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Polio Disease and Vaccine


Quick Facts

Polio

Polio
  • Poliomyelitis, or polio, is an infection caused by a virus that multiplies in the throat and gastrointestinal tract.1 There are three types of polio virus: type 1, 2 and 3. 2  Polio can be transmitted through direct person-to-person contact, or contact with infected bodily fluids, such as mucous, phlegm, and feces.3
  • In about 95 percent of cases, polio infection is subclinical and does not cause symptoms. In 4-5 percent of cases there may be minor symptoms, such as sore throat, low grade fever, headache, fatigue and nausea followed by stiff neck, meningitis (brain inflammation) and temporary paralysis of an arm or leg but there is full recovery within a few weeks.  In less than 1 percent of cases, the polio virus infects the central nervous system and paralyzes the muscles of the arms and legs or muscles needed for breathing and swallowing, which can lead to permanent paralysis or death. Some adults who appear to have fully recovered from polio as children have developed post-polio syndrome (PPS) – a syndrome that causes weakness and pain in muscles and joints.4 5 6
  • The live attenuated oral polio vaccine (OPV) can cause vaccine-strain polio in the vaccinated person or can cause vaccine-strain polio in a person who comes in contact with a recently vaccinated person’s body fluids (urine, stool, saliva) because the vaccine-strain polio virus is shed for several weeks after vaccination. OPV has also caused a new strain of polio known as vaccine-derived poliovirus (VDPV) to emerge. VDPV is transmissible to others and can cause symptoms which are indistinguishable from wild-type poliovirus. 7 8 9
  • The use of OPV was discontinued in the U.S. as of 2000 and replaced with inactivated, injectable polio vaccine, which cannot cause vaccine-strain polio. However, OPV is used widely in annual polio vaccine campaigns targeting children in many parts of Asia, Africa and the Middle East.10
  • Wild-type polio was declared eradicated in the U.S. in 1979 and eradicated in the western hemisphere in 1994.11 12 Today, it is an infectious disease that affects children living in poverty in socioeconomically disadvantaged areas, where sanitation and hygiene is poor and access to clean water and food is limited.13

Polio Vaccine 

  • Two different kinds of polio vaccines have been given to children in the U.S. since the 1950’s and 1960’s: a live attenuated oral polio vaccine (OPV), which is no longer used in the U.S.  but is given to children in other parts of the world; and an inactivated, injectable polio vaccine (IPV), which has been given to children in the U.S. since 2000. Inactivated polio vaccines contain poliovirus type 1, 2 and 3; however, the OPV currently in use is a bivalent vaccine containing only type1 and type 3 poliovirus.14 15
  • There are six inactivated, injectable polio vaccines licensed and marketed in the U.S. by pharmaceutical companies. Five of the polio containing vaccines are combination vaccines that include additional vaccines to prevent other viral or bacterial infections.16 The CDC recommends that infants and children receive a total of four doses of IPV with a dose at two and four months, between 6 and 18 months and between four and six years old.17
  • Commonly reported IPV reactions include fever, irritability and crying, local reactions (pain, redness, swelling at injection site), drowsiness, vomiting and loss of appetite.18 However, because most IPV is included with other vaccines in combination shots in the U.S., the vaccine manufacturer product insert for each combination vaccine should be reviewed to learn about vaccine reaction symptoms and contraindications before vaccination.19
  • The live attenuated oral polio vaccine (OPV) can cause vaccine-strain polio in the vaccinated person or can cause vaccine-strain polio in a person, who comes in contact with a recently vaccinated person’s body fluids (urine, stool, saliva) because the vaccine-strain polio virus is shed for several weeks after vaccination. OPV has also caused a new strain of polio known as vaccine-derived poliovirus (VDPV) to emerge. VDPV is transmissible to others and can cause symptoms which are indistinguishable from wild-type poliovirus. Vaccine- strain polio continues to occur in countries where children receive OPV, especially in areas where poor sanitation and hygiene facilitate the spread the virus.20 21 22
  • As of February 1, 2020, there have been 310 claims filed in the federal Vaccine Injury Compensation Program (VICP) for injuries and deaths following OPV containing vaccines, including 28 deaths and 282 serious injuries. There have been 489 claims for injuries and deaths following IPV containing vaccines, including 73 deaths and 416 serious injuries. Using the MedAlerts search engine, as of November 30, 2019 there have been 24,797 adverse events reported following OPV with 1,033 deaths (nearly 90% in children under age six). There have been 72,130 reports of adverse events associated with IPV containing vaccines with 1,573 deaths (more than 93% in children under age six).

NVIC “Quick Facts” is not a substitute for becoming fully informed about Polio and the Polio vaccine. NVIC recommends consumers read the more complete information following the "Quick Facts", as well as the vaccine manufacturer product information inserts, and speak with one or more trusted health care professionals before making a vaccination decision for yourself or your child.

Food & Drug Administration (FDA) 

Centers for Disease Control (CDC) 

National Institute of Allergy & Infectious Diseases (NIAID)

NIAID Workshop Development of Guillain Barre Syndrome

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Reporting a Vaccine Reaction 

Since 1982, the NVIC has operated a Vaccine Reaction Registry, which has served as a watchdog on VAERS. Reporting vaccine reactions to VAERS is the law. If your doctor will not report a reaction, you have the right to report a suspected vaccine reaction to VAERS. 

Vaccine Reaction Symptoms & Ingredients 

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What is Polio?        

Polio (poliomyelitis) is a disease caused by the poliovirus which in rare cases affects the nervous system and can lead to paralysis or death. The term ‘poliomyelitis’ used to describe the effects that the disease has on the body’s spinal cord comes from the Greek words of polio (grey) and myelin (marrow).23

There are three types of poliovirus - type 1, 2, and 3 - and immunity to one type of poliovirus does not provide immunity to the additional types. The poliovirus is an enterovirus that is unique to humans and usually inhabits the gastrointestinal tract.24

Approximately 95 percent of all polio infections are asymptomatic. This means that most people who are exposed to the virus will have no clinical symptoms of illness. Between 4 and 8 percent of individuals exposed to the poliovirus will develop mild symptoms, which often include flu-like illness, respiratory tract infections, and gastroenteritis. Approximately 1 percent of polio cases present as aseptic meningitis, and symptoms generally include severe back, neck, or leg spasms. Full recovery usually occurs within 10 days.25 For non-paralytic polio, the incubation period (time from exposure to the onset of illness) is generally between 3 and 6 days.26

Less than 1 percent of children exposed to polio will develop paralytic polio, the most severe form of polio. Paralytic polio usually begins within 1 and 18 days of initial infection, and paralysis symptoms usually progress for 2 to 3 days. In some cases, an asymptomatic period of 7 to 10 days may occur between the earliest symptoms of illness and the presentation of more severe symptoms. Severe symptoms can include excruciating muscle pain and spasms of the back or limbs, and the loss of superficial reflexes. Asymmetrical paralysis will follow, and the disease will progress to flaccid paralysis and loss of deep tendon reflexes. This condition will usually persist for days to weeks; however, most people will recover fully. If muscle weakness or paralysis persists for longer than 1 year, the condition will likely be permanent. 27

There are 3 types of paralytic polio – spinal, bulbar, and bulbospinal. Spinal paralysis, the most common form and seen in nearly 80 percent of all cases of paralytic polio, is most often recognizable by asymmetric paralysis of the lower limbs. Bulbar paralysis, which occurs in approximately 1-2 percent of cases, involves the cranial nerves and is associated with higher fatality rates. Bulbospinal paralysis, a combination of both bulbar and spinal paralysis, accounts for approximately 19 percent of all cases of paralytic polio.28

Individuals who recover from paralytic polio may be at risk for post-polio syndrome, a condition which begins with a slow progressive new weakening of the muscles previously involved in the initial case of polio. Additional symptoms often include fatigue, muscle atrophy, skeletal deformities, and joint degradation. Symptoms of post-polio syndrome can range from mild, with minor impairments, to severe, where a person’s activities of daily living are significantly impacted. There are no available tests to definitively confirm a diagnosis of post-polio syndrome, and the prevalence and incidence rates of this condition are not known. It is estimated by researchers that this condition may affect between 25 to 40 percent of persons who have recovered from paralytic polio.29

Wild-type polio was declared eradicated in the U.S. in 1979; however, between 1980 and 1998, there were 152 reported 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.30  

VAPP was associated with use of the oral polio vaccine (OPV) immediately after the vaccine’s introduction in the early 1960s.31 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 2000.32 OPV, however, remains in use globally, and is the primary vaccine used in global campaigns aimed at eradicating polio.33

In recent years, vaccine-derived poliovirus (VDPV) has emerged to cause cases and outbreaks of paralytic polio. OPV is a live attenuated (weakened) virus vaccine and after it is administered, the virus replicates in the intestine and is excreted in the stool. This excreted live vaccine virus has the potential to circulate in the environment, undergo genetic changes, and cause paralytic polio. VDPVs are classified into 3 categories: 34 35

  • Circulating VDPV (cVDPV) – this occurs in communities where individuals remain susceptible to either wild-type polio or VDPV because of inadequately administrated polio vaccination campaigns or due to a lack of immunity to polio;
  • Immunodeficiency (iVDPV) – these strains are found in individuals with primary immunodeficiency (PID)
  • Ambiguous VDPV (aVDPV) – these are strains isolated from individuals who are not immunodeficient or else found in sewage where the source is not known.

Type 2 wild-type polio was declared eradicated worldwide in 2015 36 and on October 24, 2019, the Global Polio Eradication Initiative (GPEI) announced the global eradication of type 3 wild-type polio.37

In September 2015, following the announcement that type 2 wild-type 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 replaced it with a bivalent OPV containing only vaccine-strain poliovirus types 1 and 3.38 This initiative was implemented to stop the spread of type 2 VDPV (cVDPV2), which had caused multiple polio outbreaks in several countries.39 Since 2000, there have been 1,085 cases of paralytic polio associated with cVDPV and most cases  - 932 (86 percent) – have been caused by cVDPV2.40

Despite removing type 2 polio from OPV in the spring of 2016,41 cVDPV2 associated paralytic polio cases have continued to occur. In 2019, cVDPV2 outbreaks were reported in the Philippines, and several African countries.42 This has prompted health officials to reintroduce a type 2 OPV and since April 2016, approximately 300 million doses have been administered in regions experiencing outbreaks of cVDPV2. Problems associated with the reintroduction of the live type 2 OPV have included the risk that its use will potentially lead to additional cases and outbreaks of cVDPV2. 43

Type 1 wild-type polio is the only poliovirus strain currently circulating and in 2018, there were 33 cases detected globally – 12 in Pakistan and 21 in Afghanistan.44 However, in 2018, there were 6,732 cases of VAPP associated with the use of the Sabin OPV and 104 cases of paralysis from VDPV. These cases were detected after testing was completed on the stool specimens of 190,055 persons diagnosed with acute flaccid paralysis (AFP).45

AFP or acute flaccid myelitis (AFM) is often referred to as a “polio-like” illness. This neurological disease affects the grey matter of the spinal cord and causes weakness in the reflexes and muscles. Symptoms of AFM include sudden loss of reflexes and muscle tone and extremity weakness. Additional symptoms may include swallowing impairments, slurred speech, eyelid and facial drooping, and eye movement disorder. AFM can affect the respiratory muscles and when this occurs, mechanical ventilation is required. There is no specific treatment for AFM and long-term outcomes for individuals affected by this disease are not known at this time.46

The exact cause of AFM is currently unknown, but researchers are focusing on the theory that a virus is responsible for the disease. AFM is most commonly seen in children, but public health officials believe that this disease can affect persons of any age.47

The CDC began tracking AFM in the U.S. in August 2014 and as of January 2020, 603 confirmed cases have been reported.48 In the U.S., cases of AFM appear to occur more frequently between August and October, every 2 years.49

On October 3rd, 2019, the World Health Organization (WHO) reported a significant increase in wild-type poliovirus type 1 (WPV1), from 33 cases in 2018, to 73 cases. Multiple cVDPV2 outbreaks in Africa were also reported by health officials and noted to be at the highest levels in history. Additionally, cVDPV2 had also been detected in the Philippines and China and had spread undetected for approximately a year in China and even longer in the Philippines. 50

Is Polio contagious?

The poliovirus is contagious and transmissible from person-to-person.  The most common route of transmission is through contact with the stool of an infected person; however, it can also be spread through respiratory secretions (coughing, sneezing) but this mode of transmission occurs less frequently. The poliovirus enters the body through the mouth, replicates in the pharynx and gastrointestinal system, and is excreted from the body through the stool.51 52 Vaccine-strain and vaccine-derived polio are also contagious and transmitted the same way as wild-type polio.53 54

In households with children, the transmission rate among susceptible individuals is nearly 100 percent. Transmission rates in household with adults is estimated to be over 90 percent. Approximately 95 percent of people who contract the poliovirus have no symptoms but are still contagious to others. Asymptomatic spreading of poliovirus from infected persons who have no apparent symptoms, to susceptible contacts, occurs most often.55

 An infected person is most contagious to others from 7 to 10 days before and after symptoms of illness occur, but the virus can still be found in the stool for up to 6 weeks or longer.56 In some cases, shedding of the poliovirus has occurred for months and even years. This usually occurs in persons who are immunodeficient; however, this has also been reported in healthy individuals.57 58 59 60 61 Persons who are immunodeficient can shed vaccine-strain poliovirus for several years. When this occurs, the vaccine-strain usually mutates into a vaccine-derived poliovirus and can cause cases and outbreaks in communities.62

In temperate climates, poliovirus infection occurs most frequently in the summer months. No seasonal pattern has been noted in tropical climates. 63 The poliovirus can be rendered inactive with chlorine, formaldehyde, heat, and ultraviolet light.64

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

The first documented cases of what is now believed to be poliomyelitis was recorded in 1789 by British physician Michael Underwood.65 66Underwood described polio as “…the debility of the lower extremities which gradually become more infirm, and after a few weeks are unable to support the body67 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.68 69  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. 70

The first outbreak of polio in the U.S. occurred in 1841 in Feliciana, Louisiana and caused paralysis in 10 children. 71 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.72

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.73 74 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.75 76

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.77 78

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.79

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.”80 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.81

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.82 Humans are the only known carriers of the poliovirus,83 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.84 This product was widely used in the U.S. and initially used against the gypsy moth that had invaded Boston by the 1890’s.85 However, when it was discovered that Paris Green could not be applied in “sufficient quantity to kill the caterpillars without seriously injuring the foliage” 86 a chemist with the Gypsy Moth Commission suggested that lead arsenate be used. 87 Coincidently, the first outbreak of paralysis in the U.S. in over 50 years occurred in Boston during this time.88

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.89

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.90

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.91 However, by 1913, after additional experiments could not reproduce earlier findings, health officials reported that transmission likely occurred between ‘passive human carriers.’92

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.93

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. 94

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.95

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.96 97

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.98

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.99

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.100

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.101 102 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.103

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.104

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.105

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.106

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.107

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.108

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. 109 110 111 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 1929.112 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.113 114

Vaccine development was also underway in the 1930s, however, the experimental vaccines used were found to be both ineffective and harmful.115

In the mid-1930s, an experimental nose spray containing picric acid, a highly toxic and explosive chemical compound, 116 117 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. 118  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.119 120

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.121 122 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.123

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.124 125 The lengthy limb immobilization would frequently result in the need for orthopedic surgical procedures which included contracture release and tendon transfers.126  

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.127

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.128

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.129

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.130 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.131

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. 132 133 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.” 134 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.135

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.136

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.”137 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.138

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.”139

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.140

During World War II, the U.S. armed forces began using DDT (Dichlorodiphenyl-trichloroethane), 141  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.142 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.143 144

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.”145 Massive fumigation campaigns to exterminate the mosquito population, suspected by health officials to be responsible for the spread of polio, began in 1945. 146 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 25,191.147

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.148

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.149

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.150 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.151

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:152

“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: 153

“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. 154

This is evidenced by a study published in 1960 which reported on an epidemic of poliomyelitis in Michigan that noted:155

“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. 156 157 Further, polio was being reported in persons who had received one or more vaccine doses, including those who had received three and four doses. 158

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, 159 there were 792 cases of paralytic polio and 148 cases of non-paralytic polio.160

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.161 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.162

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.163  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. 164

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 2000.165

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.166

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.167

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.168

In 1988, the World Health Assembly set a goal to globally eradicate polio by 2000.169 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 2005.170

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”.171 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.172

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.173

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.174

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.175

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.176 Further, children diagnosed with non-polio AFP were more likely to die than those who developed paralysis from wild-type polio.177

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.178

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.179 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.180

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 3.181 This initiative was implemented to stop the spread of type 2 circulating VDPV (cVDPV2), which had caused multiple outbreaks of polio globally.182

Despite removing type 2 polio from OPV in the spring of 2016,183 cVDPV2 associated paralytic polio cases have continued to occur. In 2019, cVDPV2 outbreaks were reported in the Philippines, and multiple African countries.184 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. 185

On October 24, 2019, the Global Polio Eradication Initiative (GPEI) announced the global eradication of type 3 wild-type polio.186 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. 187

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: 188

“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.189

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.”190

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.”191

The GPEI has set 2023 as their new goal for eradicating wild-type polio and circulating vaccine-derived poliovirus.192

Can Polio cause injury and/or death?

According to poliovirus researchers, approximately 95 percent of all polio cases are asymptomatic. This means that most people who are exposed to the virus will have no clinical symptoms of illness. Between 4 and 8 percent of individuals exposed to the poliovirus will develop mild symptoms, which often include flu-like illness, respiratory tract infections, and gastroenteritis. Approximately 1 percent of polio cases present as aseptic meningitis, and symptoms generally include severe back, neck, or leg spasms. Full recovery usually occurs within 10 days.193

The CDC reports that 72 percent of poliovirus infections among children occur asymptomatically and that 24 percent of children infected with poliovirus will develop a non-specific illness with symptoms that frequently include sore throat and low-grade fever. This non-specific illness is referred to as abortive poliomyelitis and when this occurs, no laboratory or clinical findings of central nervous system impairments are noted.194

Less than 1 percent of children exposed to polio will develop paralytic polio, the most severe form of polio. Paralytic polio usually begins within 1 and 18 days of initial infection with the virus, and paralysis symptoms usually progress for 2 to 3 days. In some cases, an asymptomatic period of 7 to 10 days may occur between the earliest symptom of illness and the presentation of more severe symptoms. Severe symptoms can include excruciating muscle pain and spasms of the back or limbs, and the loss of superficial reflexes. Asymmetrical paralysis will follow, and the disease will progress to flaccid paralysis, and loss of deep tendon reflexes. This condition will usually persist for days to weeks; however, most people will recover fully. If muscle weakness or paralysis persists for longer than 1 year, the condition will likely be permanent. 195

There are 3 types of paralytic polio – spinal, bulbar, and bulbospinal. Spinal paralysis, the most common form and seen in nearly 80 percent of all cases of paralytic polio, is most often recognizable by asymmetric paralysis of the lower limbs. Bulbar paralysis, which occurs in approximately 1-2 percent of cases, involves the cranial nerves and is associated with higher fatality rates. Bulbospinal paralysis, a combination of both bulbar and spinal paralysis, accounts for approximately 19 percent of all cases of paralytic polio.196

Between 2 and 5 percent of paralytic polio cases in children are fatal, while the death rate among adults ranges from 15 to 30 percent.197

Individuals who recover from paralytic polio may be at risk for post-polio syndrome, a condition which begins with a slow progressive new weakening of the muscles previously involved in the initial case of polio. Additional symptoms often include fatigue, and muscle atrophy, skeletal deformities, and joint degradation. Symptoms of post-polio syndrome can range from mild, with impairments, to severe, impacting a person’s activities of daily living. There are no available tests to definitively confirm a diagnosis of post-polio syndrome, and the prevalence and incidence rates of this condition are not known. It is estimated by researchers that this may affect between 25 to 40 percent of persons who have recovered from paralytic polio.198

The live oral poliovirus vaccine (OPV) can also cause paralytic polio. When this occurs, it is referred to as vaccine-acquired paralytic poliovirus (VAPP). VAPP was acknowledged immediately following the introduction of the live virus OPV and is currently responsible for most cases of paralytic polio globally.199 200

In recent years, vaccine-derived poliovirus (VDPV) has emerged to cause cases and outbreaks of paralytic polio. OPV is a live attenuated (weakened) virus vaccine and after it is administered, the virus replicates in the intestine and is excreted through the stool. This excreted live vaccine virus can circulate in the environment, undergo genetic changes, and cause paralytic polio. VDPVs have been classified into 3 separate categories: 201 202

  • Circulating VDPV (cVDPV) – this occurs in communities where individuals remain susceptible to either wild-type or VDPV because of inadequately administrated polio vaccination campaigns or due to a lack of immunity to polio;
  • Immunodeficiency (iVDPV) – these strains are found in individuals with primary immunodeficiency (PID)
  • Ambiguous VDPV (aVDPV) – these are strains isolated from individuals who are not immunodeficient or else found in sewage where the source is not known.

Paralysis caused by wild-type poliovirus, OPV, and VDPV cannot be distinguished through clinical symptoms.203

Who is at highest risk for getting Polio? 

Children under the age of 5 are considered most at risk for polio.204

Other risk factors for polio may include:205 206 207 208

  • Travel to an area where an outbreak of polio has recently occurred or where polio is common
  • Having an immune system disorder (primary immunodeficiency, HIV infection)
  • Taking care of or living with someone who is infected with polio
  • History of tonsillectomy
  • Strenuous physical activity or extreme stress after exposure to the poliovirus
  • Pregnancy

Individuals who receive an intramuscular injection within 30 days of exposure to the poliovirus (wildtype, vaccine strain, vaccine derived) are at higher for developing paralytic polio.209 210 211 212

Who is at highest risk for suffering complications from Polio?         

Most people infected with the poliovirus show no clinical signs of illness. Fewer than 1 percent of persons infected with polio develop paralysis, the most severe complication of polio and many who develop paralysis recover with few or no permanent residual adverse health conditions. 213

Bulbar polio, the most severe and rarest form of paralytic polio (1-2 percent of all cases of paralytic polio), involves the cranial nerves and usually results in permanent paralysis with death in 25 to 75 percent of cases.214

Can Polio be prevented and are there treatment options?

