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Poliomyelitis, also known as infantile spinal paralysis, or more colloquially as polio, is an acute, contagious, and specifically human infectious disease caused by the poliovirus. The infection, transmitted via the digestive tract, is most often asymptomatic or presents with symptoms that are usually mild and non-specific. Acute anterior poliomyelitis, specifically, is an affliction of the spinal cord. It can lead to paralysis, most frequently affecting the lower limbs, and can even impact the respiratory system. In the former case, the prognosis is functional with a risk of paralytic sequelae; in the latter, the prognosis can be life-threatening with a risk of respiratory arrest. In all instances, the treatment is symptomatic, as there is no curative treatment for the disease.
Studied and described by Heine and Medin in the 19th century, polio ravaged the globe epidemically from the 1880s until the latter half of the 20th century, incapacitating or killing millions. Advances in hygiene and, most significantly, vaccination have considerably reduced its incidence. The work of Salk in the 1950s, followed by Sabin, led to the creation of two effective vaccines – the first injectable and the second oral – thereby enabling the fight against the disease. Since 1988, the eradication of polio has been the focus of a global initiative under the auspices of the World Health Organization, UNICEF, and Rotary International. This program has reduced the annual incidence of wild virus polio from 350,000 cases in 1988 to 37 cases in 2016, with the disease remaining endemic in only two countries: Pakistan and Afghanistan. Since 2017, cases caused by vaccine-derived poliovirus have outnumbered those caused by wild poliovirus.
While the first identified polio epidemics occurred in the 20th century, the poliovirus has likely been pathogenic to humans for millennia. Dating major epidemics prior to the 20th century is difficult, as the official requirement to report polio cases in each country was only established in the early twentieth century. Until the 19th century, poliovirus was an endemic and quiescent agent. From around 1910 onwards, epidemics became regular throughout the industrialized world, primarily in cities and during the summer months. The evolution of medical understanding, coupled with the dramatic and sometimes devastating epidemic crises, shaped both physicians' and the public's perception of the disease.
Ancient Egyptian engravings depict individuals with motor impairments exhibiting characteristics suggestive of polio, such as adults with atrophied limbs and children walking with canes. English Egyptologists in the 1960s identified traces of polio on a skeleton dating back to 3400 BC. Mentions of paralysis, possibly polio, can be found in the traditions attributed first to Hippocrates and then to Galen. While physicians Michael Underwood in 1784 and Giovanni Battista Monteggia in 1813 are credited with the first descriptions of polio—an illness characterized by a febrile period of a few days followed by leg paralysis—it wasn't until the 1860s that physicians began to describe the specific spinal cord damage caused by the disease.
The disease was officially named "poliomyelitis" in 1874, derived from the Greek words "polios" (gray) and "myelos" (marrow), with the suffix "-itis" indicating inflammation. Thus, it signifies "inflammation of the gray matter of the spinal cord." Before this, polio symptoms were described under various names like "dental paralysis," "infantile spinal paralysis," "essential paralysis of children," and "morning paralysis." Jakob Heine provided the first precise, though incomplete, description in his 1840 work, "Beobachtungen über Lähmungszustände." He introduced the term "Spinale Kinderlähmung" (spinal infantile paralysis) in the second edition of 1860.
This German orthopedist established polio as a distinct clinical entity, differentiating it from cerebral palsy and hemiplegia. He hypothesized its epidemic nature and suggested lesions in the anterior horn of the spinal cord. This hypothesis, also proposed by Guillaume Duchenne de Boulogne, was confirmed by autopsies performed by Victor André Cornil in 1863 and his student Jean-Martin Charcot in 1870, revealing histological alterations. It's believed that before Duchenne, the anterior horn localization was accepted for infantile spinal paralysis; Duchenne's innovation was suggesting it for adult spinal paralysis as well.
In the autumn of 1881, Swedish physician Nils August Bergenholtz diagnosed thirteen cases of acute anterior poliomyelitis and suggested its epidemic character. This observation, remaining unpublished, went unnoticed by his contemporaries. In 1885, German neurologist Adolf Strümpell described a familial spastic paraplegia, which he initially believed to be a cerebral form of polio. Then, in 1887, experienced Swedish pediatrician Karl Oskar Medin encountered 44 cases at the Stockholm Polyclinic. His meticulous observations allowed him to establish that the paralysis, previously defining the disease, was actually the second phase of a process initially signaled by fever, headaches, and malaise. He also noted that the illness could be limited to this first phase, and crucially, Medin was the first to report the epidemic nature of the disease, publishing his findings in 1890.
Based on systematic observations during the 1905 Swedish epidemic, which affected 1,031 individuals, Dr. Ivar Wickman provided epidemiological evidence for the contagiousness previously noted by Oskar Medin. Investigating over a thousand cases and visiting more than 300 patient homes, Wickman concluded that polio was often transmitted by seemingly healthy individuals with minor, subclinical infections, which he termed "abortive poliomyelitis." Wickman's originality lay not just in noting these mild cases but in highlighting their high frequency and their role in disease propagation. He also established different incubation periods and noted its seasonality, expressing surprise that it affected adults as well, with 21.4% of his patients being over 14 years old. He is also credited with naming it the "Heine-Medin disease." His work led Sweden to make polio case notification mandatory, and subsequent epidemics confirmed his findings, leading to international recognition.
The definitive proof of the disease's infectious nature, however, came from Karl Landsteiner and Erwin Popper in 1908. Landsteiner injected an extract from the spinal cord of a young boy who died of polio into rats, guinea pigs, mice, and two monkeys. Only the monkeys rapidly became paralyzed, and microscopic examination revealed their spinal cords to be identical to those of children who had died of polio. During these experiments, Landsteiner and Popper couldn't demonstrate contagiousness, failing to transmit the disease from monkey to monkey. This transmission was achieved in 1909 by several teams, including Römer, Flexner and Lewis, Leiner and von Wiesner, and Landsteiner and Levaditi.
The exact nature of the infectious agent remained elusive. Lacking evidence of a bacterial agent, Flexner and Lewis concluded it must be a filterable virus, a notion that persisted even as late as 1952 for some researchers. Despite these discoveries, major newspapers in the United States continued to assert for years that the polio germ had not yet been found. Based on experiments with monkeys by Flexner and Lewis, and Leiner and Von Wiesner, the two teams posited in 1910 that poliovirus reached the central nervous system along nerve pathways from the nasal mucosa. A flaw in this concept stemmed from Flexner's experiments being conducted on one of the few monkey species susceptible only to injection into the central nervous system.
Furthermore, as only became evident after Enders' discoveries in 1949, Flexner's repeated experiments led to the selection of viral strains that could only develop on nerve tissue and thus induced only a low-grade viremia. This view of poliovirus's exclusive neurotropism and its nasal entry, dominant until the 1930s, obscured results that didn't fit this explanatory framework. This was the case with the work of Carl Kling in Sweden, who, extending Landsteiner's 1909 experiments, showed that injecting extracts from the throat, larynx, or intestines of adolescents who died of polio also caused paralysis in monkeys. He concluded that contamination could occur through a virus present in the saliva or intestines of infected individuals, supporting the theory of the intestinal route, or fecal-oral transmission.
