Polio or Poliomyelitis - Symptoms, Diagnosis, Treatments, Cure & Causes

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Poliomyelitis-From Wikipedia, the free encyclopedia

(Redirected from Polio)

Poliomyelitis

Classification & external resources

ICD-10 A80., B91.

ICD-9 045, 138

DiseasesDB 10209

MedlinePlus 001402

eMedicine ped/1843 pmr/6

MeSH C02.182.600.700

This article is about the disease. For the virus which causes poliomyelitis, see Poliovirus.

Poliomyelitis, often called polio or infantile paralysis, is an acute viral infectious disease which is spread from person-to-person via the fecal-oral route.[1] The majority of polio infections are asymptomatic. In about 1% of cases the virus enters the central nervous system (CNS) via the blood stream. Within the CNS, poliovirus preferentially infects and destroys motor neurons. The destruction of motor neurons causes muscle weakness and flaccid paralysis.

An ancient disease, polio was first recognized as a medical entity by Jakob Heine in 1840.[2] In the early part of the twentieth century, the United States, and much of the world, were experiencing a huge increase in the number of polio cases. These epidemics, which left thousands of children and adults paralyzed, initiated a "Great Race" towards the development of a vaccine. The polio vaccines developed in 1955, by Dr. Jonas Salk, and in 1962 by Dr. Albert Sabin are credited with reducing of the annual number of polio cases from many hundreds of thousands to around a thousand. In recent years enhanced vaccination efforts have been led by Rotary International, UNICEF and the World Health Organization, and may soon result in global eradication of the disease.

Contents

1 Ancient disease, modern killer

2 Poliovirus

3 Pathogenesis

4 Clinical presentation

4.1 Paralytic polio

4.1.1 Spinal polio

4.1.2 Bulbar polio

4.2 Post-polio syndrome

5 Diagnosis

6 Treatment

6.1 The iron lung

6.2 Antibody serum

7 Vaccine

7.1 Salk's "inactivated polio vaccine"

7.2 Sabin's "oral polio vaccine"

8 Eradication

9 Legacy

9.1 Philanthropy

9.2 Rehabilitation therapy

9.3 Disability rights movement

10 Famous polio survivors

11 Notes and references

11.1 Further reading

12 External links

Ancient disease, modern killer

An Egyptian stele thought to represent a Polio victim. 18th Dynasty (1403 - 1365 BC).The effects of a polio infection have been known since prehistory: Egyptian paintings and carvings depict otherwise healthy people with withered limbs, and children walking with canes at a young age.[3] It has been theorized that the Roman Emperor Claudius was stricken as a child, and this caused him to walk with a limp for the rest of his life. In 1789 the first clinical description of poliomyelitis was provided by the British physician Michael Underwood—he refers to polio as “a debility of the lower extremities".[4] The first medical report on poliomyelitis was by Jakob Heine in 1840. Karl Oskar Medin was the first to empirically study a poliomyelitis epidemic in 1890.[3] The work of these two physicians led to the disease being known as Heine-Medin disease.

Around 1900 small, localized paralytic polio epidemics began to appear in Europe and the United States.[5] The first polio epidemic reported in the United States occurred in Vermont in 1894 and consisted of 132 total cases, including several cases in adults.[3] In 1907 approximately 2500 cases of poliomyelitis were reported in New York City.[6] On Saturday, June 17, 1916 an official announcement of the existence epidemic polio infection was made in Brooklyn, New York. That year, there would be nearly 30,000 cases and more than 6,000 deaths due to polio in the United States (2,407 deaths in New York City alone).[7] The names and addresses of individuals with confirmed polio cases were published daily in the press, their houses were identified with placards, and their families were quarantined.[8] The 1916 epidemic caused widespread panic and thousands fled the city to nearby mountain resorts; movie theaters were closed, meetings were canceled, public gatherings were almost nonexistent, and children were warned not to drink from water fountains, and told to avoid amusement parks, swimming pools, and beaches.[7] From 1916 onward, a polio epidemic appeared each summer in at least one part of the country, with the most serious occurring in the 1940s and 1950s.[5]