Polio can be prevented by avoiding travel to countries where cases and outbreaks of wild-type and vaccine-derived polio are occurring.215

Additional preventative measures also include –

  • Frequent, thorough handwashing with soap and clean water
  • Hand sanitizer use if soap and clean water are not available
  • Reducing the risk of potential exposure by avoiding hand contact with the mouth, nose or eyes
  • Avoiding close contact with persons who are sick
  • Refraining from sharing personal items with persons who are ill
  • Using a tissue or sleeve to cover the nose and mouth when sneezing or coughing
  • Avoidance of any food and drinks that could be contaminated with feces

Polio can also be prevented by avoiding intramuscular (IM) injections and tonsillectomies in areas where the poliovirus may be circulating. Published medical research has associated both IM injections and tonsillectomies with an increased rate of paralytic polio.216 217 218 219 220 221

Approximately 95 percent of all polio cases are asymptomatic. This means that most people who are exposed to the virus will have no clinical symptoms of illness. Between 4 and 8 percent of individuals exposed to the poliovirus will develop mild symptoms, which often include flu-like illness, respiratory tract infections, and gastroenteritis.222

Approximately 1 percent of polio cases present as aseptic meningitis, and symptoms generally include severe back, neck, or leg spasms. Full recovery usually occurs within 10 days.223 Most cases of aseptic meningitis can be treated at home with the use of analgesics and anti-nausea medications; however, hospitalization may be necessary if symptoms are severe and additional medical interventions, including the use of intravenous fluids (IV), are necessary to prevent and treat complications.224

Less than 1 percent of children exposed to polio will develop paralytic polio, the most severe form of polio. 225 Treatment of paralytic polio is supportive and can include medications for pain relief, physical therapy to prevent muscle loss and deformity, and mechanical ventilation to assist with breathing, if necessary.226

Vitamin C may also be effective at treating and curing polio. In July 1949, Dr. Fred Klenner published a paper reporting that he was able to cure 100 percent of his polio patients using high doses of vitamin C.227 228

Diet has also been suggested as a way to prevent polio and researchers have reported that diets high in refined flour and sugar can increase a person’s chance of developing polio.229 230

What is Polio vaccine?      

In the U.S. today, the polio vaccine is usually administered in a combination shot that also contain vaccines for tetanus (T), diphtheria (D), pertussis (whooping cough) (P). Additional vaccines may also include Haemophilus Influenzae Type B (HIB) and/or hepatitis B vaccine.  The CDC’s Advisory Committee on Immunization Practices (ACIP) currently recommends administration of a polio containing vaccine at two, and four months old; between 6 and 18 months old; and between four and six years old.

Polio Vaccines Licensed for Use in the U.S.

Following is a list of currently available vaccines that contain the polio vaccine with links to the manufacturer product inserts (click on the name of the product):

  • IPOL, a polio vaccine containing inactive poliovirus (Monkey Kidney Cell) for individuals 6 weeks of age and older.
  • Pediarix, a 5 in 1 combination shot containing diphtheria and tetanus toxoids and acellular pertussis, hepatitis B recombinant and inactivated poliovirus vaccines for children under 7 years of age. It is manufactured by GlaxoSmithKline.
  • Kinrix, a 4 in 1 combination vaccine containing diphtheria and tetanus toxoids, acellular pertussis and inactivated poliovirus vaccines for children 4 to 6 years old. It is manufactured by GlaxoSmithKline.
  • Quadracel, a 4 in 1 combination vaccine containing diphtheria and tetanus toxoid, acellular pertussis and inactivated poliovirus vaccine for children 4 to 6 years old. It is manufactured by Sanofi Pasteur
  • Pentacel, a 5 in 1 combination shot containing diphtheria and tetanus toxoids and acellular pertussis, inactivated poliovirus and Haemophilus b conjugate (tetanus toxoid conjugate) vaccine for children under four years old. It is manufactured by Sanofi Pasteur Ltd.
  • VAXELIS, a 6 in 1 combination shot containing diphtheria and tetanus toxoids and acellular pertussis, inactivated poliovirus, Haemophilus b conjugate, and hepatitis B recombinant vaccine for children under 5 years of age. It is manufactured by MCM Vaccine Company. (Not currently available for use)

Combination Vaccines

There are some doctors who limit the numbers of vaccines given simultaneously on the same day and will work as partners with parents to choose certain vaccine products and develop individualized schedules for vaccination. If you want your child to receive polio vaccine but would prefer the vaccine to be administered alone, talk with your doctor.

If your doctor or the nurse administering vaccines refuses to have a discussion with you about vaccine products or schedules, you may want to consider consulting one or more other trusted health care professionals before making a vaccine decision.

Not all polio-containing vaccines have been studied in clinical trials to prove the safety and effectiveness of giving the shot simultaneously with other licensed vaccines. Check the product inserts for more information about administering vaccines at the same time with other vaccines.

About IPOL in Brief

  • Ages: IPOL inactivated poliovirus vaccine is approved for use in individuals 6 weeks of age and older (see Sanofi Pasteur product insert for recommended schedule and other indications.)
  • Vaccine Ingredients: VERO cells (a continuous line of monkey kidney cells), calf bovine serum albumin, polymyxin B, M-199 medium, 2-phenoxyethanol, formaldehyde, neomycin, streptomycin.
  • Estimated Efficacy: After two doses of IPOL (or IPOL in combination with DTP vaccine) was given during the first year of life, 84 to 100 percent of vaccine recipients developed antibodies considered to be protective against poliovirus (Poliovirus type 1- 88 to 100 percent) (Poliovirus type 2- 84 to 100 percent) (Poliovirus type 3 – 94 to 100 percent) depending on the study. When three doses of IPOL were given during the first year of life, 89 to 100 percent of children developed antibodies considered protective against polio (Poliovirus type 1 - 93 to 100 percent) (Poliovirus type 2 - 89 to 100 percent) (Poliovirus type 3 -97 to 100 percent). After a fourth dose of IPOL was administered between 12 and 18 months of age, 100 percent of vaccine recipients developed antibodies considered protective against all three strains of poliovirus.
  • Use with Other Vaccines: In pre-licensing clinical trials, IPOL was given with whole cell DTP vaccine. The IPOL package insert reports that IPOL can be administered simultaneously with hepatitis B, HIB, and DTaP; however, no information is available on administering IPOL with MMR, pneumococcal (PCV13), hepatitis A, or influenza vaccine.
  • Pre-licensing Clinical comparison studies: Clinical trials to assess the safety of IPOL prior to licensing did not include a placebo-control group. According to the package insert, in pre-licensing clinical trials, IPOL was administered at the same time as diphtheria and tetanus toxoids and pertussis vaccine adsorbed (DTP) vaccine – Because IPV was given in a different site but concurrently with Diphtheria and Tetanus Toxoids and Pertussis Vaccine Adsorbed (DTP), these systemic reactions could not be attributed to a specific vaccine. However, these systemic reactions were comparable in frequency and severity to that reported for DTP given alone without IPV.”231
  • Commonly Reported Adverse Events: Local injection site reactions (pain, redness, and induration); fever; sleepiness; irritability; fussiness; crying; anorexia; vomiting; and fatigue.
  • Other Serious Reported Adverse Events: convulsion, including febrile convulsion; somnolence; paresthesia; headache; injection site rash and mass; agitation; lymphadenopathy; anaphylactic reaction and anaphylactic shock; hypersensitivity; rash; urticaria; arthralgia; myalgia; and death.
  • Contraindications and precautions (Some reasons why IPOL should not be given – See Sanofi Pasteur product insert for complete list):
  • Hypersensitivity to any ingredient found within the vaccine, including polymyxin B, neomycin, streptomycin, formaldehyde, and 2-phenoxyethanol
  • Anaphylaxis or anaphylactic shock occurring within 24 hours of a previous vaccine dose
  • Acute febrile illness – vaccination should be deferred until a person has recovered

NVIC NOTE: Some doctors only vaccinate children who are healthy and are not sick with a coinciding viral or bacterial infection at the time of vaccination. If you do not want your acutely ill baby vaccinated and your doctor disagrees with you, you may want to consider consulting one or more other trusted health care professionals before vaccinating.

Animal reproduction studies have not been conducted with IPOL. It is not known whether IPOL can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. It is not known if IPOL is excreted in human milk.  IPOL has not been evaluated for carcinogenic or mutagenic potential, or for impairment of fertility.

About Pediarix Vaccine in Brief

  • Ages: Pediarix is a 5 in 1 shot (diphtheria, tetanus, acellular pertussis, inactivated polio and recombinant hepatitis B vaccines) given to children under age 7 (see GlaxoSmithKline product insert for recommended schedule and other indications.)
  • Vaccine Ingredients: Aluminum hydroxide, aluminum phosphate, aluminum salts, sodium chloride, polysorbate 80 (Tween 80), neomycin sulfate, polymyxin B, yeast protein, VERO cells, a continuous line of monkey kidney cells, calf serum and lactalbumin hydrolysate, fenton medium containing a bovine extract, modified Latham medium derived from bovine casein, formaldehyde, glutaraldehyde, modified Stainer-Scholte liquid medium.
  • Estimated Efficacy: Antibody responses to polio were tested one month following 3 doses of Pediarix administered in concomitantly with Hib vaccine and PCV7 (Prevnar 7) vaccine at 2, 4, and 6 months. At this time, 100 percent of vaccine recipients were found to have blood antibody levels considered to be protective against all three poliovirus strains.
  • Use with Other Vaccines: In clinical trials, Pediarix was given with HIB conjugate vaccine (no longer licensed in the U.S.) or pneumococcal vaccines (PCV7). There is no information in the product insert about the safety or effectiveness of giving Pediarix simultaneously with inactivated or live influenza, rotavirus, or hepatitis A vaccines.
  • Pre-licensing Clinical comparison studies: Clinical trials to assess the safety of Pediarix prior to licensing did not include a placebo-control group.
  • Commonly Reported Adverse Events: Local injection site reactions (pain, redness, or swelling); fussiness, high fever (Pediarix is associated with higher rates of fever relative to separately administered vaccines. The prevalence of fever was highest on the day of vaccination and the day following vaccination).
  • Other Serious Reported Adverse Events: High fever that required medical attention (In a safety study that evaluated medically attended fever after Pediarix or separately administered vaccines when co-administered with 7-valent pneumococcal and Hib conjugate vaccines, infants who received Pediarix had a higher rate of medical encounters for fever within the first 4 days following the first vaccination); febrile and afebrile convulsions (seizures); gastroenteritis, bronchiolitis; asthma, diabetes mellitus, and chronic neutropenia; anaphylactic reactions (hives, swelling, difficulty breathing, hypotension or shock); and demyelinating diseases.
  • Contraindications and precautions (Some reasons why Pediarix should not be given to a child – See GlaxoSmithKline product insert for complete list):
    • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
    • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
    • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
    • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
    • Serious allergic reaction to a previous pertussis vaccination;
    • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
    • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
    • Sensitivity to any component of Pediarix, including yeast or neomycin and polymyxin B (antibiotics);
    • Apnea following intramuscular vaccination has been observed in some infants born prematurely. Pediarix vaccine product insert warns that the decision to vaccinate an infant born prematurely should take into consideration both the potential risks and possible benefits of vaccination;
    • The tip caps of prefilled Pediarix syringes contain latex and may cause an allergic reaction in persons sensitive to latex;
    • If Guillain-Barré syndrome (GBS) occurred within 6 weeks of receiving a tetanus containing vaccine, careful assessment of the possible risks and potential benefits should be completed prior to considering Pediarix vaccine.

NVIC NOTE: Some doctors only vaccinate children who are healthy and are not sick with a coinciding viral or bacterial infection at the time of vaccination. If you do not want your acutely ill baby vaccinated and your doctor disagrees with you, you may want to consider consulting one or more other trusted health care professionals before vaccinating.

Animal reproduction studies have not been conducted with Pediarix. It is not known whether Pediarix can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. Pediarix has not been evaluated for carcinogenic or mutagenic potential, or for impairment of fertility.

About Kinrix Vaccine in Brief

  • Ages: Kinrix is a 4 in 1 shot (diphtheria, tetanus, acellular pertussis, inactivated polio vaccines) given to children 4 to 6 years old (see GlaxoSmithKline product insert for recommended schedule and other indications).
  • Vaccine Ingredients: Aluminum hydroxide, VERO cells, a continuous line of monkey kidney cells, calf serum, lactalbumin hydrolysate, fenton medium containing a bovine extract, modified Latham medium derived from bovine casein, formaldehyde, modified Stainer-Scholte liquid medium, glutaraldehyde, sodium chloride, polysorbate 80 (Tween 80), neomycin sulfate, polymyxin B.
  • Estimated Efficacy: Antibody responses to poliovirus type 1, type 2, and type 3 were tested in children between 4 and 6 years of age who previously received doses of IPV vaccine, 4 doses of INFANRIX (DTaP), and 1 dose of MMR vaccine. Kinrix was administered simultaneously with the second dose of MMR vaccine and antibodies levels were tested one-month post-vaccination. At this time, nearly 100 percent vaccine recipients were found to have blood antibody levels considered to be protective against all three poliovirus strains (type 1 – 99.9 percent; Type 2 – 100 percent; Type 3 – 100 percent).
  • Pre-licensing Clinical comparison studies: Clinical trials to assess the safety of Kinrix prior to licensing did not include a placebo-control group.
  • Use with Other Vaccines: In clinical trials, Kinrix was administered simultaneously with the second dose of MMR or MMR and varicella vaccine. There is no information in the product insert about the safety or effectiveness of giving Kinrix simultaneously with inactivated or live influenza, hepatitis B, or hepatitis A vaccines.
  • Commonly Reported Adverse Events: Injection site pain, including redness, swelling and increase in arm circumference; drowsiness; fever; and loss of appetite.
  • Other Serious Reported Adverse Events: Gastroenteritis, dehydration, and cellulitis. After licensure (post-marketing), reported adverse event have also included apnea, collapse or shock-like state (hypotonic-hyporesponsive episode), convulsions (with or without fever), injection site vesicles, pruritus (intense itching), allergic reactions, including anaphylaxis, urticaria, angioedema, lympadenopathy, and thrombocytopenia.
  • Contraindications and precautions (Some reasons why Kinrix should not be given to a child – See GlaxoSmithKline product insert for complete list):
    • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
    • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
    • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
    • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
    • Serious allergic reaction to a previous pertussis vaccination;
    • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
    • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
    • Severe allergic reaction to any component of Kinrix, including neomycin and polymyxin B (antibiotics);
    • The tip caps of prefilled Kinrix syringes contain latex and may cause an allergic reaction in persons sensitive to latex;
    • If Guillain-Barré syndrome (GBS) occurred within 6 weeks of receiving a tetanus containing vaccine, careful assessment of the possible risks and potential benefits should be completed prior to considering Kinrix vaccine.

NVIC NOTE: Some doctors only vaccinate children who are healthy and are not sick with a coinciding viral or bacterial infection at the time of vaccination. If you do not want your acutely ill baby vaccinated and your doctor disagrees with you, you may want to consider consulting one or more other trusted health care professionals before vaccinating.

Animal reproduction studies have not been conducted with Kinrix. It is not known whether Kinrix can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. Kinrix has not been evaluated for carcinogenic or mutagenic potential, or for impairment of fertility.

About Quadracel Vaccine in Brief

  • Ages: Quadracel is a 4 in 1 shot (diphtheria, tetanus, acellular pertussis, inactivated polio vaccines) given to children 4 to 6 years old (see Sanofi Pasteur product insert for recommended schedule and other indications).
  • Vaccine Ingredients: Aluminum phosphate, Stainer-Scholte medium, casamino acids, dimethyl-beta-cyclodextrin, MRC-5 cells, normal human diploid cells, CMRL 1969 medium supplemented with calf serum, modified Mueller’s growth medium, ammonium sulfate, modified Mueller-Miller casamino acid medium without beef heart infusion, formaldehyde, 2-phenoxyethanol, polysorbate 80, glutaraldehyde, neomycin, polymyxin B sulfate.
  • Estimated Efficacy:  Antibody responses to poliovirus (Type 1, Type 2, Type 3) were tested in children between 4 and 6 years of age 28 days following Quadracel administered simultaneously MMR, and varicella vaccines. At this time, 100 percent of vaccine recipients were found to have blood antibody levels considered to be protective against all three poliovirus strains.
  • Pre-licensing Clinical comparison studies: Clinical trials to assess the safety of Quadracel prior to licensing did not include a placebo-control group.
  • Use with Other Vaccines: In clinical trials, Quadracel was administered simultaneously with the MMR and varicella. There is no information in the product insert about the safety or effectiveness of giving Quadracel simultaneously with inactivated or live influenza, hepatitis A, or hepatitis B vaccines.
  • Commonly Reported Adverse Events: Injection site pain, including redness, swelling and increase in arm circumference; malaise; muscle pain; headache.
  • Other Serious Reported Adverse Events: After licensure (post-marketing) reported adverse event reports have also included cyanosis; convulsions (with or without fever); injection site abscess; injection site cellulitis; pallor; screaming; allergic reactions, including anaphylaxis; urticarial, and dyspnea.     
  • Contraindications and precautions (Some reasons why Quadracel should not be given to a child – See Sanofi Pasteur product insert for complete list):
    • Serious allergic reaction following administration of a pertussis, tetanus, diphtheria, or polio containing vaccine or any ingredient of Quadracel vaccine;
    • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
    • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
    • Seizures within 3 days of a previous pertussis vaccination;
    • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
    • If Guillain-Barré syndrome (GBS) occurred within 6 weeks of receiving a tetanus containing vaccine, careful assessment of the possible risks and potential benefits should be completed prior to considering Quadracel vaccine.

NVIC NOTE: Some doctors only vaccinate children who are healthy and are not sick with a coinciding viral or bacterial infection at the time of vaccination. If you do not want your acutely ill baby vaccinated and your doctor disagrees with you, you may want to consider consulting one or more other trusted health care professionals before vaccinating.

Animal reproduction studies have not been conducted with Quadracel. It is not known whether Quadracel can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. Quadracel has not been evaluated for carcinogenic or mutagenic potential, or for impairment of fertility.

About Pentacel Vaccine in Brief

  • Ages: Pentacel is a 5 in 1 shot (diphtheria, tetanus, acellular pertussis, inactivated polio and Haemophilus influenzae b conjugate vaccines) for children under age 5 (see Sanofi Pasteur product insert for recommended schedule and other indications).
  • Vaccine Ingredients: Aluminum phosphate, polysorbate 80, sucrose, formaldehyde, glutaraldehyde, bovine serum albumin, 2-phenoxyethanol, MRC-5 cells (a line of normal human diploid cells), CMRL 1969 medium supplemented with calf serum, Medium 199 without calf serum, modified Mueller and Miller medium, neomycin, polymyxin B sulfate, modified Mueller’s growth medium, ammonium sulfate, modified Mueller-Miller casamino acid medium without beef heart infusion, Stainer-Scholte medium, casamino acids, dimethyl-beta-cyclodextrin.
  • Estimated Efficacy: Antibody responses to polio were tested one month following 3 doses of Pentacel at 2, 4, and 6 months. At this time, 99.4 percent of vaccine recipients were found to have blood antibody levels considered to be protective against poliovirus.
  • Pre-licensing Clinical comparison studies: Clinical trials to assess the safety of Pentacel prior to licensing did not include a placebo-control group.
  • Use with Other Vaccines: In clinical trials, Pentacel was given with hepatitis B, pneumococcal, MMR or varicella vaccines. There is no information in the product insert about the safety or effectiveness of giving Pentacel simultaneously with inactivated or live influenza, rotavirus, or hepatitis A vaccines
  • Commonly Reported Adverse Events: Systemic reactions that occurred in clinical trials in more than 50 percent of participants following any dose included: fussiness/irritability and inconsolable crying; fever; injection site reactions, including tenderness, abscess and increase in arm circumference. Cases of encephalopathy and death occurred in clinical trials but were not causally attributed to Pentacel vaccine by investigators.
  • Other Serious Reported Adverse Events: After licensure (post marketing), there have been reports of febrile and afebrile convulsions (seizures); bronchiolitis, gastroenteritis, dehydration, pneumonia, lethargy/somnolence; hypotonic/hyporesponsive episode (collapse); apnea; cyanosis; and asthma.
  • Contraindications and precautions (Some reasons why Pentacel should not be given to a child – See Sanofi Pasteur product insert for complete list):
    • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
    • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
    • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
    • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
    • Serious allergic reaction to a previous pertussis vaccination;
    • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
    • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
    • Severe allergic reaction to any component of Pentacel, including neomycin and polymyxin B (antibiotics);
    • Apnea following intramuscular vaccination has been observed in some infants born prematurely. The Pentacel vaccine product insert warns that the decision to vaccinate an infant born prematurely should take into consideration both the potential risks and possible benefits of vaccination;
    • If Guillain-Barré syndrome (GBS) occurred within 6 weeks of receiving a tetanus containing vaccine, careful assessment of the possible risks and potential benefits should be completed prior to considering Pentacel vaccine.

NVIC NOTE: Some doctors only vaccinate children who are healthy and are not sick with a coinciding viral or bacterial infection at the time of vaccination. If you do not want your acutely ill baby vaccinated and your doctor disagrees with you, you may want to consider consulting one or more other trusted health care professionals before vaccinating.

Animal reproduction studies have not been conducted with Pentacel. It is not known whether Pentacel can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. Pentacel has not been evaluated for carcinogenic or mutagenic potential, or for impairment of fertility.

