Poliomyelitis is an acute viral infectious disease spread from person to person, primarily via the fecal-oral route. The term derives from the Greek polio (πολίός), meaning "grey", myelon (µυελός), referring to the "spinal cord", and -itis, which denotes inflammation. Although around 90% of polio infections cause no symptoms at all, affected individuals can exhibit a range of symptoms if the virus enters the blood stream. In about 1% of cases the virus enters the central nervous system, preferentially infecting and destroying motor neurons, leading to muscle weakness and acute flaccid paralysis. Different types of paralysis may occur, depending on the nerves involved. Spinal polio is the most common form, characterized by asymmetric paralysis that most often involves the legs. Bulbar polio leads to weakness of muscles innervated by cranial nerves. Bulbospinal polio is a combination of bulbar and spinal paralysis


Although polio can cause paralysis and death, the vast majority of people who are infected with the poliovirus don't become sick and are never aware they've been infected with polio.

Nonparalytic polio

Some people who develop symptoms from the poliovirus contract nonparalytic polio — a type of polio that doesn't lead to paralysis (abortive polio). This usually causes the same mild, flu-like signs and symptoms typical of other viral illnesses.

Signs and symptoms, which generally last one to 10 days, include:

  • Fever
  • Sore throat
  • Haedeach
  • Vomiting
  • Fatigue
  • Back pain or stiffness
  • Neck pain or stiffness
  • Pain or stiffness in the arms or legs
  • Muscle weakness or tenderness
  • Meningitis

Paralytic polio

In rare cases, poliovirus infection leads to paralytic polio, the most serious form of the disease. Paralytic polio has several types, based on the part of your body that's affected — your spinal cord (spinal polio), your brainstem (bulbar polio) or both (bulbospinal polio).

Initial signs and symptoms of paralytic polio, such as fever and headache, often mimic those of nonparalytic polio. Within a week, however, signs and symptoms specific to paralytic polio appear, including:

  • Loss of reflexes
  • Sever muscle aches or weakness
  • Loose and floopy limbs(flaccid paralysis),often worse on one side of the body

Post-polio syndrome

  • Post-polio syndrome is a cluster of disabling signs and symptoms that affect some people several years - an average of 35 years - after they had polio. Common signs and symptoms include:
  • Progressive muscle or joint weakness and pain
  • General fatigue and exhaustion after minimal activity
  • Muscle atrophy
  • Breathing or swallowing problems
  • Sleep-related breathing disorders, such as sleep apnea
  • Decreased tolerance of cold temperatures
  • Cognitive problems, such as concentration and memory difficulties
  • Depression or mood swings



Poliomyelitis is caused by infection with a member of the genus Enterovirus known as poliovirus (PV). This group of RNA viruses prefers to inhabit the gastrointestinal tract. PV infects and causes disease in humans alone. Its structure is very simple, composed of a single (+) sense RNA genome enclosed in a protein shell called a capsid. In addition to protecting the virus’s genetic material, the capsid proteins enable poliovirus to infect certain types of cells. Three serotypes of poliovirus have been identified—poliovirus type 1 (PV1), type 2 (PV2), and type 3 (PV3)—each with a slightly different capsid protein. All three are extremely virulent and produce the same disease symptoms. PV1 is the most commonly encountered form, and the one most closely associated with paralysis


Passive immunization

In 1950, William Hammon at the University of Pittsburgh purified the gamma globulin component of the blood plasma of polio survivors. Hammon proposed the gamma globulin, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. The results of a large clinical trial were promising; the gamma globulin was shown to be about 80% effective in preventing the development of paralytic poliomyelitis. It was also shown to reduce the severity of the disease in patients who developed polio. The gamma globulin approach was later deemed impractical for widespread use, however, due in large part to the limited supply of blood plasma, so the medical community turned its focus to the development of a polio vaccine.


Two types of vaccine are used throughout the world to combat polio. Both types induce immunity to polio, efficiently blocking person-to-person transmission of wild poliovirus, thereby protecting both individual vaccine recipients and the wider community (so-called herd immunity).

