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Infectious disease caused by poliovirus

Polio occurs naturally only in humans. (e. g. poor hygiene, or by ingestion of food or water contaminated by human feces), or via the oral–oral route. and the virus that causes it was first identified in 1909 by the Austrian immunologist Karl Landsteiner. Major outbreaks started to occur in the late 19th century in Europe and the United States, Following the introduction of polio vaccines in the 1950s, polio incidence declined rapidly. to 30 confirmed cases in 2022, confined to just three countries. There are rare incidents of disease transmission and/or of paralytic polio associated with the attenuated oral vaccine and for this reason the injected vaccine is preferred.

Poliomyelitis does not affect any species other than humans. The disease is caused by infection with a member of the genus Enterovirus known as poliovirus (PV). This group of RNA viruses colonize the gastrointestinal tract – specifically the oropharynx and the intestine. Its structure is quite simple, composed of a single (+) sense RNA genome enclosed in a protein shell called a capsid. All three are extremely virulent and produce the same disease symptoms. WPV2 was certified as eradicated in 2015 and WPV3 certified as eradicated in 2019. The incubation period (from exposure to the first signs and symptoms) ranges from three to six days for nonparalytic polio. If the disease progresses to cause paralysis, this occurs within 7 to 21 days. Infection or vaccination with one serotype of poliovirus does not provide immunity against the other serotypes, and full immunity requires exposure to each serotype. The oral polio vaccine contains weakened viruses that can replicate. On rare occasions, these may be transmitted from the vaccinated person to other people, who may display symptoms of polio. In communities with good vaccine coverage transmission is limited, and the virus dies out. In communities with low vaccine coverage, this weakened virus may continue to circulate. Polio arising from this cause is referred to as circulating vaccine derived polio (cVDPV) in order to distinguish it from the natural or "wild" poliovirus (WPV).

Poliomyelitis is highly contagious. The disease is transmitted primarily via the fecal–oral route, by ingesting contaminated food or water. It is occasionally transmitted via the oral–oral route. the very old and the very young, immune deficiency, and malnutrition. Although the virus can cross the maternal fetal barrier during pregnancy, the fetus does not appear to be affected by either maternal infection or polio vaccination. Maternal antibodies also cross the placenta, providing passive immunity that protects the infant from polio infection during the first few months of life.

Poliovirus enters the body through the mouth, infecting the first cells with which it comes in contact – the pharynx and intestinal mucosa. It gains entry by binding to an immunoglobulin like receptor, known as the poliovirus receptor or CD155, on the cell membrane. The virus then hijacks the host cell's own machinery, and begins to replicate. Poliovirus divides within gastrointestinal cells for about a week, from where it spreads to the tonsils (specifically the follicular dendritic cells residing within the tonsilar germinal centers), the intestinal lymphoid tissue including the M cells of Peyer's patches, and the deep cervical and mesenteric lymph nodes, where it multiplies abundantly. The virus is subsequently absorbed into the bloodstream. Known as viremia, the presence of a virus in the bloodstream enables it to be widely distributed throughout the body. Poliovirus can survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks. In a small percentage of cases, it can spread and replicate in other sites, such as brown fat, the reticuloendothelial tissues, and muscle. This sustained replication causes a major viremia, and leads to the development of minor influenza like symptoms. Rarely, this may progress and the virus may invade the central nervous system, provoking a local inflammatory response. In most cases, this causes a self limiting inflammation of the meninges, the layers of tissue surrounding the brain, which is known as nonparalytic aseptic meningitis. The mechanisms by which poliovirus spreads to the CNS are poorly understood, but it appears to be primarily a chance event – largely independent of the age, gender, or socioeconomic position of the individual. The destruction of neuronal cells produces lesions within the spinal ganglia; these may also occur in the reticular formation, vestibular nuclei, cerebellar vermis, and deep cerebellar nuclei. The likelihood of developing paralytic polio increases with age, as does the extent of paralysis. In children, nonparalytic meningitis is the most likely consequence of CNS involvement, and paralysis occurs in only one in 1000 cases. In adults, paralysis occurs in one in 75 cases. In children under five years of age, paralysis of one leg is most common; in adults, extensive paralysis of the chest and abdomen also affecting all four limbs – quadriplegia – is more likely. Paralysis rates also vary depending on the serotype of the infecting poliovirus; the highest rates of paralysis (one in 200) are associated with poliovirus type 1, the lowest rates (one in 2,000) are associated with type 2.