Kling also experimentally confirmed Wickman's conclusion that asymptomatic individuals could harbor the virus in their throat or intestines. When Kling's team presented their findings at a conference in Washington in 1912, Simon Flexner, director of the Rockefeller Institute for Medical Research and a leading polio research center, gave them no credibility. Unable to replicate the Swedish results, American researchers turned away from the intestinal route theory for a considerable time. It wasn't until the work of Trask and Paul at Yale, and especially Albert Sabin and Robert Ward in 1941, that the importance of the intestinal route became definitively established, though by the 1920s in Sweden, Flexner's views were, to some extent, accommodating Kling's.
Kling's work likely suffered from arriving in the US at a time when American researchers, influenced by Milton Rosenau and under pressure from polio epidemics in 1916, were inclined to view the stable fly as the disease vector. Around the same time, Simon Flexner discovered "germicidal substances," now known as antibodies. He extracted serum from convalescent monkeys and injected it into other monkeys alongside infected marrow, observing no paralysis in the experimental subjects. Arnold Netter had a similar discovery in 1909-1910 with Constantin Levaditi. In 1915, Netter promoted this serum, derived from human or simian convalescents, which was widely used during the severe 1916 US epidemic. Lacking robust evaluations and alternative treatments, this serotherapy was used in the US until 1935 and in Canada until 1940.
Between 1928 and 1931, Pierre Lépine demonstrated the survival of the poliovirus in external environments, particularly in water, its transmission to monkeys via the digestive route, and the effect of chlorine on the virus. In 1929, within the framework of the International Office of Public Hygiene, Carl Kling and Constantin Levaditi, based on epidemiological studies in Saxony and Romania, showed that the majority of polio cases occurred near watercourses, leading to the "hydric hypothesis." In 1931, by comparing the Rockefeller MV strain with a local strain from Melbourne, Frank Macfarlane Burnet and Jean MacNamara revealed the existence of at least two virus strains. These findings, from researchers in a distant continent, were met with skepticism, but their significance was later recognized by Hammon, Francis, and Rivers in light of the 1935 vaccine failures.
In 1934 and 1935, two rival and independent American vaccines emerged: an "inactivated" one by Dr. Maurice Brodie and an "attenuated" version by Dr. John Kolmer. Their hasty use in parts of the US proved ineffective and, in some cases, fatal. For the next two decades, researchers hesitated to develop or test another vaccine. It was during this period that Dr. Claus W. Jungeblut proposed a preventive and curative treatment with vitamin C. Albert Sabin, already an authority, could not replicate these results, and the idea was abandoned. Similarly, at this time, various nasal instillation treatments were proposed and evaluated, but subsequently rejected due to their ineffectiveness and harmfulness. In 1939, Charles Armstrong succeeded in multiplying the Lansing strain in mice, which facilitated research. Max Theiler and Maurice Brodie had seemingly achieved this earlier without it being noted at the time.
In 1941, a team at Johns Hopkins Hospital in Baltimore detailed the virus's cycle in the human body, demonstrating that the virus must enter the bloodstream before reaching the spinal cord. This discovery opened prospects for a future vaccine: if antibodies could be induced in the blood, the virus could be neutralized before causing bulbar damage. In 1945, physicians were still questioning the possibility of animal reservoirs for the virus beyond monkeys, such as dogs. In a related vein, in 1946, Thomas Francis reiterated that African American populations were not less exposed to polio, contrary to common belief.
In 1949, at a time when two eminent polio specialists, Sir MacFarland Burnet and William Hammon, expressed pessimism about controlling the disease, three Americans made a major discovery. In a short article published in the journal Science on January 28, 1949, Enders, Weller, and Robbins announced their success in cultivating the poliovirus (Lansing strain) on human embryonic cells, foreskins, human kidneys, and monkey kidneys. This discovery, not immediately perceived by all researchers, quickly revitalized research. From then on, researchers had access to large quantities of virus at a lower cost. Until then, despite Armstrong's discovery and Sabin and Olitsky's 1936 publication, the virus was multiplied only in vivo, and in monkeys. Constantin Levaditi had however shown as early as 1913 that it was possible to cultivate the virus on cells of non-nervous origin.
In the context of vaccine development, this also provided a safety guarantee. The risks of paralysis and death (0.4% of inoculated subjects) associated with Pasteur's rabies vaccine were known, and cultivating the vaccine virus on non-nervous cells could eliminate this risk. In their work, Enders, Weller, and Robbins also demonstrated a way to easily detect and measure the effective multiplication of the invisible poliovirus: the tissue cells in inoculated test tubes visibly degraded over time, whereas previously, the virus's presence was only confirmed when a monkey became paralyzed after injection. These discoveries earned them the Nobel Prize in Physiology or Medicine in 1954.
Shortly thereafter, in 1952, Lederle Laboratories announced that two of their teams had successfully cultivated one of the poliovirus types (MEFI strain) on chicken embryos. Also in 1949, Bodian, Morgan, and Howe established that fourteen different poliovirus strains could be grouped into three serotypes. In 1951, a committee of the National Foundation for Infantile Paralysis specified that all strains fell into only three serotypes. The discovery in 1948 by Gilbert Dalldorf and Grace Sickles of a virus distinct from poliovirus, but capable of causing similar paralysis, briefly caused confusion among researchers. This confusion was quickly dispelled by the development and distribution of the Salk and Sabin vaccines.
In Japan, in the 1960s, a disease with polio-like symptoms appeared, officially named "Subacute Myelo-Optic Neuropathy" (SMON) in 1964. Although a viral origin was initially sought, it was later identified as being caused by a medication, Clioquinol, which resulted in 11,007 fatalities. The era of vaccines marked a turning point. Early attempts to develop a vaccine began in 1913 with Römer and Flexner, followed by Brodie, Kolmer, Jungeblut, Sanders, and later Blanc and Martin in 1950, exploring various forms of serovaccination. However, it was in the 1950s that the scientific, technical, and financial conditions aligned for the creation of sufficiently safe and effective vaccines, starting with Salk's, followed by Lépine's in France, and then Sabin's, which built upon the work of Koprowski and competed with Cox's vaccine.
In 1948, Isabel Morgan demonstrated the effectiveness of an inactivated vaccine in monkeys, a significant theoretical breakthrough at a time when the scientific consensus held that only a live vaccine could confer immunity against polio. On February 17 and 27, 1950, Hilary Koprowski, assisted by Jervis and Norton, successfully inoculated several children with an attenuated live vaccine (TN strain). At a congress in 1951, his results were met with disbelief but caught the attention of Sabin, whose work would be highlighted later. Koprowski continued his trials in the US from 1952 to 1955.
