polio
Information about polio
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| ||
|---|---|---|
| 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 (from the Greek polio (πολίός), meaning grey, myelon (µυЄλός), referring to the spinal cord, and -itis denotes inflammation[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.
While polio-like symptoms have been identified in ancient cultures , poliomyelitis was first recognized as a distinct condition by Jakob Heine in 1840.[5] In the early 20th century much of the world experienced a dramatic increase in the number of polio cases, leading to a series of epidemics. These epidemics—which left thousands of children and adults paralyzed—provided the impetus for a "Great Race" towards the development of an effective vaccine. The development of polio vaccines by Jonas Salk (1952) and Albert Sabin (1962), are credited with reducing of the annual number of polio cases from many hundreds of thousands to around a thousand today.[6] Recently, enhanced vaccination efforts led by the World Health Organization, UNICEF and Rotary International may soon result in global eradication of the disease.[7]
Cause
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A TEM micrograph of poliovirus.
Transmission
Poliomyelitis is a highly contagious disease which spreads easily via human-to-human contact.[8] In endemic areas wild polioviruses can infect virtually the entire human population.[9] In temperate climates poliomyelitis is a seasonal disease, with periods of peak transmission in the summer and autumn and reduced levels during winter.[9] In tropical areas seasonal differences in transmission are far less pronounced.[9]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.[10] Following the initial poliovirus infection, virus particles are excreted in the feces for several weeks.[10] The infection is transmitted via the fecal-oral route: poor hand washing allows the virus to remain on the hands after eating or using the bathroom. While the risk of transmission is highest seven to 10 days before and after the onset of symptoms, transmission is possible as long as the virus remains in the throat or feces.[10]
Factors which increase the risk of polio infection or affect the severity of the disease include immune deficiency,[11] malnutrition,[12] tonsillectomy,[13] physical activity immediately following the onset of paralysis,[14] intramuscular injection,[15] and pregnancy.[15] 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.[16] 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.[17]
Classification
| 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 term "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.[18] 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 involving the CNS, which may be paralytic or non-paralytic.
In the majority of immunocompetent individuals (those with a normal immune system), a poliovirus infection is abortive, producing either no– or 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.[19]
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.[10][20]
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).[20] Depending on the site of paralysis, paralytic poliomyelitis is classified as spinal, bulbar, or bulbospinal.
In rare cases, encephalitis (an infection of the brain tissue itself) can occur. This form is usually restricted to infants and is characterized by confusion, changes in mental status, headaches, and fever; seizures and spastic paralysis may also occur.[21]
Mechanism
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Poliovirus enters the body through the mouth, infecting the first cells it comes into contact with—follicular dendritic cells residing within the germinal centers of the tonsils and intestinal M cells—by binding to a immunoglobulin-like receptor known as the poliovirus receptor (CD155) on the cell surface.[22] Once inside a human cell the virus hijacks the host cell's own machinery, and begins to replicate. Poliovirus 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 virus enters the bloodstream it becomes a viremia and is widely-distributed throughout the body. Poliovirus can survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks.[23] In a small percentage of cases the virus spreads and replicates in other sites such as brown fat, the reticuloendothelial tissues, and muscle.[24] This sustained replication causes a secondary major viremia, and leads to the development of minor influenza-like symptoms.
Rarely, the major viremia progresses and the virus invades the central nervous system (CNS), causing a local inflammatory response. In most cases this causes a self limiting inflammation of the meninges, the layers of tissue surrounding the brain, causing non-paralytic aseptic meningitis.[10] Penetration of the CNS provides no known benefit to the virus, and is quite possibly an "accidental" deviation of a normal gastrointestinal infection.[25] The mechanisms by which poliovirus spreads to the CNS are poorly understood, but it appears to be primarily a chance event—largely independent of the age, gender, or socioeconomic position of the individual.[25]
Paralytic polio
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Denervation of skeletal muscle tissue secondary to poliovirus infection can lead to paralysis.
In approximately 1% of infections poliovirus spreads along certain nerve fiber pathways, preferentially replicating in and destroying motor neurons within the spinal cord, brain stem, or motor cortex, which leads to the development of paralytic poliomyelitis. The various forms of paralytic poliomyelitis (spinal, bulbar, and bulbospinal) vary only with the amount of neuronal damage and inflammation that occurs, and the region of the CNS that is affected.
The destruction of neuronal cells produces lesions within the spinal ganglia; lesions can also be found in the reticular formation, vestibular nuclei, cerebellar vermis, and deep cerebellar nuclei.[25] Inflammation associated with nerve cell destruction often alters the color and appearance of the gray matter in the spinal column, causing it to appear reddish and swollen.[1] Other changes associated with paralytic disease occur in the hypothalamus and thalamus.[25] The molecular mechanisms by which poliovirus causes paralytic disease are poorly understood.