The first candidate polio vaccine, based on one serotype of a live but attenuated (weakened) virus, was developed by the virologist Hilary Koprowski. Koprowski's prototype vaccine was given to an eight-year-old boy on 27 February 1950. Koprowski continued to work on the vaccine throughout the 1950s, leading to large-scale trials in the then Belgian Congo and the vaccination of seven million children in Poland against serotypes PV1 and PV3 between 1958 and 1960.

The second inactivated virus vaccine was developed in 1952 by Jonas Salk at the University of Pittsburgh, and announced to the world on 12 April 1955. The Salk vaccine, or inactivated poliovirus vaccine (IPV), is based on poliovirus grown in a type of monkey kidney tissue culture (vero cell line), which is chemically inactivated with formalin. After two doses of IPV (given by injection), 90% or more of individuals develop protective antibody to all three serotypes of poliovirus, and at least 99% are immune to poliovirus following three doses.

Subsequently, Albert Sabin developed another live, oral polio vaccine (OPV). It was produced by the repeated passage of the virus through nonhuman cells at subphysiological temperatures. The attenuated poliovirus in the Sabin vaccine replicates very efficiently in the gut, the primary site of wild poliovirus infection and replication, but the vaccine strain is unable to replicate efficiently within nervous system tissue. A single dose of Sabin's oral polio vaccine produces immunity to all three poliovirus serotypes in about 50% of recipients. Three doses of live-attenuated OPV produce protective antibody to all three poliovirus types in more than 95% of recipients. Human trials of Sabin's vaccine began in 1957, and in 1958 it was selected, in competition with the live vaccines of Koprowski and other researchers, by the US National Institutes of Health. Licensed in 1962, it rapidly became the only polio vaccine used worldwide.

Because OPV is inexpensive, easy to administer, and produces excellent immunity in the intestine (which helps prevent infection with wild virus in areas where it is endemic), it has been the vaccine of choice for controlling poliomyelitis in many countries. On very rare occasions (about one case per 750,000 vaccine recipients), the attenuated virus in OPV reverts into a form that can paralyze. Most industrialized countries have switched to IPV, which cannot revert, either as the sole vaccine against poliomyelitis or in combination with oral polio vaccine.


Paralytic poliomyelitis may be clinically suspected in individuals experiencing acute onset of flaccid paralysis in one or more limbs with decreased or absent tendon reflexes in the affected limbs, that cannot be attributed to another apparent cause, and without sensory or cognitive loss.[38] A laboratory diagnosis is usually made based on recovery of poliovirus from a stool sample or a swab of the pharynx. Antibodies to poliovirus can be diagnostic, and are generally detected in the blood of infected patients early in the course of infection.[4] Analysis of the patient's cerebrospinal fluid (CSF), which is collected by a lumbar puncture ("spinal tap"), reveals an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level. Detection of virus in the CSF is diagnostic of paralytic polio, but rarely occurs.


Patients with abortive polio infections recover completely. In those that develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery. In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; cells that are not destroyed but lose function temporarily may recover within four to six weeks after onset. Half the patients with spinal polio recover fully, one quarter recover with mild disability and the remaining quarter are left with severe disability. The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of viremia, and inversely proportional to the degree of immunity. Spinal polio is rarely fatal


There is no cure for polio. The focus of modern treatment has been on providing relief of symptoms, speeding recovery and preventing complications. Supportive measures include antibiotics to prevent infections in weakened muscles, analgesics for pain, moderate exercise and a nutritious diet. Treatment of polio often requires long-term rehabilitation, including occupational therapy, physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery.

Portable ventilators may be required to support breathing. Historically, a noninvasive, negative-pressure ventilator, more commonly called an iron lung, was used to artificially maintain respiration during an acute polio infection until a person could breathe independently (generally about one to two weeks). Today, many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators worn over the chest and abdomen.

Other historical treatments for polio include hydrotherapy, electrotherapy, massage and passive motion exercises, and surgical treatments, such as tendon lengthening and nerve grafting.