Prior to the 20th century polio infections were rarely seen in infants before 6 months of age and most cases occurred in children 6 months to 4 years of age.[9] Young children who contract polio generally suffer only mild symptoms, but as a result they become permanently immune to the disease.[10] In developed countries during the late 19th and early 20th centuries, improvements were being made in community sanitation, including improved sewage disposal and clean water supplies. Better hygiene meant that infants and young children had fewer opportunities to encounter and develop immunity to polio. Exposure to poliovirus was therefore delayed until late childhood or adult life, when it was more likely to take the paralytic form.[9]

By 1950, the peak age incidence of paralytic poliomyelitis in the United States had shifted from infants to children aged 5 to 9 years; about one-third of the cases were reported in persons over 15 years of age.[11] Accordingly, the rate of paralysis due to polio infection also increased during this time.[5] In the United States, the 1952 polio epidemic would be the worst outbreak in the nation's history. Of the nearly 58,000 cases reported that year; 3,145 died and 21,269 were left with mild to disabling paralysis.[12]

Poliovirus

Main article: Poliovirus

Poliovirus, isolated in 1909 by Karl Landsteiner and Erwin Popper[13], is a small RNA enterovirus composed of an RNA genome enclosed in a non-enveloped capsid. The poliovirus genome is limited and only large enough to encode about 10 genes which encode the small number of viral proteins critical for the virus to invade and replicate within human cells.[14]

An Electron micrograph of poliovirus.There are three separate serotypes of polio, poliovirus type 1 (PV1), poliovirus type 2 (PV2), and poliovirus type 3 (PV3); each with a slightly different capsid protein.[1] PV1 is the most common form encountered in nature, however all three forms are extremely infectious. Poliovirus is strictly a human pathogen, and it cannot naturally infect other species.[1]

Pathogenesis

Polio is highly contagious, and spreads through human-to-human contact, usually through the mouth due to fecally contaminated water or food (fecal-oral transmission).[15] Following ingestion, poliovirus begin to replicate in the cells it first comes into contact with (the tonsils and intestinal M cells), eventually penetrating the intestinal lining. From there, it enters into the lymphatic system via the Peyer's patches and the bloodstream via the mesentery and becomes a viremia.[10] The incubation period of polio, from the time of first exposure to first symptoms, is 2-20 days, with a range of 3 to 35 days. A number of factors increase the risk of polio infection or affect the severity of the disease including: immune deficiency,[16] malnutrition,[17] intramuscular injection,[18] pregnancy,[18] and physical activity immediately following the onset of paralysis.[19]

Following an initial infection (either apparent or inapparent) with poliovirus, virus particles are excreted in the feces for several weeks.[20] This increases transmission the disease, as the infected person may be unaware that they have had the disease, and make no effort to prevent passing it on to others. In endemic areas wild polioviruses can infect virtually the entire population. In temperate climates polio is a seasonal disease, the period of peak transmission of polio is in the summer and autumn and transmission of the virus is reduced during winter.[15] In tropical areas seasonal differences in transmission are far less pronounced.

During pregnancy, the virus can cross the placenta; however, it does not appear that the fetus is affected by either maternal infection with wild poliovirus, or by polio vaccination.[21] Maternal antibodies are also able to cross the placenta, providing passive immunity that protects the infant from polio infection during the first few months of life.[22]

Clinical presentation

In individuals with a functioning immune system, polio infection is often subclinical.[10] Approximately 4%–8% of polio infections consist of a minor, nonspecific illness and may cause upper respiratory tract infection (sore throat and fever), gastrointestinal tract disturbances (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhea), and influenza-like illnesses. In some cases, there may be no significant symptoms whatsoever. Together the subclinical and mild forms of polio account for nearly 95% of all cases.

