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Added innovative polio sequelae treatment from china on paralytic and/or deformed limbs
→Treatment: Removing "Chinese Cure" - see talk page.
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[[Image:Womanonsideinlung.jpg|thumb|200px|left|A modern negative pressure ventilator (iron lung).]]
[[Image:Womanonsideinlung.jpg|thumb|200px|left|A modern negative pressure ventilator (iron lung).]]


No direct cure for polio exists, and 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, moderate exercise and a nutritious diet.<ref name=MayoTreat>{{cite web |author = Mayo Clinic Staff | date=2005-05-19 | url =http://www.mayoclinic.com/health/polio/DS00572/DSECTION=8 | title = Polio: Treatment| publisher = Mayo Foundation for Medical Education and Research (MFMER)| accessdate=2007-02-26}}</ref>
No cure for polio exists, and 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, moderate exercise and a nutritious diet.<ref name=MayoTreat>{{cite web |author = Mayo Clinic Staff | date=2005-05-19 | url =http://www.mayoclinic.com/health/polio/DS00572/DSECTION=8 | title = Polio: Treatment| publisher = Mayo Foundation for Medical Education and Research (MFMER)| accessdate=2007-02-26}}</ref>


Portable [[ventilator]]s may be required to support breathing. Historically, a noninvasive negative-pressure ventilator (more commonly called an [[iron lung]]) was used to artificially maintain respiration during an acute polio infection, generally for about one to two weeks, or until a person can breathe independently. Today many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators that are worn over the [[chest]] and [[abdomen]].<ref name= Goldberg/>
Portable [[ventilator]]s may be required to support breathing. Historically, a noninvasive negative-pressure ventilator (more commonly called an [[iron lung]]) was used to artificially maintain respiration during an acute polio infection, generally for about one to two weeks, or until a person can breathe independently. Today many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators that are worn over the [[chest]] and [[abdomen]].<ref name= Goldberg/>


In [[China]], where over 2 million paralytic polio survivors live <ref name=Qin>{{cite book | last = Qin | first = Sihe | title = The Surgical Care Of The Post-Poliomyelitis Sequelae. 2006 | isbn = 7-117-06998-8 | year = 2006 | url=http://www.qinsihe.net | }}</ref>, the surgical care of the post-poliomyelitis sequelae has offered means of reducing or eliminating the paralytic and bones deformity/atrophy associated with polio. To regenerate nerves and muscle activity in dead muscles, for example a dead [[quadriceps]], part of the [[hamstring]] may be surgically removed and grafted into the paralytic [[quadriceps]]. Bones deformity or atrophy are generally corrected by [[osteotomy]].
A pioneer in the field, Dr. Qin Sihe (See: http://www.qinsihe.net) has pioneered many techniques to address the various post polio sequelae observed.<ref name=Qin>{{cite book | last = Qin | first = Sihe | title = The Surgical Care Of The Post-Poliomyelitis Sequelae. 2006 | isbn = 7-117-06998-8 | year = 2006 | url=http://www.qinsihe.net | }}</ref>




Other [[History of poliomyelitis#Historical treatments|historical treatments for polio]] have included [[hydrotherapy]], [[electrotherapy]] and surgical treatments such as tendon lengthening and nerve grafting.<ref name= Henry1/> The use of devices such as rigid [[brace]]s and body casts, which tended to cause [[muscle atrophy]] due to the limited movement of the user, were also touted as effective treatments.<ref name= Oppewal>{{cite journal |author=Oppewal S |title=Sister Elizabeth Kenny, an Australian nurse, and treatment of poliomyelitis victims |journal=Image J Nurs Sch |volume=29 |issue=1 |pages=83-7 |year=1997 |pmid=9127546}}</ref> Massage, passive motion exercises, and [[vitamin C]] were also used to treat polio victims.<ref name= Henry1/><ref>{{cite journal | last=Klenner | first=Fred R. | authorlink=Fred R. Klenner | title=The Treatment of Poliomyelitis and Other Virus Diseases with Vitamin C | url= http://www.orthomed.com/polio.htm | journal=Southern Medicine & Surgery | volume=111 | issue=7 | date=July 1949 }}</ref>
Other [[History of poliomyelitis#Historical treatments|historical treatments for polio]] have included [[hydrotherapy]], [[electrotherapy]] and surgical treatments such as tendon lengthening and nerve grafting.<ref name= Henry1/> The use of devices such as rigid [[brace]]s and body casts, which tended to cause [[muscle atrophy]] due to the limited movement of the user, were also touted as effective treatments.<ref name= Oppewal>{{cite journal |author=Oppewal S |title=Sister Elizabeth Kenny, an Australian nurse, and treatment of poliomyelitis victims |journal=Image J Nurs Sch |volume=29 |issue=1 |pages=83-7 |year=1997 |pmid=9127546}}</ref> Massage, passive motion exercises, and [[vitamin C]] were also used to treat polio victims.<ref name= Henry1/><ref>{{cite journal | last=Klenner | first=Fred R. | authorlink=Fred R. Klenner | title=The Treatment of Poliomyelitis and Other Virus Diseases with Vitamin C | url= http://www.orthomed.com/polio.htm | journal=Southern Medicine & Surgery | volume=111 | issue=7 | date=July 1949 }}</ref>