Early symptoms of paralytic polio include a high fever, headache, stiffness in the back and neck, asymmetrical weakness of various muscles, sensitivity to touch, difficulty swallowing, muscle pain, loss of superficial and deep reflexes, paresthesia, irritability, constipation, or difficulty urinating. Paralysis generally develops 1 to 10 days after early symptoms begin, and progresses for 2 to 3 days. Paralysis is usually complete when the fever breaks.[26]
The likelihood of developing paralytic polio and the extent of paralysis increase with age. In children non-paralytic meningitis is the most likely consequence of CNS involvement, and paralysis occurs in only 1 in 1000 cases. In adults paralysis occurs in 1 in 75 cases.[27] In children under 5 years of age paralysis of one leg is most common, while in adults extensive paralysis in the trunk and muscles of the chest and abdomen and affecting all four limbs—quadriplegia—is more likely.[28] 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 type 2.[29]
Spinal polio
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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.[30]
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.[30] With the destruction of nerve cells, the muscles no longer receive signals from the brain or spinal cord; without nerve stimulation, the muscles begin to atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed.[20] Progression to maximum paralysis is rapid (two to four days), and is usually associated with fever and muscle pain.[31] 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.[30]
The extent of spinal paralysis depends on the part of the spinal cord affected, which may be cervical, thoracic, or lumbar.[32] 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.[32] 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).[32]
Bulbar polio
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The location and anatomy of the bulbar region (in orange).
Bulbar polio is a form of paralytic poliomyelitis which 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.[32]
The bulbar region is a white matter pathway which connects the cerebral cortex to the brainstem. In bulbar polio the destruction of these nerves weakens the muscles supplied by the cranial nerves, producing symptoms of encephalitis, and causing breathing, speaking and swallowing to become difficult.[32] Critical nerves affected are 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. Due to the effect on swallowing, secretions of mucus may build up in the airway causing suffocation.[32] Other signs and symptoms of bulbar polio include: facial weakness caused by destruction of the trigeminal nerve and facial nerve which innervate cheeks, tear ducts, gums, and muscles of the face, among others; double vision, difficulty in chewing, and abnormal respiratory rate, depth, and rhythm, which may lead to respiratory arrest. Pulmonary edema and shock are also possible, and may be fatal.[32][33]
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.[32] 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.[33]
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.[33] In cases of spinal polio, if the nerve cells affected by polio are completely destroyed, paralysis will be permanent; cells that are not destroyed but lose function temporarily may recover within 4–6 weeks after onset.[33] Fifty percent of patients with spinal polio recover fully, 25% recover with mild disability and 25% are left with a severe disability.[35] The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of viraemia, and inversely proportional to the degree of immunity.[25] Spinal polio is rarely fatal.[32])
A child displaying a deformity of her right leg due to polio.
Without respiratory support, poliomyelitis with respiratory involvement is likely to result in suffocation, or aspiration of secretions and resulting pneumonia.[37] 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.[32] Without mechanical ventilation, the bulbar form of paralytic poliomyelitis often results in death.[32] With respiratory support the mortality rate of bulbar polio ranges from 25% to 75%, depending on the age of the patient.[32]
Recovery
Many cases of poliomyelitis result in only temporary paralysis.[20] Within a month, nerve impulses begin to return to the apparently paralyzed muscle; recovery is usually complete within six to eight months.[20] 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.[38] Paralysis remaining after one year is likely to be permanent, but modest recoveries of muscle strength are possible 12 to 18 months after infection.[37]One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts.[39] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[40] restoring the capacity of muscle fibers to contract and improving strength.[41] Terminal sprouting may result in a few significantly enlarged motor neurons doing work previously performed by as many as four or five units:[41] a single motor neuron that once controlled 200 muscle cells might control 800 to 1000 cells. Other mechanisms that occur during the rehabilitation phase and contribute to muscle strength restoration include Myofiber hypertrophy—enlargement of muscle fibers through exercise and activity—and transformation of type II muscle fibers to type I muscle fibers.[42][42]
In addition to these physiological processes, the body possesses a number of compensatory mechanisms to maintain function in the presence of residual paralysis, including the use of weaker muscles at a higher than usual intensity relative to the muscle's maximal capacity, enhancing athletic development of previously little-used muscles, and using ligaments for stability, which results in greater mobility.[42]
Complications