In 1952, Dorothy Horstmann of Yale University demonstrated the presence of the virus in the blood, a finding later confirmed by David Bodian at Johns Hopkins Hospital. On October 21, 1952, Dr. Howard Howe of Johns Hopkins University reported on a trial of a trivalent inactivated formaldehyde vaccine administered to six disabled children, with five other children serving as controls. The children were not exposed to the virus; rather, their antibody levels were measured following the inoculation of the vaccine strains.
By late 1952, using Hanks' medium 199, Salk administered the vaccine to residents of an institution for disabled children after injecting it into himself and his family. He conducted another trial at a Pennsylvania school and, in the fall of 1953, tested his vaccine on 600 people in the Pittsburgh area. The same year, he published the results of these trials, drawing criticism for using an inactivated virus, a method deemed ineffective. The National Foundation for Infantile Paralysis then requested viral fluid from manufacturers to conduct an unprecedented double-blind field trial in the US, commencing April 26, 1954.
This trial was one of the most extensive medical experiments in history, involving the detailed follow-up of nearly 1.8 million children aged 5 to 8, who received either Medium 199 as a placebo or the actual vaccine, to observe whether they contracted polio. On April 12, 1955, the announcement of the experiment's success was a massive media event. American manufacturers hastily launched their vaccine to meet demand under the Poliomyelitis Vaccination Assistance Act.
However, on April 25, 1955, the "Cutter Incident" occurred. In California, Cutter Laboratories, one of the manufacturers distributing the Salk vaccine, began distribution almost immediately after the trial's success announcement. A few days later, children became ill. Analysis revealed that some batches still contained live viruses. On April 27, the US Surgeon General ordered all Cutter vaccines withdrawn, and on May 8, following a vast investigation, the entire US vaccination program was halted due to fears of a broader defect involving all vaccines. The Cutter incident led to 220,000 people being affected, with 70,000 sick, 164 severe paralyses, and 10 deaths. Some Salk batches produced by Wyeth also caused a few polio cases.
Between 1955 and 1963, millions of people were exposed to simian virus 40 present in polio vaccines. Discovered in 1960, this potent oncogenic virus (cancer-inducing) was eventually eliminated from polio vaccines. The long-term consequences of this contamination are still debated in 2000. In South Africa, James Gear produced a Salk-type vaccine and inoculated 15,000 children in 1955.
In 1956, Albert Sabin inoculated 9,000 monkeys, 150 chimpanzees, and 133 young adults in an Ohio prison with his vaccine. That same year, George Frederick Dick, known for his work on the yellow fever attenuated vaccine, invited Hilary Koprowski to conduct a large trial in Ireland. Dick halted the trial after observing that the attenuated vaccine strain had regained some virulence. In 1957, Salk and Pierre Lépine published their findings within weeks of each other. To prevent any risk of infection, Lépine, using a different strain, employed a double inactivation process for the virus, first with formalin and then with beta-propiolactone.
In July 1957, the World Health Organization (WHO) called for large-scale trials of attenuated vaccines adhering to six safety criteria. Following this declaration, Albert Sabin's oral vaccine was tested from 1957 onwards under WHO's auspices outside the US on 80 million people across Russia, the Netherlands, Mexico, Chile, Sweden, and Japan. On August 18, 1958, Hilary Koprowski launched a vast vaccination campaign in the Belgian Congo, which continued until 1960. From 1958 to 1960, he also vaccinated 40,000 children in Germany and over 7 million in Poland. Trials took place in Switzerland in 1960-1961 and in Croatia in 1961.
Trials conducted by Cox in Florida and Berlin showed vaccine strains regaining virulence, leading Lederle Laboratories to abandon research with Cox's strains. In 1959, a special committee established a year earlier by the National Institutes of Health to evaluate strains for the oral vaccine concluded that Sabin's strains were superior to those of Koprowski and Cox (and those cultured at Yale University), prompting the Surgeon General to recommend their use. On April 24, 1960, marked "Sabin Sunday," the first massive test of the Sabin vaccine in the United States. Monovalent oral polio vaccines of type 1 (mOPV1) and type 2 (mOPV2) were authorized in the US in 1961, followed by mOPV3 in 1962.
In May 1962, the US Congress examined a bill to establish the framework for future mass vaccination campaigns. During hearings, Congress was apprised of Dr. Bernard Greenberg's critical stance, who pointed out statistical biases that had overestimated the effect of early Salk polio vaccinations, suggesting they actually contributed to an increase in polio cases. Nevertheless, the law was adopted that same year as the Vaccination Assistance Act, allocating federal funds for vaccine purchase and statistics. In 1963, the trivalent oral Sabin vaccine (tOPV) received authorization. The use of the Salk vaccine rapidly declined, accounting for only 2% of annual polio vaccines used in the US.
In France, vaccination became mandatory and therefore free in 1964, having been introduced into the French vaccination schedule in 1958 (Salk) and then in 1962 (Sabin). Twenty years later, in 1987, the "enhanced-potency IPV" received authorization in the US, developed in 1978 using human diploid cell culture. In 1997, the Advisory Committee on Immunization Practices (ACIP) recommended the use of inactivated vaccine for the first two injections, with oral vaccine for the latter two. By June 17, 1999, the ACIP exclusively recommended the inactivated vaccine.
In the 2000s, following a hypothesis from the 1990s, journalist Edward Hooper posited that the origin of AIDS could be traced to Koprowski's polio vaccination campaigns in the Belgian Congo in the late 1950s, but this hypothesis was rejected by specialists. Turning to treatments, in 1948, Dr. Fred R. Klenner developed a curative approach based on injecting massive doses of vitamin C, tens of grams per day. Among 60 patients during the 1948 North Carolina epidemic, all recovered without sequelae in 3 to 5 days. He shared his method at the American Medical Association's annual session and later published articles on the subject. However, due to a lack of interest from scientific press and authoritative specialists, at a time when vaccination was the primary focus, his method was not widely adopted and eventually fell into obscurity.
Around the same time, a treatment using magnesium chloride was proposed by Dr. Auguste Neveu, based on the work of Dr. Pierre Delbet, who also claimed cases of recovery. In 1950, William Hammon purified gamma globulins from the blood plasma of polio survivors. He proposed injecting anti-polio serum to prevent the disease and reduce symptom severity in affected patients. A large clinical trial yielded encouraging results, suggesting that anti-polio gamma globulins could prevent paralytic polio in about 80% of cases.
However, passive immunization via serotherapy proved impractical to implement on a large scale, primarily due to insufficient serum availability. Research then shifted away from this strategy and focused on vaccine development. Historically, the most severe polio cases necessitated the use of negative-pressure non-invasive ventilation, commonly known as the "iron lung." This method allowed thousands of patients to be ventilated acceptably while awaiting recovery of respiratory autonomy, typically within one to two weeks in favorable cases.