In 1-2% of poliovirus infections, patients develop nonparalytic aseptic meningitis, with symptoms of stiffness of the neck, back, and/or legs. Typically these symptoms will last from 2 to 10 days, and are usually followed by complete recovery.[23]

Paralytic polio

In approximately 1 in 200 to 1 in 1000 cases poliovirus infection leads to paralytic disease, in which patients develop flaccid paralysis. Depending on the site of paralysis, poliomyelitis can be classified as spinal, bulbar, or spino-bulbar. Paralytic attack rates vary by the serotype of the infecting poliovirus, the highest rates of paralysis (1 in 200) are associated with poliovirus type 1, the lowest rates (1 in 2,000) are associated with poliovirus type 2.[24] Up to 0.2% of all polio infections (but nearly 20% of paralytic polio cases) require mechanical ventilation of the patient during the acute stage, and permanent quadriplegia or respiratory paralysis occur in only 0.01% (1 in 10,000) of all poliovirus infections.[23]

Spinal polio

The location of motor neurons in the anterior horn cells of the spinal column.The poliovirus affects the motor neurons of the anterior horn cells, or the ventral (front) grey matter section in the spinal column, which control movement of the trunk and limb muscles including the intercostal muscles.[25] The color and appearance of the grey matter of the spinal cord are often altered by polio infection, appearing reddish and swollen due to extensive inflammation, caused by replication of polio virus within the motor neurons of the anterior horn and brain stem. This inflammation results in damage or destruction of motor neuron ganglion within the grey matter; causing the typical clinical symptoms of poliomyelitis.[25]

When spinal neurons die Wallerian degeneration takes place, resulting in muscle weakness of those muscles that had once been innervated by the now dead neurons.[26] Destroyed motor neurons do not regenerate and the affected motor units of muscles will not be able to contract. An affected limb becomes floppy and poorly controlled — causing the condition of acute flaccid paralysis (AFP); the classic later appearance (as seen in ancient Egyptian illustrations) is of muscle wasting in a leg. Progression to maximum paralysis is rapid (2–4 days), and is usually associated with fever and muscle pain.[26] Spinal paralysis is typically asymmetric, and is often more severe proximally than distally. Deep tendon reflexes are also affected and are usually absent or diminished.[26] Extensive paralysis of the trunk and muscles of the thorax and abdomen, (quadriplegia) may occur.[10]

A blockage lumbar of the anterior spinal cord artery due to polio (PV3).This presentation of poliomyelitis can lead to permanent paralysis of the body, yet it only occurs in around 1% of cases. In most cases, paralysis due to polio infection is temporary, and nearby surviving neurons sprout to reinnervate the denervated muscle, by growing "superclustered" axons, to replace those that have died.[25] The usual recovery period is three to six months.[27] The additional stress of recovery on the surviving motor neurons may precipitate the development of symptoms of post-polio syndrome.

The degree of paralysis due to polio infection is directly correlated to the number of neurons that have died, which is likely to be proportional to the degree of viraemia, and inversely proportional to the degree of immunity.[28] Fifty percent of patients with paralytic polio recover fully, 40% recover only partially (of these 25% are left with temporary paralysis and 15% are left with permanent paralysis); 2%–5% of children, and up to 15%–30% of adults die.[23] Any paralysis remaining after one year is likely to be permanent, but recoveries even after a decade have been known.

Bulbar polio

The location and anatomy of the bulbar region (in orange).Bulbar polio and spinal polio are part of a continuum of anatomy and disease (paralytic polio). Bulbar polio occurs in 2% of cases of paralytic polio, and describes the form of the disease which affects the bulbar region of the brain stem.

The brain stem is homologous to the spinal cord, but the motor neurons arising from there and passing in the various cranial nerves control the muscles related to eyeball movement; the trigeminal nerve and facial nerve which innervate cheeks, tear ducts , gums, and muscles of the face, among others; the glossopharyngeal nerve which in part controls swallowing and functions in the throat, tongue movement and taste; the vagus nerve that sends signals to the heart, intestines, and lungs; and the accessory nerve that controls upper neck movement.[29] In bulbar polio, the virus infiltrates and destroys these nerves reducing breathing capacity and causing difficulty in swallowing and speaking. Without respiratory support, bulbar polio often results in death.[29] The mortality rate of bulbar polio currently ranges from 25% to 75%,[23] according to the age of the person.