Revision as of 14:45, 28 July 2007

Polio
SpecialtyInfectious diseases, neurology, orthopedic surgery Edit this on Wikidata
This article is about the disease. For the virus which causes poliomyelitis, see Poliovirus.

Poliomyelitis (from the Greek words πολίός (polio), meaning gray, and µυЄλός (myelon), referring to the spinal cord[1]) often called polio or infantile paralysis, is an acute viral infectious disease spread from person-to-person, primarily via the fecal-oral route.[2] While roughly 90% of polio infections are asymptomatic, affected individuals can exhibit a range of more severe symptoms if the virus enters the blood stream.[3] In less than 1% of polio cases the virus enters the central nervous system (CNS), preferentially infecting and destroying motor neurons.[4] The destruction of motor neurons causes muscle weakness and acute flaccid paralysis.

An ancient disease, polio was first recognized as a distinct condition by Jakob Heine in 1840. In the early part of the twentieth century much of the world experienced a huge increase in the number of polio cases. The disease tended to strike white, affluent individuals without warning: it was impossible to tell who would get the disease and who would be spared. 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 Jonas Salk and in 1962 by 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 led by Rotary International, UNICEF and the World Health Organization may soon result in global eradication of the disease.

Cause

A TEM micrograph of poliovirus.
Main article: poliovirus

Poliomyelitis is caused by infection with poliovirus. Poliovirus is a human pathogen and it cannot naturally infect other species.[3] A small RNA enterovirus,[2] poliovirus is structurally very simple; it is composed of an RNA genome enclosed in a non-enveloped capsid.[3] There are three different serotypes of poliovirus, poliovirus type 1 (PV1), type 2 (PV2), and type 3 (PV3), each with a slightly different capsid protein. All three forms are extremely virulent and produce the same disease symptoms.[3] PV1 is the most commonly encountered form.

Transmission

Poliomyelitis is a highly contagious disease which spreads easily via human-to-human contact.[5] In endemic areas wild polioviruses can infect virtually the entire human population.[6] In temperate climates poliomyelitis 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.[5] In tropical areas seasonal differences in transmission are far less pronounced.[6]

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.[7] Following an initial infection with poliovirus, virus particles are excreted in the feces for several weeks.[7] The infection is passed on to others via the fecal-oral route: poor hand washing allows the virus to remain on the hands after eating or using the bathroom. The risk of transmission is highest seven to 10 days before and after the onset of symptoms, but transmission is possible as long as the virus remains in the throat or feces.[1] A number of factors increase the risk of polio infection or affect the severity of the disease including: immune deficiency,[8] malnutrition,[9] intramuscular injection,[10] pregnancy,[10] tonsillectomy,[11] and physical activity immediately following the onset of paralysis.[12]

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.[13] Maternal antibodies to poliovirus are able to cross the placenta, providing passive immunity that protects the infant from polio infection during the first few months of life.[14]

Classification

Forms of poliomyelitis
Form Proportion of cases[4]
Asymptomatic 90-95%
Minor illness 4-8%
Non-paralytic aseptic
meningitis 		1-2%
Paralytic poliomyelitis 0.1-0.5%
— Spinal Polio 79% of paralytic cases
— Bulbospinal Polio 19% of paralytic cases
— Bulbar Polio 2% of paralytic cases

The name poliomyelitis is used to identify all conditions caused by any of three poliovirus serotypes. During the acute polio epidemics in the early 20th century, several categories of poliomyelitis were defined to classify the extent and seriousness of the disease.[15] Two basic patterns of polio infection are described: a minor illness which does not involve the central nervous system (CNS), sometimes called abortive polio, and a major illness, which may be paralytic or non-paralytic.

In the majority of individuals with a functioning immune system polio infection is abortive; producing either no symptoms or relatively minor symptoms such as: upper respiratory tract infection (sore throat and fever), gastrointestinal tract disturbances (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhea), and influenza-like illnesses.[16]

In about 3% of poliovirus infections, the virus enters the central nervous system. In 1–2% of infections patients develop non-paralytic aseptic meningitis, with symptoms of headache, neck, back, abdominal and extremity pain, fever, vomiting, lethargy and irritability.[1][17]

In approximately 1 in 200 to 1 in 1000 cases poliovirus infection leads to the development of paralytic disease, in which the muscles become weak, floppy and poorly controlled, and finally completely paralyzed; this condition is known as acute flaccid paralysis (AFP).[18] Depending on the site of paralysis, paralytic poliomyelitis is classified as spinal, bulbar, or bulbospinal.