During the major polio epidemic in Denmark in 1952, Danish anesthesiologist Björn Ibsen developed long-term respiratory support using positive-pressure invasive ventilation, initially manually with a bellows. The patient mortality rate dropped from 87% to approximately 25% within weeks. Since then, patients with respiratory distress require intensive care management and may need home ventilatory assistance with portable artificial respirators. Beyond its significant contribution to advancing virology and immunology, the study of polio also led to important advances in rehabilitation, benefiting individuals with traumatic brain injuries, strokes, and neurodegenerative diseases.
In France, following the creation of the National Center for the Treatment of Polio Sequelae in Garches in 1949, which is now part of the Raymond-Poincaré Hospital, hydrotherapy, balneotherapy, respiratory physiotherapy, and medicalized transport were developed. The dissemination and improvement of limb and spine orthoses, knowledge regarding the evolution of scoliosis and spinal deformities, and the birth of functional surgery also stemmed from the efforts made during that period.
In 1985, the Pan American Health Organization (PAHO), the regional office of the World Health Organization (WHO), decided to eradicate polio from the Americas. In 1988, the 41st World Health Assembly, comprising delegates from 166 member states, adopted a resolution aiming for the global eradication of polio. Thus, the Global Polio Eradication Initiative was born, led by the WHO, UNICEF, the US Centers for Disease Control and Prevention (CDC), and Rotary International. This program was established following the certification of smallpox eradication in 1980, progress made in the 1980s through polio virus elimination operations in the Americas, and Rotary International's commitment to mobilize funds to protect all children from this disease.
Polio surveillance is conducted through a network of laboratories that test for wild polioviruses in all children under 15 years old presenting with acute flaccid paralysis (AFP), the characteristic symptom of the disease. Since AFP can be a symptom of other illnesses, stool samples must be rapidly collected and analyzed in laboratories to confirm the cause of paralysis. In 1992, a polio outbreak was discovered in the Netherlands among a group refusing vaccination. By the end of 1999, cases had decreased by 95%, with 7,094 new cases reported out of a total of 20,000 patients, and the number of affected countries dropped from 125 to 30.
To implement the intensified polio eradication effort in 2007-2008, traditional partner funding for development aid was significantly supplemented by domestic resources from the remaining endemic countries. India, Nigeria, and Pakistan announced commitments to fighting poliovirus. Rotary International and the Bill & Melinda Gates Foundation announced a partnership in November 2007 to inject $200 million into the program, with Rotary stating its participation would exceed $1.2 billion. Cases were primarily geographically confined to areas with suboptimal vaccination coverage, around 30% of children unvaccinated in Nigeria, with Indian cases also limited to a region resistant to vaccinations.
The presence of sporadic cases in fully vaccinated individuals raised questions. The WHO recommends a vaccination coverage rate of 90%, which is achieved in most wealthy nations. In 2009-2010, a significant resurgence of cases occurred in Tajikistan, a country recently certified polio-free, becoming the first to see the disease reappear, accounting for 75% of global polio cases – a rate far exceeding those in India and Nigeria. The vaccination rate in Tajikistan was around 75% but declined due to public doubts about vaccine safety, fueled by religious or anti-government movements. The WHO encouraged a vaccination campaign there, and some authors feared the virus's spread to other regions, even as tourism developed in some at-risk countries.
By 2012, the disease remained endemic in three countries: Nigeria, Pakistan, and Afghanistan, which accounted for nearly all cases. A first case of polio on US territory was detected in July 2013, shortly after the discovery of cases in London and Jerusalem. Genetic studies suggested that the American and Israeli viruses were imported from London, highlighting three regions previously thought to be free of the disease. In 2014, during the usual period of low virus circulation, dissemination occurred in several regions: Central Asia, the Middle East, and Central Africa, with virus circulation affecting a total of 10 countries. The WHO deemed this risk a public health emergency of international concern and issued specific recommendations.
In August 2020, the WHO announced the eradication of wild poliovirus in Africa, with Nigeria having no cases for four years. Only two countries still reported wild virus infections: Afghanistan (29 cases) and Pakistan (58 cases). However, over 200 cases caused by a vaccine-derived virus occurred in Africa in 2019-2020, including those reported in Sudan in August 2020. The WHO indicated that at this point, a budget of $19 billion had been committed to the eradication program over 30 years.
Nevertheless, on April 2, 2020, the leadership of The Global Polio Eradication Initiative announced a pause in its vaccination activities for several months to prioritize resources for the fight against COVID-19 in affected countries. Only critical polio control functions, namely surveillance and vaccine management, were maintained. Some argue that this pursuit of eradication is disproportionately costly and comes at the expense of other interventions, such as general health improvements, that would yield better benefits.
In September 2022, the spread of the virus necessitated declaring a state of emergency in upstate New York to curb the epidemic that had been ongoing since 2013. In France, on March 30, 2023, for diphtheria, tetanus, and polio, the High Authority of Health recommended that DTP vaccination no longer be mandatory for healthcare professionals but strongly recommended, except in Mayotte where it should remain mandatory. On the same day, the Minister of Health and Prevention announced immediate compliance with this recommendation.
Poliomyelitis is caused by polioviruses, which are RNA viruses belonging to the Enterovirus genus within the Picornaviridae family. They resemble the Hepatitis A virus in size and family, sharing similar properties and a tropism for the intestines, with transmission occurring through the mouth. Humans are the sole reservoir for the virus. Polioviruses have a preferential tropism for the digestive tract. Their structure is very simple, comprising a positive-sense RNA genome surrounded by a capsid. The capsid protects the genetic material and enables the virus to infect certain cell types.
Three serotypes of poliovirus have been identified: poliovirus type 1 (PV1), type 2 (PV2), and type 3 (PV3), each differing slightly in their capsid proteins. All three are extremely virulent and produce the same symptoms. PV1 is the most frequently encountered form and is most often associated with paralysis. In rare circumstances, poliomyelitis can arise from infections caused by enteroviruses other than polioviruses. Although it can survive in aqueous environments, poliovirus, like all viruses, requires living cells for multiplication; in the external environment, without hosts to replicate in, it is destined to disappear within a few months.
Polio is highly contagious and easily transmitted through human-to-human contact. In epidemic zones, wild poliovirus strains are theoretically capable of infecting the entire human population. Transmission is typically seasonal in temperate climates, with a peak in summer and autumn, though these seasonal variations are much less pronounced in tropical climates. The incubation period, separating initial exposure from the first symptoms, is usually between six and twenty days, with extremes ranging from three to thirty-five days. Viral particles are shed in feces for several weeks after initial infection.
Therefore, disease transmission is primarily fecal-oral, via the ingestion of contaminated food or water. Occasionally, the disease can be transmitted oro-orally through saliva, a route that seems predominant in areas with high hygiene levels. Transmission can also occur through respiratory secretions, such as droplets from coughing or sneezing, from an infected person as they shed the virus in nasopharyngeal secretions during the initial days of infection. Contagiousness is highest between seven to ten days before and seven to ten days after symptom onset, but transmission is possible as long as the virus persists in saliva and feces.