Bulbospinal polio is a combination of the symptoms of both bulbar and paralytic spinal polio. This form can lead to paralysis of the arms and legs and may also affect breathing, swallowing and heart functions.[29] In bulbospinal cases the virus affects the upper part of the cervical spinal cord (C3-4-5), and paralysis of the diaphragm occurs. The critical nerves affected are the phrenic nerve (the nerve driving the diaphragm to inflate the lungs) and the innervation of muscles needed for swallowing. Of all paralytic polio cases, 19% are spinal with bulbar symptoms (i.e. bulbospinal).[23]

In extremely rare cases, usually in immunocompromised indiviuals, an uncontrolled infection of the entire brain, called fulminating encephalitis, can develop.[30] Even with intravenous antiviral therapy and intensive care the mortality rate for these cases is extremely high.

Post-polio syndrome

People who have survived polio in childhood have developed additional symptoms decades after they were infected with poliovirus, notably muscle weakness, extreme fatigue or paralysis; this is referred to as post-polio syndrome (PPS).[31] The symptoms of PPS are thought to involve a failure of the over-sized motor units created during recovery from paralytic poliomyelitis. PPS is observed in approximately 25% to 28% of patients who had recovered from an acute polio infection.[32] Factors that increase the risk of post-polio syndrome include: the length of time since acute poliovirus infection, the presence of permanent residual impairment after recovery from the acute illness, and overuse and disuse of neurons.[31] Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.[23]

Diagnosis

Polio is a rare disease in much of the world, and few doctors have ever seen a case of polio. If polio is suspected, however, the usual follow-up test is a lumbar puncture, or "spinal tap", to collect the patient's cerebrospinal fluid (CSF). The CSF of individuals with polio contains an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level.[29]

A laboratory diagnosis of poliomyelitis is usually made based on recovery of poliovirus from the stool or pharynx. Detection of virus from the CSF is diagnostic of paralytic polio, but rarely occurs. Neutralizing antibodies to poliovirus appear in the blood of infected patients early in the course of infection.[23]

When poliovirus is isolated from a patient experiencing acute flaccid paralysis, it is then further tested, using oligonucleotide mapping (genetic fingerprinting), or more recently by by PCR amplification, to determine if the virus is “wild type” (that is, the virus encountered in nature) or vaccine type (is derived from a strain of poliovirus used to produce polio vaccine).[33] Isolation of wild poliovirus constitutes a public health emergency, and appropriate control efforts must be initiated immediately.[26]

Treatment

In 1916, spurred by recent epidemics and experiencing little success in treating polio patients, researchers set out to find new and better treatments for the disease. Several therapies were explored in an effort to prevent deformities and a number of them were tried on children until the 1940s, including hydrotherapy, electrotherapy; surgical treatments such as tendon lengthening and nerve grafting,[25] and the use of devices such as rigid braces and body casts that tended to cause muscle atrophy due to the limited movement of the user, were also touted as effective treatments[34] Massage and passive motion exercises were also used to treat polio victims.[25] In 1935, American inventor and scientist, George Washington Carver developed a peanut oil derivative which he would rub into withered muscles as a remedy for paralytic polio.[35]

Because no cure for polio exists, the focus of modern polio treatment has been on increasing comfort, speeding recovery and preventing complications. Supportive measures include: antibiotics for infections, analgesics for pain, portable ventilators to support breathing, moderate exercise and a nutritious diet. [29] The two most effective and principle supportive measures for the treatment of polio are the iron lung and a gamma globulin antibody serum preparation derived from the blood of human and animal polio survivors.[36]

The iron lung

This iron lung was donated to the CDC by the family of Mr. Barton Hebert of Covington, Louisiana, who’d used the device from the late 1950s until his death in 2003.Without respiratory support, poliomyelitis affecting respiration is likely to result in suffocation, or aspiration of secretions and resulting pneumonia.[37] A noninvasive negative-pressure ventilator (more commonly called an iron lung) was used to maintain respiration artificially until a person could breathe independently, generally about one to two weeks. The machine was powered by an electric motor attached to two vacuum cleaners, and worked by changing the pressure inside the machine, pulling air in and out of the lungs.