Residual complications of paralytic polio often result following the initial recovery process.[32] Muscle paresis and paralysis can sometimes result in skeletal deformities, tightening of the joints and movement disability. Once the muscles in the limb become flaccid, they may interfere with the function of other muscles. A typical manifestation of this problem is equinus foot (similar to club foot). This deformity results when the muscles that pull the toes downward are working, but those that pull it upward are not, and foot naturally tends to drop toward the ground. If the problem is left untreated, the Achilles tendons at the back of the foot retract and the foot cannot take on a normal position. Polio victims that develop equinus foot cannot walk properly because they cannot put their heel on the ground. A similar situation can develop if the arms become paralyzed.[43]In some cases the growth of an affected leg is slowed by polio, while the other leg continues to grow normally. The result is that one leg is shorter than the other and the person limps, and leans to one side, in turn leading to deformities of the spine (such as scoliosis).[43] Osteoporosis and increased likelihood of bone fractures may occur. Extended use of braces or wheelchairs may cause compression neuropathy, as well as a loss of proper function of the veins in the legs, due to pooling of blood in paralyzed lower limbs.[44]
Complications resulting from prolonged immobility involving the lungs, kidneys and heart include pulmonary edema, aspiration pneumonia, urinary tract infections, kidney stones, paralytic ileus, myocarditis and cor pulmonale.[44]
Post-polio syndrome
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.[32] Analysis of the patient's cerebrospinal fluid (CSF), which is collected by a lumbar puncture ("spinal tap") reveals an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level.[48] 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).[49] For each reported case of paralytic polio caused by wild poliovirus, it is estimated that another 200 to 3,000 contagious asymptomatic carriers exist.[50] Therefore, isolation of wild poliovirus constitutes a public health emergency, and appropriate efforts to control the spread of the disease must be initiated immediately.[31]
Treatment
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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 to prevent infections in weakened muscles, analgesics for pain, moderate exercise and a nutritious diet.[51] Treatment of polio also often requires long-term rehabilitation including physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery.[51]
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 until a person could breathe independently; generally about one to two weeks. Today many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators that are worn over the chest and abdomen.[51]
Other historical treatments for polio have included hydrotherapy, electrotherapy and surgical treatments such as tendon lengthening and nerve grafting.[20] 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.[52] Massage, passive motion exercises, and vitamin C were also used to treat polio victims, with varying degrees of success.[30][53]
Prevention
Antibody serum
In 1950 William Hammon at the University of Pittsburgh isolated a serum from the blood of polio survivors.[54] Hammon proposed 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.[55] The serum was also shown to reduce the severity of the disease in patients that developed polio.[55] 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 its focus to the development of a polio vaccine.[56])
A child receives oral polio vaccine.
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 (so-called herd immunity).[57]
The first polio vaccine was developed in 1952 by Jonas Salk at the University of Pittsburgh, and announced to the world on April 12, 1955.[58] 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 chemically-inactivated with formalin.[9] 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.[32] 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 sub-physiological temperatures.[59] Human trials of Sabin's vaccine began in 1957 and it was licensed in 1962.[60] 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.[61] OPV produces excellent immunity in the intestine, which helps prevent infection with wild virus in areas where the virus is endemic.[62] 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.[32]
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.[63] 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.[64] 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.[65]
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.[66] In 2000 polio was officially eradicated in 36 Western Pacific countries, including China and Australia.[67]<ref name="D'Souza_2002">D'Souza R, Kennett M, Watson C (2002). "Australia declared polio free". Commun Dis Intell 26 (2): 253-60. PMID 12206379. Europe was declared polio-free in 2002.[68] Today, polio remains endemic in just four countries: Nigeria, India, Pakistan, and Afghanistan.[64]
History
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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.[72] Poorer sanitation of the time resulted in a constant exposure to the virus, which enhanced a natural immunity within the population. In developed countries during the late 19th and early 20th centuries, improvements were made in community sanitation, including improved sewage disposal and clean water supplies. These changes also drastically increased the proportion of children and adults at risk of paralytic polio infection, by reducing childhood exposure and immunity to the disease.
Around 1900, small, localized paralytic polio epidemics began to appear in Europe and the United States.[73] Outbreaks reached pandemic proportions in Europe, North America, Australia, and New Zealand during the first half of the 20th century. By 1950 the peak age incidence of paralytic poliomyelitis in the United States had shifted from infants to children aged five to nine years, when the risk of paralysis is greater; about one-third of the cases were reported in persons over 15 years of age.[74] Accordingly, the rate of paralysis and death due to polio infection also increased during this time.[73] 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.[75]
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.[76] In 1977 there were 254,000 persons living in the United States who had been paralyzed by polio.[77] 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.[76]
See also
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38. ^ 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.
39. ^ 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.
40. ^ 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.