Factors that increase infection risk or adversely affect disease severity have included immunodeficiency, malnutrition, tonsillectomy, physical activity immediately following paralysis onset, intramuscular injection of vaccines or medications, and pregnancy. Although the virus crosses the placenta during pregnancy, the fetus appears unaffected by maternal infection or vaccination. Maternal antibodies also cross the placental barrier, providing passive protective immunity to the fetus during pregnancy and the first months of life.
The poliovirus enters the body through the mouth and infects the initial cells it contacts in the pharynx and then the intestinal lining. It infects cells via a transmembrane glycoprotein belonging to the immunoglobulin family, located on the cell surface, known as the CD155 or poliovirus receptor. The virus then takes control of the host cell's genetic processes and begins replication. Poliovirus multiplies within gastrointestinal cells for about a week, then migrates to the tonsils, intestinal lymphoid tissue, and cervical and mesenteric lymph nodes, where it actively replicates. It can then enter the bloodstream.
This phase of blood circulation of the virus, or viremia, allows its distribution to various sites in the body. Poliovirus can survive and multiply in the blood and lymph for extended periods, sometimes up to 17 weeks. Viremia is responsible for the flu-like syndrome generally observed in the initial phase of symptomatic poliovirus infections. In a small proportion of cases, it can migrate and replicate in adipose tissue, the mononuclear phagocyte system, and muscles. The virus's passage into the central nervous system triggers a local inflammatory response. In most cases, this is limited to the meninges, defining a non-paralytic aseptic meningitis. Infection of the cerebral parenchyma defines acute encephalitis.
The mechanism by which poliovirus infects the central nervous system was not fully elucidated as of 2005, but it appears independent of the subject's age, sex, or socioeconomic status. Exposure to the virus, either through infection or vaccination, confers immunity. In immunized individuals, IgA antibodies are secreted in the tonsils and digestive mucosa, capable of blocking viral replication. IgG and IgM antibodies are protective against motoneuron damage. Infection or vaccination by one poliovirus serotype does not confer immunity against the other two; complete immunity thus requires exposure to each serotype.
Polio primarily affects children, without distinction of sex. Among adults, immunocompromised individuals are also at risk. It is generally accepted that in temperate climates, polio occurs most often in summer, while in tropical climates, there is no seasonal variability. However, other sources suggest two polio transmission peaks in Africa, from February to May and August to November, with the latter being more significant; in temperate countries, transmission is reportedly higher in winter. Regarding mortality, for paralytic polio, it is higher in adults, estimated at 15-30%, compared to 2-5% in children. For the bulbar form, the rate is higher than for the paralytic form, estimated around 25-75%.
In the Americas, polio (wild virus) was officially declared eradicated in 1994, followed by the Western Pacific in 2000, Europe in 2002, South-East Asia and India in 2014, and Africa in 2020. It now persists only in Pakistan and Afghanistan. In France, the last indigenous polio case dates back to 1989, and the last imported case was declared in 1995. Wild virus type 2 was certified eradicated in 2015 (last case in 1999), and wild type 3 in 2019 (last case in 2012). Thus, type 1 virus is the only wild virus type still in circulation. However, with the decline in wild virus cases, vaccine-derived virus cases have become the majority. In 2018, 33 global wild virus cases were reported (21 in Afghanistan and 12 in Pakistan), and 104 vaccine-derived cases (77 in Africa and 27 in Asia).
In 2019, there were 176 wild virus cases, 29 in Afghanistan and 147 in Pakistan, and 378 vaccine-derived cases in 19 countries. In 2020, there were 140 wild virus cases, 56 in Afghanistan and 84 in Pakistan, and 1,039 vaccine-derived cases in 26 countries, mostly in Africa. For most immunocompetent individuals, poliovirus infection remains asymptomatic, as neutralizing antibodies secreted in the digestive tract provide protection against the virus. The term "poliomyelitis" refers to a symptomatic infection caused indiscriminately by the three poliovirus serotypes. Two main forms of symptomatic infection are described: an extra-neurological form, sometimes called "abortive poliomyelitis" (97% of cases), which usually has a favorable outcome, and a neurological form involving the central nervous system (about 3% of cases), which can be paralytic or non-paralytic.
In the extra-neurological forms, if the virus crosses the digestive barrier, the infection manifests as minor, non-specific general symptoms ranging from respiratory tract infections (sore throat, cough, fever) to digestive signs (nausea, vomiting, abdominal pain, constipation, or rarely diarrhea), and flu-like symptoms. Myocarditis and pericarditis are possible and sometimes associated.
In about 3% of cases, the virus reaches the central nervous system. Among these, a majority develop a febrile meningeal syndrome (headaches, neck and back pain, fever, nausea, vomiting, lethargy), indicating aseptic meningitis with clear cerebrospinal fluid, which usually resolves favorably. Paralysis is typically absent in these cases. Encephalitic forms are rare and occur almost exclusively in infants, accompanied by high fever, behavioral changes, generalized seizures, and spastic paralysis. Isolated peripheral facial paralysis is also possible.
De-innervation of skeletal muscle tissue secondary to poliovirus infection can lead to paralysis. Between 1 in 200 and 1 in 1,000 individuals progress to paralytic disease, characterized by increasing muscle weakness culminating in complete paralysis. After incubation, the disease presents as a non-specific febrile infectious syndrome (pharyngitis, digestive disturbances), followed by the rapid onset of flaccid paralysis within hours, with no sensory involvement. The involvement is always asymmetrical. The poliovirus migrates along nerve pathways and reaches the motoneurons in the anterior horn of the spinal cord, brainstem, or motor cortex, where it replicates and destroys them.
The resulting paralysis defines paralytic poliomyelitis, with its various forms (spinal, bulbar, spinobulbar) differing in the extent of damage to motoneurons, subsequent inflammation, and the affected regions of the central nervous system. Lesions extend to the spinal ganglion, sometimes the reticular formation, vestibular nuclei, cerebellar vermis, and basal ganglia. Inflammation associated with neuronal destruction often alters the color and appearance of the spinal cord's gray matter, rendering it reddish and swollen. Lesions of the forebrain are also associated with paralytic poliomyelitis, particularly affecting the thalamus and hypothalamus.
In 2008, the molecular mechanisms leading to paralysis remained poorly understood. The propensity to develop paralytic poliomyelitis increases with age, as does the risk of widespread paralysis. In children, non-paralytic meningitis is the most common consequence of central nervous system infection. Paralysis occurs in only about 1 in 1,000 cases, and before the age of five, it typically affects only one lower limb. In adults, paralysis occurs in about 1 in 75 cases. It more readily affects the muscles of the thorax and abdomen, or even all four limbs (quadriplegia). The rate of paralysis also varies by viral serotype, with PV1 being the most frequent cause (1 in 200 cases), followed by PV3 and PV2 (1 in 2,000 cases).