The first iron lung used in the treatment of polio victims was the Drinker iron lung, invented by Philip Drinker, Louis Agassiz Shaw, and James Wilson at Harvard.[38] The Drinker iron lung was first tested October 12, 1928 at Children’s Hospital, Boston. The design of the iron lung was subsequently improved by John Haven Emerson in 1931.[38] The Emerson Iron Lung was produced until 1970.

The iron lung saved many thousands of lives, but was large and cumbersome and the price of the machine was enormous. The cost of running the machine was also prohibitive, as patients were encased in the metal chambers for months, years and sometimes for life. Permanent respiratory paralysis occurs in approximately 1 in 1000 people who developed paralytic polio, and require constant mechanical ventilation. Some polio survivors still use an iron lung to this day.[39]

During the polio epidemics of the 1950s, even with an iron lung, the fatality rate for patients with bulbar polio exceeded 90%.[40] The modern positive-pressure ventilator and the use of positive-pressure ventilation by tracheostomy was first used to treat bulbar patients in Blegdamshospital, Copenhagen, Denmark during a polio outbreak in 1952.[40] Positive pressure ventilators reduced mortality in bulbar polio from 90% to 20%.[37] The Copenhagen epidemic polio of 1952 has been described as the start of intensive care, when large numbers of patients were ventilated by hand ("bagged") by medical students and anyone else on hand.[41] With the advent of modern ventilators, however, many patients with permanent respiratory paralysis use more modern cuirass type mechanical ventilators that are worn over thorax and abdomen, and control breathing via the direct intubation of the airway.[37]

Antibody serum

In 1950—three years before the arrival of the Salk vaccine—William Hammon at the University of Pittsburgh isolated serum from the blood of polio survivors.[36] The serum contained antibodies to poliovirus and was used to prevent the spread of polio and to reduce the severity of disease in polio patients. The results of a large clinical trial were promising; the serum was shown to be about 80% effective in preventing the development of paralytic poliomyelitis, and protection was shown to last for 5 weeks if given under tightly controlled circumstances.[42] The serum was also shown to reduce the severity of the disease in patients that developed polio.[36] The large scale use of antibody serum to prevent and treat polio had a number of drawbacks, however, including the observation that the immunity provided by the serum did not last long, and the protection offered by the antibody was incomplete, that reinjection was required during each epidemic outbreak, and that the optimal time frame for administration was unknown.[43] The antibody serum was widely administered, but obtaining the serum was an expensive and time-consuming process, and the focus of the medical community soon shifted to the development of a polio vaccine.

Vaccine

Main article: Polio vaccine

United States postage stamp celebrating the development of the Polio vaccine.In 1935 Maurice Brodie, a research assistant at New York University, had attempted to produce a polio vaccine, procured from ground up monkey spinal cords, and killed by formaldehyde. Brodie first tested the vaccine on himself and several of his assistants. He then gave the vaccine to three thousand children, many developed allergic reactions, but none of the children developed an immunity to polio.[44] During the late 1940s and early 1950s, a research group headed by John Enders at the Boston Children's Hospital successfully cultivated the poliovirus in human tissue. This highly significant breakthrough ultimately allowed for the development of vaccines against polio. Enders and his colleagues, Thomas H. Weller and Frederick C. Robbins, were recognized for their labors with a Nobel Prize in 1954.[45]

In 1952 and 1953 the U.S. experienced large outbreaks of poliomyelitis (58,000 and 35,000 cases, up from a typical number of around 20,000 cases). Amid this U.S. polio epidemic, millions of dollars were invested in finding and marketing a polio vaccine. The development of two polio vaccines would lead to the first modern mass inoculations. The last cases of paralytic poliomyelitis caused by endemic transmission of wild virus in the United States were in 1979, when an outbreak occurred among the Amish in several Midwest states. The disease was entirely eradicated in the Americas by 1994.

