Polio: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
No edit summary
No edit summary
Line 39: Line 39:
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.<ref name=UK>{{cite book |author=Joint Committee on Vaccination and Immunisation, David Salisbury (Editor), Mary Ramsay (Editor), Karen Noakes (Editor) |title=Immunisation Against Infectious Disease 2006 Chapter 26:Poliomyelitis | url=http://www.immunisation.nhs.uk/files/GB_26_polio.pdf |publisher=Stationery Office |location=Edinburgh |year= |pages=313-329|isbn=0-11-322528-8 |oclc= |doi=}}</ref> Maternal antibodies are also able to cross the placenta, providing [[passive immunity]] that protects the infant from polio infection during the first few months of life.<ref>{{cite journal |author=Sauerbrei A, Groh A, Bischoff A, Prager J, Wutzler P |title=Antibodies against vaccine-preventable diseases in pregnant women and their offspring in the eastern part of Germany |journal=Med Microbiol Immunol |volume=190 |issue=4 |pages=167-72 |year=2002 |pmid=12005329 |issn=}}</ref>
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.<ref name=UK>{{cite book |author=Joint Committee on Vaccination and Immunisation, David Salisbury (Editor), Mary Ramsay (Editor), Karen Noakes (Editor) |title=Immunisation Against Infectious Disease 2006 Chapter 26:Poliomyelitis | url=http://www.immunisation.nhs.uk/files/GB_26_polio.pdf |publisher=Stationery Office |location=Edinburgh |year= |pages=313-329|isbn=0-11-322528-8 |oclc= |doi=}}</ref> Maternal antibodies are also able to cross the placenta, providing [[passive immunity]] that protects the infant from polio infection during the first few months of life.<ref>{{cite journal |author=Sauerbrei A, Groh A, Bischoff A, Prager J, Wutzler P |title=Antibodies against vaccine-preventable diseases in pregnant women and their offspring in the eastern part of Germany |journal=Med Microbiol Immunol |volume=190 |issue=4 |pages=167-72 |year=2002 |pmid=12005329 |issn=}}</ref>


== Clinical presentation ==
{| class = "prettytable" style = "float:right; font-size:90%; margin-left:15px"
|+'''Forms of Poliomyelitis'''<ref name = PinkPages/>
|-
! style="background:#efefef;" | Form
! style="background:#efefef" | Proportion of cases
|-
| Asymptomatic
| align="center" |90-95%
|-
| Minor illness
|align="center" |4-8%
|-
|Non-paralytic aseptic<br/> meningitis
| align="center" |1-2%
|-
|Paralytic poliomyelitis
| align="center" |about 1%
|-
|— Spinal Polio
|align="center" |79% of paralytic cases
|-
|— Bulbospinal Polio
|align="center" |19% of paralytic cases
|-
|— Bulbar Polio
|align="center" |2% of paralytic cases
|}


Following ingestion, poliovirus begins to replicate in the cells it first comes into contact with, the [[tonsil]]s and intestinal [[M cell]]s. It divides within these 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]]. The virus can survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks.<ref>{{cite web| last = Todar | first = Ken | title = Polio | work = Ken Todar's Microbial World | publisher = University of Wisconsin - Madison | date = 2006 | url = http://www.bact.wisc.edu/themicrobialworld/Polio.html | accessdate = 04-23-07 }}</ref> Once polio enters the bloodstream it becomes a [[viremia]] and is widely distributed throughout the body.

There are two basic patterns of polio infection: ''abortive polio'', a minor illness which does not involve the [[central nervous system]] (CNS), and a major illness, which may be paralytic or non-paralytic. In 90–95% of individuals with a functioning [[immune system]] polio infection is abortive; the virus is cleared from the body, and the polio infection is [[asymptomatic]]. In 4-8% of cases the virus spreads and replicates in other sites such as [[brown fat]], the [[reticuloendothelial]] tissues, and [[muscle]].<ref>{{cite journal |author=Sabin A |title=Pathogenesis of poliomyelitis; reappraisal in the light of new data |journal=Science |volume=123 |issue=3209 |pages=1151-7 |year=1956 |pmid=13337331 |issn=}}</ref> This sustained replication causes a secondary viremia, and leads to the development of 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.<ref name=Baron />

In about 3% of poliovirus infections, the virus enters enters the [[central nervous system]]. In 1–2% of infections patients develop non-paralytic [[aseptic meningitis]], with symptoms of stiffness of the neck, back, and/or legs. Typically these symptoms last for 2 to 10 days, and are followed by complete recovery.<ref name= TG/> About 1% of poliovirus infections result in the most serious form of the disease: paralytic poliomyelitis.

