Ethiopia, and Somalia.
Mortality observed in paralytic polio is due to respiratory failure, although this has not occurred in the United States since 1979. Incidence is equal in males and females. Poliomyelitis tends to be a disease mainly of children; however, it can affect individuals of any age, especially those who are immunocompromised.
PV is transmitted feco-orally by the ingestion of contaminated water or, during epidemics, via pharyngeal spread. PV infects and causes disease only in humans. It is highly contagious. In temperate climates, infection is seasonal, with peak transmission occurring in summer and autumn. Three serotypes of PV have been identified: PV types 1 (PV1), 2 (PV2), and 3 (PV3). All are extremely virulent and produce the same symptoms. PV1 is the most common and is most frequently associated with paralysis.
After entering the mouth, the organism tends to infect the cells of the mouth, nose, and throat. It binds to an immunoglobulin-like receptor, known as the PV receptor or CD155, on the cell membrane. 90%-95% of PV infections are asymptomatic. There is an incubation period of 3-35 days (minimum range 6-20 days), during which the virus undergoes primary replication in the lymphatic tissues of the gastrointestinal tract using the host cells' own machinery. An asymptomatic primary (minor) transient viremia occurs, with spread of virus to the systemic reticuloendothelial tissue throughout the body. In 4%-8% of individuals, a second (major) viremia occurs, which manifests as influenza-like symptoms; this may rarely progress to invasion of the CNS, resulting in a local inflammatory response in the form of nonparalytic aseptic meningitis. In about 1% of these patients, the PV then causes selective destruction of motor neurons in the spinal cord, brain stem, or motor cortex leading to the development of various forms of paralytic poliomyelitis (spinal, bulbar, or bulbospinal, respectively). The mechanism of spread of PV to the CNS is unclear. It may occur by direct passage of the virus from blood by crossing the blood-brain barrier, or it may occur by retrograde axonal transport from muscle to spinal cord and brain. After invading the CNS, the virus uncoats, viral replication occurs, and the motor neuron dies, leading to paralysis of muscle fibers supplied by this motor neuron. Spread of the virus to neighboring motor neurons may occur laterally, independent of axonal transport, or by transneuronal spread in a retrograde transport-dependent fashion. Other neurons can be infected as well, producing brainstem encephalitis and respiratory insufficiency.
The virus can cross the placenta during pregnancy but does not seem to affect the fetus, either by maternal infection or vaccination. Maternal antibodies also cross the placenta, providing passive immunity during the first few months of life.
Risk factors for infection as well as severe disease include:
- Immune deficiency
- Physical activity immediately after the onset of paralysis
Primary viremia (abortive polio) is asymptomatic. In 4%-8% of patients, this is followed by a second major viremia manifesting as a flu-like illness with headache, sore throat, fever, nausea, vomiting, malaise, and fatigue. A fraction of patients in this group can have invasion of the CNS and inflammation of the meninges, causing neck stiffness, headache, fever, and vomiting and, in some patients, selective destruction of motor neurons; depending on the anatomical site, this causes severe back pain, neck/muscle pain, and the development of motor weakness. Such paralysis occurs in only about 0.1% of all PV infections. Weakness may vary, from 1 muscle or group of muscles to quadriplegia and respiratory failure.
- Spinal polio – Tone is reduced, nearly always in an asymmetric manner, with lower motor neuron destruction. Proximal muscles usually are affected more than distal muscles, and legs more commonly than arms. Reflexes are decreased or absent. The sensory examination is normal. Weakness typically worsens over 2-3 days, although sometimes worsening can progress for up to a week. Muscle atrophy is generally observed several weeks after onset of symptoms. Recovery may be complete, partial, or absent.
- Bulbar polio – Bulbar involvement occurs in 5%-35% of patients, producing dysphagia, dysarthria, and difficulty handling secretions. Approximately 19% of all paralytic polio cases have both bulbar and spinal symptoms.
- Respiratory polio (bulbospinal polio) – Bulbospinal polio affects the upper part of the cervical spinal cord (C3 through C5), and causes paralysis of the diaphragm along with difficulty in swallowing. There may be encephalitis, usually in infancy.
- Post-polio syndrome – Recurrences of weakness or fatigue may occur in some patients decades (20-40 years) after initial infection and disease. The same groups of muscles are usually involved, but weakness can extend to muscles that were not involved during the initial infection. The prognosis is generally good, though the actual cause of the syndrome is poorly understood. It is, at least, not secondary to persistent or reactivated PV infection. Patients may also experience chronic pain, contractures, depression, fatigue, and sleep problems.
- VAPP – Usually occurs after the first dose of OPV, and its estimated incidence is 1 person per 2.5 million doses. It is thought to be due to mutation of the vaccine virus to a neurovirulent type. The disease may occur in the vaccinated individual or a close contact of that person. Predisposing factors include B-cell immunodeficiencies and hypogammaglobulinemia.
- Vaccine-derived poliomyelitis – Refers to outbreaks of poliomyelitis in regions with low immunization rates when OPV vaccination starts. The mechanism appears to be mutation of vaccine virus to naturally occurring wild-type PV.
A80.9 – Acute poliomyelitis, unspecified
398102009 – Acute poliomyelitis
- Infection with other enteroviruses (eg, coxsackie virus, echovirus)
- Guillain-Barré syndrome
- West Nile virus infection
- Spinal cord disease (infarction, transverse myelitis, space-occupying lesions, etc)
- Acute intermittent porphyria
- Mononeuritis multiplex
- Myasthenia gravis
- Lambert-Eaton myasthenic syndrome
- Inflammatory myopathy