Acute anterior poliomyelitis manifests with early symptoms that combine high fever, headaches, neck and back stiffness, muscle pain, asymmetrical muscle weakness, tenderness to touch, swallowing difficulties, disappearance of deep tendon reflexes, paresthesias, irritability, and constipation, and urinary difficulties. Paralysis generally occurs one to ten days after symptom onset, progresses for two or three days, and ceases to spread as the fever subsides.
Spinal polio is the most common form of paralytic poliomyelitis. It results from the poliovirus invading the motoneurons in the anterior horn of the spinal cord (the ventral part of the gray matter), which transmit motor commands and are responsible for movement. Spinal motor nerves innervate the muscles of the trunk, including the intercostal muscles and diaphragm, and the limbs. Viral infection causes inflammation of the nerve cells, leading to partial or complete destruction of the motoneuron cell body. The death of motoneurons causes their Wallerian degeneration. Muscle cells, no longer receiving signals from the motor cortex or spinal cord, atrophy, weaken, and rapidly become inactive.
The partial or complete destruction of a muscle's innervation determines the intensity of its paralysis. The progression to maximal paralysis is rapid, usually over two to four days, and is generally accompanied by fever and muscle pain. Since the deep tendon reflex arc is interrupted, these reflexes are abolished. Conversely, the integrity of sensory nerves preserves somatosensory function. The distribution of spinal paralysis depends on the affected spinal cord segment, which can be cervical, thoracic, lumbar, or a combination. The involvement can be bilateral but is always asymmetrical. Paralysis is often more pronounced in proximal muscles (closer to the limb's root) than in distal muscles (fingers and toes).
Bulbar polio accounts for 2% of paralytic polio cases. It results from the poliovirus invading and destroying the motoneurons in the bulbar region of the brainstem, leading to paralysis of muscles innervated by cranial nerves, signs of encephalitis, respiratory difficulties, and problems with speech and swallowing. The three most critical cranial nerves involved are the glossopharyngeal nerve (IX), controlling oropharyngeal movements and swallowing; the vagus nerve (X), playing a major role in phonation; and the accessory nerve (XI), innervating the sternocleidomastoid and trapezius muscles. Involvement of the trigeminal nerve (V) and facial nerve (VII) can lead to chewing difficulties and facial paralysis. Involvement of the oculomotor nerves (III and VI) results in double vision.
Spinobulbar polio, a combined form of the previous two, represents 19% of paralytic polio cases. It is sometimes referred to as "respiratory polio." The virus attacks the upper part of the cervical spinal cord (C2 to C5), leading to diaphragmatic paralysis due to phrenic nerve involvement. This formidable form can necessitate mechanical ventilation. It can also lead to limb paralysis, swallowing difficulties, and cardiac dysfunction.
Recovery is the norm in individuals with abortive poliomyelitis. In cases of aseptic meningitis, symptoms may persist for two to ten days, but the outcome is almost always favorable. In spinal polio, paralysis is permanent if the motor innervation of the muscle is completely destroyed. Damaged but surviving cells can regain some function four to six weeks after the initial signs. Half of patients with spinal polio recover completely, a quarter recover with moderate sequelae, and a quarter have severe disabilities. The degree of paralysis in the acute phase and residual paralysis appears proportional to the intensity of the viremia and inversely proportional to the level of immunity.
Spinal polio is rarely fatal. In the absence of respiratory support, forms accompanied by respiratory involvement evolve towards aspiration pneumonia and asphyxia. In total, 5 to 10% of paralytic poliomyelitis cases result in death due to paralysis of the respiratory muscles. Mortality rates vary by age: 2 to 5% of children and 15 to 30% of adults die from the disease. Bulbar polio is the most lethal, being constantly fatal without treatment and respiratory assistance, killing 25 to 75% of managed patients. Positive-pressure mechanical ventilation, the standard artificial ventilation method in 1994, reduces mortality to 15%.
Thirty to forty years after the acute phase of the disease, when their general condition has long been stabilized, patients may experience extreme fatigue, progressive muscle weakness, and joint pain. Sometimes these symptoms are accompanied by breathing difficulties or muscle atrophy. This is known as post-polio syndrome, first described by neurologists Jean-Martin Charcot and Fulgence Raymond in 1875, but only named in the 1980s. It is estimated to affect one in two survivors. In 2002, 55,000 people in France were reported to have polio sequelae, 700,000 in Europe, and over a million in the United States. Dr. Richard L. Bruno notes the similarity of post-polio syndrome to chronic fatigue syndrome, suggesting it may result from cerebral lesions related to a prior poliovirus or other viral infection.
Humans are the only known natural hosts in whom the virus causes disease, which enabled the consideration of an eradication program. While it was established as early as 1909 that certain species of monkeys could develop the disease after inoculation, it took time to determine not only the sensitivity of each monkey species to the virus and its different serotypes but also whether they could harbor the virus and be a source of contagion under natural conditions. This inventory was still ongoing in 1948. Monkeys and chimpanzees develop paralysis when the virus is inoculated into their brain or spinal cord. Chimpanzees and cynomolgus monkeys can be infected orally but rarely show clinical signs, though they can sometimes develop viremia and, in very rare cases, paralysis.
Paralytic poliomyelitis has been described in captive chimpanzees, orangutans, and gorillas, as well as in wild chimpanzees. However, these species are likely accidental hosts, and their wild populations are too small and geographically dispersed to sustain poliovirus transmission or pose a threat of reintroducing the virus to human populations once eradication is achieved. Rhesus monkeys (Macaca Mulatta) are among the rare species of monkeys that do not develop infection after ingesting poliovirus, as it simply does not replicate in their digestive system. Flexner's defense of his erroneous neurotropism hypothesis was largely based on his experiments with these rhesus monkeys.
Serums neutralizing poliovirus have been found in other vertebrates, such as cows, horses, chickens, dogs, goats, and sheep, but without signs of infection. Analysis of cerebrospinal fluid (CSF) obtained by lumbar puncture typically reveals clear fluid, moderate to predominantly lymphocytic pleocytosis (increased cell count), normal glucose (glycorachia), and normal or moderately increased protein levels (proteinorachia), indicating aseptic meningitis. Repeat examination 15 days later generally shows a decrease in cell count and an increase in protein. However, lumbar puncture is not without risks, especially during an established epidemic.
Polio serology is sensitive and early, but definitive diagnosis requires direct demonstration of the poliovirus from a pharyngeal swab, stool, or CSF. This is performed exceptionally in endemic areas due to cost and lack of necessity, but it is essential in cases of doubt, especially in regions where the disease has disappeared. Identifying viral genetic material by polymerase chain reaction also allows for distinguishing between wild and vaccine strains used in oral vaccination. This distinction is important because for every reported case of paralytic poliomyelitis, it is estimated that there are 200 to 3,000 other asymptomatic but contagious cases.