Mechanism

The virus enters the body through the mouth, and infects the first cells it comes into contact with, the tonsils and intestinal M cells, by binding to a immunoglobulin-like receptor (called the poliovirus receptor or CD155) on the cells' surface.[19] Once inside a human cell the virus begins to replicate, and divides within gastrointestinal cells for about one week before penetrating the intestinal lining. Following penetration, the virus is absorbed into the blood via the mesentery, and into the lymphatic system via the Peyer's patches. Once the poliovirus enters the bloodstream it becomes a viremia and is widely distributed throughout the body. The virus can survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks.[20] In a small percentage of cases the virus spreads and replicates in other sites such as brown fat, the reticuloendothelial tissues, and muscle.[21] This sustained replication causes a secondary viremia, and leads to the development of minor symptoms (see above).

A blockage of the lumbar anterior spinal cord artery due to polio (PV3).

Rarely the virus invades the central nervous system (CNS), causing a local inflammatory response. The mechanisms by which poliovirus spreads to the CNS are poorly understood.[22] In one to two percent of poliovirus infections, the virus causes a self limiting inflammation of the meninges, the layers of tissue surrounding the brain, causing non-paralytic aseptic meningitis.[1]

In approximately 1% of poliovirus infections, the virus replicates in motor neurons within the spinal cord, brain stem, or motor cortex; leading to the development of paralytic poliomyelitis. Early symptoms of paralytic polio include a high fever, headache, stiffness in the back and neck, muscle weakness, sensitivity to touch, difficulty swallowing, muscle pain, irritability, constipation, or difficulty urinating. Paralysis generally develops 1 to 10 days after early symptoms develop and progresses for 2 to 3 days. Paralysis is usually complete when the fever breaks.[23]

Both the likelihood of developing paralytic polio and the extent of paralysis increase with age. In children, paralysis occurs in 1 in 1000 cases, while in adults, paralysis occurs in 1 in 75.[24] In children under 5 years of age paralysis of one leg is most common. In adults extensive paralysis in the trunk and muscles of the chest and abdomen and affecting all four limbs—quadriplegia—is more common.[25] Paralysis rates also vary depending on 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.[26]

Spinal polio

The location of motor neurons in the anterior horn cells of the spinal column.

Spinal polio is the most common form of paralytic poliomyelitis. This form of the disease results from viral invasion of the motor neurons of the anterior horn cells, or the ventral (front) gray matter section in the spinal column, which are responsible for movement of the muscles, including the trunk, limb and intercostal muscles.[18]

Poliovirus invasion causes inflammation of the nerve cells, and results in damage or destruction of motor neuron ganglia. When spinal neurons die Wallerian degeneration takes place, resulting in weakness of those muscles formerly innervated by the now dead neurons.[27] The destruction of nerve cells means that the muscles no longer receive any messages from the brain or spinal cord. Without nerve stimulation, the muscles begin to atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed.[18] Progression to maximum paralysis is rapid (two to four days), and is usually associated with fever and muscle pain.[27] Deep tendon reflexes are also affected and are usually absent or diminished; sensation, the ability to feel, however, is not affected in the paralyzed limbs.[27] The inflammation caused by poliovirus often also alters the color and appearance of the gray matter, causing it to appear reddish and swollen.[1]

The degree of paralysis due to spinal polio infection depends on where the virus strikes within the spinal cord and 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.[22] The virus may affect muscles on both sides of the body, but more often the paralysis is asymmetric and affects unbalanced parts of the body.[16] Any limb or combination of limbs may be affected—one leg, one arm, or both legs and both arms. Paralysis is often more severe proximally (where the limb joins the body) than distally (i.e. the fingertips and toes).[16] Spinal polio rarely results in death.[23]

Bulbar polio

The location and anatomy of the bulbar region (in orange).

Bulbar polio describes a form paralytic poliomyelitis that occurs when poliovirus invades and destroys nerves within the bulbar region of the brain stem. This form of the disease occurs in approximately 2% of cases of paralytic polio.[4]

The bulbar region is a white matter pathway which connects the cerebral cortex to the brainstem. 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.[28] In bulbar polio the destruction of these nerves reduces breathing capacity and causes difficulty in speaking and swallowing. Due to the affect on swallowing, secretions of mucous may build up in the airway causing suffocation.[23]

Nineteen percent of all paralytic polio cases appear as a combination of the symptoms of both bulbar and spinal polio, this form of the disease is called respiratory polio or bulbospinal polio.[4] 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. By destroying these nerves this form of polio affects breathing, making it difficult or impossible for the patient to breathe without the support of a respirator. It can lead to paralysis of the arms and legs and may also affect swallowing and heart functions.[28]

In extremely rare cases, usually in immunocompromised individuals, an uncontrolled infection of the entire brain, called fulminating encephalitis, can develop.[29] Even with intravenous antiviral therapy and intensive care the mortality rate for these cases is extremely high.

