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What is the history of Polio in America and other countries?

Updated August 15, 2022


The first documented cases of what is now believed to be poliomyelitis was recorded in 1789 by British physician Michael Underwood.   Underwood described polio as “…the debility of the lower extremities which gradually become more infirm, and after a few weeks are unable to support the body  and noted that it was not a common disorder.

In 1834, the first outbreak of paralysis was reported on the South Atlantic island of St. Helena and one year later, John Badham described the onset of acute paralysis affecting four English children.     Five years later, Jacob von Heine published an analysis of unique form of paralysis and referred to it as infantile paralysis. Later, in 1890, Swedish physician Medin would report on epidemics of paralysis and for a brief period, the disease would be known as Heine-Medin disease.  

The first outbreak of polio in the U.S. occurred in 1841 in Feliciana, Louisiana and caused paralysis in 10 children.   This outbreak was referred to as ‘teething paralysis’ as it had affected children under the age of 2, all of whom eventually improved or recovered. 

In 1855, French physician Duchenne reported that polio impacted the anterior horn cells of the spinal column. His findings were also supported by Charcot and Joffroy, who discovered atrophy of the anterior horns in the grey matter of the spinal cord.    The term “acute anterior poliomyelitis” was first introduced by Erb in 1875.

Sporadic outbreaks of paralysis were reported in Sweden and Norway during the latter part of the 19th century but the U.S. would not report an outbreak until 1893, when 26 cases were reported in Boston, Massachusetts. One year later, a larger outbreak of 132 cases occurred in Vermont, with 18 reported deaths. The outbreak in Vermont affected more than just humans as there were reports of paralysis occurring in dogs, horses, and fowls.   

It was during this outbreak that Dr. Charles Caverly discovered that there were likely two forms of polio – paralytic and nonparalytic (abortive). Unlike those who developed paralytic polio, persons who developed abortive polio had a mild illness but recovered fully and quicky. Caverly also stated that the term ‘infantile paralysis’ was inaccurate, as most who developed the disease were children, not infants. He also believed that the illness was not especially contagious because the disease rarely affected more than one person within a household. Males were much more affected than females which led Caverly to suggest that activities which might lower a person’s ability to fight off disease - such as playing hard on a hot day or chilling the body when it was heated – might be responsible for causing the disease.

In 1905, Sweden experienced an epidemic of polio with twelve-hundred reported cases. After extensive investigation, Swedish pediatrician Dr. Ivar Wickman, declared that polio was contagious and could be spread by people who did not realize that they were infected.

The cause of polio was not yet known as microscopes were not strong enough to detect the virus. However, this changed in 1908 when Karl Landsteiner created an emulsion derived from the spinal cord of a boy who had succumb to the disease and injected it into the stomach of two rhesus monkeys – who both died from the disease. The spinal cords of both monkeys showed similar damage to that of the boy who had died.  Landsteiner’s experiment proved that a virus was responsible for disease and he has been credited for isolating the poliovirus.   

At the beginning of the 20th century, cases of polio began increasing in both the U.S. and abroad. In a public health report published in 1910, the rate of polio was found to have increased significantly in the U.S. between 1907 and 1909. In 1907, most polio cases occurred in and around New York City; however, in 1908 and 1909, outbreaks were reported in other states. In 1910, the rate of polio was not considered alarming when compared with other infectious diseases and the mortality rate was considered low at between 10 and 15 percent. It was noted, however, that most people who developed polio would be permanently disabled. 

In this 1910 report, public health officials noted that medical researchers had found that the disease could be transmitted from humans to monkeys and from monkey to monkey, but that transmission between animals other than monkeys had not been widely observed by most researchers - except that a few researchers had observed it among rabbits. This report also noted the paralysis that had occurred among dogs, horses, and fowl during the Vermont epidemic in 1894, but concluded that cases of “paralysis in animals did not correspond to the distribution of human poliomyelitis.”  In fact these same health officials went on to state that paralysis among domestic animals was a common occurrence at turn of the 20th century. 