Differential diagnosis is challenging in non-paralytic forms, as the disease is often mistaken for a common nasopharyngeal or digestive infection. When a meningeal syndrome is present, it resembles other viral meningitis. Paralytic poliomyelitis is clinically suspected based on the acute onset of flaccid paralysis in one or more limbs with diminished or absent deep tendon reflexes, without sensory loss or cognitive impairment. Other clinical features of acute flaccid paralysis that might suggest polio include asymmetry, rapid progression, association with fever, and the occurrence of sequelae. The diagnosis is easily evoked in indigenous populations of endemic areas but less so in non-immunized travelers.
Diagnosing polio requires excluding other causes, particularly inflammatory conditions like Guillain-Barré syndrome or acute transverse myelitis, or mechanical causes like spinal cord or nerve root compression, or injury from intramuscular injection. Other enterovirus types can also cause polio-like paralysis, as can arboviruses such as West Nile virus. Bacterial diseases like diphtheria or botulism should also be considered. Other potential diagnoses include Kugelberg-Welander syndrome or myotonic dystrophy.
There is no curative treatment for polio. Extra-neurological forms and aseptic meningitis, once diagnosed, only require symptomatic management. In cases of paralytic poliomyelitis, therapeutic goals focus on alleviating symptoms, accelerating recovery, and preventing complications. Treatment includes analgesics for pain, antibiotics for bacterial superinfections, moderate physical exercise, and an adapted diet. The treatment often necessitates prolonged convalescence with physical rehabilitation, the use of orthoses, orthopedic footwear, mobility aids like wheelchairs or canes, and, in some cases, orthopedic surgery.
Non-specific prevention relies primarily on adherence to food hygiene rules and hand cleanliness. Vaccination constitutes the only specific means of prevention. In France, mandatory polio vaccination was instituted by law in 1964. Two antipolio vaccines are available: one inactivated, administered by subcutaneous or intramuscular injection, and one live attenuated, administered orally. Both provide effective immunity against poliovirus infection, but the live attenuated vaccine offers better gut immunity.
The inactivated polio vaccine (IPV), developed in 1952 by Jonas Salk's team and announced in 1955, is made from polioviruses cultured in simian cell lines, then chemically inactivated by formaldehyde. It confers protective immunity in 90% of subjects after two injections and over 99% after three injections. It is trivalent, protecting against all three poliovirus strains (PV1, PV2, and PV3). It can be administered as early as six weeks of age. This vaccine essentially induces serum immunity but little to no local immunity, thus having a limited effect on intestinal multiplication, virus excretion, and the potential number of virus carriers.
Although IPV requires booster injections and is more costly than the live attenuated vaccine, it is still used because the oral vaccine may not suffice under certain conditions. Despite its limited local immunity induction, IPV has been capable of eliminating polio in industrialized countries that exclusively used it, such as the Netherlands, Sweden, and Finland. IPV is recommended for imminent risk of exposure to poliovirus as a first-line measure, not for combating an outbreak.
The injectable vaccine is contraindicated in cases of allergy to any of its constituents and not recommended during intercurrent infections. Adverse effects include localized reactions at the injection site, such as pain, swelling, or redness. According to the National Academy of Medicine, no serious adverse events have been associated with the vaccine. The oral polio vaccine (OPV), developed in 1957 by Albert Sabin, uses a live but attenuated poliovirus, weakened through repeated passage in non-human cells at sub-physiological temperatures.
It was tested from 1957 and authorized in 1962. Administered orally, it mimics a mild intestinal infection and stimulates the active synthesis of protective antibodies by the digestive barrier. Monovalent oral polio vaccines (mOPV) are specific against wild poliovirus types 1 (mOPV1), 2 (mOPV2), and 3 (mOPV3). The trivalent oral polio vaccine (tOPV), against all three wild poliovirus types, has efficacy comparable to the attenuated OPV (95% protection after three doses) and can be administered from birth. Inexpensive, effective, and easy to administer, the oral vaccine is best suited for mass vaccination and is most widely used globally, particularly in developing countries. Viral interference phenomena are sometimes responsible for failures.
The bivalent oral polio vaccine (bOPV), against serotypes 1 and 3, based on WHO data in 2009, yields similar results to mOPV but is more effective than tOPV against these two virus types. Contraindications for OPV, like any live vaccine, include immunodeficiency and pregnancy. Rare cases of vaccine-associated paralytic polio can occur in vaccinated individuals or their close contacts. Furthermore, viruses derived from vaccine strains (VDPVs) can emerge in areas with low vaccination coverage. These can cause epidemics (circulating VDPV - cVDPV) or persist long-term in individuals with B-lymphocyte immunodeficiency (iVDPV). Isolated cases without an immunodeficiency context (ambiguous VDPV - aVDPV) are also identified.
Thus, in 2013, cVDPV was found in 117 cases and 27 contacts across 7 countries; iVDPV affected 10 new individuals in 8 countries, while aVDPV was found in 11 people in 13 countries. These cases are relatively rare; between 2005 and 2015, there were nearly 500 cases of paralysis among 2.5 billion vaccinated children. Detection of these strains typically necessitates intensification of vaccination campaigns. The majority of cases are linked to the type 2-derived virus (VDPV2). Therefore, the WHO plans to remove this valence from the vaccine, especially since the last detected case of wild poliovirus type 2 was in 1999. A prerequisite, however, would be the cessation of the derived strain's circulation. In the interim, to reduce risk, another option is to replace one dose of OPV with a dose of IPV.
In endemic countries, the trivalent oral vaccine has not been used since April-May 2016 and has been replaced by the bivalent oral vaccine (types 1 and 3), which is planned for discontinuation in 2019-2020. The WHO proposes a universal transition to the inactivated injectable vaccine (at least one dose, intramuscularly or intradermally). As of August 31, 2016, 173 out of 194 WHO member states (89%) used the injectable polio vaccine. In 2020, the WHO still recommends that all children worldwide be vaccinated, even though wild polio virus only circulates in Afghanistan and Pakistan. It justifies this position by stating that as long as all strains are not eradicated globally, the incredible progress made against polio will remain threatened.
The Roman Emperor Claudius was considered by mid-20th-century authors to have had polio, but given he showed no deformity, he likely suffered from cerebral palsy. The writer Walter Scott probably contracted polio at age two, experiencing a severe fever during teething that left him with weakness in his right leg. US President Franklin Delano Roosevelt believed he contracted it in 1921, but it is more probable he suffered from Guillain-Barré syndrome. Others include musician Neil Young, painter Frida Kahlo, violinist Itzhak Perlman, writer Arthur C. Clarke, filmmaker Francis Ford Coppola, actress Mia Farrow, actor Jean Lefebvre, French author and cartoonist Charlie Schlingo, businessman Franklin Clarence Mars, golfer Jack Nicklaus, likely Pharaoh Siptah of the 19th Dynasty, American athlete Wilma Rudolph, Albert Craig, Cecil Spence, and Lascele Bulgin of the reggae trio Israel Vibration, hip-hop dancer Junior Bosila Banya, June Middleton, who lived 60 years in an iron lung, prima ballerina Tanaquil Le Clercq, whose career was interrupted at 27 by the disease.