About VAXELIS Vaccine in Brief

  • Ages: VAXELIS is a 6 in 1 shot (diphtheria, tetanus, acellular pertussis, inactivated poliomyelitis, Haemophilus influenzae b (Meningococcal Protein Conjugate) and hepatitis B (recombinant vaccines) for infants and children 6 weeks through 4 years of age (prior to the 5th birthday) (see MCM company product insert for recommended schedule and other indications).
  • Vaccine Ingredients: Aluminum, polysorbate 80, glutaraldehyde, formaldehyde, bovine serum albumin, neomycin, streptomycin sulfate, polymyxin B sulfate, yeast protein, ammonium thiocyanate, Mueller’s growth medium, Mueller-Miller casamino acid medium without beef heart infusion, ammonium sulfate, aluminum phosphate, Stainer-Scholte medium, Vero cells, extract of yeast, soy peptone, dextrose, amino acids, mineral salts, amorphous aluminum hydroxyphosphate sulfate.
  • Estimated Efficacy: One month following the administration of 3 doses of VAXELIS, 100 percent of vaccine recipients were found to have antibodies considered protective against all 3 strains of poliovirus.
  • Pre-licensing Clinical comparison studies: Clinical trials to assess the safety of VAXELIS prior to licensing did not include a placebo-control group.
  • Use with Other Vaccines: In clinical trials, VAXELIS was given with pneumococcal (Prevnar 13) and rotavirus (RotaTeq) vaccines. There is no information in the product insert about the safety or effectiveness of giving VAXELIS simultaneously with inactivated or live influenza, hepatitis A, measles, mumps, rubella (MMR), varicella, or measles, mumps, rubella and varicella (MMR-V) vaccines.
  • Commonly Reported Adverse Events: Systemic reactions that occurred in clinical trials following any dose included: injection site redness, swelling, and pain; fever; crying; decreased appetite; irritability; vomiting; and somnolence.
  • Other Serious Reported Adverse Events: In the two U.S. clinical trials, 6 deaths were reported but were determined by trial investigators not to be caused by VAXELIS. These deaths included sepsis, asphyxia, hydrocephalus, unknown cause, and two cases of sudden infant death syndrome (SIDS). As VAXELIS is not currently available for use in the United States, post-marketing data on serious adverse events are limited to those events considered to have a causal link to the vaccines containing the antigens of VAXELIS. These include anaphylaxis, hypersensitivity, seizures, including febrile seizures, and excessive swelling of the injected limb.
  • Contraindications and precautions (Some reasons why VAXELIS should not be given to a child – See MCM Vaccine Company product insert for complete list):
    • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
    • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
    • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
    • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
    • Serious allergic reaction to a previous dose of VAXELIS, any ingredient found in VAXELIS, or any other tetanus toxoid, diphtheria toxoid, pertussis-containing vaccine, hepatitis B vaccine, inactivated poliovirus vaccine, or H. influenzae type b vaccine;
    • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
    • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
    • If Guillain-Barré syndrome (GBS) occurred within 6 weeks of receiving a tetanus containing vaccine, careful assessment of the possible risks and potential benefits should be completed prior to considering VAXELIS vaccine;
    • Apnea following intramuscular vaccination has been observed in some infants born prematurely. The decision to vaccinate an infant born prematurely should be careful based on both the possible benefits and potential risks of vaccination.

NVIC NOTE: Some doctors only vaccinate children who are healthy and are not sick with a coinciding viral or bacterial infection at the time of vaccination. If you do not want your acutely ill baby vaccinated and your doctor disagrees with you, you may want to consider consulting one or more other trusted health care professionals before vaccinating.

Animal reproduction studies have not been conducted with VAXELIS. It is not known whether VAXELIS can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. VAXELIS has not been evaluated for carcinogenic or mutagenic potential, or for impairment of fertility.

What is the history of Polio vaccine use in America?

Early vaccine development

The first use of a poliovirus vaccine in the United States occurred in 1934, prior to the discovery that there were 3 poliovirus types, type 1, 2, and 3. This unlicensed experimental vaccine contained a poliovirus obtained from the nerve tissue of an infected monkey which was then ground up and mixed with formalin, a formaldehyde agent, in an attempt to inactivate the poliovirus without impairing its ability to stimulate antibody production.

William Park and Maurice Brodie, the two researchers responsible for the experimental poliovirus vaccine, published their findings in the Journal of the American Medical Association (JAMA) in 1935 and after vaccinating a dozen children, reported that their vaccine appeared to be safe.232

Following publication of their findings, health officials experiencing polio outbreaks requested that this vaccine be tested on a larger number of individuals. While some officials involved in the vaccine trials reported the experimental poliovirus vaccine to be effective at preventing polio, others blamed cases of polio on the vaccine itself. The vaccine trials were poorly run, and no accurate information could be gathered to determine the vaccine’s effectiveness.233 234

At the same time as Park and Brodie were conducting clinical trials on their inactivated poliovirus vaccine, John A. Kolmer, a pathologist from Philadelphia began testing his live virus vaccine. This experimental vaccine was reportedly weakened with chemicals that included two highly toxic mercury containing compounds -mercurophen and merthiolate.235   After testing the live virus vaccine on a few monkeys, Kolmer vaccinated himself, his 2 sons, and 23 additional children before expanding its use to include over 10,000 individuals. Nine people who received his vaccine died and dozens were paralyzed.236 237

In the late 1940s, research aimed at determining how many poliovirus types were circulating in the environment began. By 1949, a team led by Dr. David Bodian reported that at least 3 distinct poliovirus types existed but researchers continued to study polio strains by collecting samples of throat cultures, stool, and even nerve tissue, from persons who developed or died of polio.238 Between 1949 and 1951, more than $1.2 million dollars was spent on poliovirus typing, with most of the money used to purchase and transport monkeys for experimental purposes.239

Poliovirus researchers used monkeys for polio research, and during the typing experiments, stool samples from persons who had developed polio were injected into the brains of monkeys. These monkeys were monitored for symptoms of polio and when these occurred, they were killed so that their poliovirus-infected spinal cords and brain tissues could be collected. Over 17,000 monkeys were killed between 1949 and 1951 but no additional poliovirus types were isolated.240

Researchers had already concluded that the poliovirus could be grown in the nervous tissue of monkeys but were aware that they could not use this tissue to develop a vaccine because monkey nervous tissue was known to cause an inflammation of the spinal cord and brain (encephalomyelitis) in humans.241 In 1949, however, a team of researchers from the Children’s Hospital of Boston led by microbiologist Dr. John Enders, discovered that the poliovirus could also be grown in kidney, skin, and muscle tissue and in a test tube, instead of in the spinal cord or brain of a monkey.242 243

Once it was determined that only three poliovirus types existed, and that cultures could be grown in a test tube in other tissues besides monkey nervous tissues, work on a killed virus vaccine began.

At this time, however, research on a live attenuated poliovirus vaccine was already underway, led by Dr. Hilary Koprowski, a scientist with Lederle pharmaceuticals. In 1950, Koprowski tested his vaccine on institutionalized children residing at New York’s Letchworth Village without permission from New York state officials. Koprowski reported that children involved in the secretive trial developed antibodies against type 2 poliovirus without experiencing paralysis. His experiment was, however, criticized by fellow researchers who questioned the ethics of experimenting on institutionalized children.244

Salk’s Inactivated poliovirus vaccine

By 1950, University of Pittsburgh poliovirus researcher Dr. Jonas Salk had begun working on a killed poliovirus vaccine derived from monkey kidney cells seeded with live poliovirus. Researchers working with Salk had found monkey kidneys to be ideal for developing cell cultures and that one monkey kidney could produce several thousand poliovirus vaccine doses.245

The killed poliovirus vaccine would contain all 3 poliovirus types selected from strains isolated in the samples submitted to laboratories from poliovirus patients. Salk selected type 1 from the Mahoney strain, isolated in 1941 and responsible for over 80 percent of all cases of paralytic polio; type 2 from the Middle East Forces strain, isolated from the spinal tissue of a British soldier who died from polio in Egypt in 1943; and type 3 from the Saukett strain, isolated by Salk himself, from the stool of a child with polio.246 247

The selected strains were then inactivated by a process that used formaldehyde in a 250:1 ratio at a temperature of one degree Celsius. This process was required to be perfect to ensure that the poliovirus could produce an immune response but be incapable of causing paralytic polio.248 249

Early testing of Salk’s killed poliovirus vaccine began in 1952 at two different institutions in Pennsylvania – the D.T. Watson Home for Crippled Children and the Polk School for the Retarded and Feeble-Minded.250  The Watson Home, a stately facility for persons recovering from paralytic polio, was considered one of the best rehabilitation centers, and patients administered Salk’s experimental vaccine were considered at low risk due to previous exposure to polio. With this experiment, Salk tested each patient to determine what poliovirus type had likely caused the paralysis and then injected them with an experimental vaccine containing only that particular strain. This experiment was done to see whether his vaccine could raise antibody levels even higher than what was previously found and whether they would remain elevated for an extended period.251

The Polk School, however, housed individuals with intellectual disabilities, and was considered a depressing institution that was poorly staffed and overcrowded. While some residents had measurable antibody to at least one type of poliovirus, others did not, and this put them at a high-risk for developing polio from an incorrectly inactivated experimental vaccine.252

Salk continued to change his vaccine formulation during the vaccine trial process. Some formulations contained mineral oil while others did not. He tried a single type poliovirus vaccine on some residents and gave others a vaccine containing all 3 types. He even experimented with the process by which the poliovirus was inactivated. Salk reported that his killed vaccine was safe for human use and capable of producing an antibody response to all 3 poliovirus types that persisted for several months.253 254

Coincidentally, the worst poliovirus year in history also occurred in 1952, with over 57,000 reported cases in the United States, and 3,000 deaths.255 Some attributed the rise in reported 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 causing an increase in polio.256

In March 1954, Salk appeared on the cover of Time magazine and an article accompanied his photo which reported on the success of the small vaccine trials. His findings had not yet been published in any medical journal and Salk reported that his vaccine would not be available for the public before the next polio season.257

Preparations for a large-scale vaccine trial that would begin in the early part of the spring in 1954 began after the publicity Salk received in Time magazine. The Vaccine Advisory Committee, the committee charged with overseeing the trials, wanted a double-blind placebo study to ensure that the vaccine was indeed safe and effective. Salk, on the other hand, initially refused to agree to this condition, as he felt that he would not be able to live with himself if a child who received the placebo contracted polio and it could have been prevented by his vaccine. Salk eventually agreed to have a control group as part of the field trial after his former mentor, Thomas Francis, was selected to evaluate the trial’s results. 258

Connaught Laboratories in Toronto cultivated the live poliovirus for use in the vaccines and shipped them to Parke-Davis pharmaceuticals in Detroit for vaccine production.259 Vaccine manufacturing problems occurred immediately and were blamed on the complex process involved to ensure that the poliovirus was inactivated. Additionally, Salk was still refining his vaccine product even though it was supposed to be in the manufacturing stages for use in the vaccine field trials slated to begin in 1954.260

By the fall of 1953, after several failed attempts by Parke-Davis to consistently duplicate Salk’s vaccine, additional pharmaceutical companies were approached to assist in vaccine development, including Cutter Laboratories, Eli Lilly, Wyeth, and Sharp and Dohme. Stricter quality controls were also established and would require each batch of poliovirus vaccine be triple-tested – by the pharmaceutical company, by Salk’s lab, and by the Public Health Service – to ensure that the vaccine was safe and effective for use.261

Questions about the safety of Salk’s vaccine began to surface, by both the media and by other scientists. Oral poliovirus vaccine (OPV) developer, Dr. Albert Sabin, who was actively working on a rival vaccine, voiced concerns about the size of the study population, the poliovirus type 1 strain selected for use in the vaccine, and the speed at which the vaccine had gone from being an experiment in a laboratory, to one expected to be injected into hundreds of thousands of children. Further, the media was told that certain vaccine batches were found to contain live poliovirus.262

Due to the negative publicity, an additional safeguard was initiated that would require the vaccine manufacturer to produce eleven consecutive vaccine lots free of live poliovirus prior to allowing the use of one lot by the public. Salk was also required to complete a smaller field test involving 5,000 children to ensure that the vaccine was safe prior to starting the mass vaccination trial.

Salk reported his smaller vaccine trial as successful and on April 26, 1954, the large-scale clinical trial began. Problems did occur during the clinical trial and included the administration of multiple doses to a single child, the reuse of needles between children, the loss of records, and even illness and death following vaccination.263

The trial, which involved over 1.3 million children of whom over 600,000 received at least one dose of vaccine, ended in late spring of 1954. It took, however, nearly a year for the results to be evaluated and publicly presented. On April 12, 1955, at an official press conference scheduled specifically to discuss the outcomes of the field trial, Dr. Thomas Francis reported Salk’s vaccine to be between 60 and 70 percent effective at preventing paralytic polio.264 265 266 The 1954 vaccine was, however, reported to be ineffective at preventing non-paralytic polio.267

Within 2 hours of the announcement, the U.S Department of Health, Education, and Welfare (HEW), a newly formed government agency which encompassed the Public Health Service, voted to approve the vaccine for use. Even though it was not yet known if Salk’s vaccine would be approved for use, preparations had already been made to ensure that the vaccine would be available immediately for commercial use. Six pharmaceutical companies had manufactured 9 million vaccines in advance and these vaccines became available for use by the American public right after approval. 268

Immediately following the vaccine’s approval, the safety provisions which required each vaccine lot to be triple-tested were no longer enforced, and vaccine manufacturers were the only ones screening their products. 269 270  As a result, vaccine lots containing live poliovirus were not caught and within 2 weeks, the consequences would be apparent – when recently vaccinated children began developing polio.271 272  

Cases of paralytic polio following vaccination were reported in several states including California and Idaho. All cases occurred within 10 days of vaccination and paralysis frequently began in the limb where the injection had been administered – not in the lower limbs of the body as what was classically seen with paralytic polio. It was also discovered that most cases of paralysis had occurred in children vaccinated with a poliovirus vaccine manufactured by Cutter Laboratories.273

Public health officials did not immediately halt the poliovirus vaccination program or even stop Cutter Laboratories from manufacturing or distributing the poliovirus vaccine. Instead, U.S. Surgeon General Leonard A. Scheele called Cutter Laboratories executives on April 27th and requested that they recall all their poliovirus vaccines. Publicly, Scheele stated that there was no correlation between paralytic polio and use of the vaccine, but few believed him. Polio had also occurred in persons vaccinated with vaccines manufactured by both Eli Lilly and Wyeth, though less frequently.274 Additionally, cases of polio were also reported among family members of children who were administered the polio vaccine, particularly those who received vaccines made by Cutter Laboratories.275

The incidence of polio following vaccination continued to rise and by May 8, 1955, Scheele ordered that all poliovirus vaccination programs be halted until a review of the six poliovirus vaccine makers could be completed. Five days after Scheele halted use of all poliovirus vaccines, the vaccines manufactured by Parke-Davis and Eli Lilly were cleared for use. As questions remained about the safety of the vaccine, the demand for the vaccine was much less.276

What was not known at the time of this incident was that National Institutes of Health (NIH) microbiologist, Dr. Bernice Eddy, had reported to her NIH supervisors that vaccines manufactured by Cutter Laboratories in 1954-1955 were causing paralysis in laboratory monkeys. NIH director, Dr. William Sebrell chose to ignore Eddy’s findings and her immediate supervisor called her “an alarmist”.277

While lots of poliovirus vaccine manufactured during the 1954 field trials were required to undergo strict testing prior to use, vaccines made for commercial use were not and after the vaccine was licensed for use, Cutter Laboratories would not report problems and would simply discard vaccine lots found to be contaminated with the live poliovirus.278

The poliovirus vaccine manufactured by Cutter was found to be responsible for 40,000 cases of polio – including 200 cases of severe polio and 10 deaths.279

There were 18,308 cases of paralytic polio and 20,168 cases of non-paralytic polio in 1954. In 1955, the year that Salk’s vaccine received approval, this number had decreased to 13,850 paralytic cases and 15,135 non-paralytic cases.280 Incidentally, diagnosing criteria for polio also changed. 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:281

“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: 282

“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.”

While Salk’s vaccine is credited with decreasing the number of polio cases immediately following its 1955 approval, public health experts noted that polio, like other infectious diseases, have natural variability, and in 1955, rates of infectious hepatitis, an infection with no vaccine at the time, also declined at a similar rate as polio.283

Additionally, prior to the introduction of the Salk vaccine, an epidemic of polio was considered 20 or more cases of polio per 100,000 population. After the Salk vaccine became available, a polio epidemic was defined as 35 cases per 100,000. This definition change artificially decreased the number of epidemics in the U.S.  Further, there were few efforts made to differentiate between paralysis cause by the poliovirus or paralysis caused by other factors such as enteroviruses (ECHO and Coxsackie), transverse myelitis, Guillain-Barre Syndrome, DDT and arsenic toxicity, and more. 284 285

This is evidenced by a study published in 1960 which reported on a polio epidemic in Michigan that noted:286

“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 began to increase in 1958 and again in 1959. Public health officials quickly blamed the rise in polio rates on a lack of vaccination – yet by 1958, vaccination rates had significantly increased from those reported between 1955 and 1957. 287 288 Further, polio was being reported in persons who had received one or more vaccine doses, including those who had received three and four doses. 289

By 1960, some poliovirus experts were even hypothesizing that the use of the Salk vaccine might actually put a person at a higher risk of paralytic polio, when a 1959 polio epidemic in Massachusetts reported that 47 percent of the cases that involved paralysis had occurred in persons who had received three or more vaccine doses. 290  By 1961, over 47 percent of individuals who developed paralytic polio but recovered without residual paralysis and over 27 percent who had developed paralytic polio with residual paralysis had received 3 doses of the Salk vaccine.291

Many doctors were opting to vaccinate infants and children with Salk’s poliovirus vaccine at the same time as the combination diphtheria, pertussis, and tetanus vaccine (DTP), a vaccine which had been in use since the 1940s. As a result, Parke-Davis pharmaceuticals developed Quadrigen, a combination vaccine containing DTP and Salk’s inactivated poliovirus vaccine.292 The vaccine was approved for use in 1959 but was removed from the market in 1968 after multiple lawsuits found that it caused severe injuries in children.293 294 Additional combination vaccines containing DTP and polio were also approved for use in 1959, but by 1968, all had been removed from the market.295

By 1962, approximately 400 million doses of Salk’s IPV vaccine had been administered in the U.S., but public health officials estimated that most children had not received the four recommended vaccine doses. Polio in persons who had received 3 and 4 IPV doses were still occurring sporadically but public health officials reported that most cases occurred among under-vaccinated and unvaccinated individuals.296

The first dose of IPV was recommended at 6 weeks to 3 months of age, with 2 more doses recommended at least 6 weeks apart. A fourth dose was also recommended, and this dose was supported to be administered at least 6 months after the third dose. The same schedule was also recommended for use in other age groups.297

After 1963, and the approval of the live oral poliovirus vaccine (OPV), IPV usage decreased and in 1968, only 2.7 million IPV doses were distributed in the U.S.298 In 1969, the CDC published its first Advisory Committee on Immunization Practices (ACIP) recommendations and reported that IPV use had essentially been replaced by OPV due this vaccine’s ease of use, superior immune response, and lack of booster requirements.299

Live Oral Poliovirus Vaccine Development

Salk was not the only poliovirus vaccine researcher in the 1950s. Dr. Albert Sabin, another researcher who had begun working on a live-virus polio vaccine by 1951, was still actively developing his product when Salk’s killed vaccine was approved for use in the U.S.300

Sabin had always believed that a live-virus oral polio vaccine, attenuated enough to produce a mild infection but weak enough not to cause harm, was the only way to stop polio. Many scientists also considered this live-virus vaccine to be preferential because it could be administered orally and mimic the way that the poliovirus enters and replicates in the body. His vaccine would contain all 3 types of poliovirus strains and he attenuated the virus by passing each one through the tissue of monkeys. The first testing of his live-virus vaccine took place in 1954- 1955 among adult prisoners, and Sabin reported that all 30 prisoners who received his vaccine safely developed antibodies to all 3 types of polio. He was, however, aware that his live-virus vaccine could revert to being virulent and capable of causing polio.301

This, in fact, was what had occurred when Lederle pharmaceutical researcher, Dr. Hilary Koprowski was permitted to begin testing his live-virus vaccine in Belfast, Northern Ireland. Early in the study, stool samples acquired post-vaccination of monkeys found poliovirus vaccine particles that had become problematic and even capable of producing paralysis. When this was discovered, the vaccine trial was halted.302

Sabin was also aware that he would not be able to run a large-scale vaccine trial in the U.S. because this had already occurred. Polio cases, however, were increasing in the Soviet Union, and researchers from Russia were looking to the U.S. for information on the poliovirus vaccine. Russian scientists at the time were not convinced that Salk’s vaccine was all that effective, and production and administration of the vaccine was expensive. Further, at times, the final product was not always acceptable for use due to manufacturing issues.303

Sabin was permitted to go to the Soviet Union to continue work on his vaccine and in 1959, millions of Russian children were vaccinated with Sabin’s live-virus vaccine. By the end of the year, Russia declared the vaccine effective and their health ministry announced that all persons under the age of 20 years would receive Sabin’s vaccine. 304  

Sabin was not the only live-virus poliovirus vaccine researcher in the 1950s and early 60s. Koprowski, who had initially failed to develop a safe oral polio vaccine in Belfast, continued to expand on his earlier work. By this time, he was working for the Wistar Institute and had developed 2 separate vaccines – the CHAT-type1 oral polio vaccine and the W-Fox- type 3 oral polio vaccine. Koprowski’s vaccines were used to mass vaccinate children in the Belgian Congo,305 Poland306 307 and Croatia.308 Double-blind placebo-controlled studies of his experimental vaccine were not completed, and in most cases, government officials mandated the vaccine without even knowing whether it was safe or effective.

Additionally, a team of scientists from Lederle Pharmaceuticals led by Dr. Herald Cox, Koprowski’s former boss, tested another experimental oral polio vaccine on a small group of volunteers in Minnesota in 1958,309 before administering it to hundreds of thousands of individuals in South America.310

In 1960, Sabin and Cox were granted permission to proceed with vaccine trials in the U.S.311 Sabin chose to test his oral polio vaccines near his home in Cincinnati, Ohio and administered his vaccine to nearly 200,000 people – even though most in the area had already received the Salk vaccine and polio was no longer an issue.312 313

Cox chose to run his trial in Dade County, Florida, and administered his trivalent oral polio vaccine to over 400,000 individuals. The vaccine was reported as effective and even preferred over Sabin’s vaccine as it contained all 3 types of polio in a single dose; however, 6 cases of severe polio occurred within 7-14 days of vaccination. As a result, Cox’s vaccine failed to receive approval for licensing. 314 315

The U.S. Surgeon General approved Sabin’s poliovirus vaccine to be manufactured on a trial basis in August 1960.316 Four major pharmaceutical companies, including Cox’s employer, Lederle pharmaceutical, announced plans to manufacture Sabin’s vaccine.

Salk and Sabin were known rivals, with Sabin a frequent critic of Salk and his vaccine. Sabin was quick to discount the killed vaccine as ineffective and after the ‘Cutter Incident,’ he had called for the complete removal of the Salk vaccine from the market.

With both vaccines licensed for use, the controversy and competition became even more fierce. Also, doctors were not sure what vaccine would be best for their patients and were requesting to have information provided to them from a ‘neutral’ source. In 1961, the American Medical Association (AMA) entered the polio vaccine discussions and stated that their “Council on Drugs” would evaluate the situation and issue a report.