In 1910, another polio outbreak occurred again in Vermont. And while most cases were still being reported in children, persons of all ages were being affected. In this outbreak, Dr. Charles Caverly reported that outbreaks of polio had also occurred again in animals, but this time in pigs and calves.  Humans are the only known carriers of the poliovirus,  and therefore it is reasonable to believe that these early epidemics of paralysis were not necessarily caused by the poliovirus.

In fact, one of the early pesticides used at the time was an arsenic based product frequently referred to as Paris Green or Schwein-Furth Green. By 1882, it was already known that exposure to arsenic, including the arsenic contained in these pesticides, could cause paralysis and lesions of the spinal cord in both humans and animals.  This product was widely used in the U.S. and initially used against the gypsy moth that had invaded Boston by the 1890’s.  However, when it was discovered that Paris Green could not be applied in “sufficient quantity to kill the caterpillars without seriously injuring the foliage”   a chemist with the Gypsy Moth Commission suggested that lead arsenate be used.   Coincidently, the first outbreak of paralysis in the U.S. in over 50 years occurred in Boston during this time. 

Paris Green would remain in use in the U.S. until the 1940s when it was replaced by synthetic organic insecticides, including dichlorodiphenyltrichloroethane or DDT. 

In a May 1912 article published in The Medical Times, Jacolyn Van Vliet Manning reported that “a close relationship between paralytic cases in man and animal during epidemics of poliomyelitis has been observed in nine Western states of the United States” as well as abroad, in Sweden, England, and Northwestern Germany. 

Also, in 1912, public health officials reported that polio was transmissible through the stable fly but that further investigations needed to be completed to determine whether the other modes of transmission occurred in nature.  However, by 1913, after additional experiments could not reproduce earlier findings, health officials reported that transmission likely occurred between ‘passive human carriers.’ 

Epidemiological studies conducted between 1910 and 1912 concluded that poliovirus exposure was likely common, but few people were affected enough to show signs of clinical disease. It was during the 1916 New York City polio epidemic that researchers realized that the disease could be spread asymptomatically. 

In 1916, health officials reported that the virus could be found in the secretions and tissues of a person who had died from the disease; in the secretions of an acutely ill individual; in the intestinal and nasopharyngeal secretions of a person recovering from the disease; and in the nasopharyngeal secretions of healthy individuals who had exposure to persons with the disease (carriers). Outside of the human body, the virus was reportedly found in the dust within the rooms of a person with disease. It was also believed that the virus could be spread through the respiratory system and digestive tract.  

As outbreaks of polio were being reported in many countries worldwide, under varying circumstances, and in both urban and rural settings, in 1916, public health officials reported that no set conditions were necessary for an epidemic to occur. They also noted that smaller towns or rural areas were usually more affected than larger ones within the same geographical region. Between 50 and 90 percent of cases occurred in children under the age of 5, but public health officials had no explanation for why children were primarily impacted - but suggested that this was because children were more susceptible to illness than adults. 

The 1916 polio epidemic originated in New York City and researchers have estimated that this epidemic paralyzed 27,000 individuals and caused 6,000 deaths. This number however, is not necessarily accurate because the reporting of polio cases to public health officials was not a requirement in 1916. It is also believed that some cases might have been missed because parents chose to keep their affected children at home out of fear of hospitals. Additionally, not all cases of polio treated in hospitals were paralytic, but as there were no reporting systems in place for polio, there were also no systems in place that differentiated between paralytic and non-paralytic polio.   

In addition to the high number of polio cases, the 1916 epidemic was also noted for its high fatality rates. In 1907, approximately 5 percent of reported cases were fatal, whereas in 1916, death rates were estimated to be as high as 25 percent. It is possible that treatment protocols for the disease may have led to high fatality rates because little was known about the disease, and treatments at the time varied between hospitals and practitioners. In hospitals, polio treatment options included: lumbar punctures, external and internal use of disinfectants, hydrogen peroxide nasal sprays, and administration of the tetanus and diphtheria antitoxins – in the belief that since poliomyelitis affected nerve cells, the antitoxins would block this from occurring. Adrenaline was also used and frequently injected into the spinal cord or given intramuscularly. Other treatments included intraspinal injections of quinine, urea hydrochloride, and even human serum. Many who were treated with these early protocols died, which likely contributed to the high fatality rate of the illness. 