The analysis of cerebrospinal fluid collected by lumbar puncture typically reveals clear fluid, moderate to predominantly lymphocytic pleocytosis, normal glucose and protein levels, indicating aseptic meningitis. Repeat examination 15 days later usually shows a decrease in cell count and an increase in protein. However, lumbar puncture is not without risk, particularly during an established epidemic. Polio serology is sensitive and early, but definitive diagnosis requires direct isolation of poliovirus from pharyngeal swabs, feces, or CSF. This is performed exceptionally in endemic areas due to cost and lack of necessity, but it is essential in cases of doubt, especially in regions where the disease has disappeared. Identifying viral genetic material by polymerase chain reaction also allows for distinguishing between wild and vaccine strains.
This distinction is important because for every reported case of paralytic poliomyelitis, it's estimated there are 200 to 3,000 other asymptomatic but contagious cases. Differential diagnosis is challenging in non-paralytic forms, often mistaken for common upper respiratory or digestive infections. When a meningeal syndrome is present, it resembles other viral meningitis. Paralytic poliomyelitis is clinically suspected with the acute onset of flaccid paralysis in one or more limbs, with diminished or absent deep tendon reflexes, and no sensory impairment or cognitive disorder.
Other clinical features suggestive of polio in acute flaccid paralysis include asymmetry, rapid progression, association with fever, and the occurrence of sequelae. The diagnosis is readily considered in indigenous populations of endemic areas, but less so in non-immunized travelers. Diagnosing polio necessitates ruling out other causes, particularly inflammatory conditions like Guillain-Barré syndrome or acute transverse myelitis, or mechanical causes like spinal cord or nerve root compression, or injury from intramuscular injection. Other enterovirus types can also cause polio-like paralysis, as can arboviruses like West Nile virus. Bacterial diseases like diphtheria or botulism should also be considered. Other potential diagnoses include Kugelberg-Welander syndrome or myotonic dystrophy.
There is no curative treatment for poliomyelitis. Extra-neurological forms and aseptic meningitis, once diagnosed, only require symptomatic management. In cases of paralytic poliomyelitis, therapeutic goals focus on alleviating symptoms, accelerating recovery, and preventing complications. Treatment includes analgesics for pain, antibiotics for bacterial superinfections, moderate physical exercise, and an adapted diet. The treatment often necessitates prolonged convalescence with physical rehabilitation, the use of orthoses, orthopedic footwear, mobility aids like wheelchairs or canes, and, in some cases, orthopedic surgery.
Non-specific prevention relies primarily on adherence to food hygiene rules and hand cleanliness. Vaccination constitutes the only specific means of prevention. In France, mandatory polio vaccination was instituted by law in 1964. Two antipolio vaccines are available: one inactivated, administered by subcutaneous or intramuscular injection, and one live attenuated, administered orally. Both provide effective immunity against poliovirus infection, but the live attenuated vaccine offers better gut immunity.
The inactivated polio vaccine (IPV), developed in 1952 by Jonas Salk's team and announced in 1955, is made from polioviruses cultured in simian cell lines, then chemically inactivated by formaldehyde. It confers protective immunity in 90% of subjects after two injections and over 99% after three injections. It is trivalent, protecting against all three poliovirus strains (PV1, PV2, and PV3). It can be administered as early as six weeks of age. This vaccine essentially induces serum immunity but little to no local immunity, thus having a limited effect on intestinal multiplication, virus excretion, and the potential number of virus carriers.
Although IPV requires booster injections and is more costly than the live attenuated vaccine, it is still used because the oral vaccine may not suffice under certain conditions. Despite its limited local immunity induction, IPV has been capable of eliminating polio in industrialized countries that exclusively used it, such as the Netherlands, Sweden, and Finland. IPV is recommended for imminent risk of exposure to poliovirus as a first-line measure, not for combating an outbreak. The injectable vaccine is contraindicated in cases of allergy to any of its constituents and not recommended during intercurrent infections. Adverse effects include localized reactions at the injection site, such as pain, swelling, or redness. According to the National Academy of Medicine, no serious adverse events have been associated with the vaccine.
The oral polio vaccine (OPV), developed in 1957 by Albert Sabin, uses a live but attenuated poliovirus, weakened through repeated passage in non-human cells at sub-physiological temperatures. It was tested from 1957 and authorized in 1962. Administered orally, it mimics a mild intestinal infection and stimulates the active synthesis of protective antibodies by the digestive barrier. Monovalent oral polio vaccines (mOPV) are specific against wild poliovirus types 1 (mOPV1), 2 (mOPV2), and 3 (mOPV3). The trivalent oral polio vaccine (tOPV), against all three wild poliovirus types, has efficacy comparable to the attenuated OPV (95% protection after three doses) and can be administered from birth. Inexpensive, effective, and easy to administer, the oral vaccine is best suited for mass vaccination and is most widely used globally, particularly in developing countries. Viral interference phenomena are sometimes responsible for failures.
The bivalent oral polio vaccine (bOPV), against serotypes 1 and 3, based on WHO data in 2009, yields similar results to mOPV but is more effective than tOPV against these two virus types. Contraindications for OPV, like any live vaccine, include immunodeficiency and pregnancy. Rare cases of vaccine-associated paralytic polio can occur in vaccinated individuals or their close contacts. Furthermore, viruses derived from vaccine strains (VDPVs) can emerge in areas with low vaccination coverage. These can cause epidemics (circulating VDPV - cVDPV) or persist long-term in individuals with B-lymphocyte immunodeficiency (iVDPV). Isolated cases without an immunodeficiency context (ambiguous VDPV - aVDPV) are also identified.
Thus, in 2013, cVDPV was found in 117 cases and 27 contacts across 7 countries; iVDPV affected 10 new individuals in 8 countries, while aVDPV was found in 11 people in 13 countries. These cases are relatively rare; between 2005 and 2015, there were nearly 500 cases of paralysis among 2.5 billion vaccinated children. Detection of these strains typically necessitates intensification of vaccination campaigns. The majority of cases are linked to the type 2-derived virus (VDPV2). Therefore, the WHO plans to remove this valence from the vaccine, especially since the last detected case of wild poliovirus type 2 was in 1999. A prerequisite, however, would be the cessation of the derived strain's circulation. In the interim, to reduce risk, another option is to replace one dose of OPV with a dose of IPV.
In endemic countries, the trivalent oral vaccine has not been used since April-May 2016 and has been replaced by the bivalent oral vaccine (types 1 and 3), which is planned for discontinuation in 2019-2020. The WHO proposes a universal transition to the inactivated injectable vaccine (at least one dose, intramuscularly or intradermally). As of August 31, 2016, 173 out of 194 WHO member states (89%) used the injectable polio vaccine. In 2020, the WHO still recommends that all children worldwide be vaccinated, even though wild polio virus only circulates in Afghanistan and Pakistan. It justifies this position by stating that as long as all strains are not eradicated globally, the incredible progress made against polio will remain threatened.
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