The chair of the AMA’s Council on Drugs, however, was the former medical director of Pfizer pharmaceuticals, one of the four drug companies involved in the manufacturing of Sabin’s oral poliovirus vaccine. In July 1961, the AMA officially recommended that Sabin’s vaccine be used instead of Salk’s killed vaccine, even though Sabin’s vaccine had not yet been officially licensed.317

Sabin’s type 1 oral poliovirus vaccine received approval for use within a month of the AMA’s decision and his type 2 and type 3 vaccines would receive licensing within a year. In the U.S., Sabin’s oral polio vaccine would replace Salk’s killed vaccine; however, Salk’s vaccine would still be used globally, in countries such as the Netherlands,318 and Sweden.319

Sabin’s monovalent type 1 OPV was first licensed in August of 1961 and two months later, his type 2 OPV received approval. By the spring of 1962, Sabin’s type 3 had received approval and Subcommittee One of the Advisory Committee on Poliomyelitis Control recommended that in infants, each of the three types of OPV be administered sequentially, beginning with type 1 OPV between 6 weeks and 3 months of age. Type 3 OPV was recommended 6 weeks later, followed by type 2 OPV after another 6 weeks. A fourth dose of a trivalent OPV was recommended 6 months or more after administration of the type 2 OPV. This schedule was similar for other age groups except that a fourth OPV dose was not recommended.320

Reports of paralysis after administration of Sabin’s vaccine, like Cox’s vaccine, were also being reported, but public health officials did not express concern.321 322 323 By December of 1962, the Special Advisory Committee on Oral Poliomyelitis to the Surgeon General of the Public Health Service announced that communities should move forward with vaccination plans using all three types of OPV, with a special focus on vaccine administration in children and young adults. OPV associated paralysis was noted in the report but in nearly all cases, public health officials stated that most cases were inconclusive and the risk of acquiring polio from the vaccine was small.324

In 1962, Wistar Institute researcher Leonard Hayflick announced that he had developed an alternative to monkey kidney cells for use in the production of the poliovirus vaccine.325 Hayfield had developed a cell substrate from human diploid lung fibroblasts – WI-38- taken from the lung cells of a 12-week-old female fetus.326 This cell line was reportedly free of viruses and Hayfield believed it to be a safer option to monkey kidney cells with their known simian viruses- such as the recently discovered Simian Virus 40 (SV40), which was found capable of causing cancer in small animals. 327  

Federal health regulatory agencies, however, were not convinced that this cell line would be safe and declined to make any changes to polio vaccine production. Their rationale was that while this cell line appeared safe and free of adventitious ingredients, they did not feel there was enough evidence that could prove that it would remain so.

Hayfield chose to distribute vials of his cell substrate to laboratories in Europe and even the Soviet Union. The first poliovirus vaccine produced using WI-38 was approved for use in Yugoslavia in 1967, and approvals followed in the Soviet Union, Great Britain, and France. It took until 1972 for the U.S. to approve Diplovax; however, issues with supply of the vaccine limited its use, and by 1976, it was no longer available in the U.S.328

In 1969, the CDC published its first Advisory Committee on Immunization Practices (ACIP) recommendations, and at this time OPV was considered the preferred vaccine, due to the ease of use, superior immune response, and lack of booster requirements.329

The use of OPV was again considered the preferred vaccine in both 1982 and 1987, when the CDC’s ACIP committees updated their recommendations for the use of poliovirus vaccines. Persons with immunodeficiencies or with conditions which altered their immune response such as those with cancer or those undergoing corticosteroid treatments were, however, recommended to receive IPV due to the potential risk of vaccine-induced paralysis.330 331

Wild-type polio was declared eradicated in the U.S. 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.332 

VAPP was associated with the use of OPV nearly immediately following the vaccine’s introduction. When OPV was in use in the U.S., 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. At the June 1996 ACIP meeting, committee members voted to increase the use of IPV and to gradually decrease OPV usage over the next 3-5 years because of the risk of VAPP.333

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 2000.334 OPV, however, remains in use in certain countries, and continues to be the preferred vaccine for use in global campaigns aimed at eradicating polio.335

Current Poliovirus Vaccines and Recommendations in the United States

In 2000, two IPV products were licensed for use in the U.S. – Poliovax and IPOL. These two vaccines remain licensed for use in the U.S; however, Poliovax, which contains all 3 poliovirus types grown on MRC-5 human diploid cells, has been discontinued by the manufacturer.336 At this time, the CDC’s Advisory Committee on Immunization Practices (ACIP) recommended that all children receive 4 doses of IPV at 2, 4, 6-18 months, and 4-6 years. 337

IPOL is an inactivated poliovirus vaccine containing all 3 poliovirus types grown on monkey kidney cells (Vero cells), a cell line derived from African green monkey kidneys in the 1960s. Additional ingredients include calf bovine serum albumin, 2-phenoxyethanol, formaldehyde, polymyxin B, neomycin, and streptomycin.338 339 This vaccine was licensed for use in the U.S. without any clinical trials that involved a placebo-control group, and safety studies were limited to monitoring children for only 3 days post- administration.340 341 342

On December 13, 2002, the FDA approved Pediarix, a combination vaccine containing diphtheria, tetanus, acellular pertussis (DTaP), hepatitis B (Hep B), and poliovirus vaccine (IPV) manufactured by GlaxoSmithKline. The poliovirus vaccine in Pediarix contains the same quantity and strains of poliovirus type 1, 2, and 3 found in IPOL. Following approval, ACIP recommended the vaccine for use but noted that its use caused higher fever rates when compared to rates of those who received the vaccine doses separately. Additionally, when administered as recommended at 2, 4, and 6 months, an infant who received the birth dose of Hep B vaccine would be given an extra fourth Hep B dose. This, however, was declared acceptable by ACIP.343

In June 2008, Pentacel, a combination vaccine manufactured by Sanofi Pasteur containing DTaP, Haemophilus Influenzae Type B (HIB), and IPV, received FDA approval for use in infants and toddlers.344 When administered as recommended at 2, 4, 6, and 15-18 months, an additional IPV dose would be given, because all children are recommended to receive another IPV dose between 4-6 years of age per CDC’s guidelines. Again, this extra fifth IPV dose was declared acceptable by ACIP. 345  

Also, in June 2008, the FDA approved Kinrix, a combination vaccine manufactured by GlaxoSmithKline containing DTaP and IPV. This vaccine was approved for use in children aged 4 through 6 years as a fifth booster dose of DTaP and a fourth booster dose of IPV who had previously received either INFANRIX DTaP and/or Pediarix combination vaccine containing DTaP, Hep B, and IPV.346 ACIP quickly recommended this vaccine for use and stated that it could be used in children whose previous vaccine type was not known even though safety and immunogenicity data of interchanging DTaP vaccine brands was not known.347

On March 24, 2015, the FDA approved Quadracel, a combination vaccine containing DTaP and IPV. This vaccine, manufactured by Sanofi Pasteur, was approved for use in children 4 through 6 years of age who had previously received DAPTACEL DTaP vaccine and/or Pentacel combination vaccine containing DTaP, HIB, and IPV.348 Quadracel was also recommended for use by ACIP and again, the committee stated that even though data on safety and immunogenicity of interchanging vaccine brands was limited, the vaccine could be used when the DTaP brand type previously used was not known.349

On December 21, 2018, the FDA approved VAXELIS, a combination 6 in 1 vaccine containing DTaP, HIB, Hep B, and IPV as a 3-dose series for use in children 6 weeks through 4 years of age.350 This vaccine, manufactured through a joint partnership between Sanofi Pasteur and Merck (MCM Vaccine Company), is not expected to be available for use until 2021; however, ACIP has already voted to recommend the vaccine as an option for use through its Vaccines For Children (VFC) program, to be administered at 2, 4, and 6 months of age. The use of VAXELIS in children who receive the recommended birth dose of Hep B vaccine will result in an extra fourth Hep B dose.351

SV40 and Poliovirus vaccine

All early poliovirus vaccines were made using monkey kidneys, and primarily from the kidneys of rhesus monkeys. Kidneys from monkeys, like those of humans, filter contaminates from the body and therefore contain waste products that include bacteria, viruses, toxins and more. Early poliovirus researchers were aware that rhesus monkeys, even those who were seemingly healthy, were reservoirs for novel viruses. Monkey kidneys, however, were readily available at the time due to the widespread use of monkeys in poliovirus research. Once removed from the body, the monkey would be killed, and the kidneys would be chopped up and placed into bottles containing a nutrient. This was the process by which the tissue cultures used in poliovirus vaccine development began.352

Researchers, however, quickly realized that these unknown viruses found in monkey kidneys could cause damage and death to the tissue cultures. The first monkey virus (simian virus), SV1, was isolated in February 1954 by researcher Robert Hull of Eli Lilly after the virus had caused the destruction of 17 percent of the company’s tissue cultures.353 354

Hull began to catalogue each newly discovered simian virus, but few concerns were expressed about the possible presence of these viruses in the poliovirus vaccine. It was believed that the formaldehyde used to inactivate the poliovirus would also kill any other viruses that might be present. When Salk’s vaccine was licensed for use in April of 1955, researchers did not express any concerns about the possibility that the vaccine might also contain simian viruses or other contaminants.355

By 1959, National Institutes of Health (NIH) microbiologist, Dr. Bernice Eddy, who had previously reported her concerns regarding the Cutter poliovirus vaccine, was researching the hypothesis that viruses might be capable of causing cancer. In 1959, Eddy and fellow researcher Sarah Stewart discovered that a mouse virus could cause cancer in other small mammals.356 357

Through her previous work at NIH on vaccine safety testing, Eddy had been forced to discard hundreds of tissue cultures due to viral contamination. With her recent discovery that viruses could cause cancer in other species, the idea that a simian virus (SV) might be capable of causing cancer was now of interest to her. Without support from her superiors, Eddy began testing her theory by injecting newborn hamsters with ground up and filtered rhesus monkey cell cultures and compared them with a control group who were injected with human and feline tumor extracts.358 359

Hamsters who received the cat and human tumor extracts did not develop any issues; however, 70 percent of hamsters who received rhesus monkey kidney cell cultures developed tumors and eventually died from cancer. Most hamsters developed tumors later in their lives, which suggested that these tumors might have a long latency period.360

In July of 1960, Eddy presented her findings to her boss, Joe Smadel, who was now in charge of vaccine safety testing within the Division of Biologic Standards (DBS), a new agency formed following the Cutter Incident. Smadel dismissed Eddy’s findings and would not support any efforts to have her research published or publicized. Eddy, however, was not the only scientist looking at monkey kidney cell cultures.361

By 1960, Merck, headed by vaccine researcher Maurice Hilleman, was working on an inactivated poliovirus vaccine that would be more effective than Salk’s vaccine formulation. Prior to the vaccine’s approval, however, fellow researcher Ben Sweet discovered that during the testing phase of a rhesus kidney cell derived adenovirus vaccine, the cells would balloon in size and fill with holes. During his investigation, Sweet realized that while the tissue cultures were being cultivated in rhesus monkey kidneys, they were being tested on African green monkey kidney tissue cultures – a completely different species.362

This simian virus, now referred to as simian virus 40 (SV40), was almost impossible to locate in its natural host – the rhesus monkey – but once transplanted into tissue cultures from another species and grown out, problems were visible. Sweet tested all his adenovirus stock and discovered that it was completely contaminated with this new virus. Sweet, at the request of Hilleman, tested the polio seed stock from samples of Sabin’s experimental OPV vaccine, and found that it was also contaminated.363 364

In June 1960, Hilleman announced his findings and reported that this virus was nearly always present in the rhesus monkey kidney cells, frequently found in kidney cultures from the cynomolgus monkey, but rarely seen in African green monkeys.365 366 Scientists who heard about Hilleman’s findings either expressed concerns or else dismissed the findings as inconsequential. Some stated that since Sabin’s vaccine had been administered to millions of individuals in the Soviet Union without evidence of harm, the presence of this virus was not concerning. Others, however, voiced concerns of the potential harmful effects that might not yet be known.367

Publicly, Hilleman began recommending that African green monkeys be used in vaccine development while privately expressing to Sabin his concerns over the long-term health implications that this virus might have in persons who had received Sabin’s OPV. Hilleman had reportedly developed an antiserum against this virus and told Sabin that if he treated his seed stock with this antiserum, the virus would be rendered harmless and safe for use in vaccine production.368

When Eddy heard about Sweet and Hilleman’s findings she suspected that this was the same virus that she had isolated several months earlier. Eddy repeated her studies and after completing a yearlong series of tests, she was able to prove that the cancer-causing virus that she had discovered was in fact SV40 – the same virus isolated by Sweet and Hilleman. Despite multiple attempts by Eddy to request that the DBS act to ensure that all vaccines were free of SV40, no initiatives were implemented.369

The concern over SV40 was initially limited to the oral poliovirus vaccine which was soon to be licensed for use in the U.S. It was widely believed that the formaldehyde used in the inactivation process of the Salk vaccine would neutralize SV40 and render it safe from contaminants. But by the spring of 1961, this theory would be challenged when researchers from Britain reported that SV40 was resistant to formaldehyde and that persons who had received the Salk vaccine had been found to have antibodies to SV40.370

The Public Health Service’s Technical Committee on Poliomyelitis Vaccine, a committee appointed by the U.S. Surgeon General in 1955 after the Cutter Incident, was asked to weigh in on these findings. In 1961, the committee consisted of eight scientists, and included Salk and five members with close personal ties to the Salk vaccine. In May 1961, this committee reported that while evidence supported that many poliovirus vaccine lots contained SV40, there was no proof that exposure to the virus was harmful. They did, however, decide that going forward, all new Salk vaccines would need to be free of SV40 but that no recall of potentially contaminated vaccines was necessary.371

Yet within the month, Merck scientists had proof that SV40 could cause cancer in laboratory animals. On June 20th, 1961, Hilleman presented his findings to the same committee and recommended that all inactivated poliovirus vaccines be taken off the market until changes could be made to ensure that the vaccines did not contain SV40. Once again, the committee chose not to act, and did not express any concern over the SV40 findings.372

On June 30, 1961, the DBS went ahead and notified all poliovirus vaccine manufacturers that beginning on August 1, 1961, they would be required to show test results to confirm that each poliovirus vaccine lot was free of live SV40 contaminants. SV40, however, could still be present if it was inactivated. It would be another two years before stricter requirements involving SV40 would be required of manufacturers. Again, no recall was issued and contaminated vaccine lots remained in use until 1963.373

For many years, the common belief was that the techniques used to inactivate SV40 in the manufacturing process of the oral polio vaccine were enough to ensure that this contaminant was not present in the final product. In recent years, however, evidence has been presented to show that SV40 was in the OPV until the 1990s.374 375 376 Health officials have only acknowledged that between 1955 and 1963, nearly 100 million Americans who received IPV may have also been exposed to SV40.377

By 1998, published medical research had noted the presence of SV40 in brain, bone, bladder and lung cancers. 378 379 380 381 382 383 384 385 Further, 45 percent of sperm from healthy men were also found to contain SV40. Researchers concluded that “multiple SV40 strains can infect humans”386 and that SV40 infection may be spread by “blood transfusion and sexual transmission in the human population.”387  In 2002, the Institute of Medicine (IOM) concluded that “the biological evidence is strong that SV40 is a transforming virus” and that “the biological evidence is of moderate strength that SV40 exposure could lead to cancer in humans under natural conditions”. It also concluded that "the evidence is inadequate to accept or reject a causal relationship between SV40-containing polio vaccines and cancer." 388

Between 1997 and 2005, efforts were made to deny any association between SV40 and the development of human cancer.389 390

On January 27-28, 1997, the National Institutes of Health (NIH) hosted a Workshop on Simian Virus-40 (SV40): A Possible Human Polyomavirus in Bethesda, Maryland. This gathering, which included government scientists from the FDA, CDC, NIH, NIP and NVPO, as well as independent non-government scientist working in labs globally, was scheduled to allow for an open discussion on SV40 and its possible connection to cancer. Several independent scientists presented data which linked SV40 to cancer, but they were dismissed by government scientists who reported that they were unable to find any association and that their data did not support an increased risk of cancer in persons who may have received SV40 contaminated poliovirus vaccines.391

In September 2003, the Subcommittee on Human Rights and Wellness of the U.S. House Government Reform Committee met to discuss SV40 and its link to the rising rates of cancer. While U.S public health officials acknowledged that live SV40 did contaminate both inactivated and live polio vaccines between 1955 and 1963, they continued to deny that the monkey virus infecting humans was causing human cancers.392

The 2002 IOM committee recommended that additional research be completed to determine whether a causal relationship exists between SV40 and cancer but have not published any further reports on this subject. 

Simian Immunodeficiency Virus, Human Immunodeficiency Virus and Poliovirus Vaccines

In the 1980’s, after acquired immune deficiency syndrome (AIDS) emerged and was associated with the human immunodeficiency virus (HIV), the live oral polio vaccine (OPV) was associated with another monkey virus contamination scandal as a search for the origins of HIV began. Beginning in the early 1990s, several hypotheses were published in the mainstream media and medical literature. Some authors provided evidence that experimental live oral polio vaccines tested on children in central Africa in the late 1950’s and early 1960’s had been produced using monkey cells from chimpanzees or African green monkeys infected with simian immunodeficiency virus (SIV). They alleged that the HIV-1 virus currently circulating among humans is a hybrid monkey-human virus that was created when there was a cross-species transmission of SIV from non-human African primates to humans in Africa via SIV-contaminated oral polio vaccines.393 394 395

By 2009, the origins of HIV-1 group M, the most prevalent form circulating in humans, was traced to a monkey virus (SIV), residing in chimpanzees in central Africa.396 While most scientists and vaccine manufacturers involved in the research and development of live polio vaccines and government health officials defending the use of OPV continue to deny that SIV contaminated oral polio vaccines were involved in the creation of HIV-1, those who disagree maintain that there is good evidence to the contrary.397

Global Vaccine Use

A live-virus oral poliovirus vaccine (OPV) containing type 1 and type 3 poliovirus continues to be used by most health officials in campaigns aimed at eradicating polio. Wild poliovirus type 2 was declared eradicated in 2015 and health officials moved quickly to remove this strain from the OPV because it was known to cause cases and outbreaks of circulating vaccine-derived poliovirus (cVDPV2). 398  

Health experts believed that the removal of type 2 poliovirus from the OPV would eventually stop cVDPV2 outbreaks, and that in instances where an outbreak was occurring, a monovalent OPV type 2 (mOPV2) vaccine could be used to halt the spread of cVDPV2. While circulation of cVDPV2 appeared to stop in many countries after an mOPV2 vaccine was used, the opposite occurred in Africa.399  

In Africa, use of mOPV2 caused an increase in the number of cases of cVDPV2 and health officials were forced to admit that its use caused more cases of polio than likely would have occurred if they had not used the vaccine.400

Global health officials hope that the two new mOPV2 vaccines currently under development will receive quick approval for use in countries experiencing cVDPV2 outbreaks. Both mOPV2 vaccines are in the early stages of development and made through genetic engineering and vaccine researchers believe that these novel vaccines will lower the risk of cVDPV2.401 402

Public health officials acknowledge that polio will not be eradicated until OPV is no longer in use; however, experts are not certain whether the exclusive use of IPV will be able to maintain eradication status. Concerns include the vaccine’s inability to fully halt poliovirus transmission, and the fact that some individuals can shed the poliovirus for years. 403 404

How effective is Polio vaccine? 

According to the CDC, 99 percent of people develop blood antibodies considered to be protective against polio after 3 doses of inactivated poliovirus vaccine (IPV); however, the duration of vaccine-acquired immunity is not known.405

IPV is limited in its ability to induce mucosal immunity and is less effective at preventing the poliovirus from replicating and shedding in the intestines. As a result, persons who receive IPV, the only poliovirus vaccine available for use in the US, may be personally protected from developing paralytic polio but remain capable of transmitting the poliovirus to others through fecal-oral transmission.406

The oral poliovirus vaccine (OPV), while not in use in the United States, continues to be administered in most developing countries as part of the Global Polio Eradication Initiative (GPEI). This live vaccine is used in developing countries for several reasons, including cost effectiveness (less than 20 cents per dose) and ease of administration (oral vs. injection).407

Persons vaccinated with OPV, however, can still be infected, shed, and transmit wildtype poliovirus.