A paper on the 1916 New York City epidemic published in 2011 has suggested that this epidemic may have been caused by the inadvertent release of the poliovirus from the Rockefeller laboratories, which was actively experimenting with the virus at the time.  The first cases of polio occurred only blocks away from the facility and the epidemic began in May – much earlier in the year than all previously reported epidemics of polio. 

This epidemic also prompted a push to increase sanitation in the immigrant areas of New York City, as it was widely believed that immigrants were the cause of the disease. Quarantines were enacted, and thousands of stray animals were killed for fear that they were responsible for the spread of the disease. Children leaving the city were required to get proof from the health department of being ‘polio-free’; however, many communities refused to allow newcomers to enter their towns. 

During this epidemic most people assumed that the poor living conditions were responsible for disease outbreak; however, this assumption was challenged when rates in affluent areas were found to be significantly higher than those found in poorer and more congested areas. This finding then led to the common belief that living in unsanitary conditions was protective against the disease and that individuals living in areas of poor sanitation were exposed to the virus at a young age and would therefore developed naturally immunity.    This, of course, directly contradicts the current belief on polio which reports the disease to be problematic in areas that lack proper hygiene and adequate sanitation. 

The exact number of polio cases that occurred prior to 1932 is not known. In August 1910, the U.S. Surgeon General requested that national reporting on the incidence of polio be completed and submitted, however many states did not comply. Public health officials only consider polio data collected from 1932 and later to be accurate. 

Former President Franklin D. Roosevelt, who was diagnosed with polio in August 1921, is credited with launching efforts aimed at learning more about the disease and for providing those afflicted with the financial support to cover disease-associated costs.

In 1924, Roosevelt first visited the declining resort of Warm Springs in Georgia at the suggestion of a friend, who told him of a young boy’s complete recovery that had occurred from swimming in the resort’s pools. Roosevelt’s experience prompted him to purchase the resort in 1926 and to start the Warm Springs Foundation - the first treatment center for polio in the world. 

This treatment center, however, was for whites only, which was the cultural norm during this time, especially in the South. In fact, for a decade, the scientific consensus was that blacks were not susceptible to polio. The reality was, however, that blacks, especially those living in the south, were neglected and nearly always subjected to medical racism. The few health care professionals who were even available to black families lacked the training needed to adequately diagnose polio symptoms. 

The first large-scale fundraising event for polio occurred in 1934, with the launching of the annual Birthday Ball campaign that would be held on Roosevelt’s birthday – January 30th – to raise funds for his Warm Springs Foundation. Within a few years, the money raised through the balls would no longer be sent to Warm Springs but would remain in the local communities to help pay the medical costs of those affected by polio.

Eventually, the association between the Birthday Balls and President Roosevelt became a sore point for persons who disagreed with the President’s politics. Articles critical of the fundraising efforts soon appeared in the media, and this led Roosevelt to form the National Foundation for Infantile Paralysis in 1938, as a nonpartisan organization focused on generating financial support for research and treatment of polio. This foundation would eventually become known as The March of Dimes, when a highly successful fundraising campaign was launched to encourage people to mail their dimes to the White House to support those affected by polio. This fundraiser netted the organization millions of dollars and the dime quickly became the fundraising symbol of polio. 

In addition to the criticism surrounding the Birthday Balls, the ‘whites only’ policy enforced at Warm Springs had also become an issue. At least $100,000 had been raised by the black community for the Warm Springs Foundation - and yet blacks were not permitted to receive treatment at the facility.

It would be 1941 before the black community would have a treatment center available for polio. In January of 1941, the Tuskegee Infantile Paralysis Center opened its doors on the campus of the Tuskegee Institute. The facility, however, was limited to 36 beds and most who sought treatment would be denied care. 

Some researchers now believe that President Roosevelt may not have had polio but rather Guillain-Barre Syndrome (GBS), as his reported symptoms were more aligned with this diagnosis.       While it will never be known for certain what caused Roosevelt’s paralysis, history will remember him as the person who launched the efforts to stop this rare, but terrifying disease.