Spinal polio, the most common form of paralytic poliomyelitis, results from viral invasion of the motor neurons of the anterior horn cells, or the ventral (front) grey matter section in the spinal column, which are responsible for movement of the muscles, including those of the trunk, limbs, and the intercostal muscles. Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron ganglia. When spinal neurons die, Wallerian degeneration takes place, leading to weakness of those muscles formerly innervated by the now dead neurons. With the destruction of nerve cells, the muscles no longer receive signals from the brain or spinal cord; without nerve stimulation, the muscles atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed. The extent of spinal paralysis depends on the region of the cord affected, which may be cervical, thoracic, or lumbar. The virus may affect muscles on both sides of the body, but more often the paralysis is asymmetrical. A laboratory diagnosis is usually made based on the recovery of poliovirus from a stool sample or a swab of the pharynx. Rarely, it may be possible to identify poliovirus in the blood or in the cerebrospinal fluid. Poliovirus samples are further analysed using reverse transcription polymerase chain reaction (RT PCR) or genomic sequencing to determine the serotype (i. e., 1, 2, or 3), and whether the virus is a wild or vaccine derived strain. 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 percent effective in preventing the development of paralytic poliomyelitis. It was also shown to reduce the severity of the disease in patients who developed polio.

Two types of vaccine are used throughout the world to combat polio: an inactivated poliovirus given by injection, and a weakened poliovirus given by mouth. Both types induce immunity to polio and are effective in protecting individuals from disease. The inactivated polio vaccine (IPV) was developed in 1952 by Jonas Salk at the University of Pittsburgh, and announced to the world on 12 April 1955. The Salk vaccine is based on poliovirus grown in a type of monkey kidney tissue culture (vero cell line), which is chemically inactivated with formalin. 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 OPV produces immunity to all three poliovirus serotypes in about 50 percent of recipients. Three doses of OPV produce protective antibody to all three poliovirus types in more than 95 percent of recipients. 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, IPV confers good immunity but is less effective at preventing spread of wild poliovirus by the fecal–oral route. Because the oral polio vaccine 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, the attenuated virus in the Sabin OPV can revert into a form that can paralyze. In 2017, cases caused by vaccine derived poliovirus (cVDPV) outnumbered wild poliovirus cases for the first time, due to wild polio cases hitting record lows. Most industrialized countries have switched to inactivated polio vaccine, which cannot revert, either as the sole vaccine against poliomyelitis or in combination with oral polio vaccine. An improved oral vaccine (Novel oral polio vaccine type 2 nOPV2) began development in 2011 and was granted emergency licencing in 2021, and subsequently full licensure in December 2023. This has greater genetic stability than the traditional oral vaccine and is less likely to revert to a virulent form. Treatment of polio often requires long term rehabilitation, including occupational therapy, physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery. and due to the eradication of polio in most of the world. Other historical treatments for polio include hydrotherapy, electrotherapy, massage and passive motion exercises, and surgical treatments, such as tendon lengthening and nerve grafting. 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. Overall, 5 to 10 percent of patients with paralytic polio die due to the paralysis of muscles used for breathing. The case fatality rate (CFR) varies by age: 2 to 5 percent of children and up to 15 to 30 percent of adults die. When intermittent positive pressure ventilation is available, the fatalities can be reduced to 15 percent.

Many cases of poliomyelitis result in only temporary paralysis. Paralysis remaining after one year is likely to be permanent, although some recovery of muscle strength is possible up to 18 months after infection. These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection, restoring the fibers' capacity to contract and improving strength. In addition to these physiological processes, the body can compensate for residual paralysis in other ways. Weaker muscles can be used at a higher than usual intensity relative to the muscle's maximal capacity, little used muscles can be developed, and ligaments can enable stability and mobility. In some cases the growth of an affected leg is slowed by polio, while the other leg continues to grow normally. The result is that one leg is shorter than the other and the person limps and leans to one side, in turn leading to deformities of the spine (such as scoliosis). Complications from prolonged immobility involving the lungs, kidneys and heart include pulmonary edema, aspiration pneumonia, urinary tract infections, kidney stones, paralytic ileus, myocarditis and cor pulmonale. notably new muscle weakness and extreme fatigue. This condition is known as post polio syndrome (PPS) or post polio sequelae. The symptoms of PPS are thought to involve a failure of the oversized motor units created during the recovery phase of the paralytic disease. Contributing factors that increase the risk of PPS include aging with loss of neuron units, the presence of a permanent residual impairment after recovery from the acute illness, and both overuse and disuse of neurons. PPS is a slow, progressive disease, and there is no specific treatment for it.