41. ^ Trojan DA, Cashman NR (2005). "Post-poliomyelitis syndrome". Muscle Nerve 31 (1): 6-19. PMID 15599928.
42. ^ 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.
43. ^ Sanofi Pasteur. Poliomyelitis virus (picornavirus, enterovirus), after-effects of the polio, paralysis, deformations. Polio Eradication. Retrieved on 2007-07-31.
44. ^ Mayo Clinic Staff (2005-05-19). Polio: Complications. Mayo Foundation for Medical Education and Research (MFMER). Retrieved on 2007-02-26.
45. ^ Trojan D, Cashman N (2005). "Post-poliomyelitis syndrome". Muscle Nerve 31 (1): 6-19. PMID 15599928.
46. ^ Ramlow J, Alexander M, LaPorte R, Kaufmann C, Kuller L (1992). "Epidemiology of the post-polio syndrome". Am. J. Epidemiol. 136 (7): 769-86. PMID 1442743.
47. ^ 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.
48. ^ Mayo Clinic Staff (2005-05-19). Polio: Screening and diagnosis. Mayo Foundation for Medical Education and Research (MFMER). Retrieved on 2007-02-26.
49. ^ Chezzi C (1996). "Rapid diagnosis of poliovirus infection by PCR amplification". J Clin Microbiol 34 (7): 1722-5. PMID 8784577.
50. ^ Gawande A (2004-01-12). "The mop-up: eradicating polio from the planet, one child at a time": 34–40. ISSN 0028-792X. Retrieved on 2007-05-13.
51. ^ Mayo Clinic Staff (2005-05-19). Polio: Treatment. Mayo Foundation for Medical Education and Research (MFMER). Retrieved on 2007-02-26.
52. ^ Oppewal S (1997). "Sister Elizabeth Kenny, an Australian nurse, and treatment of poliomyelitis victims". Image J Nurs Sch 29 (1): 83-7. PMID 9127546.
53. ^ Klenner FR (1949). "The Treatment of Poliomyelitis and Other Virus Diseases with Vitamin C". Southern Medicine & Surgery 111 (7).
54. ^ Hammon W (1955). "Passive immunization against poliomyelitis". Monogr Ser World Health Organ 26: 357-70. PMID 14374581.
55. ^ Hammon W, Coriell L, Ludwig E, et al (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.
56. ^ 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.
57. ^ 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.
58. ^ Spice B. "Tireless polio research effort bears fruit and indignation", The Salk vaccine: 50 years later- second of two parts, Pittsburgh Post-Gazette, April 04, 2005. Retrieved on 2007-04-30.
59. ^ Sabin AB, Boulger LR (1973). "History of Sabin attenuated poliovirus oral live vaccine strains". J Biol Stand 1: 115–8.
60. ^ A Science Odyssey: People and Discoveries. PBS (1998). Retrieved on 2007-08-14.
61. ^ Sabin A, Ramos-Alvarez M, Alvarez-Amezquita J, et al (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.
62. ^ (1997) "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. PMID 9024465.
63. ^ Mastny, Lisa (January 25, 1999). Eradicating Polio: A Model for International Cooperation. Worldwatch Institute. Retrieved on 2007-02-02.
64. ^ (2006) "Update on vaccine-derived polioviruses". MMWR Morb Mortal Wkly Rep 55 (40): 1093-7. PMID 17035927.
65. ^ Smallpox. WHO Factsheet. Retrieved on 2006-09-23.
66. ^ (1994) "International Notes Certification of Poliomyelitis Eradication -- the Americas, 1994". Morbidity and Mortality Weekly Report 43 (39): 720-722. PMID 7522302.
67. ^ (2001) "General News. Major Milestone reached in Global Polio Eradication: Western Pacific Region is certified Polio-Free" (PDF). Health Educ Res 16 (1): p. 109.
68. ^ "Europe achieves historic milestone as Region is declared polio-free", Press release, European Region of the World Health Organization, 2002-06-21. Retrieved on 2007-02-02.
69. ^ Sass Ej, Gottfried G, Sorem, A (eds.) (1996). Polio's legacy: an oral history. Washington, D.C: University Press of America. ISBN 0-7618-0144-8.
70. ^ 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) (fee required), Early American Imprints, 1st series, no. 26291 (filmed); Copyright 2002 by the American Antiquarian Society, Philadelphia: Printed by T. Dobson, no. 41, South Second-Street, pp. 254–6. Retrieved on 2007-02-23.
71. ^ Pearce J (2005). "Poliomyelitis (Heine-Medin disease)" (fee required). J Neurol Neurosurg Psychiatry 76 (1): 128. PMID 15608013.