One of the earliest polio treatment modalities was the iron lung, an airtight coffin-like tank that could force the diaphragm to contract and expand, invented by two researchers from Harvard University in 1929.  The idea behind the invention was to help sustain the life of someone with respiratory difficulties until they could resume breathing on their own. Though widely associated with polio, these machines were also used for other respiratory disorders including gas asphyxiation and severe pneumonia. Iron lungs have since evolved and are now referred to as ventilators. They are frequently used in both hospitals and home settings, to sustain the life of individuals with complex medical conditions who require assistance with breathing.   

Vaccine development was also underway in the 1930s, however, the experimental vaccines used were found to be both ineffective and harmful. 

In the mid-1930s, an experimental nose spray containing picric acid, a highly toxic and explosive chemical compound,     was developed for use as a polio preventative. In the early part of the 20th century, many in the scientific community believed that polio entered the body through the nose and directly impacted the brain and nervous system.    The use of the nose spray was an attempt to stop paralysis by preventing the virus from entering the brain and nervous system. Clinical trials of a nasal spray containing a combination of picric acid and aluminum sulphate were conducted in Alabama, but the formulation was found to be ineffective.   

Zinc sulfate, another experimental chemical, was sprayed intranasally during an outbreak in Toronto in the late 1930s, but like picric acid, it was not effective, and several children who received the spray permanently lost their sense of smell.    It took researchers until 1941 to confirm that the poliovirus rarely entered the body through the nasal passages, but rather through the nasopharynx and digestive tract. 

In the 30s and early 40s, the standard treatment of paralytic polio in the U.S. was for doctors to immobilize the affected limbs in splints or plaster for weeks to months and to ensure constant rest and joint restrictions. While this treatment was not scientifically supported, it was widely accepted as the standard of care at the time.    The lengthy limb immobilization would frequently result in the need for orthopedic surgical procedures which included contracture release and tendon transfers.  

In Australia, however, new treatment protocols were being employed that would challenge the orthodoxy. In 1911, Sister Elizabeth Kenny, a woman from the Australian Outback with no formal nursing training but experience as care provider in the remote areas encountered infantile paralysis for the first time in children living in the communities that she served. Kenny, who had no knowledge of the condition, applied therapies used at the time to treat injured limbs – gentle movements of the affected limbs and warm poultices.  All 6 children who had developed paralysis and received care from Kenny recovered from the disease. 

Her techniques were not well received by many, both in Australia, and abroad. While some embraced her new therapeutic model, others were highly critical and considered them to be ineffective. Kenny came to the U.S. in 1940 to share her methods with the National Foundation for Infantile Paralysis but she did not receive a warm welcome. Instead, she was provided with a copy of the 1939 Public Health Bulletin entitled Care During the Recovery Period in Paralytic Poliomyelitis, which endorsed the need for long periods of rest and immobilization though splinting as the treatment for paralytic polio. 

After being dismissed by the Foundation, Kenny traveled to Chicago to meet with the American Medical Association’s Council on Physical Therapy but again, her unconventional methods did not impress officials. Her last attempt to introduce her therapy modules in the U.S., however would be successful. At the prompting of her daughter, Kenny would travel to Minnesota where she would be afforded the opportunity to demonstrate her methods of using heat and gentle range of motion exercises at the Minnesota General Hospital. Her techniques proved to be highly effective and many initial skeptics became huge supporters of her methods. 

Though her methods would eventually be recognized in the media and by some in the medical community as revolutionary, her strong personality and ego would keep many from supporting her efforts.  Her clinic and the Sister Kenny Foundation, under the leadership of Dr. Frank Krusen, one of her earliest supporters, would remain a leader in rehabilitative medicine for many years. 

Between 1933 and 1942, polio rates fluctuated, with the highest number of reported cases occurring in 1935 (10,839) with an incidence rate of 8.5 per 100,000 population, and the lowest occurring in 1938 (1,705) with an incidence rate of 1.3 per 100,000 population.     Death rates from polio were highest in 1940 (1,004) and lowest in 1938 (478). Public health officials also reported that several of the states who reported a large ratio of cases to death “also reported a fairly large proportion of nonparalytic cases.”   While public health officials were able to report that a total of 69,451 cases and approximately 7,800 polio deaths had occurred during this 10-year period, they were still not differentiating between paralytic and nonparalytic polio. 