Prognosis

Patients with abortive polio infections recover completely. In those patients that develop aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery.[30] In cases of spinal polio 50% of patients recover fully, 25% recover with mild disability and 25% are left with a severe disability.[31]

A child displaying a deformity of her right lower extremity due to polio.

Without respiratory support, poliomyelitis affecting respiration is likely to result in suffocation, or aspiration of secretions and resulting pneumonia.[32] Overall 5–10% of patients with paralytic polio die due to the paralysis of muscles used for breathing. The mortality rate varies by age; 2%–5% of children, and up to 15%–30% of adults die.[4] Without mechanical ventilation, the bulbar form of paralytic poliomyelitis often results in death.[28] With respiratory support the mortality rate of bulbar polio ranges from 25% to 75%, depending on the age of the patient.[4]

Recovery

If the nerve cells affected by polio are completely destroyed, paralysis will be permanent. Many cases of poliomyelitis, however, result in only temporary paralysis.[18] Within a month, nerve impulses begin to return to the apparently paralyzed muscle; recovery is usually complete within six to eight months.[30] The neurophysiological processes involved in recovery following acute paralytic poliomyelitis are quite effective; muscles are able to retain normal strength even after 50 percent of the original motor neurons have been lost.[33] Any paralysis remaining after one year is likely to be permanent, but modest recoveries of muscle strength are possible 12 to 18 months after infection.[30]

One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons elaborate new branches, or axonal sprouts.[34] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[35] restoring the capacity of muscle fibers to contract and improving strength.[36] Terminal sprouting may result in a few significantly enlarged motor neurons doing work previously performed by as many as 4 or 5 units.[24] This means that a single motor neuron that once controlled 200 muscles might now control 800 to 1000 muscles. Other mechanisms that occur during the rehabilitation phase and contribute to muscle strength restoration are Myofiber hypertrophy—enlargement of muscle fibers through exercise and activity—and transformation of type II muscle fibers to type I muscle fibers.[37][35]

In addition to these physiological processes, the body possesses a number of compensatory mechanisms to maintain function in the presence of residual paralysis, including: use of weak muscles at a higher level of capacity, substituting strong muscles with increased energy expenditure for tasks, and the use of ligaments for stability which results in greater mobility.[37]

Complications

Residual complications of paralytic polio often result following the initial recovery process, and may include:[17]

Post-polio syndrome

Main article: Post-polio syndrome

Some people who have survived paralytic 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).[39] 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.[40] 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.[39] Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.[4]

Diagnosis

A laboratory diagnosis of poliomyelitis is usually made based on recovery of poliovirus from the stool or pharynx. Neutralizing antibodies to poliovirus can be diagnostic and are generally detected in the blood of infected patients early in the course of infection.[4]

Analysis of the patient's cerebrospinal fluid (CSF), which is collected by a lumbar puncture, or "spinal tap" reveals an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level.[41] Detection of virus from the CSF is diagnostic of paralytic polio, but rarely occurs.

If poliovirus is isolated from a patient experiencing acute flaccid paralysis it is further tested, using oligonucleotide mapping (genetic fingerprinting), or more recently 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).[42] For each reported case of paralytic polio caused by wild poliovirus, it is estimated that another 200 to 3,000 contagious asymptomatic carriers exist.[43] Therefore, isolation of wild poliovirus constitutes a public health emergency, and appropriate efforts to control the spread of the disease must be initiated immediately.[27]

Treatment

File:Womanonsideinlung.jpg
A modern negative pressure ventilator (iron lung).

No cure for polio exists, and 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, moderate exercise and a nutritious diet.[44]

Portable ventilators may be required to support breathing. Historically, a noninvasive negative-pressure ventilator (more commonly called an iron lung) was used to artificially maintain respiration during an acute polio infection, generally for about one to two weeks, or until a person can breathe independently. Today many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators that are worn over the chest and abdomen.[32]

Other historical treatments for polio have included hydrotherapy, electrotherapy and surgical treatments such as tendon lengthening and nerve grafting.[18] The use of devices such as rigid braces and body casts, which tended to cause muscle atrophy due to the limited movement of the user, were also touted as effective treatments.[45] Massage, passive motion exercises, and vitamin C were also used to treat polio victims.[18][46]

Prevention

Antibody serum

In 1950 William Hammon at the University of Pittsburgh a isolated serum from the blood of polio survivors.[47] Hammon reasoned that the serum, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. 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.[48] The serum was also shown to reduce the severity of the disease in patients that developed polio.[47] The antibody approach was later deemed impractical for widespread use, however, due in large part to the limited supply of blood plasma, and the medical community turned it's focus to the development of a polio vaccine.[49]

A child receives oral Polio vaccine.