In 2010, researchers studying asymptomatic wild-type poliovirus transmission in India among healthy vaccinated children admitted that “mucosal immunity induced by OPV is imperfect” and concluded that:

“Although OPV is protective against infection with poliovirus, the majority of healthy contacts who excreted wild-type poliovirus were well vaccinated. This is consistent with a potential role for OPV-vaccinated children in continued wildtype poliovirus transmission and requires further study.” 408

In July 2014, a study by European and U.S. researchers investigating wild-type polio outbreaks in 2010 among older children and adults in the Republic of Congo and Tajikistan, concluded that “intestinal immunity to poliovirus wanes over time, allowing individuals vaccinated with oral polio vaccine (OPV) to become re-infected and shed poliovirus.”409 Additionally, study authors stated that the “Global Polio Eradication Initiative is considering expanding the age range of vaccination campaigns even in the absence of adult cases, because of concerns about imperfect, waning intestinal immunity.”410

OPV can cause vaccine-strain paralytic polio (VAPP) but according to the GPEI, the estimated rate of 2 to 4 cases of paralytic polio per 1 million births is considered an acceptable risk for most public health officials.411

In addition to VAPP, OPV can also cause vaccine-derived poliovirus (VDPV). OPV is a live virus vaccine and individuals who receive the vaccine will shed vaccine-strain poliovirus in the stool for several weeks after vaccination. In areas with poor sanitation, the vaccine-strain virus can spread within a community for an extended period. When this occurs, the vaccine-strain polio virus will undergo genetic changes and, in some cases, transform into circulating VDPV (cVDPV) and cause paralysis. Public health officials report that cVDPV occurs in communities that lack immunity, or due to poorly administered vaccination programs.412

In 2008, U.S. and European health officials analyzed eight outbreaks of paralytic polio between 2000 and 2005 in Hispaniola, Indonesia, Egypt, Philippines, Madagascar (2), China and Cambodia that were caused by circulating vaccine-derived poliovirus (cVDPV). Health officials admitted that “it is now known that vaccine viruses can be serially transmitted through human hosts, and may revert genetically toward wild-type transmissibility and virulence.” 413 They also reported that:

“Although only 114 virologically confirmed paralytic cases were identified in the eight cVDPV outbreaks, it is likely that a minimum of hundreds of thousands, and more likely several million individuals were infected during these events, and that many thousands more have been infected by VDPV lineages within outbreaks which have escaped detection.”414

They concluded by stating that “Our estimates of the extent of cVDPV circulation suggest widespread transmission in some countries, as might be expected from endemic wild poliovirus transmission in these same settings.” 415

In September 2015, following the announcement that type 2 wild-type 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 replace it with a bivalent OPV containing only vaccine-strain poliovirus types 1 and 3.416 This initiative was implemented to stop the spread of type 2 cVDPV (cVDPV2) that had caused multiple cases and outbreaks of polio in several countries.417

Despite removing type 2 polio from OPV in the spring of 2016,418  cVDPV2 associated paralytic polio cases have continued to occur. In 2019, cVDPV2 outbreaks were reported in the Philippines, and multiple African countries.419 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 have included the risk that its use will potentially lead to additional cases and outbreaks of cVDPV2. 420

Public health officials acknowledge that polio will not be eradicated until OPV is no longer in use; however, experts are not certain whether the exclusive use of IPV will be able to maintain eradication status. Concerns include the vaccine’s inability to fully halt poliovirus transmission, and the fact that some individuals can shed the poliovirus for years. 421 422

Certain people vaccinated with OPV can excrete poliovirus in their feces for months to years after vaccination. While this occurs primarily in children who are immunocompromised,423 424 it has also been reported to have occurred in healthy individuals.425 426

Persons who excrete the vaccine-acquired poliovirus vaccine long-term usually have B-cell-related primary immunodeficiency diseases and what is referred to as infectious VDPV (iVDPV). In these individuals, the vaccine-acquired poliovirus frequently reverts into a virulent strain which often causes paralysis. Individuals who shed the poliovirus for extended periods of time can reintroduce and spread poliovirus within a community. According to the published literature, as of 2018, 107 individuals have been identified as having iVDPV.427 428 429

While the GPEI plans to stop use of the OPV after wild-type poliovirus has been declared eradicated, the risk of VDPV will continue because of individuals with iVDPV. Polio experts report that surveillance of poliovirus shedding in persons with primary immunodeficiency will be crucial because of their potential to restart polio outbreaks within the population.430

In 2019, following numerous outbreaks of cVDPV, some infectious disease experts strongly 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.”431

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.”432

In a WHO statement published in October 2019, health officials reported an increase in wild-type 1 poliovirus cases (WPV1) in Pakistan and Afghanistan, and a significant increase in cases of cVDPV2 this year in multiple countries giving children the OPV and stated the following: 433

“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.”

Although there were five times as many cases of wild-type polio in 2019 than in 2018, most of the paralytic polio cases identified and reported in 2019 were caused by outbreaks of cVDPV2 that occurred in Niger, Nigeria, Cameroon, Benin, Ghana, Ethiopia, Somalia, China, Myanmar, Kenya, Central African Republic (CAR), Angola, Somalia, and Papua New Guinea, Indonesia.434

These countries have been among those that have been targeted since 1988 by the GPEI, which have repeated mass vaccination campaigns among child populations using the trivalent OPV, sometimes giving children six to eight doses of the vaccine every year. After the WHO declared type 2 polio eradicated in 2015, polio vaccination campaigns in Africa and Asia have been administering a bivalent OPV that only contains type 1 and type 3 attenuated polioviruses.435

WHO officials have reported that the risk of international transmission of wild poliovirus type 1 is increasing and that there is “a rising risk of cVDPV spread” of vaccine-strain poliovirus 2 as cVDPV has spread from Nigeria to Ghana, Benin, and Niger, and from Somalia to Ethiopia.436

Despite the increasing risk of both wild-type and cVDPV, the GPEI has set a goal of global polio eradication for the year 2023. 437

Can Polio vaccine cause injury and death?

The Institute of Medicine (IOM) has acknowledged that there is individual susceptibility to vaccine reactions for genetic, biological and environmental reasons, but that vaccine providers cannot accurately predict prior to a vaccine’s administration who will suffer complications, injury or death from vaccination.438 However, a person who has previously had a serious reaction to a vaccination or is acutely or chronically ill should become informed about all potential risks associated with vaccination and discuss any concerns with a trusted health care professional before receiving a poliovirus vaccine or any other vaccine.

The poliovirus vaccine is commonly administered in a combination vaccine which includes the diphtheria, tetanus, and acellular pertussis vaccine (DTaP), hepatitis B and Haemophilus influenzae type b (Hib) vaccines. It is important to review the manufacturer product insert prior to receiving a combination vaccine that contains the poliovirus vaccine.

Adverse reactions reported by vaccine manufacturers as listed in the vaccine product inserts:

Pediarix (Diphtheria and tetanus toxoids and acellular pertussis, hepatitis B recombinant and inactivated poliovirus vaccine manufactured by GlaxoSmithKline.)

  • Frequently Reported Adverse Events: Local injection site reactions (pain, redness, or swelling); fussiness, high fever (Pediarix is associated with higher rates of feverrelative to separately administered vaccines. The prevalence of fever was highest on the day of and the day following vaccination.)
  • Serious Reported Adverse Events: High fever requiring medical attention (In a safety study that evaluated medically attended fever after Pediarix or separately administered vaccines when co-administered with 7-valent pneumococcal and Hib conjugate vaccines, infants who received Pediarix had a higher rate of medical encounters for fever within the first 4 days following the first vaccination); febrile and afebrile convulsions (seizures); gastroenteritis; bronchiolitis; asthma; diabetes mellitus; and chronic neutropenia; anaphylactic reactions (hives, swelling, difficulty breathing, hypotension or shock); and demyelinating diseases.

Kinrix (Diphtheria and tetanus toxoids, acellular pertussis and inactivated poliovirus vaccine manufactured by GlaxoSmithKline.)

  • Frequently Reported Adverse Events: Injection site pain, including redness, swelling and increase in arm circumference; drowsiness; fever; loss of appetite.
  • Serious Reported Adverse Events:Gastroenteritis; dehydration; and cellulitis. After licensure (post-marketing), reported adverse event have also included apnea, collapse or shock-like state (hypotonic-hyporesponsive episode), convulsions (with or without fever), injection site vesicles, pruritus (intense itching), allergic reactions, including anaphylaxis, urticaria, angioedema, lympadenopathy, and thrombocytopenia.

Quadracel (Diphtheria and tetanus toxoid, acellular pertussis and inactivated poliovirus vaccine manufactured by Sanofi Pasteur.)

  • Frequently Reported Adverse Events: Injection site pain, including redness, swelling and increase in arm circumference; malaise; muscle pain; headache.
  • Serious Reported Adverse Events: After licensure (post-marketing), reported adverse event have also included cyanosis, convulsions (with or without fever), injection site abscess, injection site cellulitis, pallor, screaming, allergic reactions, including anaphylaxis, urticaria, and dyspnea.

Pentacel (Diphtheria and tetanus toxoids and acellular pertussis, inactivated poliovirus and Haemophilus b conjugate (tetanus toxoid conjugate) vaccine manufactured by Sanofi Pasteur.)

  • Frequently Reported Adverse Events: Systemic reactions that occurred in clinical trials in more than 50 percent of participants following any dose included: fussiness/irritability and inconsolable crying; fever; injection site reactions, including tenderness, abscess and increase in arm circumference.
  • Serious Reported Adverse Events: Cases of encephalopathy and death also occurred during clinical trials. After licensure (post marketing), there have been reports of febrile and afebrile convulsions (seizures), bronchiolitis, gastroenteritis, dehydration, pneumonia, lethargy/somnolence, hypotonic/hyporesponsive episode (collapse), apnea, cyanosis, and asthma.

VAXELIS (Diphtheria and tetanus toxoids and acellular pertussis, inactivated poliovirus, Haemophilus b conjugate, and hepatitis B recombinant vaccine manufactured by MCM Vaccine Company.)

  • Frequently Reported Adverse Events: Systemic reactions that occurred in clinical trials following any dose included: injection site redness, swelling, and pain, fever, crying, decreased appetite, irritability, vomiting, and somnolence
  • Serious Reported Adverse Events: In the two U.S. clinical trials, 6 deaths were reported but were determined by trial investigators not to be caused by VAXELIS. These deaths included sepsis, asphyxia, hydrocephalus, unknown cause, and two cases of sudden infant death syndrome. As VAXELIS is not currently available for use in the United States, post-marketing data on serious adverse events are limited to those events considered to have a causal link to the vaccines containing the antigens of VAXELIS. These include anaphylaxis, hypersensitivity, seizures, including febrile seizures, and excessive swelling of the injected limb.

IPOL (inactive poliovirus (Monkey Kidney Cell) manufactured by Sanofi Pasteur)

  • Frequently Reported Adverse Events: Local injection site reactions (pain, redness, and induration); fever; sleepiness; irritability; fussiness; crying; anorexia; vomiting; and fatigue;
  • Serious Reported Adverse Events: convulsion, including febrile convulsion; somnolence; paresthesia; headache; injection site rash and mass; agitation; lymphadenopathy; anaphylactic reaction and anaphylactic shock; hypersensitivity; rash; urticaria; arthralgia; myalgia; and death.

In 1994, the Institute of Medicine (IOM) reported that there was compelling scientific evidence to establish a causal relationship between the oral poliovirus vaccine (OPV) and paralytic and non-paralytic polio. The committee also affirmed that OPV could cause vaccine-strain polio in the contacts of vaccinated individuals. Additionally, the IOM committee also favored acceptance of an association between OPV and Guillain-Barre Syndrome (GBS). An immune mediated painful and disabling neurological disorder that can occur after viral infection or vaccination, GBS involves inflammation of the peripheral nervous system and can cause temporary or permanent paralysis that may lead to death. The committee, however, reported that there was insufficient evidence to accept or reject a causal relationship between the inactivated, injectable poliovirus vaccine (IPV) and GBS. A potential association between poliovirus vaccines, both OPV and IPV, and transverse myelitis, a rare neurological condition which causes spinal inflammation, was also evaluated in this report. Committee members reported that the evidence was insufficient to accept or reject a causal relationship between OPV and transverse myelitis and that there was no evidence to determine a relationship between IPV and this serious neurological condition.439

Vaccine-acquired paralytic polio (VAPP) was associated with OPV immediately following the vaccine’s introduction. When OPV was in use in the U.S., 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 2000.440 OPV, however, remains in use globally, and is the vaccine primarily used in global campaigns that are focused on eradicating polio.441

In addition to VAPP, OPV can also cause vaccine-derived poliovirus (VDPV). OPV is a live virus vaccine and individuals who receive the vaccine will shed vaccine-strain poliovirus in the stool for several weeks following vaccination. In areas with poor sanitation, the vaccine-strain virus can spread within a community for an extended period. When this occurs, the vaccine-strain polio virus will undergo genetic changes and, in some cases, transform into circulating VDPV (cVDPV) and cause paralysis. Public health officials report that cVDPV occurs in under-vaccinated communities or due to poorly administered vaccination programs.442

In 2019, the majority of reported paralytic polio cases were caused by outbreaks of type 2 cVDPV (cVDPV2) which were reported in Niger, Nigeria, Cameroon, Benin, Ghana, Ethiopia, Somalia, China, Myanmar, Kenya, Central African Republic (CAR), Angola, Somalia, and Papua New Guinea, Indonesia.443

The U.S. government recognizes the following as OPV vaccine injuries – 444

  • Paralytic polio occurring within 30 days of vaccine administration in an immunocompetent individual
  • Paralytic polio occurring within 6 months of vaccine administration in an immunodeficient individual
  • Paralytic polio in a vaccine-associated case within the community
  • Vaccine-strain polio infection occurring within 30 days of vaccine administration in an immunocompetent individual
  • Vaccine-strain polio infection occurring within 6 months of vaccine administration in an immunodeficient individual
  • Vaccine-strain polio infection associated case within the community

The U.S. government recognizes the following as IPV vaccine injuries – 445

  • Anaphylaxis occurring within 4 hours of vaccine administration
  • Shoulder injury related to vaccine administration within 48 hours of receiving the vaccine
  • Vasovagal syncope within 1 hour of vaccine administration

As of November 30, 2019, there have been 24,797 adverse events reported following OPV including 1,033 deaths (nearly 90% in children under age six). There have also been more than 72,130 reports of adverse events associated with IPV containing vaccines including 1,573 deaths. However, the number of vaccine-related injuries and deaths reported to VAERS may not reflect the true number of serious health problems that occur after polio vaccination.

Even though the National Childhood Vaccine Injury Act of 1986 legally required pediatricians and other vaccine providers to report serious health problems following vaccination to federal health agencies (VAERS), many doctors and other medical workers giving vaccines to children and adults fail to report vaccine-related health problem to VAERS. There is evidence that only between one and 10 percent of serious health problems that occur after use of prescription drugs or vaccines in the U.S. are ever reported to federal health officials, who are responsible for regulating the safety of drugs and vaccines and issue national vaccine policy recommendations. 446 447 448 449 450

As of February 1, 2020, there had been 310 claims filed in the federal Vaccine Injury Compensation Program (VICP) for injuries and deaths following OPV containing vaccines, including 28 deaths and 282 serious injuries. There had been 489 claims for injuries and deaths following IPV containing vaccines, including 73 deaths and 416 serious injuries. Of that number, the U.S. Court of Claims administering the VICP has compensated 228 children and adults, who have filed claims for polio vaccine associated injury and death.451

SV40 and Poliovirus vaccine

In 1960, Dr. Bernice Eddy discovered that the rhesus monkey kidney cells used to make the first injectable poliovirus vaccine, and the first experimental oral polio vaccines, could cause cancer when injected into lab animals. Later that year, the cancer-causing virus in the rhesus monkey kidney cells was identified as simian virus 40 (SV40), the 40th monkey virus to be discovered. Public health officials, who were aware of the virus and its potential to cause cancer, chose not to make this information public. Further, they allowed the contaminated vaccine to be injected into millions of Americans between 1955 and 1963.452

The U.S. government and vaccine manufacturers have reported that all SV40 tainted poliovirus vaccines were removed from the market by 1963; however, there is evidence that SV40 was still present in the OPV and administered to children from 1963 through the 1990’s.453 454 455

In 2002, the Institute of Medicine (IOM) concluded that “the biological evidence is strong that SV40 is a transforming virus” and that “the biological evidence is of moderate strength that SV40 exposure could lead to cancer in humans under natural conditions”. It also concluded that "the evidence is inadequate to accept or reject a causal relationship between SV40-containing polio vaccines and cancer." 456 SV40 associated cancers include - brain cancers, bone cancers, malignant mesothelioma, and non-Hodgkin's lymphoma. 457 458

The 2002 IOM committee recommended that additional research be completed to determine whether a causal relationship exists between SV40 and cancer, but they have not published any further reports on this subject. U.S public health officials have acknowledged that live SV40 contaminated both inactivated and live polio vaccines between 1955 and 1963, but they continue to deny that SV40 causes cancer in humans.459

Who is at highest risk for complications from Polio vaccine?

There is a gap in medical knowledge in terms of doctors being able to predict who will have an adverse reaction to polio vaccination, and who will not.

In the U.S. today, the polio vaccine is usually administered in a combination shot that also contain vaccines for diphtheria (D), tetanus (T), and pertussis (whooping cough) (P). Additional vaccines may also include Haemophilus influenzae Type B (HIB) and/or hepatitis B vaccine. 

Pediarix (Diphtheria and tetanus toxoids and acellular pertussis, hepatitis B recombinant and inactivated poliovirus vaccine manufactured by GlaxoSmithKline.)

Children most at risk for complications from Pediarix include:

  • Premature infantsApnea following intramuscular vaccination has been observed in some infants born prematurely. Pediarix vaccine product insert warns that the decision to vaccinate an infant born prematurely should take into consideration both the potential risks and possible benefits of vaccination.
  • Children with latex allergies - The tip caps of prefilled Pediarix syringes contain latex and may cause an allergic reaction in persons sensitive to latex;
  • Previous health history of Guillain-Barré syndrome (GBS) occurring within 6 weeks of receiving a tetanus containing vaccine. Pediarix vaccine package insert states that assessment of the possible risks and potential benefits of receiving Pediarix should be carefully considered prior to vaccination.
  • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
  • Allergy or sensitivity to any component of Pediarix, including yeast or neomycin and polymyxin (antibiotics);
  • Having a temperature of 105 F or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
  • Collapse or shock-like state within 48 hours of a previous pertussis vaccination;
  • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
  • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
  • Serious allergic reaction to a previous pertussis vaccination;
  • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;

Kinrix (Diphtheria and tetanus toxoids, acellular pertussis and inactivated poliovirus vaccine manufactured by GlaxoSmithKline.)

Children most at risk for complications from Kinrix include:

  • Children with latex allergies - The tip caps of prefilled Kinrix syringes contain latex and may cause an allergic reaction in persons sensitive to latex;
    • Previous health history of Guillain-Barré syndrome GBS) occurring within 6 weeks of receiving a tetanus containing vaccine. Kinrix vaccine package insert states that assessment of the possible risks and potential benefits of receiving Kinrix should be carefully considered prior to vaccination.
    • Severe allergic reaction to any component of Kinrix, including neomycin and polymyxin B (antibiotics);
    • Serious allergic reaction to a previous pertussis vaccination;
    • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
    • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
    • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
    • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
    • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
    • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);

Quadracel (Diphtheria and tetanus toxoid, acellular pertussis and inactivated poliovirus vaccine manufactured by Sanofi Pasteur.)

Children most at risk for complications from Quadracel include:

  • Serious allergic reaction following administration of a pertussis, tetanus, diphtheria, or polio containing vaccine or any ingredient of Quadracel vaccine;
  • Previous history of Guillain-Barré syndrome (GBS) occurring within 6 weeks of receiving a tetanus containing vaccine. The Quadracel package insert states that assessment of the possible risks and potential benefits of receiving Quadracel should be carefully considered prior to vaccination. 
  • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
  • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
  • Seizures within 3 days of a previous pertussis vaccination;
  • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;

Pentacel (Diphtheria and tetanus toxoids and acellular pertussis, inactivated poliovirus and Haemophilus b conjugate (tetanus toxoid conjugate) vaccine manufactured by Sanofi Pasteur.)

Children most at risk for complications from Pentacel include:

  • Premature infants - Apnea following intramuscular vaccination has been observed in some infants born prematurely. The Pentacel vaccine product insert warns that the decision to vaccinate an infant born prematurely should take into consideration both the potential risks and possible benefits of vaccination;
  • Severe allergic reaction to any component of Pentacel, including neomycin and polymyxin B (antibiotics);
  • Serious allergic reaction to a previous pertussis vaccination;
  • Previous history of Guillain-Barré syndrome (GBS) occurring within 6 weeks of receiving a tetanus containing vaccine. The Pentacel package insert states that assessment of the possible risks and potential benefits of receiving Pentacel should be carefully considered prior to vaccination. 
  • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy)
  • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
  • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
  • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
  • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
  • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;

VAXELIS (Diphtheria and tetanus toxoids and acellular pertussis, inactivated poliovirus, Haemophilus b conjugate, and hepatitis B recombinant vaccine manufactured by MCM Vaccine Company.)

Children most at risk for complications from VAXELIS include:

  • Premature infants - Apneafollowing intramuscular vaccination has been observed in some infants born prematurely. The VAXELIS vaccine product insert warns that the decision to vaccinate an infant born prematurely should take into consideration both the potential risks and possible benefits of vaccination;
  • Previous history ofGuillain-Barré syndrome (GBS) occurring within 6 weeks of receiving a tetanus containing vaccine. The VAXELIS vaccine product insert warns that the decision to vaccinate an infant born prematurely should take into consideration both the potential risks and possible benefits of vaccination;
  • Serious allergic reaction to a previous dose of VAXELIS, any ingredient found in VAXELIS, or any other tetanus toxoid, diphtheria toxoid, pertussis-containing vaccine, hepatitis B vaccine, inactivated poliovirus vaccine, or influenzae type b vaccine;
  • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
  • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
  • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
  • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
  • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
  • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;

IPOL (inactive poliovirus (Monkey Kidney Cell) manufactured by Sanofi Pasteur)

Persons most at risk for complications from IPOL include:

  • Persons with an allergy or hypersensitivity to any ingredient found within the vaccine, including polymyxin B, neomycin, streptomycin, formaldehyde, and 2-phenoxyethanol;
  • Persons who experience anaphylaxis or anaphylactic shock occurring within 24 hours of vaccine administration;
  • Persons who receive the vaccine when they are experiencing an acute febrile illness.

Oral Poliovirus Vaccine

While not in use in the United States, the oral poliovirus vaccine (OPV) can cause complications, which include paralytic polio. Persons most at risk for developing vaccine-acquired paralytic polio (VAPP) are those who are immunosuppressed with B-cell deficiencies. In this population, the risk is reported to be 3200-times greater than that of the general population. Vaccine-strain type 3 poliovirus is most frequently found in previously healthy individuals who develop VAPP. VAPP in persons with immunosuppression is commonly attributed to vaccine-strain type 2 poliovirus;460 however, OPV containing type 2 poliovirus are no longer in use globally.461

Children who receive intramuscular (IM) injections, usually within 30 days of receiving OPV, are at a greater risk of developing VAPP. This risk also extends to children within the community who have received IM injections and who are exposed to vaccine-strain poliovirus through shedding from OPV recipients.462 463 464

Household contacts and members of the community are also at risk for complications from OPV if they come into contact with the vaccine-strain poliovirus through direct or indirect vaccine-strain shedding and transmission.465 466   

Who should not get Polio vaccine?

In the U.S. today, the polio vaccine is usually administered in a combination shot that also contain vaccines for diphtheria (D), tetanus (T), and pertussis (whooping cough) (P). Additional vaccines may also include Haemophilus influenzae Type B (HIB) and/or hepatitis B vaccine.  

Contraindications and precautions to vaccination as listed in the vaccine manufacturer product inserts

Pediarix (Diphtheria and tetanus toxoids and acellular pertussis, hepatitis B recombinant and inactivated poliovirus vaccine manufactured by GlaxoSmithKline.)

  • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
  • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
  • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
  • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
  • Serious allergic reaction to a previous pertussis vaccination;
  • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
  • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
  • Sensitivity to any component of Pediarix, including yeast or neomycin and polymyxin B (antibiotics);
  • Apnea following intramuscular vaccination has been observed in some infants born prematurely. The Pediarix vaccine product insert warns that the decision to vaccinate an infant born prematurely should take into consideration both the potential risks and possible benefits of vaccination.
  • The tip caps of prefilled Pediarix syringes contain latex and may cause an allergic reaction in persons sensitive to latex;
  • If Guillain-Barré syndrome (GBS) occurred within 6 weeks of receiving a tetanus containing vaccine, assessment of the possible risks and potential benefits of receiving Pediarix should be carefully considered prior to vaccination.

Pediarix is FDA approved for use in infants and children 6 weeks through 6 years of age. Pediarix should not be administered to infants younger than 6 weeks or children older than 6 years of age.

Kinrix (Diphtheria and tetanus toxoids, acellular pertussis and inactivated poliovirus vaccine manufactured by GlaxoSmithKline.)

  • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
  • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
  • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
  • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
  • Serious allergic reaction to a previous pertussis vaccination;
  • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
  • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
  • Severe allergic reaction to any component of Kinrix, including neomycin and polymyxin B (antibiotics);
  • The tip caps of prefilled Kinrix syringes contain latex and may cause an allergic reaction in persons sensitive to latex;
  • If Guillain-Barré syndrome (GBS) occurred within 6 weeks of receiving a tetanus containing vaccine, assessment of the possible risks and potential benefits of receiving Kinrix should be carefully considered prior to vaccination.

Kinrix is FDA approved for use in children between the ages of 4 and 6 years. Kinrix should not be administered to children younger than 4 years or older than 6 years of age.

Quadracel (Diphtheria and tetanus toxoid, acellular pertussis and inactivated poliovirus vaccine manufactured by Sanofi Pasteur.)

  • Serious allergic reaction following administration of a pertussis, tetanus, diphtheria, or polio containing vaccine or any ingredient of Quadracel vaccine;
  • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
  • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
  • Seizures within 3 days of a previous pertussis vaccination;
  • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
  • If Guillain-Barré syndrome (GBS) occurred within 6 weeks of receiving a tetanus containing vaccine, assessment of the possible risks and potential benefits of receiving Quadracel should be carefully considered prior to vaccination.

Quadracel is FDA approved for use in children between the ages of 4 and 6 years. Quadracel should not be administered to children younger than 4 years or older than 6 years of age.

Pentacel (Diphtheria and tetanus toxoids and acellular pertussis, inactivated poliovirus and Haemophilus b conjugate (tetanus toxoid conjugate) vaccine manufactured by Sanofi Pasteur.)

  • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
  • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
  • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
  • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
  • Serious allergic reaction to a previous pertussis vaccination;
  • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
  • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy)
  • Severe allergic reaction to any component of Pentacel, including neomycin and polymyxin B (antibiotics);
  • Apnea following intramuscular vaccination has been observed in some infants born prematurely. Pentacel vaccine product insert warns that the decision to vaccinate an infant born prematurely should take into consideration both the potential risks and possible benefits of vaccination;
  • If Guillain-Barré syndrome (GBS) occurred within 6 weeks of receiving a tetanus containing vaccine, assessment of the possible risks and potential benefits of receiving Pentacel should be carefully considered prior to vaccination.

Pentacel is FDA approved for use in infants and children 6 weeks through 4 years of age. Pentacel should not be administered to infants younger than 6 weeks or children older than 4 years of age.

VAXELIS (Diphtheria and tetanus toxoids and acellular pertussis, inactivated poliovirus, Haemophilus b conjugate, and hepatitis B recombinant vaccine manufactured by MCM Vaccine Company.)

  • Temperature of 105 F. or higher within 48 hours of a previous pertussis vaccination, not attributable to another identifiable cause;
  • Collapse or shock-like state (hypotonic-hyporesponsive episodes) within 48 hours of a previous pertussis vaccination;
  • Persistent crying lasting 3 hours or more within 48 hours of a previous pertussis vaccination;
  • Convulsions with or without fever, occurring within 3 days of a previous pertussis vaccination;
  • Serious allergic reaction to a previous dose of VAXELIS, any ingredient found in VAXELIS, or any other tetanus toxoid, diphtheria toxoid, pertussis-containing vaccine, hepatitis B vaccine, inactivated poliovirus vaccine, or H. influenzae type b vaccine;
  • Encephalopathy (coma, decreased level of consciousness, prolonged convulsions) within 7 days of a previous pertussis vaccination not attributable to another identifiable cause;
  • Children with a progressive neurologic disorder (such as infantile spasms, uncontrolled epilepsy, or progressive encephalopathy);
  • Apnea following intramuscular vaccination has been observed in some infants born prematurely. The VAXELIS vaccine product insert warns that the decision to vaccinate an infant born prematurely should take into consideration both the potential risks and possible benefits of vaccination;
  • If Guillain-Barré syndrome (GBS) occurred within 6 weeks of receiving a tetanus containing vaccine, assessment of the possible risks and potential benefits of receiving VAXELIS should be carefully considered prior to vaccination.

VAXELIS is FDA approved for use in infants and children 6 weeks through 4 years of age. VAXELIS should not be administered to infants younger than 6 weeks or children older than 4 years of age.

IPOL (inactive poliovirus (Monkey Kidney Cell) manufactured by Sanofi Pasteur)

  • Hypersensitivity to any ingredient found within the vaccine, including polymyxin B, neomycin, streptomycin, formaldehyde, and 2-phenoxyethanol
  • Anaphylaxis or anaphylactic shock occurring within 24 hours of a previous vaccine dose
  • Acute febrile illness – vaccination should be deferred until a person has recovered

IPOL is FDA approved for use in individuals 6 weeks of age and older. IPOL should not be administered to infants younger than 6 weeks.

What questions should I ask my doctor about the Polio vaccine? 

NVIC’s If You Vaccinate, Ask 8! Webpage downloadable brochure suggests asking eight questions before you make a vaccination decision for yourself, or for your child. If you review these questions before your appointment, you will be better prepared to ask your doctor questions.  Also make sure that the nurse or doctor gives you the relevant Vaccine Information Statement (VIS) for the vaccine or vaccines you are considering well ahead of time to allow you to review it before you or your child gets vaccinated. Copies of VIS for each vaccine are also available on the CDC's website and there is a link to the VIS for vaccines on NVIC's “Quick Facts” at the top of this page.

It is also a good idea to read the vaccine manufacturer product insert that can be obtained from your doctor or public health clinic because federal law requires drug companies marketing vaccines to include certain kinds of vaccine benefit, risk and use information in product information inserts that may not be available in other published information. Poliovirus vaccine product inserts are located on the Food and Drug Administration’s website.

Other questions that may be useful to discuss with your doctor before getting the poliovirus vaccine are: 

  • If other vaccines in addition to tetanus vaccine are scheduled for my child at this office visit, am I allowed to modify the schedule so fewer vaccines are given at once?
  • What should I do if my child has a high fever or appears very ill after vaccination?
  • What other kinds of reaction symptoms should I call to report after poliovirus vaccination?
  • If the poliovirus vaccine doesn’t protect my child, do I have any other options for preventing poliovirus infection?

Under the National Childhood Vaccine Injury Act of 1986, doctors and all vaccine providers are legally required to give you vaccine benefit and risk information before vaccination; record serious health problems following vaccination in the permanent medical record; keep a permanent record of all vaccines given, including the manufacturer’s name and lot number; and report serious health problems, injuries and deaths that follow vaccination to VAERS.

Remember, if you choose to vaccinate, always keep a written record of exactly which shots/vaccines you or your child have received, including the manufacturer’s name and vaccine lot number. Write down and describe in detail any serious health problems that develop after vaccination and keep vaccination records in a file you can access easily.  

It also is important to be able to recognize a vaccine reaction and seek immediate medical attention if the reaction appears serious, as well as know how to make a vaccine reaction report to federal health officials at the Vaccine Adverse Reporting System (VAERS). NVIC’s Report Vaccine Reactions—It’s the Law webpage can help you file a vaccine reaction report yourself to VAERS if your doctor fails or refuses to make a report.

NVIC Press Releases, Statements & Commentaries Related to Polio

NVIC Polio Video Playlist

View the collection of video resources within the player below for more information on polio and the polio vaccine.

To view the entire video collection, click the hamburger menu in the upper left corner of the video player above. This will expand a full list of videos. You may also open the video player in full screen mode for optimal display.

Hearings, Workshops and NVIC Testimony

 NVIC Press Releases

The Vaccine Reaction

Selected medical literature and resources

Selected Books

  • Maready F The moth in the iron lung: a biography of polio. United States: Feels Like Fire.2018
  • Humphries S Bystrianyk R Dissolving illusions: disease, vaccines and the forgotten history. United States: CreateSpace, 2015
  • Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006.
  • Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. Martin’s Press, 2004
  • Paul, JR. A History of Poliomyelitis. New Haven, Yale University Press, 1971

References

1 Medline Plus Polio Jan. 6, 2020

2 CDC Poliomyelitis – Poliovirus Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

3 Medline Plus Polio Jan. 6, 2020

4 Mehndiratta MM, Mehndiratta P, Pande R Poliomyelitis Historical Facts, Epidemiology, and Current Challenges in Eradication Neurohospitalist. 2014 Oct; 4(4): 223–229

5 Johnson S Polio Healthline Oct 15. 2016

6 Medline Plus Polio and Post-Polio Syndrome Jan.9, 2020

7 Mehndiratta MM, Mehndiratta P, Pande R Poliomyelitis Historical Facts, Epidemiology, and Current Challenges in Eradication Neurohospitalist. 2014 Oct; 4(4): 223–229

8 Lopalco PL Wild and vaccine-derived poliovirus circulation, and implications for polio eradication. Epidemiol Infect. 2017 Feb;145(3):413-419

9 CDC Vaccine-derived Poliovirus - Questions and Answers May 4, 2018

10 CDC Polio Vaccination May 4, 2018

11 CDC Poliomyelitis – Epidemiology  Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

12 CDC International Notes Certification of Poliomyelitis Eradication -- the Americas, 1994 MMWR Oct. 7, 1994; 43(39);720-722

13 WHO Poliomyelitis Feb. 9, 2017

14 CDC Poliomyelitis – Poliovirus Vaccines Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

15 WHO Replacing trivalent OPV with bivalent OPV No date (accessed Jan. 19, 2020)

16 FDA Vaccines Licensed for Use in the United States Jan. 16, 2020

17 CDC Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP) Regarding Routine Poliovirus Vaccination MMWR August 7, 2009; 58(30);829-830

18 FDA IPOL - Poliovirus Vaccine Inactivated (Monkey Kidney Cell) Package Insert Aug. 6, 2015

19 FDA Vaccines Licensed for Use in the United States Jan. 16, 2020

20 Lopalco PL Wild and vaccine-derived poliovirus circulation, and implications for polio eradication. Epidemiol Infect. 2017 Feb;145(3):413-419

21 CDC Vaccine-derived Poliovirus - Questions and Answers May 4, 2018

22 Beaubien J Mutant Strains Of Polio Vaccine Now Cause More Paralysis Than Wild Polio National Public Radio Jun. 28, 2017

23 CDC Poliomyelitis – Poliovirus Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

24 Ibid

25 Mehndiratta MM, Mehndiratta P, Pande R Poliomyelitis Historical Facts, Epidemiology, and Current Challenges in Eradication Neurohospitalist. 2014 Oct; 4(4): 223–229

26 CDC Poliomyelitis – Clinical Features Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

27 Mehndiratta MM, Mehndiratta P, Pande R Poliomyelitis Historical Facts, Epidemiology, and Current Challenges in Eradication Neurohospitalist. 2014 Oct; 4(4): 223–229

28 Ibid

29 National Institute of Health Post-Polio Syndrome Fact Sheet National Institute of Neurological Disorders and Stroke Aug 13, 2019

30 CDC Poliomyelitis Prevention in the United States - Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR May 19, 2000; 49(RR05);1-22

31 Henderson DA, Witte JJ, Morris L, Langmuir AD. PARALYTIC DISEASE ASSOCIATED WITH ORAL POLIO VACCINES. JAMA. 1964 Oct 5; 190:41-8.

32 CDC Poliomyelitis Prevention in the United States - Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR May 19, 2000; 49(RR05);1-22

33 Global Polio Eradication Initiative (GPEI) OPV – Oral Polio Vaccine No date. (accessed Jan.30, 2020)

34 WHO What is vaccine-derived polio? Apr. 2017

35 Guo J, Bolivar-Wagers S, Srinivas N et al. Immunodeficiency-related vaccine-derived poliovirus (iVDPV) cases: a systematic review and implications for polio eradication. Vaccine. 2015 Mar 3;33(10):1235-42

36 CDC Progress Toward Polio Eradication — Worldwide, January 2017–March 2019 MMWR 68(20):458-462

37 Global Polio Eradication Initiative (GPEI) TWO OUT OF THREE WILD POLIOVIRUS STRAINS ERADICATED Oct. 24, 2019

38 CDC Cessation of Trivalent Oral Poliovirus Vaccine and Introduction of Inactivated Poliovirus Vaccine — Worldwide, 2016 MMWR Sep 9, 2016; 65(35);934–938

39 CDC Update on Vaccine-Derived Polioviruses — Worldwide, January 2015–May 2016 MMWR Aug. 5, 2016; 65(30);763–769

40 CDC Update on Vaccine-Derived Poliovirus Outbreaks — Worldwide, January 2018–June 2019 MMWR Nov. 15, 2019; 68(45);1024–1028

41 CDC Cessation of Trivalent Oral Poliovirus Vaccine and Introduction of Inactivated Poliovirus Vaccine — Worldwide, 2016 MMWR Sep 9, 2016; 65(35);934–938

42 WHO Emergencies Preparedness, response – Poliomyelitis – Disease outbreak news No Date (accessed Jan. 19, 2020)

43 CDC Update on Vaccine-Derived Poliovirus Outbreaks — Worldwide, January 2018–June 2019 MMWR Nov. 15, 2019; 68(45);1024–1028

44 CDC Surveillance to Track Progress Toward Polio Eradication — Worldwide, 2017–2018 MMWR 68(13):312-318

45 Ibid

46 Medline Plus Acute Flaccid Myelitis Nov 13, 2019

47 Ibid

48 CDC AFM Cases in U.S. Jan. 3, 2020

49 CDC About Acute Flaccid Myelitis June 28, 2019

50 Fisher BL, Cáceres M Polio Eradication Stalls with More Wild-Type and Vaccine Strain Polio Outbreaks The Vaccine Reaction Dec. 7, 2019

51 CDC Poliomyelitis – Epidemiology Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

52 CDC Global Health – What is Polio? Oct. 24, 2019

53 CDC Vaccine-derived Poliovirus - Questions and Answers May 4, 2018

54 Global Polio Eradication Initiative (GPEI) Vaccine-associated paralytic polio (VAPP) and vaccine-derived poliovirus (VDPV) Fact Sheet Feb. 2015

55 CDC Poliomyelitis – Epidemiology Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

56 Ibid

57 Minor P Characteristics of poliovirus strains from long-term excretors with primary immunodeficiencies. Dev Biol (Basel). 2001;105:75-80.

58 Martín J Vaccine-derived poliovirus from long term excretors and the end game of polio eradication. Biologicals. 2006 Jun;34(2):117-22

59 Kew OM, Sutter RW, Nottay BK et al. Prolonged Replication of a Type 1 Vaccine-Derived Poliovirus in an Immunodeficient Patient J Clin Microbiol. 1998 Oct; 36(10): 2893–2899.

60 Martín J, Odoom K, Tuite G Long-term excretion of vaccine-derived poliovirus by a healthy child. J Virol. 2004 Dec;78(24):13839-47.

61 Hovi T, Lindholm N, Savolainen C et al. Evolution of wild-type 1 poliovirus in two healthy siblings excreting the virus over a period of 6 months. J Gen Virol. 2004 Feb;85(Pt 2):369-77.

62 Aghamohammadi A, Abolhassani H, Kutukculer N et al. Patients with Primary Immunodeficiencies Are a Reservoir of Poliovirus and a Risk to Polio Eradication. Front Immunol. 2017 Jun 13;8:685.

63 CDC Poliomyelitis – Epidemiology Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

64 CDC Poliomyelitis – Poliovirus Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

65 Ruhrah J, Mayer EE, Poliomyelitis in all its aspects New York: Lea and Febiger, 1917.

66 CDC Poliomyelitis Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

67 University of Virginia Vaulted Treasures - Michael Underwood (1736?-1820) 2007

68 Pearce JMS Poliomyelitis (Heine-Medin disease) J. Neurol. Neurosurg. Psychiatry 2005;76:128.

69 Trevelyan B, Smallman-Raynor M, Cliff AD. The Spatial Dynamics of Poliomyelitis in the United States: From Epidemic Emergence to Vaccine-Induced Retreat, 1910-1971. Ann Assoc Am Geogr. 2005 Jun;95(2):269-293.

70 Pearce JMS Poliomyelitis (Heine-Medin disease) J. Neurol. Neurosurg. Psychiatry 2005;76:128.

71 Trevelyan B, Smallman-Raynor M, Cliff AD. The Spatial Dynamics of Poliomyelitis in the United States: From Epidemic Emergence to Vaccine-Induced Retreat, 1910-1971. Ann Assoc Am Geogr. 2005 Jun;95(2):269-293.

72 Ruhrah J, Mayer EE, Poliomyelitis in all its aspects New York: Lea and Febiger, 1917.

73 Pearce JMS Poliomyelitis (Heine-Medin disease) J. Neurol. Neurosurg. Psychiatry 2005;76:128.

74 Ruhrah J, Mayer EE, Poliomyelitis in all its aspects New York: Lea and Febiger, 1917.

75 State Department of Public Health INFANTILE PARALYSIS IN VERMONT 1894-1922 The Vermont Printing Company Brattleboro, VT; 1924

76 Baicus A History of polio vaccination. World J Virol. 2012 Aug 12;1(4):108-14.

77 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap 1: 8-23

78 Paul, JR. A History of Poliomyelitis. New Haven, Yale University Press, 1971. Chap. 11: 98-106

79 CDC Weekly Reports for NOVEMBER 18, 1910 Public Health Rep. Nov. 18, 1910; 25(46):1663-1709

80 Ibid

81 Ibid

82 State Department of Public Health INFANTILE PARALYSIS IN VERMONT 1894-1922 The Vermont Printing Company Brattleboro, VT; 1924

83 CDC Poliomyelitis – Epidemiology Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

84 Seguin EC Myelitis Following Acute Arsenical Poisoning (By Paris Green or Schwein-Furth Green) Journal of Nervous and Mental Disease Oct 1882; IX no. 4:6

85 Spear, RJ. The Great Gypsy Moth War a History of the First Campaign in Massachusetts to Eradicate the Gypsy Moth, 1890-1901. Univ. of Massachusetts Press, 2005.

86 Haywood JK, McDonnell CC LEAD ARSENATE. I. Composition of lead arsenates found on the market. II. " Home-made" lead arsenate and the chemicals entering into its manufacture. III. Action of lead arsenate on foliage.  U. S. DEPARTMENT OF AGRICULTURE, BUREAU OF CHEMISTRY BULLETIN No. 131. Washington: Government Printing Office, April 6, 1910.

87 Spear, RJ. The Great Gypsy Moth War a History of the First Campaign in Massachusetts to Eradicate the Gypsy Moth, 1890-1901. Univ. of Massachusetts Press, 2005.

88 Trevelyan B, Smallman-Raynor M, Cliff AD. The Spatial Dynamics of Poliomyelitis in the United States: From Epidemic Emergence to Vaccine-Induced Retreat, 1910-1971. Ann Assoc Am Geogr. 2005 Jun;95(2):269-293.

89 Casita JE The Greening of Pesticide–Environment Interactions: Some Personal Observations Environ Health Perspect. 2012 Apr; 120(4): 487–493.

90 Manning JVV The Correlation of epidemic paralysis in animal and man The Medical Times May 1912 p134-137

91 CDC Weekly Reports for OCTOBER 25, 1912 Public Health Rep. Oct. 25, 1912; 27(43):1731-1772

92 CDC Weekly Reports for MAY 2, 1913 Public Health Rep. May 2, 1913; 28(18):833-883

93 Baicus A History of polio vaccination. World J Virol. 2012 Aug 12;1(4):108-14.

94 CDC Weekly Reports for JULY 14, 1916 Public Health Rep. July 14, 1916; 31(28):1817-1906

95 Ibid

96 Wyatt HV Before the Vaccines: Medical Treatments of Acute Paralysis in the 1916 New York Epidemic of Poliomyelitis Open Microbiol J. 2014; 8: 144–147.

97 Baicus A History of polio vaccination. World J Virol. 2012 Aug 12;1(4):108-14.

98 Wyatt HV Before the Vaccines: Medical Treatments of Acute Paralysis in the 1916 New York Epidemic of Poliomyelitis Open Microbiol J. 2014; 8: 144–147.

99 Wyatt HV The 1916 New York City Epidemic of Poliomyelitis: Where Did the Virus Come From? The Open Vaccine Journal 2011, 4: p13-17

100 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 1: 8-23

101 Ibid

102 Lien G, Heymann DL. The problems with polio: toward eradication. Infect Dis Ther. 2013 Dec;2(2):167-74.

103 WHO Poliomyelitis Feb. 9, 2017

104 CDC Poliomyelitis distribution in the United States Public Health Rep. May 1953; 68(5):453-466

105 NPS.gov Warm Springs Historic District Roosevelt’s Little White House State Historic Site and Roosevelt Warm Springs Institute for Rehabilitation Georgia. No date.

106 Rogers N Race and the Politics of Polio Warm Springs, Tuskegee, and the March of Dimes Am J Public Health. 2007 May; 97(5): 784–795.

107 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006.Chap 3: 43-60

108 Rogers N Race and the Politics of Polio Warm Springs, Tuskegee, and the March of Dimes Am J Public Health. 2007 May; 97(5): 784–795.

109 Goldman AS, Schmalstieg EJ, Freeman DH Jr et al. What was the cause of Franklin Delano Roosevelt's paralytic illness? J Med Biogr. 2003 Nov;11(4):232-40.

110 Goldman AS, Schmalstieg EJ, Dreyer CF et al. Franklin Delano Roosevelt's (FDR's) (1882-1945) 1921 neurological disease revisited; the most likely diagnosis remains Guillain-Barré syndrome. J Med Biogr. 2016 Nov;24(4):452-459.