Age distribution of polio also varied between states. Some states reported the highest number of cases among children under five years of age while others reported that the disease was prevalent among all age demographics, though less often seen among persons 20 years of age and older. 

By 1943, public health experts were reporting that the poliovirus “Infection seldom occurs by way of the olfactory tract but mainly through mucous membrane of the pharyngeal or the lower gastrointestinal tract, or both.”  It was, however, not conclusively known how the infection was transmitted from person to person. Some researchers believed that the infection was water-borne as it had been found in the sewage, and epidemics were nearly exclusive to the summer months. They also reported that there was no convincing evidence that the infection was spread by insects or that animals were reservoirs of the virus. 

Polio rates increased in 1944 to the highest number of reported cases since 1916. The cases of polio, however, were largely diagnosed as non-paralytic polio. Some cities and counties were reporting up to 80 percent of polio cases as non-paralytic polio while others did not report any, leaving public health officials to report that “the percentage probably depends more on local definitions or interpretations of a "case" of poliomyelitis.” 

In World War II, America’s military personnel also suffered from polio while serving abroad, especially in the Philippines and China. In the Philippines, paralysis rates among American troops were reportedly 20 times higher than those of troops stationed in Europe or in the U.S., yet polio was rarely found among natives of these countries. The belief at this time was that the local populations were able to harbor the virus and spread it to U.S. troops without becoming ill themselves. 

During World War II, the U.S. armed forces began using DDT (Dichlorodiphenyl-trichloroethane),    an insecticide which was eventually banned from use in the U.S. in 1972 due to the harm it caused to both humans and animals.  DDT use during the war was nearly exclusive to the armed forces and primarily used for malaria control, which was a serious problem for troops stationed in the Pacific Theatre.   

DDT became available to the general U.S. population after the war and was hailed by federal health officials a “miracle insecticide” that was “not harmful to man in the dilutions recommended.”  Massive fumigation campaigns to exterminate the mosquito population, suspected by health officials to be responsible for the spread of polio, began in 1945.   While there was a decrease in the number of polio cases in 1945 (13,619) from one year earlier, the rates in 1946 nearly doubled, to 25,191. 

Polio cases decreased again in 1947 (10,737) but rose significantly in 1948 to 27,680 and by 1949, there were over 42,000 reported cases. Again, during this time, U.S. government officials were conducting massive DDT fumigation campaigns with the belief that insects were responsible for the spread of the virus. 

Cases of paralytic and non-paralytic poliomyelitis were not differentiated in national reporting data until 1951. In 1951, there were 10,037 cases of paralytic polio and 18,349 cases of non-paralytic polio. One year later, in 1952, the U.S. would reach its peak in the number of polio cases, with 21,269 cases of paralytic polio and 36,610 cases of non-paralytic polio. 

Some attributed the rise in the number of cases to improved public health reporting systems and more accurate physician diagnosis of polio, while others believed the rise in population simply increased the number of potentially susceptible individuals. Some people even suggested that DDT and other poisonous chemicals in widespread use might be contributing to the increase in polio.  Incidentally, in 1952, DDT fumigations began subsiding and in 1953, polio cases were also decreasing at about the same rate. By 1953, the number of polio cases had dropped by nearly 40 percent. 

In 1953, there were no set criteria or guidelines for the diagnosing of poliomyelitis. A scientific report published from a panel discussion held in 1960 by the Illinois State Medical Society noted that: 

“Prior to 1954 any physician who reported paralytic poliomyelitis was doing his patient a service by way of subsidizing the cost of hospitalization and was being community-minded in reporting a communicable disease. The criterion of diagnosis at that time in most health departments followed the World Health Organization definition: “Spinal paralytic poliomyelitis: “Signs and symptoms of nonparalytic poliomyelitis with the addition of partial or complete paralysis of one or more muscle groups, detected on two examinations at least 24 hours apart.”  Note that “two examinations at least 24 hours apart” was all that was required. Laboratory confirmation and presence of residual paralysis was not required. In 1955 the criteria were changed to conform more closely to the definition used in the 1954 field trials: residual paralysis was determined 10 to 20 days after onset of illness and again 50 to 70 days after onset. The influence of the field trials is still evident in most health departments; unless there is residual involvement at least 60 days after onset, a case of poliomyelitis is not considered paralytic”