72. ^ Robertson S (1993). Module 6: Poliomyelitis (PDF). The Immunological Basis for Immunization Series.. World Health Organization. Geneva, Switzerland.. Retrieved on 2007-05-08.
73. ^ 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.
74. ^ Melnick JL (1990). Poliomyelitis. In: Tropical and Geographical Medicine, 2nd ed., McGraw-Hill, p. 558-576. ISBN 007068328X.
75. ^ Zamula E (1991). "A New Challenge for Former Polio Patients". FDA Consumer 25 (5): 21-5.
76. ^ After Effects of Polio Can Harm Survivors 40 Years Later. March of Dimes (2001-06-01). Retrieved on 2007-08-07.
77. ^ Frick NM, Bruno RL (1986). "Post-polio sequelae: physiological and psychological overview". Rehabilitation literature 47 (5-6): 106-11. PMID 3749588. Retrieved on 2007-06-04.
2. ^ Cohen JI (2004). "Chapter 175: Enteroviruses and Reoviruses", in Kasper DL, Braunwald E, Fauci AS, et al (eds.): Harrison's Principles of Internal Medicine, 16th ed., McGraw-Hill Professional, 1144. ISBN 0071402357.
3. ^ Ryan KJ, Ray CG (eds.) (2004). "Enteroviruses", Sherris Medical Microbiology, 4th ed., McGraw Hill, 535–7. ISBN 0-8385-8529-9.
4. ^ Atkinson W, Hamborsky J, McIntyre L, Wolfe S (eds.) (2007). "Poliomyelitis.", Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book) (PDF), 10th ed., Washington DC: Public Health Foundation, 101–14.
5. ^ Paul JR (1971). A History of Poliomyelitis, Yale studies in the history of science and medicine. New Haven, Conn: Yale University Press. ISBN 0-300-01324-8.
6. ^ Aylward R (2006). "Eradicating polio: today's challenges and tomorrow's legacy". Ann Trop Med Parasitol 100 (5-6): 401-13. PMID 16899145.
7. ^ Heymann D (2006). "Global polio eradication initiative". Bull. World Health Organ. 84 (8): 595. PMID 16917643.
8. ^ 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.
9. ^ Parker SP (ed.) (1998). McGraw-Hill Concise Encyclopedia of Science & Technology. New York: McGraw-Hill. ISBN 0-07-052659-1.
10. ^ Racaniello V (2006). "One hundred years of poliovirus pathogenesis". Virology 344 (1): 9-16. PMID 16364730.
11. ^ 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.
12. ^ 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.
13. ^ 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.
14. ^ 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.
15. ^ Evans C (1960). "Factors influencing the occurrence of illness during naturally acquired poliomyelitis virus infections" (PDF). Bacteriol Rev 24 (4): 341-52. PMID 13697553.
16. ^ Joint Committee on Vaccination and Immunisation (Salisbury A, Ramsay M, Noakes K (eds.) (2006). Chapter 26:Poliomyelitis. in: Immunisation Against Infectious Disease, 2006 (PDF), Edinburgh: Stationery Office, 313-329. ISBN 0-11-322528-8.
17. ^ 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.
18. ^ 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.
19. ^ Yin-Murphy M, Almond JW (1996). "Picornaviruses: The Enteroviruses: Polioviruses", Baron's Medical Microbiology (Baron S et al'', eds.), 4th ed., Univ of Texas Medical Branch. ISBN 0-9631172-1-1.
20. ^ Leboeuf C (1992). The late effects of Polio: Information For Health Care Providers.. Commonwealth Department of Community Services and Health. ISBN 1-875412-05-0.
21. ^ Wood, Lawrence D. H.; Hall, Jesse B.; Schmidt, Gregory D. (2005). Principles of Critical Care, Third Edition. McGraw-Hill Professional, 870. ISBN 0-07-141640-4.
22. ^ He Y, Mueller S, Chipman P, et al (2003). "Complexes of poliovirus serotypes with their common cellular receptor, CD155". J Virol 77 (8): 4827-35. PMID 12663789.
23. ^ Todar K (2006). Polio. Ken Todar's Microbial World. University of Wisconsin - Madison. Retrieved on 2007-04-23.
24. ^ Sabin A (1956). "Pathogenesis of poliomyelitis; reappraisal in the light of new data". Science 123 (3209): 1151-7. PMID 13337331.
25. ^ 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.
26. ^ Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers. ISBN 0-7660-1592-0.
27. ^ Gawne AC, Halstead LS (1995). "Post-polio syndrome: pathophysiology and clinical management". Critical Review in Physical Medicine and Rehabilitation 7: 147–88.
28. ^ Young GR (1989). "Occupational therapy and the postpolio syndrome". The American journal of occupational therapy 43 (2): 97-103. PMID 2522741.