Vaccine

Main article: Polio vaccine

Two polio vaccines are used throughout the world to combat polio. Both vaccines induce immunity to polio, efficiently blocking person-to-person transmission of wild poliovirus, thereby protecting both individual vaccine recipients and the wider community.[50]

The first polio vaccine was developed in 1952 by Jonas Salk at the University of Pittsburgh, and announced to the world by Salk on April 12, 1955.[51] 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 is inactivated with formalin.[5] After two doses of IPV, ninety percent or more of individuals develop protective antibody to all three serotypes of poliovirus, and at least 99% are immune to poliovirus following three doses.[4] IPV is currently the vaccine of choice in most countries.

Eight years after Salk's success, Albert Sabin developed an oral polio vaccine (OPV) using live but weakened (attenuated) virus, produced by the repeated passage of the virus through non-human cells at a sub-physiological temperature.[52] Human trials of Sabin's vaccine began in 1957 and it was licensed in 1962. The attenuated poliovirus in the Sabin vaccine replicates very efficiently in the gut, the primary site of wild poliovirus infection and replication, but the vaccine strain is unable to replicate efficiently within nervous system tissue.[53] OPV produces excellent immunity in the intestine, which helps prevent infection with wild virus in areas where the virus is endemic.[54] A single dose of oral polio vaccince produces immunity to all three poliovirus serotypes in approximately 50% of recipients. Three doses of live-attenuated OPV produce protective antibody to all three poliovirus types in more than 95% of recipients.[4]

Eradication

Main article: Poliomyelitis eradication

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.[55] 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.[56] 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.[57]

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.[58] In 2000 polio was officially eradicated in 36 Western Pacific countries, including China and Australia.[59][60] Europe was declared polio-free in 2002.[61] Today, polio remains endemic in just four countries: Nigeria, India, Pakistan, and Afghanistan.[56]

History

Main article: History of poliomyelitis
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.[62] The first clinical description of poliomyelitis was provided by the British physician Michael Underwood in 1789—he refers to polio as “a debility of the lower extremities".[63] The work of physicians Jakob Heine in 1840 and Karl Oskar Medin in 1890 led to the disease being known as Heine-Medin disease.[64][62]

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.[65] 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.

Around 1900, small, localized paralytic polio epidemics began to appear in Europe and the United States.[66] By 1950, the peak age incidence of paralytic poliomyelitis in the United States had shifted from infants to children aged five to nine years; about one-third of the cases were reported in persons over 15 years of age.[67] Accordingly, the rate of paralysis and death due to polio infection also increased during this time.[66] 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.[68]

The polio epidemics changed not only the lives of those who survived them, 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. 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.[69] In 1977 there were 254,000 persons living in the United States who had been paralyzed by polio.[70] According to doctors and local polio support groups, some 40,000 polio survivors with varying degrees of paralysis 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.[69]