111 Berciano J Additional arguments supporting that Franklin Delano Roosevelt's paralytic illness was related to Guillain-Barré syndrome. J Med Biogr. 2018 May;26(2):142-143

112 Jackson CD Mechanical Ventilation Medscape Apr. 11, 2019

113 Cáceres M “Iron Lungs” Still Around. They’re Called Ventilators. The Vaccine Reaction May 7, 2017

114 Cáceres M Market for Breathing Machines Alive and Well The Vaccine Reaction May 29, 2019

115 Paul, JR. A History of Poliomyelitis. New Haven, Yale University Press, 1971. Chap. 24: 252-262

116 CDC The National Institute for Occupational Safety and Health (NIOSH) – Picric Acid Dec. 4, 2014

117 NIH National Center for Biotechnology Information. PubChem Database. Picric acid (accessed Jan. 30, 2020)

118 CDC Weekly Reports for MARCH 6, 1936 Public Health Rep. Mar. 6, 1936; 51(10):241-262

119 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 7: 112-127

120 CDC Weekly Reports for JULY 17, 1936 Public Health Rep. Jul. 17, 1936; 51(29):947-987

121 INFANTILE PARALYSIS—ZINC SULPHATE NASAL SPRAY Cal West Med. 1937 Oct; 47(4): 286–287.

122 ZINC SULPHATE SPRAY FOR PREVENTION OF POLIOMYELITIS. Br Med J. 1938 Apr 30;1(4034):953-4.

123 CDC Weekly Reports for MAY 8, 1942 Public Health Rep. May 8, 1942; 57(19):685-727

124 Kendall HO, Kendall F. Care during the recovery period of paralytic poliomyelitis: Public Health Bulletin No. 242. Washington, DC: US Surgeon General; revised 1939.

125 Becker BE Sister Elizabeth Kenny and Polio in America: Doyenne or Demagogue in Her Role in Rehabilitation Medicine? PM R. 2018 Feb;10(2):208-217

126 Ibid

127 Ibid

128 Ibid

129 Ibid

130 Ibid

131 Cartwright RL Sister Kenny Institute Minnesota Historical Society Feb. 21, 2017

132 CDC Weekly Reports for JUNE 18, 1943 Public Health Rep. Jun 18 1943; 58(25):937-968

133 CDC Poliomyelitis distribution in the United States Public Health Rep. May 1953; 68(5):453-466

134 CDC Weekly Reports for JUNE 18, 1943 Public Health Rep. Jun 18, 1943; 58(25):937-968

135 Ibid

136 Ibid

137 Ibid

138 Ibid

139 CDC Public Health Reports; v. 60. No. 23 June 8, 1945 Public Health Rep. Jun. 8, 1945; 60(23):633-660

140 SABIN AB. Paralytic consequences of poliomyelitis infection in different parts of the world and in different population groups. Am J Public Health Nations Health. 1951 Oct;41(10):1215-30.

141 CDC Malaria Control in War Areas field bulletin: January 1945.

142 CDC Dichlorodiphenyltrichloroethane (DDT) Nov. 2009

143 Paltzer S The Other Foe: The U.S. Army’s Fight against Malaria in the Pacific Theater, 1942-45 Army Historical Foundation Apr. 30, 2016

144 CDC Malaria Control in War Areas field bulletin: January 1945.

145 CDC DDT for the control of household pests October 1945

146 Cáceres M DDT and the Rise and Fall of Polio The Vaccine Reaction July 22, 2015

147 CDC Weekly Reports for JUNE 20, 1947 Public Health Rep. June 20, 1947 62(25):901-932

148 CDC Communicable Disease Center activities, 1949-1950. 1951

149 Post-Polio Health International Incidence Rates of Poliomyelitis in the US. No Date (Accessed Jan 12, 2020)

150 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006 Chap. 10:161-173

151 Cáceres M DDT and the Rise and Fall of Polio The Vaccine Reaction Jul. 22, 2015

152 Ratner H et al. The Present Status of Polio Vaccines Illinois Medical Journal 118, no 2, 3, pp 84-93; pp160-168 Edited from a Panel Discussion presented before the Section on Preventative Medicine and Public Health at the 120th annual meeting of the Illinois State Medical Society in Chicago, May 26, 1960

153 Ibid

154 Ibid

155 Brown GC, Lenz WR, Agate GH. Laboratory data on the Detroit poliomyelitis epidemic-1958. J Am Med Assoc. 1960 Feb 20; 172:807-12.

156 Ratner H et al. The Present Status of Polio Vaccines Illinois Medical Journal 118, no 2, 3, pp 84-93; pp160-168 Edited from a Panel Discussion presented before the Section on Preventative Medicine and Public Health at the 120th annual meeting of the Illinois State Medical Society in Chicago, May 26, 1960

157 CDC National participation trends, 1955-61, in the poliomyelitis vaccination program Public Health Rep. Aug. 1962; 77(8):661-670

158 Ratner H et al. The Present Status of Polio Vaccines Illinois Medical Journal 118, no 2, 3, pp 84-93; pp160-168 Edited from a Panel Discussion presented before the Section on Preventative Medicine and Public Health at the 120th annual meeting of the Illinois State Medical Society in Chicago, May 26, 1960

159 CDC Recommendations on oral poliomyelitis vaccine Public Health Rep. Mar. 1963; 78(3):273-275

160 Post-Polio Health International Incidence Rates of Poliomyelitis in the US. No Date (Accessed Jan. 30, 2020)

161 CDC Surveillance of poliomyelitis in the United States, 1962-65. Public Health Rep. May 1967; 82(5):417-428

162 CDC Recommendations on oral poliomyelitis vaccine Public Health Rep. Mar. 1963; 78(3):273-275

163 CDC Poliomyelitis Prevention in the United States - Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR May 19, 2000; 49(RR05);1-22

164 Ibid

165 Ibid

166 Freyche M-J, Payne AM-M Poliomyelitis in 1953 Bull World Health Organ. 1955; 12: 595-649

167 Cockburn WC, Drozdov SG Poliomyelitis in the World Bull World Health Organ 1970; 42: 405-417

168 CDC Update: Progress Toward Eradicating Poliomyelitis from the Americas MMWR Aug. 24, 1990; 39(33):557-561

169 WHO WHA41.28 Global eradication of poliomyelitis by the year 2000 FORTY-FIRST WORLD HEALTH ASSEMBLY  GENEVA, 2-13 MAY 1988.

170 CDC Progress Toward Global Poliomyelitis Eradication, 2000 MMWR April 27, 2001; 50(16);320-2, 331

171 CDC Public Health Dispatch: Outbreak of Poliomyelitis --- Dominican Republic and Haiti, 2000 MMWR Dec. 08, 2000; 49(48);1094,1103

172 CDC Public Health Dispatch: Acute Flaccid Paralysis Associated with Circulating Vaccine-Derived Poliovirus --- Philippines, 2001 MMWR Oct. 12, 2001; 50(40);874-5

173 CDC Acute Flaccid Paralysis Surveillance Systems for Expansion to Other Diseases, 2003–2004 MMWR Dec. 3, 2004; 43(47): 1113-1116

174 Wringe A, Fine PE, Sutter RW, Kew OM. Estimating the extent of vaccine-derived poliovirus infection. PLoS One. 2008;3(10):e3433.

175 Performance of acute flaccid paralysis (AFP) surveillance and incidence of poliomyelitis, 2010. Wkly Epidemiol Rec. 2010 Dec 10;85(50):503-7.

176 Puliyel C, Sathyamala C, Banerji D Protective Efficacy of a Monovalent Oral Type 1 Poliovirus Vaccine Lancet 2007 July; 370 (9582): 129

177 Sathyamala C Polio Eradication Programme in India Indian J Med Res 2007 May; 125: 695-696

178 Vashisht N, Puliyel J. Polio programme: let us declare victory and move on. Indian J Med Ethics. 2012 Apr-Jun;9(2):114-7.

179 CDC Tracking Progress Toward Polio Eradication — Worldwide, 2013–2014 MMWR Apr. 24, 2015; 64(15):415-420.

180 Ibid

181 CDC Cessation of Trivalent Oral Poliovirus Vaccine and Introduction of Inactivated Poliovirus Vaccine — Worldwide, 2016 MMWR Sep 9, 2016; 65(35);934–938

182 CDC Update on Vaccine-Derived Polioviruses — Worldwide, January 2015–May 2016 MMWR Aug. 5, 2016; 65(30);763–769

183 CDC Cessation of Trivalent Oral Poliovirus Vaccine and Introduction of Inactivated Poliovirus Vaccine — Worldwide, 2016 MMWR Sep 9, 2016; 65(35);934–938

184 WHO Emergencies Preparedness, response – Poliomyelitis – Disease outbreak news No Date (accessed Jan. 30, 2020)

185 CDC Update on Vaccine-Derived Poliovirus Outbreaks — Worldwide, January 2018–June 2019 MMWR Nov. 15, 2019; 68(45);1024–1028

186 Global Polio Eradication Initiative (GPEI) TWO OUT OF THREE WILD POLIOVIRUS STRAINS ERADICATED Oct. 24, 2019

187 CDC Surveillance to Track Progress Toward Polio Eradication — Worldwide, 2017–2018 MMWR 68(13):312-318

188 WHO. Statement of the Twenty-Second IHR Emergency Committee Regarding the International Spread of Poliovirus. WHO.int Oct. 3, 2019.

189 Ibid

190 Razum O, Sridhar D, Jahn A et al. Polio: from eradication to systematic, sustained control. BMJ Glob Health. 2019 Aug 20;4(4):e001633

191 Ibid

192 GPEI Polio Endgame Strategy 2019-2023 – Eradication, integration, certification and containment 2019

193 Mehndiratta MM, Mehndiratta P, Pande R Poliomyelitis Historical Facts, Epidemiology, and Current Challenges in Eradication Neurohospitalist. 2014 Oct; 4(4): 223–229

194 CDC Poliomyelitis – Clinical Features Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

195 Mehndiratta MM, Mehndiratta P, Pande R Poliomyelitis Historical Facts, Epidemiology, and Current Challenges in Eradication Neurohospitalist. 2014 Oct; 4(4): 223–229

196 Ibid

197 CDC Poliomyelitis – Clinical Features Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

198 National Institute of Health Post-Polio Syndrome Fact Sheet National Institute of Neurological Disorders and Stroke Aug 13, 2019

199 CDC Poliomyelitis Prevention in the United States - Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR May 19, 2000; 49(RR05);1-22

200 CDC Surveillance to Track Progress Toward Polio Eradication — Worldwide, 2017–2018 MMWR 68(13):312-318

201 WHO What is vaccine-derived polio? Apr. 2017

202 Guo J, Bolivar-Wagers S, Srinivas N et al. Immunodeficiency-related vaccine-derived poliovirus (iVDPV) cases: a systematic review and implications for polio eradication. Vaccine. 2015 Mar 3;33(10):1235-42

203 CDC Vaccine-derived Poliovirus - Questions and Answers May 4, 2018

204 WHO Poliomyelitis July 22, 2019

205 Johnson S Polio Healthline Oct. 10, 2016

206 Guo J, Bolivar-Wagers S, Srinivas N et al Immunodeficiency-related vaccine-derived poliovirus (iVDPV) cases: a systematic review and implications for polio eradication. Vaccine. 2015 Mar 3;33(10):1235-42

207 Tonsillectomy and Poliomyelitis Am J Public Health Nations Health. 1954 Aug; 44(8): 1065–1067.

208 Horstmann DM. Acute poliomyelitis relation of physical activity at the time of onset to the course of the disease. J Am Med Assoc. 1950 Jan 28;142(4):236-41.

209 Mawdsley SE. Polio provocation: solving a mystery with the help of history. Lancet. 2014 Jul 26;384(9940):300-1.

210 Strebel PM, Ion-Nedelcu N, Baughman AL Intramuscular injections within 30 days of immunization with oral poliovirus vaccine--a risk factor for vaccine-associated paralytic poliomyelitis. N Engl J Med. 1995 Feb 23;332(8):500-6.

211 Gromeier M, Wimmer E. Mechanism of injury-provoked poliomyelitis. J Virol. 1998 Jun;72(6):5056-60.

212 CDC Relationship between inoculations and poliomyelitis Public Health Rep. May 1952; 67(5):495

213 Mehndiratta MM, Mehndiratta P, Pande R Poliomyelitis Historical Facts, Epidemiology, and Current Challenges in Eradication Neurohospitalist. 2014 Oct; 4(4): 223–229

214 CDC Poliomyelitis – Clinical Features Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

215 WHO Emergencies Preparedness, response – Poliomyelitis – Disease outbreak news No Date (accessed Jan. 30, 2020)

216 Mawdsley SE. Polio provocation: solving a mystery with the help of history. Lancet. 2014 Jul 26;384(9940):300-1.

217 Gromeier M, Wimmer E. Mechanism of injury-provoked poliomyelitis. J Virol. 1998 Jun;72(6):5056-60.

218 Strebel PM, Ion-Nedelcu N, Baughman AL Intramuscular injections within 30 days of immunization with oral poliovirus vaccine--a risk factor for vaccine-associated paralytic poliomyelitis. N Engl J Med. 1995 Feb 23;332(8):500-6.

219 Siegel M, Greenberg M, Magee MC. Tonsillectomy and poliomyelitis. II. Frequency of bulbar paralysis, 1944-1949. J Pediatr. 1951 May;38(5):548-58.

220 Greenberg M, Abramson H, Cooper HM, Solomon HE. The relation between recent injections and paralytic poliomyelitis in children. Am J Public Health Nations Health. 1952 Feb;42(2):142-52.

221 Tonsillectomy and Poliomyelitis Am J Public Health Nations Health. 1954 Aug; 44(8): 1065–1067.

222 Mehndiratta MM, Mehndiratta P, Pande R Poliomyelitis Historical Facts, Epidemiology, and Current Challenges in Eradication Neurohospitalist. 2014 Oct; 4(4): 223–229

223 Ibid

224 Ramachandran, TS Aseptic Meningitis Treatment & Management – Approach Considerations Medscape Jul. 17, 2018

225 Mehndiratta MM, Mehndiratta P, Pande R Poliomyelitis Historical Facts, Epidemiology, and Current Challenges in Eradication Neurohospitalist. 2014 Oct; 4(4): 223–229

226 Mayo Clinic Polio – Diagnosis & treatment Dec. 9, 2017

227 KLENNER FR. The treatment of poliomyelitis and other virus diseases with vitamin C. South Med Surg. 1949 Jul;111(7):209-14.

228 Landwehr R The Origin of the 40-Year Stonewall of Vitamin C J Orthomol Med. 1991; 6(2): 99-103

229 Sandler B Diet Prevents Polio Lee Foundation for Nutritional Research, 1951

230 van Meer F. Poliomyelitis: the role of diet in the development of the disease. Med Hypotheses. 1992 Mar;37(3):171-8.

231 FDA IPOL - Poliovirus Vaccine Inactivated (Monkey Kidney Cell) – Package Insert Aug 6, 2015

232 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap 3: 56-57

233 Brodie M, Park WH. Active Immunization Against Poliomyelitis. Am J Public Health Nations Health. 1936 Feb;26(2):119-25.

234 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap 3: 56-57

235 Kolmer JA. An Improved Method of Preparing the Kolmer Poliomyelitis Vaccine (Delivered before the Sixty-fourth Annual Meeting of the American Public Health Association in Milwaukee, Wis., October 8, 1935). Am J Public Health Nations Health. 1936 Feb;26(2):149-57.

236 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. P. 57-58

237 Kolmer JA Vaccination Against Acute Anterior Poliomyelitis Am J Public Health Nations Health. 1936 Feb; 26(2): 126–135.

238 Bodian D, Morgan IM, Howe HA. Differentiation of types of poliomyelitis viruses; the grouping of 14 strains into three basic immunological types. Am J Hyg. 1949 Mar;49(2):234-45.

239 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap.7: 112-127

240 Ibid

241 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap. 3 :p19-30

242 Enders JF, Weller TH, Robbins FC Cultivation of the Lansing Strain of Poliomyelitis Virus in Cultures of Various Human Embryonic Tissues. Science 1949 Jan 28;109(2822):85-7.

243 Vaccine Safety Committee, Institute of Medicine. Polio Vaccines. Adverse Events Associated with Childhood vaccines: Evidence Bearing on Causality. Washington D.C. National Academies Press 1994.

244 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 8: 128-144

245 Time Medicine: Closing in on Polio Mar. 29, 1954

246 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 9: 145-160

247 Time Medicine: Closing in on Polio Mar. 29, 1954

248 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 9: 145-160

249 Juskewitch JE, Tapia CJ, Windebank AJ. Lessons from the Salk polio vaccine: methods for and risks of rapid translation. Clin Transl Sci. 2010 Aug;3(4):182-5.

250 Thompson D The Salk Polio Vaccine: A medical miracle turns 60 CBS News Dec. 1, 2014

251 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006; Chap. 9: 145-160

252 Ibid

253 Juskewitch JE, Tapia CJ, Windebank AJ. Lessons from the Salk polio vaccine: methods for and risks of rapid translation. Clin Transl Sci. 2010 Aug;3(4):182-5.

254 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006; Chap. 9: 145-160

255 CDC Poliomyelitis distribution in the United States, 1952 Public Health Rep. Nov 1953; 68(11):1033-1034

256 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006 Chap. 10:161-173

257 Time Medicine: Closing in on Polio Mar. 29, 1954

258 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006: p180

259 Time Medicine: Closing in on Polio Mar. 29, 1954

260 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006; Chap. 12:188-213

261 Ibid

262 Ibid

263 Ibid

264 Ibid

265 Juskewitch JE, Tapia CJ, Windebank AJ. Lessons from the Salk polio vaccine: methods for and risks of rapid translation. Clin Transl Sci. 2010 Aug;3(4):182-5.

266 Francis T, Jr, Korns R, Voight R, et al. An evaluation of the 1954 poliomyelitis vaccine trials: summary report. Am J Public Health Nations Health. 1955 May;45(5 Pt 2):1-63.

267 Ratner H et al. The Present Status of Polio Vaccines Illinois Medical Journal 118, no 2, 3, pp 84-93 Edited from a Panel Discussion presented before the Section on Preventative Medicine and Public Health at the 120th annual meeting of the Illinois State Medical Society in Chicago, May 26, 1960

268 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 13: 214-236

269 Ratner H et al. The Present Status of Polio Vaccines Illinois Medical Journal 118, no 2, 3, pp 84-93 Edited from a Panel Discussion presented before the Section on Preventative Medicine and Public Health at the 120th annual meeting of the Illinois State Medical Society in Chicago, May 26, 1960

270 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 13: 214-236

271 CDC Poliomyelitis surveillance report number 3, May 3, 1955

272 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 13: 214-236

273 CDC An estimate of the extent of the national problem associated with Cutter vaccine Poliomyelitis surveillance special report; no. 2 May 14, 1955

274 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 13: 214-236

275 CDC Special report on cases of poliomyelitis among unvaccinated persons having familial contact with individuals who have received poliomyelitis vaccine Poliomyelitis surveillance special report; May 14, 1955; no. 1

276 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 13: 214-236

277 Cáceres M Bernice Eddy Warned of Defective Salk Polio Vaccine The Vaccine Reaction June 23, 2016

278 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 13: 214-236

279 Fitzpatrick M The Cutter Incident: How America's First Polio Vaccine Led to a Growing Vaccine Crisis J R Soc Med. 2006 Mar; 99(3): 156.

280 Post-Polio Health International Incidence Rates of Poliomyelitis in the US. No Date (Accessed Jan. 30, 2020)

281 Ratner H et al. The Present Status of Polio Vaccines Illinois Medical Journal 118, no 2, 3, pp 84-93; pp160-168 Edited from a Panel Discussion presented before the Section on Preventative Medicine and Public Health at the 120th annual meeting of the Illinois State Medical Society in Chicago, May 26, 1960

282 Ibid

283 Ibid

284 Ibid

285 Humphries S, Bystrianyk B. Dissolving Illusions: Disease, Vaccines, and the Forgotten History. July 27, 2013.

286 Brown GC, Lenz WR, Agate GH. Laboratory data on the Detroit poliomyelitis epidemic-1958. J Am Med Assoc. 1960 Feb 20; 172:807-12.

287 Ratner H et al. The Present Status of Polio Vaccines Illinois Medical Journal 118, no 2, 3, pp 84-93; pp160-168 Edited from a Panel Discussion presented before the Section on Preventative Medicine and Public Health at the 120th annual meeting of the Illinois State Medical Society in Chicago, May 26, 1960

288 CDC National participation trends, 1955-61, in the poliomyelitis vaccination program Public Health Rep. Aug. 1962; 77(8):661-670

289 Ratner H et al. The Present Status of Polio Vaccines Illinois Medical Journal 118, no 2, 3, pp 84-93; pp160-168 Edited from a Panel Discussion presented before the Section on Preventative Medicine and Public Health at the 120th annual meeting of the Illinois State Medical Society in Chicago, May 26, 1960

290 Ibid

291 CDC Surveillance of poliomyelitis in the United States, 1958-61 Public Health Rep. Dec. 1962; 77(12):1011-1020

292 Barrett CD, Timm EA, Molner JG, et al. Multiple antigen for immunization against poliomyelitis, diphtheria, pertussis, and tetanus. II. Response of infants and young children to primary immunization and eighteen-month booster. Am J Public Health Nations Health. 1959 May;49(5):644-55.

293 ChemEurope.com Parke-Davis No Date

294 Institute of Medicine (US) Immunization Safety Review Committee Adverse Effects of Pertussis and Rubella Vaccines: A Report of the Committee to Review the Adverse Consequences of Pertussis and Rubella Vaccines. Washington (DC): National Academies Press (US);1991 Pertussis and Rubella Vaccines: A Brief Chronology

295 CDC Selected Discontinued U.S. Vaccines Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book).2012

296 CDC Poliomyelitis surveillance report no. 253, Apr. 6, 1962

297 Ibid

298 CDC Immunization against infectious disease 1968 Public Health Service 1968

299 CDC ACIP recommendations 1969 : collected recommendations of the Public Health Service Advisory Committee on Immunization Practices MMWR Oct.25,1969; v. 18, no. 43, suppl.

300 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap.14: 237-254

301 Ibid

302 Ibid

303 Ibid

304 Chumakov MP Some results of the work on mass immunization in the Soviet Union with live poliovirus vaccine prepared from Sabin strains. Bull World Health Organ. 1961;25:79-91.