29. ^ 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.
30. ^ Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment. Pathology: p. 79-101. Philadelphia Davis. OCLC 2078290.
31. ^ Cono J, Alexander LN (2002). "Chapter 10, Poliomyelitis.", Vaccine Preventable Disease Surveillance Manual (PDF), 3rd ed., Centers for Disease Control and Prevention, p. 10–1.
32. ^ (2005) Professional Guide to Diseases (Professional Guide Series). Hagerstwon, MD: Lippincott Williams & Wilkins, 243-245. ISBN 1-58255-370-X.
33. ^ Mayo Clinic Staff (2005-05-19). Polio: Signs and symptoms. Mayo Foundation for Medical Education and Research (MFMER). Retrieved on 2007-02-26.
34. ^ 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.
35. ^ Cuccurullo SJ (2004). Physical Medicine and Rehabilitation Board Review. Demos Medical Publishing. ISBN 1-888799-45-5.
36. ^ 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.
37. ^ Goldberg A (2002). "Noninvasive mechanical ventilation at home: building upon the tradition". Chest 121 (2): 321-4. PMID 11834636.
38. ^ 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.
39. ^ 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.
40. ^ 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.
41. ^ Trojan DA, Cashman NR (2005). "Post-poliomyelitis syndrome". Muscle Nerve 31 (1): 6-19. PMID 15599928.
42. ^ 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.
43. ^ Sanofi Pasteur. Poliomyelitis virus (picornavirus, enterovirus), after-effects of the polio, paralysis, deformations. Polio Eradication. Retrieved on 2007-07-31.
44. ^ Mayo Clinic Staff (2005-05-19). Polio: Complications. Mayo Foundation for Medical Education and Research (MFMER). Retrieved on 2007-02-26.
45. ^ Trojan D, Cashman N (2005). "Post-poliomyelitis syndrome". Muscle Nerve 31 (1): 6-19. PMID 15599928.
46. ^ Ramlow J, Alexander M, LaPorte R, Kaufmann C, Kuller L (1992). "Epidemiology of the post-polio syndrome". Am. J. Epidemiol. 136 (7): 769-86. PMID 1442743.
47. ^ 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.
48. ^ Mayo Clinic Staff (2005-05-19). Polio: Screening and diagnosis. Mayo Foundation for Medical Education and Research (MFMER). Retrieved on 2007-02-26.
49. ^ Chezzi C (1996). "Rapid diagnosis of poliovirus infection by PCR amplification". J Clin Microbiol 34 (7): 1722-5. PMID 8784577.
50. ^ Gawande A (2004-01-12). "The mop-up: eradicating polio from the planet, one child at a time": 34–40. ISSN 0028-792X. Retrieved on 2007-05-13.
51. ^ Mayo Clinic Staff (2005-05-19). Polio: Treatment. Mayo Foundation for Medical Education and Research (MFMER). Retrieved on 2007-02-26.
52. ^ Oppewal S (1997). "Sister Elizabeth Kenny, an Australian nurse, and treatment of poliomyelitis victims". Image J Nurs Sch 29 (1): 83-7. PMID 9127546.
53. ^ Klenner FR (1949). "The Treatment of Poliomyelitis and Other Virus Diseases with Vitamin C". Southern Medicine & Surgery 111 (7).
54. ^ Hammon W (1955). "Passive immunization against poliomyelitis". Monogr Ser World Health Organ 26: 357-70. PMID 14374581.
55. ^ Hammon W, Coriell L, Ludwig E, et al (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.
56. ^ 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.
57. ^ 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.
58. ^ Spice B. "Tireless polio research effort bears fruit and indignation", The Salk vaccine: 50 years later- second of two parts, Pittsburgh Post-Gazette, April 04, 2005. Retrieved on 2007-04-30.
59. ^ Sabin AB, Boulger LR (1973). "History of Sabin attenuated poliovirus oral live vaccine strains". J Biol Stand 1: 115–8.
60. ^ A Science Odyssey: People and Discoveries. PBS (1998). Retrieved on 2007-08-14.
61. ^ Sabin A, Ramos-Alvarez M, Alvarez-Amezquita J, et al (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.
62. ^ (1997) "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. PMID 9024465.
63. ^ Mastny, Lisa (January 25, 1999). Eradicating Polio: A Model for International Cooperation. Worldwatch Institute. Retrieved on 2007-02-02.
64. ^ (2006) "Update on vaccine-derived polioviruses". MMWR Morb Mortal Wkly Rep 55 (40): 1093-7. PMID 17035927.
65. ^ Smallpox. WHO Factsheet. Retrieved on 2006-09-23.