See also

Notes and references

  1. ^ a b c d e Chamberlin SL, Narins B (editors) (2005). The Gale Encyclopedia of Neurological Disorders. Detroit: Thomson Gale. ISBN 0-7876-9150-X. {{cite book}}: |author= has generic name (help)
  2. ^ a b Cohen JI (2004). Harrison's Principles of Internal Medicine (Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, Isselbacher KJ, eds.) (16th ed. ed.). McGraw-Hill Professional. p. 1144. ISBN 0071402357. {{cite book}}: |edition= has extra text (help)
  3. ^ a b c d Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. pp. pp. 535–7. ISBN 0-8385-8529-9. {{cite book}}: |author= has generic name (help); |edition= has extra text (help); |pages= has extra text (help)
  4. ^ a b c d e f g h i j Atkinson W, Hamborsky J, McIntyre L, Wolfe S, eds. (2007). Poliomyelitis. in: Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book) (PDF) (10th ed. ed.). Washington DC: Public Health Foundation. pp. 101–14. {{cite book}}: |author= has generic name (help); |edition= has extra text (help)CS1 maint: multiple names: authors list (link)
  5. ^ a b c Kew O, Sutter R, de Gourville E, Dowdle W, Pallansch M (2005). "Vaccine-derived polioviruses and the endgame strategy for global polio eradication". Annu Rev Microbiol. 59: 587–635. PMID 16153180.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ a b Sybil P. Parker, editor in chief (1998). McGraw-Hill concise encyclopedia of science & technology. New York: McGraw-Hill. ISBN 0-07-052659-1. {{cite book}}: |author= has generic name (help)
  7. ^ a b Racaniello V (2006). "One hundred years of poliovirus pathogenesis". Virology. 344 (1): 9–16. PMID 16364730.
  8. ^ Davis L, Bodian D, Price D, Butler I, Vickers J (1977). "Chronic progressive poliomyelitis secondary to vaccination of an immunodeficient child". N Engl J Med. 297 (5): 241–5. PMID 195206.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Chandra R (1975). "Reduced secretory antibody response to live attenuated measles and poliovirus vaccines in malnourished children". Br Med J. 2 (5971): 583–5. PMID 1131622.
  10. ^ a b Evans C (1960). "Factors influencing the occurrence of illness during naturally acquired poliomyelitis virus infections" (PDF). Bacteriol Rev. 24 (4): 341–52. PMID 13697553.
  11. ^ Miller A (1952). "Incidence of poliomyelitis; the effect of tonsillectomy and other operations on the nose and throat". Calif Med. 77 (1): 19–21. PMID 12978882.
  12. ^ Horstmann D (1950). "Acute poliomyelitis relation of physical activity at the time of onset to the course of the disease". J Am Med Assoc. 142 (4): 236–41. PMID 15400610.
  13. ^ Joint Committee on Vaccination and Immunisation (Salisbury A, Ramsay M, Noakes K, editors) (2006). Chapter 26:Poliomyelitis. in: Immunisation Against Infectious Disease, 2006 (PDF). Edinburgh: Stationery Office. pp. 313–329. ISBN 0-11-322528-8. {{cite book}}: |author= has generic name (help)CS1 maint: multiple names: authors list (link)
  14. ^ Sauerbrei A, Groh A, Bischoff A, Prager J, Wutzler P (2002). "Antibodies against vaccine-preventable diseases in pregnant women and their offspring in the eastern part of Germany". Med Microbiol Immunol. 190 (4): 167–72. PMID 12005329.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Falconer M, Bollenbach E (2000). "Late functional loss in nonparalytic polio". American journal of physical medicine & rehabilitation / Association of Academic Physiatrists. 79 (1): 19–23. PMID 10678598.
  16. ^ a b c Yin-Murphy M, Almond JW (1996). Picornaviruses: The Enteroviruses: Polioviruses in: Baron's Medical Microbiology (Baron S et al, eds.) (4th ed. ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1. {{cite book}}: |edition= has extra text (help)
  17. ^ a b Charlotte Leboeuf, (1992). The late effects of Polio: Information For Health Care Providers. Commonwealth Department of Community Services and Health. ISBN 1-875412-05-0.{{cite book}}: CS1 maint: extra punctuation (link)
  18. ^ a b c d e f Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment. Pathology: p. 79-101. Philadelphia Davis. OCLC 2078290.
  19. ^ He Y, Mueller S, Chipman P, Bator C, Peng X, Bowman V, Mukhopadhyay S, Wimmer E, Kuhn R, Rossmann M (2003). "Complexes of poliovirus serotypes with their common cellular receptor, CD155". J Virol. 77 (8): 4827–35. PMID 12663789.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  20. ^ Todar, Ken (2006). "Polio". Ken Todar's Microbial World. University of Wisconsin - Madison. Retrieved 2007-04-23.
  21. ^ Sabin A (1956). "Pathogenesis of poliomyelitis; reappraisal in the light of new data". Science. 123 (3209): 1151–7. PMID 13337331.