This report also went on to state that:  

“This change in definition meant that in 1955 we started reporting a new disease, namely, paralytic poliomyelitis with a longer lasting paralysis. Furthermore, diagnostic procedures have continued to be refined. Coxsackie virus infections and aseptic meningitis have been distinguished from paralytic poliomyelitis. Prior to 1954 large numbers of these cases undoubtedly were mislabeled as paralytic poliomyelitis. Thus, simply by changes in diagnostic criteria, the number of paralytic cases was predetermined to decrease in 1955-1957, whether or not any vaccine was used. At the same time, the number of nonparalytic cases was bound to increase because any case of poliomyelitis-like disease which could not be classified as paralytic poliomyelitis according to the new criteria was classified as nonparalytic poliomyelitis.”

Prior to the introduction and widespread use of the polio vaccine, there were few efforts to differentiate between paralysis caused by the poliovirus or by other factors such as enteroviruses (ECHO and Coxsackie), transverse myelitis, Guillain-Barre Syndrome, DDT and arsenic toxicity, and more.  

This is evidenced by a study published in 1960 which reported on an epidemic of poliomyelitis in Michigan that noted: 

“During an epidemic of poliomyelitis in Michigan in 1958, virological and serologic studies were carried out with specimens from 1,060 patients. Fecal specimens from 869 patients yielded no virus in 401 cases, poliovirus in 292, ECHO (enteric cytopathogenic human orphan) virus in 100, Coxsackie virus in 73, and unidentified virus in 3 cases. Serums from 191 patients from whom no fecal specimens were obtainable showed no antibody changes in 123 cases but did show changes diagnostic for poliovirus in 48, ECHO viruses in 14, and Coxsackie virus in 6. In a large number of paralytic as well as nonparalytic patients poliovirus was not the cause. Frequency studies showed that there were no obvious clinical differences among infections with Coxsackie, ECHO, and poliomyelitis viruses. Coxsackie and ECHO viruses were responsible for more cases of "nonparalytic poliomyelitis" and "aseptic meningitis" than was poliovirus itself. This, added to the fact that two immunological types of the poliovirus were involved in the epidemic, suggests the difficulty to be anticipated in future programs of immunization.”

Between 1955 and 1957, cases of both paralytic and non-paralytic polio decreased, however, rates increased in 1958 and again in 1959. Public health officials quickly blamed the rise in incidence on low vaccine uptake – yet by 1958, vaccination rates had significantly increased from the 1955 to 1957 rates.     Further, polio was being reported in persons who had received one or more vaccine doses, including those who had received three and four doses.  

Rates of polio decreased again by 1960 and would continue to drop. By the time the live oral polio vaccine (OPV) had become available and recommended for use in the U.S. in 1962,   there were 792 cases of paralytic polio and 148 cases of non-paralytic polio. 

Between 1962 and 1965, polio cases continued to decline; however, polio was still occurring in vaccinated individuals. Additionally, persons who received the new OPV vaccines were also developing polio, with some cases occurring within 30 days of receiving the live virus vaccine.  In 1962, when OPV was recommended for use, public health officials acknowledged that the vaccine could cause paralysis in those who received the vaccine as well as in persons with close contact to the vaccine recipients. 

The last reported case of wild-type polio in the U.S. occurred in 1979; however, between 1980 and 1998, there were 152 cases of paralytic polio in the U.S.  One hundred and forty-four of these cases were confirmed as vaccine-acquired paralytic polio (VAPP), 6 were imported, and 2 cases were unknown.   When OPV was in use in the United States, VAPP was estimated to occur at a rate of one case per 2.4 million doses, or one case per 750,000 doses, if OPV was administered as the first dose.  

On June 17, 1999, the CDC’s Advisory Committee on Immunization Practices (ACIP) voted to stop the use of OPV in the U.S., by January of 2000. 