Salk's "inactivated polio vaccine"

The first effective polio vaccine was developed in 1952 by Jonas Salk at the University of Pittsburgh. The Salk vaccine, or inactivated poliovirus vaccine (IPV), is based on poliovirus grown in a type of monkey kidney tissue culture (Vero cell line), which are then inactivated with formalin. Salk's vaccine was licensed in 1955. Immediately children's vaccination campaigns were launched. In 1954, the vaccine was tested for its ability to prevent polio; the clinical trials involving the Salk vaccine would grow to be the largest medical experiment in history. The results of the field trial were announced April 12, 1955 (the tenth anniversary of the death of Franklin Roosevelt). The Salk vaccine had been 60 - 70% effective against PV1 (poliovirus type 1), over 90% effective against PV2 and PV3, and 94% effective against the development of bulbar polio.[46] In the U.S, following a mass immunization campaign promoted by the March of Dimes, the annual number of polio cases would fall to 5,600 by 1957.[3] The IPV vaccine was used extensively in the U.S. until the early 1960s. An enhanced-potency IPV was licensed in the United States in November 1987, and is currently the vaccine of choice in the United States.[23]

A child receives oral Polio vaccine.

Sabin's "oral polio vaccine"

Eight years after Salk's success, Albert Sabin developed the oral polio vaccine (OPV).[47] The OPV is a live-attenuated vaccine, produced by the passage of the virus through non-human cells at a sub-physiological temperature.[13] The attenuated poliovirus in the Sabin vaccine replicates very efficiently in the gut, the primary site of infection and replication, but is unable to replicate efficiently within nervous system tissue. The OPV proved to be superior in administration, and also provided longer lasting immunity than the Salk vaccine.[13]

In 1961, type 1 and 2 monovalent oral poliovirus vaccine (MOPV) was licensed, and in 1962, type 3 MOPV was licensed. In 1963, trivalent OPV was licensed, and would become the vaccine of choice in the United States and most other countries of the world, largely replacing the use of the inactivated polio vaccine.[44] A second wave of mass immunizations would lead to a dramatic decline in the number of polio cases. In 1961, only 161 cases were recorded in the United States.[48] The use of OPV was discontinued in the United States in 2000, but it continues to be used around the globe.[23]

Eradication

Main article: Poliomyelitis eradication

The global status of polio eradication. Note: Endemic (in red) and polio-free regions (in blue) are unchanged through 2006.Polio is one of few diseases with the potential for global eradication because the virus is transmitted only through person-to-person contact, (there is no animal reservoir, insects play no role in transmission), and the virus cannot persist in the environment for long periods of time in the absence of a human host (a few weeks at room temperature, and a few months between 0–8° Celsius (32–46° Fahrenheit).[49] Another factor that has bolstered efforts to eradicate polio is that the oral polio vaccine is both highly effective and cheap (about $1 per dose, or $3 per child); vaccination generally provides lifelong immunity to the virus.[50]

Following the widespread use of poliovirus vaccine in the mid-1950s, the incidence of poliomyelitis declined rapidly in many industrialized countries. A global effort to eradicate polio began in 1988 and was led by the World Health Organization, UNICEF and The Rotary Foundation. These efforts have reduced 99% of annual diagnosed cases from an estimated 350,000 cases in 1988 to fewer than 2,000 cases in 2006.[51] Should eradication be successful it will represent only the second time mankind has ever completely eliminated a disease. The first such disease was smallpox, which was officially eradicated in 1979.[52]

A number of eradication milestones have already been reached, and several regions of the world have been certified polio-free. The Americas were declared polio-free in 1994.[53] In 2000 polio was officially eradicated in 36 Western Pacific countries, including China and Australia.[54][55] Europe was declared polio-free in 2002.[56]

Today, polio remains endemic in just four countries: Nigeria, India, Pakistan, and Afghanistan.[51] Among the greatest obstacles to further eradication are the lack of basic health infrastructure, which limits vaccine distribution. The crippling effects of civil war, internal strife, and philosophical objection to vaccination based on religious reasons have also hindered polio eradication.