  22. ^ a b Mueller S, Wimmer E, Cello J (2005). "Poliovirus and poliomyelitis: a tale of guts, brains, and an accidental event". Virus Res. 111 (2): 175–93. PMID 15885840.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ a b c Silverstein A, Silverstein V, Silverstein Nunn L (2001). Polio. Berkeley Heights, NJ: Enslow Publishers. ISBN 0-7660-1592-0.{{cite book}}: CS1 maint: multiple names: authors list (link)
  24. ^ a b Gawne AC, Halstead LS (1995). "Post-polio syndrome: pathophysiology and clinical management". Critical Review in Physical Medicine and Rehabilitation. 7: 147–88.
  25. ^ Christopher King (2007). "Poliomyelitis". MSN Encarta. Retrieved 2007-05-12.
  26. ^ Nathanson N, Martin J (1979). "The epidemiology of poliomyelitis: enigmas surrounding its appearance, epidemicity, and disappearance". Am J Epidemiol. 110 (6): 672–92. PMID 400274.
  27. ^ a b c d Cono J, Alexander LN (2002). Chapter 10, Poliomyelitis. in Vaccine Preventable Disease Surveillance Manual (PDF) (3rd ed. ed.). Centers for Disease Control and Prevention. pp. p. 10–1. {{cite book}}: |edition= has extra text (help); |pages= has extra text (help)
  28. ^ a b c Mayo Clinic Staff (2005-05-19). "Polio: Signs and symptoms". Mayo Foundation for Medical Education and Research (MFMER). Retrieved 2007-02-26.
  29. ^ Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment. Special Types of Poliomyelitis. Philadelphia: Davis. pp. pp. 179–183. OCLC 2078290. {{cite book}}: |pages= has extra text (help)
  30. ^ a b c Neumann D (2004). "Polio: its impact on the people of the United States and the emerging profession of physical therapy" (PDF). The Journal of orthopaedic and sports physical therapy. 34 (8): 479–92. PMID 15373011.
  31. ^ Sara, M.D. Cuccurullo, Sara J., MD. Cuccurullo,. Physical Medicine and Rehabilitation Board Review. Demos Medical Publishing. ISBN 1-888799-45-5.{{cite book}}: CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
  32. ^ a b Goldberg A (2002). "Noninvasive mechanical ventilation at home: building upon the tradition". Chest. 121 (2): 321–4. PMID 11834636.
  33. ^ Sandberg A, Hansson B, Stålberg E (1999). "Comparison between concentric needle EMG and macro EMG in patients with a history of polio". Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 110 (11): 1900–8. PMID 10576485.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  34. ^ Cashman NR, Covault J, Wollman RL, Sanes JR (1987). "Neural cell adhesion molecule in normal, denervated, and myopathic human muscle". Ann. Neurol. 21 (5): 481–9. PMID 3296947.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  35. ^ a b Agre JC, Rodríquez AA, Tafel JA (1991). "Late effects of polio: critical review of the literature on neuromuscular function". Archives of physical medicine and rehabilitation. 72 (11): 923–31. PMID 1929813.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  36. ^ Trojan DA, Cashman NR (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
  37. ^ a b Grimby G, Einarsson G, Hedberg M, Aniansson A (1989). "Muscle adaptive changes in post-polio subjects". Scandinavian journal of rehabilitation medicine. 21 (1): 19–26. PMID 2711135.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  38. ^ Mayo Clinic Staff (2005-05-19). "Polio: Complications". Mayo Foundation for Medical Education and Research (MFMER). Retrieved 2007-02-26.
  39. ^ a b Trojan D, Cashman N (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
  40. ^ Lin K, Lim Y (2005). "Post-poliomyelitis syndrome: case report and review of the literature" (PDF). Ann Acad Med Singapore. 34 (7): 447–9. PMID 16123820.
  41. ^ Mayo Clinic Staff (2005-05-19). "Polio: Screening and diagnosis". Mayo Foundation for Medical Education and Research (MFMER). Retrieved 2007-02-26.
  42. ^ Chezzi C (1996). "Rapid diagnosis of poliovirus infection by PCR amplification". J Clin Microbiol. 34 (7): 1722–5. PMID 8784577.
  43. ^ Atul Gawande (January 12, 2004). "The mop-up: eradicating polio from the planet, one child at a time". New Yorker. pp. 34–40. {{cite news}}: |access-date= requires |url= (help); Cite has empty unknown parameter: |coauthors= (help)
  44. ^ Mayo Clinic Staff (2005-05-19). "Polio: Treatment". Mayo Foundation for Medical Education and Research (MFMER). Retrieved 2007-02-26.
  45. ^ Oppewal S (1997). "Sister Elizabeth Kenny, an Australian nurse, and treatment of poliomyelitis victims". Image J Nurs Sch. 29 (1): 83–7. PMID 9127546.
  46. ^ Klenner, Fred R. (July 1949). "The Treatment of Poliomyelitis and Other Virus Diseases with Vitamin C". Southern Medicine & Surgery. 111 (7).
  47. ^ a b Hammon W (1955). "Passive immunization against poliomyelitis". Monogr Ser World Health Organ. 26: 357–70. PMID 14374581.