Poliomyelitis worldwide

In 1953, polio was occurring in many countries globally; however, most cases were reported in the U.S. and other developed countries. The World Health Organization (WHO) reported that rates were rising but stated that this rise was likely due to better reporting. 

By 1970, WHO was reporting that most countries in Europe and North America had seen a significant decrease in the number of polio cases; however, multiple countries in Africa, Asia, South and Central America were experiencing increases. Additionally, researchers noted that in many instances, when infant mortality rates dropped, the incidence of polio rose. 

Initiatives were launched in May of 1985 to eradicate polio from the Americas by the end of the 1990s. Strategies to accomplish this goal included national vaccination campaigns held twice a year, improved surveillance of acute flaccid paralysis (AFP), and improved response and containment measure when new paralysis case were reported. In 1990, health officials reported that since 1986, the number of AFP cases had been increasing. In 1986, of the 1100 reported AFP cases, 930 were confirmed as polio; however, by 1989, 2094 cases of AFP were reported, yet only 130 were considered by health officials to be polio. Of these 130 cases, only 24 were confirmed by stool culture to be from wild-type polio. 

In 1988, the World Health Assembly set a goal to globally eradicate polio by 2000.  This goal was not achieved and while health officials reported a decrease in the number of countries with ongoing poliovirus transmission, they also acknowledged a rise in the number of AFP cases globally between 1999 and 2000, from 1.3 per 100,000 population to 1.5 per 100,000 population. The new date for worldwide polio eradication was set for 2005. 

By 2000, the first outbreaks associated with vaccine-derived poliomyelitis (VDPV) were reported by public health officials. In Haiti and the Dominican Republic, investigators noted that the new polio outbreaks were unusual because the virus was 97 percent similar to the OPV strain but stated that the virus “appears to have recovered the neurovirulence and transmissibility characteristics of wild poliovirus type 1”.  One year later, the CDC reported on another outbreak of VDPV, this time in the Philippines, and blamed low rates of vaccination for the outbreak. 

By 2003, WHO was reporting that there were only 6 polio-endemic countries remaining and only 784 cases of polio had occurred worldwide that year. There were, however, 34,915 reported cases of AFP. 

Outbreaks of VDPV continued to be reported and by 2008, there had been 8 confirmed VDPV outbreaks globally, with 2 more under investigation, in addition to single case reports. Researchers investigating these outbreaks estimated that millions of people had likely been infected although only 114 cases of VDPV had been confirmed. 

By late 2010, the number of cases of AFP was 81,338, over twice as many that had been reported in 2003. Of these cases, only 830 were confirmed as wild-type polio. 

In fact, by 2007, physicians in India were reporting on the significant rise in the number of non-polio AFP rates and noted that the increase had begun after vaccine campaigns using an experimental, high-potency polio vaccine were initiated.  Further, children diagnosed with non-polio AFP were more likely to die than those who developed paralysis from wild-type polio. 

AFP rates in India continued to rise and in 2012, physicians reported that the number of non-polio AFP cases had increased in relation to the number of OPV doses received in each area. Further, they stated that the significant increase in the number of AFP cases were not being investigated by health experts to find out exactly what was causing the paralysis. They went on to call for an end to monthly administration of OPV doses, and even speculated that better overall health outcomes might have occurred in India had the money spent on vaccination campaigns been used to improve sanitation and water. 

In 2014, there were over 203,000 cases of AFP reported worldwide. Of that number, over 8,000 cases were caused by OPV, 412 from wild-type polio, and 80 the result of circulating VDPV.  2014 was the year that the CDC began tracking cases of AFP (referred to as acute flaccid myelitis – or AFM) after noting a significant increase in the number of cases in the U.S. CDC Health officials currently have no definitive answer for the cause of AFM but are focusing on the theory that a virus is to blame for the disease. AFM is most commonly seen in children, but public health officials believe that this disease can affect persons of any age. 

In September 2015, following the announcement that wild-type 2 polio had been eradicated globally, public health officials moved quickly to stop use of the trivalent OPV (vaccine containing vaccine-strain poliovirus types 1, 2, and 3) and began replacing it with a bivalent OPV containing only vaccine-strain poliovirus types 1 and 3.  This initiative was implemented to stop the spread of type 2 circulating VDPV (cVDPV2), which had caused multiple outbreaks of polio globally. 