Major polio epidemics were unknown before the 20th century; up until that time, polio was an endemic disease worldwide. Mothers who had survived polio infection passed on temporary immunity to their babies in the womb and through breast milk. As a result, an infant who encountered a polio infection generally suffered only mild symptoms and acquired a long term immunity to the disease. With improvements in sanitation and hygiene during the 19th century, the general level of herd immunity in the population declined providing circumstances where epidemics of polio became frequent. Following the widespread use of poliovirus vaccine in the mid 1950s, new cases of poliomyelitis declined dramatically in many industrialized countries. Efforts to completely eradicate the disease started in 1988 and are ongoing.

The last remaining region with wild polio cases are the South Asian countries Afghanistan and Pakistan. There were attacks and deaths among vaccination workers; 66 vaccinators were killed in 2013 and 2014. These factors have set back efforts to eliminate polio by means of vaccination in these countries. In Afghanistan, 80 cases of polio were reported from 35 districts during 2011. Incidence over the subsequent 10 years has declined to just 4 cases in 2 districts during 2021. In Pakistan, cases dropped by 97 percent from 2014 to 2018; reasons include 440 million dirham support from the United Arab Emirates to vaccinate more than ten million children, changes in the military situation, and arrests of some of those who attacked polio workers.

The Americas were declared polio free in 1994. The last known case was a boy in Peru in 1991. The US Centers for Disease Control and Prevention recommends polio vaccination boosters for travelers and those who live in countries where the disease is endemic. In July 2022, the US state of New York reported a polio case for the first time in almost a decade in the country; this was subsequently attributed to a vaccine derived strain of the virus.

In 2000, polio was declared to have been officially eliminated in 37 Western Pacific countries, including China and Australia. Despite eradication ten years earlier, an outbreak was confirmed in China in September 2011, involving a strain common in Pakistan. In September 2019, the Department of Health of the Philippines declared a polio outbreak in the country after a single case in a 3 year old girl. In December 2019, acute poliomyelitis was confirmed in an infant in Sabah state, Borneo, Malaysia. Subsequently, a further three polio cases were reported, with the last case reported in January 2020. Both outbreaks were found to be linked instances of vaccine derived poliomyelitis.

Europe was declared polio free in 2002.

On 27 March 2014, the WHO announced the eradication of poliomyelitis in the South East Asia Region, which includes eleven countries: Bangladesh, Bhutan, North Korea, India, Indonesia, Maldives, Myanmar, Nepal, Sri Lanka, Thailand and Timor Leste. With the addition of this region, 80 per cent of the world population was considered to be living in polio free regions. acknowledged by the WHO in 2013. 15 cases were confirmed among children in Syria between October and November 2013 in Deir Ezzor. Later, two more cases, one each in rural Damascus and Aleppo, were identified. It was the first outbreak in Syria since 1999. Doctors and international public health agencies report more than 90 cases of polio in Syria, with fears of contagion in rebel areas from lack of sanitation and safe water services. A vaccination campaign in Syria operated literally under fire and led to the deaths of several vaccinators, but returned vaccination coverage to pre war levels. Syria is currently free of polio, but is considered "at risk".

In 2003 in northern Nigeria – a country which at that time was considered provisionally polio free – a fatwa was issued declaring that the polio vaccine was designed to render children sterile. Subsequently, polio reappeared in Nigeria and spread from there to several other countries. In 2013, nine health workers administering polio vaccine were targeted and killed by gunmen on motorcycles in Kano, but this was the only attack. Local traditional and religious leaders and polio survivors worked to revive the campaign, and Nigeria was removed from the polio endemic list in September 2015 after more than a year without any cases, only to be restored to the list in 2016 when two cases were detected. Africa was declared free of wild polio in August 2020, although cases of circulating vaccine derived poliovirus type 2 continue to appear in several countries. A single case of wild polio which was detected in Malawi in February 2022, and another in Mozambique in May 2022 were both of a strain imported from Pakistan and do not affect the African region's wild poliovirus free certification status.