  48. ^ Hammon W, Coriell L, Ludwig E, McAllister R, Greene A, Sather G, Wehrle P (1954). "Evaluation of Red Cross gamma globulin as a prophylactic agent for poliomyelitis. 5. Reanalysis of results based on laboratory-confirmed cases". J Am Med Assoc. 156 (1): 21–7. PMID 13183798.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  49. ^ Rinaldo C (2005). "Passive immunization against poliomyelitis: the Hammon gamma globulin field trials, 1951-1953". Am J Public Health. 95 (5): 790–9. PMID 15855454.
  50. ^ Fine P, Carneiro I (1999). "Transmissibility and persistence of oral polio vaccine viruses: implications for the global poliomyelitis eradication initiative". Am J Epidemiol. 150 (10): 1001–21. PMID 10568615.
  51. ^ Spice, Byron (April 04, 2005). "Tireless polio research effort bears fruit and indignation". The Salk vaccine: 50 years later- second of two parts. Pittsburgh Post-Gazette. Retrieved 2007-04-30. {{cite news}}: Check date values in: |date= (help)
  52. ^ Sabin AB, Boulger LR (1973). "History of Sabin attenuated poliovirus oral live vaccine strains". J Biol Stand. 1: 115–8.
  53. ^ Sabin A, Ramos-Alvarez M, Alvarez-Amezquita J, Pelon W, Michaels R, Spigland I, Koch M, Barnes J, Rhim J (1960). "Live, orally given poliovirus vaccine. Effects of rapid mass immunization on population under conditions of massive enteric infection with other viruses". JAMA. 173: 1521–6. PMID 14440553.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  54. ^ "Poliomyelitis prevention: recommendations for use of inactivated poliovirus vaccine and live oral poliovirus vaccine. American Academy of Pediatrics Committee on Infectious Diseases". Pediatrics. 99 (2): 300–5. 1997. PMID 9024465.
  55. ^ Mastny, Lisa (January 25, 1999). "Eradicating Polio: A Model for International Cooperation". Worldwatch Institute. Retrieved 2007-02-02.
  56. ^ a b "Update on vaccine-derived polioviruses". MMWR Morb Mortal Wkly Rep. 55 (40): 1093–7. 2006. PMID 17035927.
  57. ^ "Smallpox". WHO Factsheet. Retrieved 2006-09-23.
  58. ^ "International Notes Certification of Poliomyelitis Eradication -- the Americas, 1994". Morbidity and Mortality Weekly Report. 43 (39). Centers for Disease Control and Prevention: 720–722. 1994. PMID 7522302.
  59. ^ "General News. Major Milestone reached in Global Polio Eradication: Western Pacific Region is certified Polio-Free" (PDF). Health Educ Res. 16 (1): p. 109. 2001. {{cite journal}}: |pages= has extra text (help)
  60. ^ D'Souza R, Kennett M, Watson C (2002). "Australia declared polio free". Commun Dis Intell. 26 (2): 253–60. PMID 12206379.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  61. ^ "Europe achieves historic milestone as Region is declared polio-free". Press release. European Region of the World Health Organization. 2002-06-21. Retrieved 2007-02-02.
  62. ^ a b [edited by] Edmund J. Sass with George Gottfried, Anthony Sorem; foreword by Richard Owen (1996). Summary Polio's legacy: an oral history. Washington, D.C: University Press of America. ISBN 0-7618-0144-8. {{cite book}}: |author= has generic name (help); Check |url= value (help)CS1 maint: multiple names: authors list (link)
  63. ^ Underwood, Michael (1793). Debility of the lower extremities. In: A treatise on the dieases [sic] of children, with general directions for the management of infants from the birth (1789). Early American Imprints, 1st series, no. 26291 (filmed); Copyright 2002 by the American Antiquarian Society. Vol. 2. Philadelphia: Printed by T. Dobson, no. 41, South Second-Street. pp. pp. 254–6. Retrieved 2007-02-23. {{cite book}}: |pages= has extra text (help)
  64. ^ Pearce J (2005). "Poliomyelitis (Heine-Medin disease)". J Neurol Neurosurg Psychiatry. 76 (1): 128. PMID 15608013.
  65. ^ Robertson S (1993). "Module 6: Poliomyelitis" (PDF). The Immunological Basis for Immunization Series. World Health Organization. Geneva, Switzerland. Retrieved 2007-05-08.
  66. ^ a b Trevelyan B, Smallman-Raynor M, Cliff A (2005). "The Spatial Dynamics of Poliomyelitis in the United States: From Epidemic Emergence to Vaccine-Induced Retreat, 1910-1971". Ann Assoc Am Geogr. 95 (2): 269–293. PMID 16741562.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  67. ^ Melnick JL (1990). Poliomyelitis. In: Tropical and Geographical Medicine (2nd ed. ed.). McGraw-Hill. pp. p. 558-576. ISBN 007068328X. {{cite book}}: |edition= has extra text (help); |pages= has extra text (help)
  68. ^ Zamula, Evelyn (1991). "A New Challenge for Former Polio Patients". FDA Consumer. 25 (5).
  69. ^ a b "After Effects of Polio Can Harm Survivors 40 Years Later". 2001-06-01. Retrieved 2007-06-04.
  70. ^ Frick NM, Bruno RL (1986). "Post-polio sequelae: physiological and psychological overview". Rehabilitation literature. 47 (5–6): 106–11. PMID 3749588. {{cite journal}}: |access-date= requires |url= (help)

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