66. ^ (1994) "International Notes Certification of Poliomyelitis Eradication -- the Americas, 1994". Morbidity and Mortality Weekly Report 43 (39): 720-722. PMID 7522302.
67. ^ (2001) "General News. Major Milestone reached in Global Polio Eradication: Western Pacific Region is certified Polio-Free" (PDF). Health Educ Res 16 (1): p. 109.
68. ^ "Europe achieves historic milestone as Region is declared polio-free", Press release, European Region of the World Health Organization, 2002-06-21. Retrieved on 2007-02-02.
69. ^ Sass Ej, Gottfried G, Sorem, A (eds.) (1996). Polio's legacy: an oral history. Washington, D.C: University Press of America. ISBN 0-7618-0144-8.
70. ^ 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) (fee required), Early American Imprints, 1st series, no. 26291 (filmed); Copyright 2002 by the American Antiquarian Society, Philadelphia: Printed by T. Dobson, no. 41, South Second-Street, pp. 254–6. Retrieved on 2007-02-23.
71. ^ Pearce J (2005). "Poliomyelitis (Heine-Medin disease)" (fee required). J Neurol Neurosurg Psychiatry 76 (1): 128. PMID 15608013.
72. ^ Robertson S (1993). Module 6: Poliomyelitis (PDF). The Immunological Basis for Immunization Series.. World Health Organization. Geneva, Switzerland.. Retrieved on 2007-05-08.
73. ^ 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.
74. ^ Melnick JL (1990). Poliomyelitis. In: Tropical and Geographical Medicine, 2nd ed., McGraw-Hill, p. 558-576. ISBN 007068328X.
75. ^ Zamula E (1991). "A New Challenge for Former Polio Patients". FDA Consumer 25 (5): 21-5.
76. ^ After Effects of Polio Can Harm Survivors 40 Years Later. March of Dimes (2001-06-01). Retrieved on 2007-08-07.
77. ^ Frick NM, Bruno RL (1986). "Post-polio sequelae: physiological and psychological overview". Rehabilitation literature 47 (5-6): 106-11. PMID 3749588. Retrieved on 2007-06-04.
Further reading
- Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment: Pathology.. Philadelphia: Davis, pp. 79-101. OCLC 2078290. (Full text available from Google Books, with hundreds of pictures.)
- Huckstep RL (1975). Poliomyelitis: a guide for developing countries - including appliances and rehabilitation for the disabled. Edinburgh: Churchill Livingstone. ISBN 0443013128. (A look at the modern polio patient and polio treatment techniques.)
External links
- General:
- What ever happened to Polio? An exhibit from the Smithsonian National Museum of American History.
- The Middle-Class Plague: Epidemic Polio and the Canadian State.
- CBC Digital Archives - Polio: Combating the Crippler Video and Radio reports related to Polio.
- Poliovirus in New Zealand 1915-1997
- Polio: A Virus' Struggle - an amusing yet educational graphic novella from the Science Creative Quarterly (in pdf format).
- Fermín: Making Polio History An article about Luis Fermín Tenorio Cortez, the last case of polio reported in the Americas.
- A UK Polio survivor - An account of John Prestwich who lived 50 years in an iron lung.
- Post-Polio Health International
For other uses of "ICD", see ICD (disambiguation).
The International Statistical Classification of Diseases and Related Health Problems (most commonly known by the abbreviation ICD
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List of ICD-10 codes. The version for 2007 is available online at [1]
Chapter Blocks Title
I Certain infectious and parasitic diseases
II Neoplasms
III Diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism
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Chapter Blocks Title
I Certain infectious and parasitic diseases
II Neoplasms
III Diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism
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For other uses of "ICD", see ICD (disambiguation).
The International Statistical Classification of Diseases and Related Health Problems (most commonly known by the abbreviation ICD
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The following is a list of codes for International Statistical Classification of Diseases and Related Health Problems. These codes are in the public domain.
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See also
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The Diseases Database is a free website that provides information about the relationships between medical conditions, symptoms, and medications.
It directly integrates the Unified Medical Language System.
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It directly integrates the Unified Medical Language System.
External links
- Diseases Database
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MedlinePlus is a website containing health information from the world's largest medical library, the United States National Library of Medicine. The site is intended to be used by health care providers and patients, and designed to provide up-to-date, authoritative information.
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Poliovirus
Poliovirus, the causative agent of poliomyelitis, is a human enterovirus and member of the family of Picornaviridae.[1] Poliovirus is composed of a RNA genome and a protein capsid.
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Poliovirus, the causative agent of poliomyelitis, is a human enterovirus and member of the family of Picornaviridae.[1] Poliovirus is composed of a RNA genome and a protein capsid.
