polio polio poliomyelitis, commonly shortened to polio, is an infectious disease caused by the poliovirus. approximately 75% of cases are asymptomatic; mild symptoms which can occur include sore throat and fever; in a proportion of cases more severe symptoms develop such as headache, neck stiffness, and paresthesia. these symptoms usually pass within one or two weeks. a less common symptom is permanent paralysis, and possible death in extreme cases. years after recovery, post-polio syndrome may occur, with a slow development of muscle weakness similar to that which the person had during the initial infection. "poliomyelitis" redirects here. for the virus, see poliovirus. for other uses, see polio (disambiguation). polioother namespoliomyelitis, infantile paralysis, heine-medin diseasea man with a wasted right leg due to poliomyelitispronunciation/ˌpoʊlioʊˌmaɪəˈlaɪtɪs/ specialtyneurology, infectious diseasesymptomsfever, sore throatcomplicationsmuscle weakness resulting in paralysis; post-polio syndrometypeswild pv types 1,2 & 3; vaccine-derived pvcausespoliovirus spread by fecal–oral routerisk factorspoor hygienediagnostic methodfinding the virus in the feces or antibodies in the bloodpreventionpolio vaccinetreatmentno treatment other than supportive carefrequency30 (wild) + 856 (vaccine-derived) in 2022 polio occurs naturally only in humans. it is highly infectious, and is spread from person to person either through fecal-oral transmission (e.g. poor hygiene, or by ingestion of food or water contaminated by human feces), or via the oral-oral route. those who are infected may spread the disease for up to six weeks even if no symptoms are present. the disease may be diagnosed by finding the virus in the feces or detecting antibodies against it in the blood. poliomyelitis has existed for thousands of years, with depictions of the disease in ancient art. the disease was first recognized as a distinct condition by the english physician michael underwood in 1789, 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, and in the 20th century, it became one of the most worrying childhood diseases. following the introduction of polio vaccines in the 1950s polio incidence declined rapidly. once infected, there is no specific treatment. the disease can be prevented by the polio vaccine, with multiple doses required for lifelong protection. there are two broad types of polio vaccine; an injected vaccine using inactivated poliovirus and an oral vaccine containing attenuated (weakened) live virus. through the use of both types of vaccine, incidence of wild polio has decreased from an estimated 350,000 cases in 1988 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. signs and symptoms outcomes of poliovirus infection in children outcome proportion of cases no symptoms 72% minor illness 24% nonparalytic aseptic meningitis 1–5% paralytic poliomyelitis 0.1–0.5% — spinal polio 79% of paralytic cases — bulbospinal polio 19% of paralytic cases — bulbar polio 2% of paralytic cases the term "poliomyelitis" is used to identify the disease caused by any of the three serotypes of poliovirus. two basic patterns of polio infection are described: a minor illness which does not involve the central nervous system (cns), sometimes called abortive poliomyelitis, and a major illness involving the cns, which may be paralytic or nonparalytic. adults are more likely to develop symptoms, including severe symptoms, than children. in most people with a normal immune system, a poliovirus infection is asymptomatic. in about 25% of cases, the infection produces minor symptoms which may include sore throat and low fever. these symptoms are temporary and full recovery occurs within one or two weeks. in about 1 percent of infections the virus can migrate from the gastrointestinal tract into the central nervous system (cns). most patients with cns involvement develop nonparalytic aseptic meningitis, with symptoms of headache, neck, back, abdominal and extremity pain, fever, vomiting, stomach pain, lethargy, and irritability. about one to five in 1000 cases progress to paralytic disease, in which the muscles become weak, floppy and poorly controlled, and, finally, completely paralyzed; this condition is known as acute flaccid paralysis. the weakness most often involves the legs, but may less commonly involve the muscles of the head, neck, and diaphragm. depending on the site of paralysis, paralytic poliomyelitis is classified as spinal, bulbar, or bulbospinal. in those who develop paralysis, between 2 and 10 percent die as the paralysis affects the breathing muscles. encephalitis, an infection of the brain tissue itself, can occur in rare cases, and is usually restricted to infants. it is characterized by confusion, changes in mental status, headaches, fever, and, less commonly, seizures and spastic paralysis. cause main article: poliovirus a tem micrograph of poliovirus 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. in addition to protecting the virus' genetic material, the capsid proteins enable poliovirus to infect certain types of cells. three serotypes of poliovirus have been identified – wild poliovirus type 1 (wpv1), type 2 (wpv2), and type 3 (wpv3) – 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. 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. individuals who are exposed to the virus, either through infection or by immunization via polio vaccine, develop immunity. in immune individuals, iga antibodies against poliovirus are present in the tonsils and gastrointestinal tract and able to block virus replication; igg and igm antibodies against pv can prevent the spread of the virus to motor neurons of the central nervous system. infection or vaccination with one serotype of poliovirus does not provide immunity against the other serotypes, and full immunity requires exposure to each serotype. a rare condition with a similar presentation, nonpoliovirus poliomyelitis, may result from infections with enteroviruses other than poliovirus. 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). transmission 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. it is seasonal in temperate climates, with peak transmission occurring in summer and autumn. these seasonal differences are far less pronounced in tropical areas. polio is most infectious between 7 and 10 days before and after the appearance of symptoms, but transmission is possible as long as the virus remains in the saliva or feces. virus particles can be excreted in the feces for up to six weeks. factors that increase the risk of polio infection include pregnancy, 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. pathophysiology a photomicrograph of the lumbar spinal cord depicting an infarct due to polio type iii surrounding the anterior spinal artery 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. penetration of the cns provides no known benefit to the virus, and is quite possibly an incidental deviation of a normal gastrointestinal infection. 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. paralytic polio denervation of skeletal muscle tissue secondary to poliovirus infection can lead to paralysis. in around one percent of infections, poliovirus spreads along certain nerve fiber pathways, preferentially replicating in and destroying motor neurons within the spinal cord, brain stem, or motor cortex. this leads to the development of paralytic poliomyelitis, the various forms of which (spinal, bulbar, and bulbospinal) vary only with the amount of neuronal damage and inflammation that occurs, and the region of the cns affected. 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. inflammation associated with nerve cell destruction often alters the color and appearance of the gray matter in the spinal column, causing it to appear reddish and swollen. other destructive changes associated with paralytic disease occur in the forebrain region, specifically the hypothalamus and thalamus. the molecular mechanisms by which poliovirus causes paralytic disease are poorly understood. early symptoms of paralytic polio include high fever, headache, stiffness in the back and neck, asymmetrical weakness of various muscles, sensitivity to touch, difficulty swallowing, muscle pain, loss of superficial and deep reflexes, paresthesia (pins and needles), irritability, constipation, or difficulty urinating. paralysis generally develops one to ten days after early symptoms begin, progresses for two to three days, and is usually complete by the time the fever breaks. 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 location of motor neurons in the anterior horn cells of the spinal column 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