Despite removing type 2 polio from OPV in the spring of 2016,  cVDPV2 associated paralytic polio cases have continued to occur. In 2019, cVDPV2 outbreaks were reported in the Philippines, and multiple African countries.  As a result, since April 2016, approximately 300 million doses of a type 2 OPV have been administered in regions experiencing outbreaks of cVDPV2. Problems arising from the reintroduction of the live type 2 OPV include the risk that its use will potentially lead to additional cases and outbreaks of cVDPV2.  

On October 24, 2019, the Global Polio Eradication Initiative (GPEI) announced the global eradication of type 3 wild-type polio.  OPV containing type 3 poliovirus remains in use and it is not known whether health officials will remove the strain from the vaccine at any point in the near future.

Type 1 wild-type polio (WPV1) is the only wild polio strain currently circulating and in 2018, there were 33 cases detected – 12 in Pakistan and 21 in Afghanistan. In 2018, however, there were 6,732 cases of VAPP associated with the use of the Sabin OPV and 104 cases of VDPV which resulted in paralysis. There were also 190,055 cases of AFP – a condition which is indistinguishable from paralytic polio except through stool specimen testing.  

In October 2019, WHO officials reported an increase in WPV1 cases in Pakistan and Afghanistan, and a significant increase in cVDPV2 cases in multiple countries giving children the Sabin OPV and stated the following:  

“The Committee is gravely concerned by the significant further increase in WPV1 cases globally to 73 in 2019 year to date, compared to 15 for the same period in 2018, with most of the increase due to the ongoing outbreaks in Pakistan… The multiple cVDPV2 outbreaks on the continent of Africa are now at unprecedented levels and need to be treated by countries as a national public health emergency…Furthermore, the global nature of the risk is highlighted by the appearance of cVDPV2 in China and the Philippines, with undetected transmission for about a year in China, and much longer in the Philippines.”

While there were five times as many cases of wild-type polio in 2019 in comparison to 2018, the majority of the paralytic polio cases identified and reported in 2019 were caused by outbreaks of cVDPV2 in Niger, Nigeria, Cameroon, Benin, Ghana, Ethiopia, Somalia, China, Myanmar, Kenya, Central African Republic (CAR), Angola, Somalia, and Papua New Guinea, Indonesia. 

Some infectious disease experts have argued for a halt to the three decade WHO-led Global Polio Eradication Initiative (GPEI) and a transition to a more achievable program of systematic, sustained control of polio. In their argument, published in the BMJ Global Health Journal they state:

“…even successful eradication of poliovirus may not mean an end of polio-like illness. Other viruses from the same family (eg, enteroviruses D68, D71) may produce flaccid paralysis resembling poliomyelitis, with outbreaks reported from a number of industrialised countries in recent years. The existence of other causes of disease does not mean that eradication of one cause should not be attempted. However, it would bring about the challenge of explaining to the world community why outbreaks presenting with the clinical symptoms of a disease eradicated at substantial cost continue to occur.” 

The authors concluded that:

“In 2019, the world ‘is at a critical point in polio eradication.’ This could be the year to implement the lessons learnt from GPEI and to move from the eradication goal to sustained polio control, as had already been proposed by leading experts on smallpox eradication more than 10 years ago….. In conclusion, there are two strategies that the world should not be content with: first, unsystematic and uncoordinated polio control efforts, implemented by individual countries acting on their own. Second, continued polio eradication efforts offering simply more of the same. Urging ‘all involved in the effort to excel in their roles’ to achieve polio eradication is just such a strategy. It merely pours more money into an ultimately unsustainable vertical programme.” 

The GPEI has set 2023 as their new goal for eradicating wild-type polio and circulating vaccine-derived poliovirus. 

IMPORTANT NOTE: NVIC encourages you to become fully informed about Polio and the Polio vaccine by reading all sections in the Table of Contents, which contain many links and resources such as the manufacturer product information inserts, and to speak with one or more trusted health care professionals before making a vaccination decision for yourself or your child. This information is for educational purposes only and is not intended as medical advice.


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