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Greek}}}
Writing system: Greek alphabet
Official status
Official language of: Greece
Cyprus
European Union
recognised as minority language in parts of:
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Regulated by:
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Writing system: Greek alphabet
Official status
Official language of: Greece
Cyprus
European Union
recognised as minority language in parts of:
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Regulated by:
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spinal chord is a thin, tubular bundle of nerves that is an extension of the central nervous system from the brain and is enclosed in and protected by the bony vertebral column.
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-itis is typically used to denote an inflammation.
Inflammation Body part
Appendicitis Appendix
Arteritis Arteries
Arthritis Joint
Blepharitis Eyelids
Bronchiolitis Bronchioles
Bronchitis Bronchi
Bursitis Bursa
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List of inflammations
Inflammation Body part
Appendicitis Appendix
Arteritis Arteries
Arthritis Joint
Blepharitis Eyelids
Bronchiolitis Bronchioles
Bronchitis Bronchi
Bursitis Bursa
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Inflammation (Latin, inflammatio, to set on fire) is the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants.
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infectious disease is a clinically evident disease resulting from the presence of pathogenic microbial agents, including viruses, bacteria, fungi, protozoa, multicellular parasites, and aberrant proteins known as prions.
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fecal-oral route (or alternatively, the oral-fecal route or orofecal route).
There are, usually, intermediate steps, sometimes many of them. Amongst the more common causes are: Water that has come in contact with feces and poorly treated before drinking; food
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There are, usually, intermediate steps, sometimes many of them. Amongst the more common causes are: Water that has come in contact with feces and poorly treated before drinking; food
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In medicine, a disease is asymptomatic while the patient does not experience any noticeable symptoms. Asymptomatic diseases may not be discovered until the patient undergoes medical tests (X-rays or other investigations).
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Blood is a specialized biological fluid consisting of red blood cells (also called RBCs or erythrocytes), white blood cells (also called leukocytes) and platelets (also called thrombocytes) suspended in a complex fluid medium known as blood plasma.
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The central nervous system (CNS) represents the largest part of the nervous system, including the brain and the spinal cord. Together with the peripheral nervous system, it has a fundamental role in the control of behavior.
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Location Ventral horn of the spinal cord
Function Excitatory projection (to NMJ)
Neurotransmitter ACh
Morphology Projection neuron
Presynaptic connections M1 via the Corticospinal tract
Postsynaptic connections
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Function Excitatory projection (to NMJ)
Neurotransmitter ACh
Morphology Projection neuron
Presynaptic connections M1 via the Corticospinal tract
Postsynaptic connections
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MUSCLE (multiple sequence comparison by log-expectation) is public domain, multiple sequence alignment software for protein and nucleotide sequences.
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Flaccid paralysis is a clinical manifestation characterized by weakness or paralysis and reduced muscle tone without other obvious cause (e.g., trauma).[1]
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Causes
Polio
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Jakob (or Jacob) Heine (April 16, 1800, Lauterbach (Black Forest, Germany) – November 12, 1879, Cannstatt, Germany) was a German orthopaedist. He is most famous for his study, in 1840, into poliomyelitis, which was the first medical report on the disease, and
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In epidemiology, an epidemic (from Greek epi- upon + demos people) is a classification of a disease that appears as new cases in a given human population, during a given period, at a rate that substantially exceeds what is "expected," based on recent experience
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A vaccine is an antigenic preparation used to establish immunity to a disease. The term derives from Edward Jenner's use of cowpox ("vacca" means cow in Latin), which, when administered to humans, provided them protection against smallpox, the work which Louis Pasteur and others
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Two polio vaccines are used throughout the world to combat polio. The first was developed by Jonas Salk, first tested in 1952, and announced to the world by Salk on April 12, 1955. It consists of an injected dose of inactivated (dead) poliovirus.
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Jonas Salk
Jonas Salk during a 1988 Centers for Disease Control visit
Born September 28 1914
New York City, New York, USA
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Jonas Salk during a 1988 Centers for Disease Control visit
Born September 28 1914
New York City, New York, USA
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Albert Bruce Sabin (August 26, 1906 - March 3, 1993) was a renowned American medical researcher of Jewish ancestry who is best-known for having developed the hugely successful oral vaccine for polio.
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Vaccination is the administration of antigenic material to produce immunity to a disease. This will prevent or ameliorate the effects of infection by a pathogen. The material administrated can either be live, but weakened forms of pathogens such as bacteria or viruses,
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World Health Organization (WHO) is a specialized agency of the United Nations (UN) that acts as a coordinating authority on international public health. Established on 7 April 1948, and headquartered in Geneva, Switzerland, the agency inherited the mandate and resources of
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