305 Plotkin SA, Lebrun A, Courtois G, Koprowski H. Vaccination with the CHAT strain of type 1 attenuated poliomyelitis virus in Leopoldville, Congo. 3. Safety and efficacy during the first 21 months of study. Bull World Health Organ. 1961;24:785-92.

306 Kostrzewski J, Kulesza A, Załeska H. Vaccination against poliomyelitis in Poland with types 1 and 3 attenuated viruses of Koprowski: 2. Epidemiological evaluation of results of mass vaccination, 1959-60. Bull World Health Organ. 1962;26(6):745-58.

307 Przesmycki F, Dobrowolska, Mirski B et al Vaccination against poliomyelitis in Poland with types 1 and 3 attenuated viruses of Koprowski*-1. Virological studies of the vaccine strains and serological studies of the vaccinated population Bull World Health Organ. 1962; 26(6): 733–743.

308 Ikić D, Jancikić B, Lulić V et al. Preliminary report on vaccination in Croatia against poliomyelitis with type 1 (CHAT) and type 3 (W-Fox) attenuated polioviruses of Koprowski. Bull World Health Organ. 1963;28(2):217-23.

309 Kimball AC, Barr RN, Bauer H et al Community spread of orally administered attenuated poliovirus vaccine strains Public Health Rep. Oct 1961; 76(10):903-914

310 Roca-Garcia M, Orsi EV, Jervis GA et al. Laboratory studies associated with field trials of monovalent oral poliovirus vaccines. J Infect Dis. 1960 Nov-Dec;107:300-17.

311 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006 Chap 3: 57-58

312 Porter ER, Wehr RE Oral poliomyelitis vaccine program in Cincinnati Public Health Rep. May 1961; 76(5):369-374

313 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 15: 262-263

314 Burney LE Oral Poliovirus Vaccine Public Health Rep. Oct. 1960 75(10):869-871

315 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 15: 263

316 Burney LE Oral Poliovirus Vaccine Public Health Rep. Oct. 1960 75(10):869-871

317 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006. Chap. 15: 265-266

318 Hofman B Poliomyelitis in the Netherlands 1958-69: the influence of a vaccination programme with inactivated poliovaccine. Bull World Health Organ. 1972;46(6):735-45.

319 Böttiger M, Zetterberg B, Salenstedt CR. Seroimmunity to poliomyelitis in Sweden after the use of inactivated poliovirus vaccine for 10 years. Bull World Health Organ. 1972;46(2):141-9.

320 Ibid

321 CDC Poliomyelitis surveillance report no. 268, Sep. 21, 1962

322 CDC Poliomyelitis surveillance report no. 273, Dec. 21, 1962

323 CDC Poliomyelitis surveillance report no. 272, Nov. 30, 1962

324 CDC Recommendations on oral poliomyelitis vaccine Mar. 1963; Public Health Rep. 78(3):273-275

325 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap. 3:118-128

326 Coriell Institute for Medical Research WI-38 - NORMAL HUMAN FETAL LUNG FIBROBLAST No Date

327 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap. 3:118-128

328 Ibid

329 CDC ACIP recommendations 1969 : collected recommendations of the Public Health Service Advisory Committee on Immunization Practices MMWR Oct.25,1969; v. 18, no. 43, suppl.

330 CDC MMWR. Morbidity and mortality weekly report, Vol. 31, no. 3, January 29, 1982 MMWR; Jan. 29, 1982; v. 31, no. 3

331 CDC MMWR. Morbidity and mortality weekly report, Vol. 36, no. 48, December 11, 1987 MMWR; Dec. 11, 1987; V.36, no. 48

332 CDC Poliomyelitis Prevention in the United States - Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR May 19, 2000; 49(RR05);1-22

333 Live Polio Vaccine Voted Out National Vaccine Information Center No Date

334 CDC Poliomyelitis Prevention in the United States - Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR May 19, 2000; 49(RR05);1-22

335 Global Polio Eradication Initiative (GPEI) OPV – Oral Polio Vaccine No date. (accessed Jan.30, 2020)

336 CDC Polio Vaccine Composition, Dosage, and Administration May 4, 2018

337 CDC Poliomyelitis Prevention in the United States - Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR May 19, 2000; 49(RR05);1-22

338 FDA IPOL - Poliovirus Vaccine Inactivated (Monkey Kidney Cell) Package Insert Aug. 6, 2015

339 Ammerman NC, Beier-Sexton M, Azad AF Growth and maintenance of Vero cell lines. Curr Protoc Microbiol. 2008 Nov; Appendix 4: Appendix 4E

340 FDA Summary for Basis of Approval - IPOL No Date (accessed Jan. 30, 2020)

341 ICANDECIDE.org Clinical Trials Relied Upon to License the Polio Vaccine in 1990 No Date (accessed Jan. 30,2020)

342 FDA IPOL - Poliovirus Vaccine Inactivated (Monkey Kidney Cell) Package Insert Aug. 6, 2015

343 CDC Notice to Readers: FDA Licensure of Diphtheria and Tetanus Toxoids and Acellular Pertussis Adsorbed, Hepatitis B (Recombinant), and Poliovirus Vaccine Combined, (PEDIARIX™) for Use in Infants MMWR Mar. 14, 2003; 52(10);203-204

344 FDA June 20, 2008 Approval Letter – Pentacel June 20, 2008

345 CDC Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP) Regarding Routine Poliovirus Vaccination MMWR Aug. 7, 2009; 58(30);829-830

346 FDA June 24, 2008 Approval Letter – Kinrix June 24, 2008

347 CDC Licensure of a diphtheria and tetanus toxoids and acellular pertussis adsorbed and inactivated poliovirus vaccine and guidance for use as a booster dose MMWR. Oct. 3, 2008; 57(39):1078-9.

348 FDA March 24, 2015 Approval Letter - Quadracel Mar. 24, 2015

349 CDC MMWR. Morbidity and mortality weekly report, Vol. 64, no. 34, September 4, 2015 MMWR Sep. 4, 2015;64(34):948-9

350 FDA December 21, 2018 Approval Letter – VAXELIS Dec. 21, 2018

351 CDC Advisory Committee on Immunization Practices (ACIP) summary report : June 26-27, 2019, Atlanta, Georgia ACIP meeting Minutes Nov. 4, 2019: 65-80

352 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap. 4: 31-45

353 Hull RN, Minner JR, Smith JW. New viral agents recovered from tissue cultures of monkey kidney cells. I. Origin and properties of cytopathogenic agents S.V.1, S.V.2, S.V.4, S.V.5, S.V.6, S.V.11, S.V.12 and S.V.15. Am J Hyg. 1956 Mar;63(2):204-15.

354 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap. 4: 31-45

355 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006; Chap. 16: 269-286

356 Eddy BE, Stewart SE. Characteristics of the SE polyoma virus. Am J Public Health Nations Health. 1959 Nov;49:1486-92.

357 Stewart SE, Eddy BE. Tumor induction by SE polyoma virus and the inhibition of tumors by specific neutralizing antibodies. Am J Public Health Nations Health. 1959 Nov;49:1493-6.

358 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap. 6: 57-68

359 Oshinsky, DM. Polio: an American Story. Oxford University Press, 2006; Chap. 16: 269-286

360 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap. 6: 57-68

361 Ibid

362 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap. 7: 69-85

363 Ibid

364 Garcea RL, Imperiale MJ. Simian virus 40 infection of humans. J Virol. 2003 May;77(9):5039-45.

365 Sweet BH, Hilleman MR. The vacuolating virus, S.V. 40. Proc Soc Exp Biol Med. 1960 Nov;105:420-7.

366 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap. 7: 69-85

367 Ibid

368 Ibid

369 Ibid

370 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap.8: 86-98

371 Ibid

372 Ibid

373 Institute of Medicine (US) Immunization Safety Review Committee Immunization Safety Review: SV40 Contamination of Polio Vaccine and Cancer. Washington (DC): National Academies Press (US); 2002.

374 Kops SP Oral polio vaccine and human cancer: a reassessment of SV40 as a contaminant based upon legal documents. Anticancer Res. 2000 Nov-Dec;20(6C):4745-9.

375 Cutrone R, Lednicky J, Dunn G et al Some oral poliovirus vaccines were contaminated with infectious SV40 after 1961. Cancer Res. 2005 Nov 15;65(22):10273-9.

376 House Hearing, 108 Congress The SV-40 Virus: Has Tainted Polio Vaccine Caused an Increase in Cancer? US House Government Reform Subcommittee on Human Rights and Wellness  Sept 10, 2003

377 Institute of Medicine (US) Immunization Safety Review Committee Immunization Safety Review: SV40 Contamination of Polio Vaccine and Cancer. Washington (DC): National Academies Press (US); 2002.

378 Scherneck S, Rudolph M, Geissler E et al. Isolation of a SV40-like Papovavirus from a human glioblastoma. Int J Cancer. 1979 Nov 15;24(5):523-31.

379 Tabuchi K, Kirsch WM, Low M et al. Screening of human brain tumors for SV40-related T antigen. Int J Cancer. 1978 Jan 15;21(1):12-7.

380 Carbone M, Rizzo P, Procopio A, et al. SV40-like sequences in human bone tumors. Oncogene. 1996 Aug 1;13(3):527-35.

381 Bravo MP, del Rey-Calero J, Olivares I, Vizcaino MJ. Antibodies to simian vacuolating virus 40 in bladder cancer patients. Urol Int. 1987;42(6):427-30.

382 Carbone M, Pass HI, Rizzo P et al Simian virus 40-like DNA sequences in human pleural mesothelioma. Oncogene. 1994 Jun;9(6):1781-90.

383 Lednicky JA, Garcea RL, Bergsagel DJ, Butel JS. Natural simian virus 40 strains are present in human choroid plexus and ependymoma tumors. Virology. 1995 Oct 1;212(2):710-7.

384 Bergsagel DJ, Finegold MJ, Butel JS et al. DNA sequences similar to those of simian virus 40 in ependymomas and choroid plexus tumors of childhood. N Engl J Med. 1992 Apr 9;326(15):988-93.

385 Suzuki SO, Mizoguchi M, Iwaki T. Detection of SV40 T antigen genome in human gliomas. Brain Tumor Pathol. 1997;14(2):125-9.

386 Butel JS, Jafar S, Stewart AR, Lednicky JA. Detection of authentic SV40 DNA sequences in human brain and bone tumours. Dev Biol Stand 1998; 94: 23-32.

387 Martini F, Lazzarin L, Iaccheri L et al. Simian virus 40 footprints in normal human tissues, brain and bone tumors of different histotypes. Dev Biol Stand 1998; 94: 55-66.

388 Institute of Medicine (US) Immunization Safety Review Committee Immunization Safety Review: SV40 Contamination of Polio Vaccine and Cancer. Washington (DC): National Academies Press (US); 2002.

389 Shah KV, Galloway DA, Knowles WA, Viscidi RP. Simian virus 40 (SV40) and human cancer: a review of the serological data. Rev Med Virol. 2004 Jul-Aug;14(4):231-9.

390 Lundstig A, Eliasson L, Lehtinen M et al. Prevalence and stability of human serum antibodies to simian virus 40 VP1 virus like particles. J Gen Virol 2005; 86(6): 1703-1708.

391 Bookchin D, Schumacher J The Virus and the Vaccine – The True Story Of A Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the millions of Americans Exposed. St. Martin’s Press, 2004; Chap.15: 187-202

392 Goedert J. Research on SV40 Exposure and the Development of Cancer. NIH Testimony: Subcommittee on Wellness and Human Rights, U.S. Committee on Government Reform Sept. 10, 2003.

393 Curtis T. The Origin of AIDS. Rolling Stone Magazine Mar. 19, 1992.

394 Kyle WS. Simian retroviruses, polio vaccine, and the origin of AIDS.  Lancet 1992; 339: 600-601.

395 Hooper E. The River: A Journey to the Source of HIV and AIDS. Little Brown & Co 1999.

396 Sharp PM, Hahn BH. The evolution of HIV-1 and the origin of AIDS. Phil. Trans. R. Soc. B 2010; 365 (1552): 2487-2494.

397 Hooper E. Aids and the Polio Vaccine: Edward Hooper finds new evidence. London Review of Books Apr. 3, 2003; 25(7): 22-23.

398 CDC Cessation of Trivalent Oral Poliovirus Vaccine and Introduction of Inactivated Poliovirus Vaccine — Worldwide, 2016 MMWR Sep 9, 2016; 65(35);934–938

399 Roberts L Surging cases have dashed all hope that polio might be eradicated in 2019 Science Jul. 10, 2019

400 Ibid

401 Van Paridon B Two Novel OPV2 Vaccine Candidates Show Tolerability and Immunogenicity Infectious Disease Advisor Jul. 12, 2019

402 Van Damme P, De Coster I, Bandyopadhyay AS et al. The safety and immunogenicity of two novel live attenuated monovalent (serotype 2) oral poliovirus vaccines in healthy adults: a double-blind, single-centre phase 1 study. Lancet. 2019 Jul 13;394(10193):148-158.

403 Bandyopadhyay AS, Garon J, Seib K, Orenstein WA Polio vaccination: past, present and future. Future Microbiol. 2015;10(5):791-808.

404 Minor P The polio endgame. Hum Vaccin Immunother. 2014;10(7):2106-8

405 CDC Poliomyelitis – Poliovirus Vaccines Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). 13th ed. 2015.

406  Parker EPK, Molodecky NA, Pons-Salort M et al. Impact of inactivated poliovirus vaccine on mucosal immunity: implications for the polio eradication endgame Expert Rev Vaccines. 2015 Aug 3; 14(8): 1113–1123.

407 GPEI OPV- Oral Poliovirus Vaccines Polio Today May 7, 2016

408 Grassly NC, Jafari H, Bahl S et al. Asymptomatic Wild-Type Poliovirus Infection in India among Children with Previous Oral Poliovirus Vaccination. J Infect Dis 2010; 201 (10): 1535-1543.

409 Blake IM, Martin R, Goel A et al. The role of older children and adults in wild poliovirus transmission. PNAS 2014; 111(29): 10604–10609

410 Ibid

411 Ibid

412 WHO What is vaccine-derived polio? Apr. 2017

413 Wringe A, Fine PEM, Sutter RW, Kew OM. Estimating the Extent of Vaccine-Derived Poliovirus Infection. PLoS One. 2008;3(10):e3433.

414 Ibid

415 Ibid

416 CDC Cessation of Trivalent Oral Poliovirus Vaccine and Introduction of Inactivated Poliovirus Vaccine — Worldwide, 2016 MMWR Sep 9, 2016; 65(35);934–938

417 CDC Update on Vaccine-Derived Polioviruses — Worldwide, January 2015–May 2016 MMWR Aug. 5, 2016; 65(30);763–769

418 CDC Cessation of Trivalent Oral Poliovirus Vaccine and Introduction of Inactivated Poliovirus Vaccine — Worldwide, 2016 MMWR Sep 9, 2016; 65(35);934–938

419 WHO Emergencies Preparedness, response – Poliomyelitis – Disease outbreak news No Date (accessed Jan. 30, 2020)

420 CDC Update on Vaccine-Derived Poliovirus Outbreaks — Worldwide, January 2018–June 2019 MMWR Nov. 15, 2019; 68(45);1024–1028

421 Bandyopadhyay AS, Garon J, Seib K, Orenstein WA Polio vaccination: past, present and future. Future Microbiol. 2015;10(5):791-808.

422 Minor P The polio endgame. Hum Vaccin Immunother. 2014;10(7):2106-8

423 Martín J Vaccine-derived poliovirus from long term excretors and the end game of polio eradication. Biologicals. 2006 Jun;34(2):117-22. Epub 2006 May 2.

424 Minor P Characteristics of poliovirus strains from long-term excretors with primary immunodeficiencies. Dev Biol (Basel). 2001;105:75-80.

425 Hovi T, Lindholm N, Savolainen C et al. Evolution of wild-type 1 poliovirus in two healthy siblings excreting the virus over a period of 6 months. J Gen Virol. 2004 Feb;85(Pt 2):369-77.

426 Martín J, Odoom K, Tuite G Long-term excretion of vaccine-derived poliovirus by a healthy child. J Virol. 2004 Dec;78(24):13839-47.

427 Kalkowska DA, Pallansch MA, Thompson KM Updated modelling of the prevalence of immunodeficiency-associated long-term vaccine-derived poliovirus (iVDPV) excreters Epidemiol Infect. 2019; 147: e295.

428 Shaghaghi M, Soleyman-Jahi S, Abolhassani H et al. New insights into physiopathology of immunodeficiency-associated vaccine-derived poliovirus infection; systematic review of over 5 decades of data. Vaccine. 2018 Mar 20;36(13):1711-1719.

429 Aghamohammadi A, Abolhassani H, Kutukculer N et al. Patients with Primary Immunodeficiencies Are a Reservoir of Poliovirus and a Risk to Polio Eradication. Front Immunol. 2017 Jun 13;8:685.

430 Galal NM, Meshaal S, ElHawary R et al Poliovirus excretion following vaccination with live poliovirus vaccine in patients with primary immunodeficiency disorders: clinicians' perspectives in the endgame plan for polio eradication. BMC Res Notes. 2018 Oct 11;11(1):717

431 Razum O, Sridhar D, Jahn A et al. Polio: from eradication to systematic, sustained control. BMJ Glob Health. 2019 Aug 20;4(4):e001633

432 Ibid

433 WHO. Statement of the Twenty-Second IHR Emergency Committee Regarding the International Spread of Poliovirus. WHO.int Oct. 3, 2019.

434 Ibid

435 Razum O, Sridhar D, Jahn A et al. Polio: from eradication to systematic, sustained control. BMJ Glob Health. 2019 Aug 20;4(4):e001633

436 WHO. Statement of the Twenty-Second IHR Emergency Committee Regarding the International Spread of Poliovirus. WHO.int Oct. 3, 2019.

437 GPEI Polio Endgame Strategy 2019-2023 – Eradication, integration, certification and containment 2019

438 Institute of Medicine Committee to Review Adverse Effects of Vaccines. Adverse Effects of Vaccines: Evidence and Causality. Evaluating Biological Mechanisms of Adverse Events (p. 57-102), Increased Susceptibility (p. 82). Washington, DC: The National Academies Press 2012.

439 Vaccine Safety Committee, Institute of Medicine. Polio Vaccines. Adverse Events Associated with Childhood vaccines: Evidence Bearing on Causality. Washington D.C. National Academies Press 1994.

440 Ibid

441 Global Polio Eradication Initiative (GPEI) OPV – Oral Polio Vaccine No date. (accessed Jan. 30, 2020)

442 WHO What is vaccine-derived polio? Apr. 2017

443 Ibid

444 HRSA Vaccine Injury Table Mar. 21, 2017

445 Ibid

446 Kessler DA, the Working Group, Natanblut S, et al. A New Approach to Reporting Medication and Device Adverse Effects and Product Problems. JAMA. 1993;269(21):2765-2768.

447 FDA.gov. Kessler DA. Introducing MEDWatch: A New Approach to Reporting Medication and Device Adverse Effects and Product Problems. Reprint from JAMA. June 9, 1993.

448 Braun M. Vaccine adverse event reporting system (VAERS): usefulness and limitations. Johns Hopkins Bloomberg School of Public Health

449 Rosenthanl S, Chen R. The reporting sensitivities of two passive surveillance systems for vaccine adverse events. Am J Public Health 1995; 85: pp. 1706-9.

450 AHRQ Electronic Support for Public Health–Vaccine Adverse Event Reporting System (ESP:VAERS) Dec 1, 2007-Sep. 30, 2010

451 U.S. Department of Health and Human Services. National Vaccine Injury Compensation Program Data—February 1, 2020 National Vaccine Injury Compensation Program. Feb. 1, 2020

452 House Hearing, 108 Congress The SV-40 Virus: Has Tainted Polio Vaccine Caused an Increase in Cancer? US House Government Reform Subcommittee on Human Rights and Wellness  Sept 10, 2003

453 Kops SP Oral polio vaccine and human cancer: a reassessment of SV40 as a contaminant based upon legal documents. Anticancer Res. 2000 Nov-Dec;20(6C):4745-9.

454 Cutrone R, Lednicky J, Dunn G et al Some oral poliovirus vaccines were contaminated with infectious SV40 after 1961. Cancer Res. 2005 Nov 15;65(22):10273-9.

455 House Hearing, 108 Congress The SV-40 Virus: Has Tainted Polio Vaccine Caused an Increase in Cancer? US House Government Reform Subcommittee on Human Rights and Wellness  Sept 10, 2003

456 Institute of Medicine (US) Immunization Safety Review Committee Immunization Safety Review: SV40 Contamination of Polio Vaccine and Cancer. Washington (DC): National Academies Press (US); 2002.

457 Ibid

458 Vilchez RA, Butel JS Emergent Human Pathogen Simian Virus 40 and Its Role in Cancer Clin Microbiol Rev. 2004 Jul; 17(3): 495–508.

459 Goedert J. Research on SV40 Exposure and the Development of Cancer. NIH Testimony: Subcommittee on Wellness and Human Rights, U.S. Committee on Government Reform Sept. 10, 2003.

460 Bandyopadhyay AS, Garon J, Seib K, Orenstein WA Polio vaccination: past, present and future. Future Microbiol. 2015;10(5):791-808.

461 CDC Cessation of Trivalent Oral Poliovirus Vaccine and Introduction of Inactivated Poliovirus Vaccine — Worldwide, 2016 MMWR Sep 9, 2016; 65(35);934–938

462 Strebel PM, Ion-Nedelcu N, Baughman AL Intramuscular injections within 30 days of immunization with oral poliovirus vaccine--a risk factor for vaccine-associated paralytic poliomyelitis. N Engl J Med. 1995 Feb 23;332(8):500-6.

463 Wyatt HV Injections and poliomyelitis: what are the risks of vaccine associated paralysis? Dev Biol Stand. 1986;65:123-6.

464 Gromeier M, Wimmer E. Mechanism of injury-provoked poliomyelitis. J Virol. 1998 Jun;72(6):5056-60.

465 Strebel PM, Aubert-Combiescu A, Ion-Nedelcu N et al.  Paralytic poliomyelitis in Romania, 1984-1992. Evidence for a high risk of vaccine-associated disease and reintroduction of wild-virus infection. Am J Epidemiol. 1994 Dec 15;140(12):1111-24.

466 Örstavik I, Flugsrud LB, Lahelle O Paralytic poliomyelitis in Norway since the introduction of trivalent oral vaccine: an epidemiological and virological study Bull World Health Organ. 1971; 45(6): 733–739.


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