The effects of polio have been known since prehistory; Egyptian paintings and carvings depict otherwise healthy people with withered limbs, and young children walking with canes. The earliest known case of polio is indicated by the remains of a teenage girl discovered in a 4000 year old burial site in the United Arab Emirates, exhibiting characteristic symptoms of the condition. The first clinical description was provided by the English physician Michael Underwood in 1789, where he refers to polio as "a debility of the lower extremities". The work of physicians Jakob Heine in 1840 and Karl Oskar Medin in 1890 led to it being known as Heine–Medin disease. The disease was later called infantile paralysis, based on its propensity to affect children. Before the 20th century, polio infections were rarely seen in infants before six months of age, most cases occurring in children six months to four years of age. Poorer sanitation of the time resulted in constant exposure to the virus, which enhanced a natural immunity within the population. In developed countries during the late 19th and early 20th centuries, improvements were made in community sanitation, including better sewage disposal and clean water supplies. These changes drastically increased the proportion of children and adults at risk of paralytic polio infection, by reducing childhood exposure and immunity to the disease. Small localized paralytic polio epidemics began to appear in Europe and the United States around 1900. Outbreaks reached pandemic proportions in Europe, North America, Australia, and New Zealand during the first half of the 20th century. By 1950, the peak age incidence of paralytic poliomyelitis in the United States had shifted from infants to children aged five to nine years, when the risk of paralysis is greater; about one third of the cases were reported in persons over 15 years of age. Accordingly, the rate of paralysis and death due to polio infection also increased during this time. Intensive care medicine has its origin in the fight against polio. Most hospitals in the 1950s had limited access to iron lungs for patients unable to breathe without mechanical assistance. Respiratory centers designed to assist the most severe polio patients, first established in 1952 at the Blegdam Hospital of Copenhagen by Danish anesthesiologist Bjørn Ibsen, were the precursors of modern intensive care units (ICU). (A year later, Ibsen would establish the world's first dedicated ICU.) The polio epidemics not only altered the lives of those who survived them, but also brought profound cultural changes, spurring grassroots fund raising campaigns that would revolutionize medical philanthropy, and giving rise to the modern field of rehabilitation therapy. As one of the largest disabled groups in the world, polio survivors also helped to advance the modern disability rights movement through campaigns for the social and civil rights of the disabled. The World Health Organization estimates that there are 10 to 20 million polio survivors worldwide. In 1977, there were 254,000 persons living in the United States who had been paralyzed by polio. According to doctors and local polio support groups, some 40,000 polio survivors with varying degrees of paralysis were living in Germany, 30,000 in Japan, 24,000 in France, 16,000 in Australia, 12,000 in Canada and 12,000 in the United Kingdom in 2001. The disease was very well publicized during the polio epidemics of the 1950s, with extensive media coverage of any scientific advancements that might lead to a cure. Thus, the scientists working on polio became some of the most famous of the century. Fifteen scientists and two laymen who made important contributions to the knowledge and treatment of poliomyelitis are honored by the Polio Hall of Fame, which was dedicated in 1957 at the Roosevelt Warm Springs Institute for Rehabilitation in Warm Springs, Georgia, US. In 2008 four organizations (Rotary International, the World Health Organization, the U. S. Centers for Disease Control and UNICEF) were added to the Hall of Fame. World Polio Day (24 October) as an annual day of awareness was established by Rotary International to commemorate the birth of Jonas Salk, who led the first team to develop a vaccine against poliomyelitis. A global effort to eradicate polio – the Global Polio Eradication Initiative (GPEI) – began in 1988, led by the World Health Organization, UNICEF, and The Rotary Foundation. i. e., inflammation of the spinal cord's grey matter. The word was first used in 1874 and is attributed to the German physician Adolf Kussmaul. The first recorded use of the abbreviated version polio was in the Indianapolis Star in 1911.