Legacy

Early in the 20th century polio would become the world's most feared disease. The disease hit without warning, tended to strike white, affluent individuals, required long periods quarantine, in which parents were separated from children, and it was impossible to tell who would get the disease and who would be spared.[3] The consequences of the disease left polio victims marked for life, leaving behind vivid images of wheelchairs, crutches, leg braces, breathing devices, and deformed limbs. However, polio changed not only the lives of those who survived it, but also affected profound cultural changes: the emergence of grassroots fund-raising campaigns that would revolutionize medical philanthropy, the rise of rehabilitation therapy and, through campaigns for the social and civil rights of the disabled, polio survivors helped to spur the modern disability rights movement.

Philanthropy

March of Dimes poster cir. late 1950sIn 1921 Franklin D. Roosevelt became totally and permanently paralyzed from the waist down. Although the paralysis (whether from poliomyelitis, as diagnosed at the time, or from Guillain-Barré syndrome) had no cure at the time, Roosevelt, who had planned a life in politics, refused to accept the limitations of his disease. He tried a wide range of therapies, but none had any effect. In 1938 Roosevelt helped to found the National Foundation for Infantile Paralysis (now known as the March of Dimes), that raised money for the rehabilitation of victims of paralytic polio, and was instrumental in funding the development of polio vaccines. The March of Dimes changed the way it approached fund-raising. Rather than soliciting large contributions from a few wealthy individuals, the March of Dimes sought small donations from millions of individuals. Its hugely successful fund-raising campaigns collected hundreds of millions of dollars - more than all of the U.S. charities at the time combined (with the exception of the Red Cross).[57] By 1955 the March of Dimes had invested $25.5 million in research; [58] funding both Jonas Salk’s and Albert Sabin’s vaccine development; the 1954–55 field trial of vaccine, and supplies of free vaccine for thousands of children.[59]

In truth, however poliomyelitis was never the monstrous killer it was portrayed as in the media, not even at its height during the 1940s and 1950s. In 1952 during the worst recorded epidemic, 3,145 people, including 1,873 children, in the United States would die from polio.[60] That same year over 200,000 people (including 4,000 children) would die of cancer and 20,000 (including 1,500 children) would die of tuberculosis.[60] According to David Oshinsky’s book Polio: An American Story: “There is evidence that the March of Dimes over-hyped polio, and promoted an image of immediately curable polio victims, which was not true. The March of Dimes refused to partner with other charity organizations like the United Way.”[57]

Rehabilitation therapy

Prior to the polio scares of the 20th century, most rehabilitation therapy was focused on treating injured soldiers returning from war. The crippling effects of polio lead to heightened awareness and public support of physical rehabilitation, and in response a number of rehabilitation centers specifically aimed at treating polio patients were opened, with the task of restoring and building the remaining strength of polio victims and teaching new, compensatory skills to large numbers of newly paralyzed individuals.[61] The cost of polio rehabilitation was often more than the average family could afford, and more than 80% of the nation’s polio patients would receive funding through the March of Dimes.[57] Some families also received support through philanthropic organizations such as the Shrine fraternity, which established a network of pediatric hospitals in 1919, the Shriners Hospitals for Children, to provide care free of charge for children with polio.[62]

A physical therapist assists two polio-stricken children while they exercise their lower limbs.In 1926 Franklin Roosevelt, convinced of the benefits of hydrotherapy, bought a resort at Warm Springs, Georgia, where he founded the first modern rehabilitation center for treatment of polio patients which still operates as the Roosevelt Warm Springs Institute for Rehabilitation.[63] Another well known advocate of polio rehabilitation is Elizabeth Kenny, an Australian army nurse, who between 1928 and 1940 developed a controversial polio treatment - that instead of immobilizing afflicted limbs - advocated massage, exercise and applying warm, moist heat to stimulate muscles and improve mobility.[34] Kenny's therapy is still used in the treatment of paralytic poliomyelitis (in combination with antispasmodic medications to reduce muscular contractions).

Disability rights movement

As thousands of polio survivors with varying degrees of paralysis left the rehabilitation hospitals and went home, to school and to work, many were frustrated by a lack of accessibility and discrimination they experienced in their communities. In the early 20th century the use of a wheelchair at home or out in public was a daunting prospect as no public transportation system accommodated wheelchairs and most public buildings including schools, were inaccessible to those with disabilities. Many children left disabled by polio were forced to attend separate institutions for "crippled children" or had be carried up and down stairs.[63]

As people who had had polio matured, they began to demand the right to participate in the mainstream of society. By pushing legislation such as the Rehabilitation Act of 1973 which protected qualified individuals from discrimination based on their disability, and the Americans with Disabilities Act of 1990, polio survivors helped to bring about a revolution: the disability rights movement.[63] Other political movements lead by polio survivors include the Independent Living and Universal design movements of the 1960s and 1970s.[64]

Today, polio survivors are one of the largest disabled groups in the world. The World Health Organization estimates that there are 10 to 20 million polio survivors worldwide.[65] In 1977, the National Health Interview Survey reported that there were 254,000 persons living in the United States who had been paralyzed by polio.[66] According to local polio support groups and doctors, some 40,000 polio survivors live in Germany, 30,000 in Japan, 24,000 in France, 16,000 in Australia, 12,000 in Canada and 12,000 in the United Kingdom.[65]

Famous polio survivors

Franklin D. Roosevelt may have contracted polio in 1921.Franklin D. Roosevelt, U.S. president, has been by far the most famous polio survivor in the public mind. However, his age (39 years) and many features of his illness are more consistent with a diagnosis of Guillain-Barré syndrome.[67] (See Franklin D. Roosevelt's paralytic illness article for more information.)

Several athletes have survived polio including several track and field Olympic games gold medalists Wilma Rudolph, Ray Ewry and Walter "Buddy" Davis. Physician and Olympic gold medalist figure skater Tenley Albright, Cricket champion Bhagwat Chandrasekhar, Baseball All-Star Bud Daley, and golfer Jack Nicklaus, are also polio survivors.

Actors, filmmakers and media personalities including: Alan Alda, Francis Ford Coppola, Bill Cullen, Mia Farrow, Martin Milner, and Peg Phillips; actor, broadcaster, and writer Michael Flanders and Australian publishing, media and gaming tycoon Kerry Packer.

Musicians CeDell Davis, Donovan, Ian Dury, Joni Mitchell, Itzhak Perlman, Ray Peterson, David Sanborn, Dinah Shore, Neil Young, composers Dmitri Shostakovich, and Doc Pomus and opera singers Marjorie Lawrence and Renata Tebaldi.

Authors J. D. Beresford, Richmal Crompton, Alan Marshall, Sir Walter Scott and Robert Anton Wilson.

Artists Frida Kahlo, Dorothea Lange, Margarete Steiff and Brooks Stevens.

Scientists including psychiatrist Milton Erickson, physiologist Arthur Guyton and science fiction writer Sir Arthur C. Clarke.

Other polio survivors include US Congressman Steve Cohen and US Senator John Porter East, architect Patrick Nuttgens and several well known disability rights activists including: Justin Whitlock Dart, Jr., Hugh Gallagher, John H. Hager, Judith Heumann and Ed Roberts.

Notes and references

^ a b c Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill, pp. 535–7. ISBN 0838585299.

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