=== Paralytic polio ===

In approximately 1 in 200 to 1 in 1000 cases poliovirus infection leads to the development of [[paralytic]] disease, in which patients develop ''flaccid paralysis''. Depending on the site of paralysis, paralytic poliomyelitis is classified as ''spinal'', ''bulbar'', or ''bulbospinal''. Paralytic attack rates vary by the serotype of the infecting poliovirus, the highest rates of paralysis (1 in 200) are associated with poliovirus type 1, the lowest rates (1 in 2,000) are associated with poliovirus type 2.<ref name=Nathanson>{{cite journal |author=Nathanson N, Martin J |title=The epidemiology of poliomyelitis: enigmas surrounding its appearance, epidemicity, and disappearance |journal=Am J Epidemiol |volume=110 |issue=6 |pages=672-92 |year=1979 |pmid=400274}}</ref>

==== Spinal polio ====

Spinal polio is the most common form of paralytic poliomyelitis. This form of the disease results from viral invasion of the [[motor neuron]]s of the [[Anterior horn (spinal cord)|anterior horn cells]], or the [[ventral]] (front) [[grey matter]] section in the [[spinal column]], which are responsible for movement of the muscles, including the [[trunk]], [[limb]] and [[intercostal muscle]]s.<ref name= Henry1>{{cite book | author = Henry WA Frauenthal and Jacolyn Van Vliet Manning| title = Manual of infantile paralysis, with modern methods of treatment. Pathology: p. 79-101 | publisher = Philadelphia Davis | year = 1914| url= http://books.google.com/books?vid=029ZCFMPZ0giNI1KiG6E&id=piyLQnuT-1YC&printsec=titlepage | oclc= 2078290}}</ref> [[Image:Polio spinal diagram.PNG|thumb|230px|left|The location of [[motor neuron]]s in the [[Anterior horn (spinal cord)|anterior horn cells]] of the [[spinal column]].]]
Poliovirus invasion causes inflammation of the nerve cells within the spinal column, which often alters the color and appearance of the grey matter, causing it to appear reddish and swollen, and results in damage or destruction of [[motor neuron]] [[ganglion]].<ref name= TG/>

When spinal neurons die a process known as [[Wallerian degeneration]] takes place, resulting in muscle weakness of those muscles that had once been [[innervate]]d by the now dead neurons.<ref name= Cono/> The destruction of nerve cells means that the muscles no longer receive any messages from the brain or spinal cord. The muscles become weak, floppy and poorly controlled; and finally completely paralyzed, this condition is known as acute flaccid paralysis (AFP).<ref name= Henry1/> Without nerve stimulation, the muscle begins to [[atrophy]], or shrink. Progression to maximum paralysis is rapid (2–4 days), and is usually associated with fever and muscle pain.<ref name= Cono>Cono, Joanne and Lorraine N. Alexander. (2002). VPD (Vaccine Preventable Disease) Surveillance Manual, 3rd Edition, [http://www.cdc.gov/nip/publications/surv-manual/chpt10_polio.pdf Chapter 10, Poliomyelitis] p.10-1.</ref> 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. Spinal paralysis is often more severe [[proximal]]ly than [[distal]]ly. Extensive paralysis of the trunk and muscles of the [[thorax]] and [[abdomen]], ([[quadriplegia]]) may occur.<ref name=Baron/> 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.<ref name= Cono/>

The degree of paralysis due to 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 (medical)|immunity]].<ref name= Mueller>{{cite journal |author=Mueller S, Wimmer E, Cello J |title=Poliovirus and poliomyelitis: a tale of guts, brains, and an accidental event |journal=Virus Res |volume=111 |issue=2 |pages=175-93 |year=2005 |id=PMID 15885840}}</ref>

==== Bulbar polio ====

[[Image:Brain bulbar region.PNG|thumb|right|180px|The location and anatomy of the bulbar region (in orange).]]

Bulbar polio describes a form of the disease that occurs when poliovirus invades the [[bulbar]] region of the [[brain stem]], which occurs in approximately 2% of cases of paralytic polio.<ref name = PinkPages>{{cite book | author = Atkinson W, Hamborsky J, McIntyre L, Wolfe S, eds. | title = Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book) | edition = 10th ed. | publisher = Washington DC: Public Health Foundation | year = 2007 | url = http://www.cdc.gov/nip/publications/pink/polio.pdf | id = ISBN }}</ref>

The brain stem is homologous to the spinal cord, but the motor neurons arising from there and passing in the various [[cranial nerves]] control the muscles related to eyeball movement; the [[trigeminal nerve]] and facial nerve which innervate cheeks, [[tear duct]]s , 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.<ref name=Mayo>{{cite web |author = Mayo Clinic Staff | date=2005-05-19 | url = http://www.mayoclinic.com/health/polio/DS00572/DSECTION=2 | title = Polio: Signs and symptoms | publisher = Mayo Foundation for Medical Education and Research (MFMER)| accessdate=2007-02-26}}</ref> In bulbar polio, the virus infiltrates and destroys these nerves reducing breathing capacity and causing difficulty in swallowing and speaking. Without respiratory support, poliomyelitis affecting [[respiration]] is likely to result in [[suffocation]], or [[aspiration]] of secretions and resulting [[pneumonia]].<ref name= Goldberg>{{cite journal |author=Goldberg A |title=Noninvasive mechanical ventilation at home: building upon the tradition |url= http://www.chestjournal.org/cgi/content/full/121/2/321 |journal=Chest |volume=121 |issue=2 |pages=321-4 |year=2002 |id=PMID 11834636}}</ref>

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 ''bulbospinal polio''.<ref name= PinkPages/> In bulbospinal cases, the virus affects the upper part of the [[cervical spine|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. This form can lead to paralysis of the arms and legs and may also affect breathing, swallowing and heart functions.<ref name= Mayo/>

In extremely rare cases, usually in [[immunocompromise]]d individuals, an uncontrolled infection of the entire brain, called fulminating [[encephalitis]], can develop.<ref name= Henry2>{{cite book | author = Henry WA Frauenthal and Jacolyn Van Vliet Manning| title = Manual of infantile paralysis, with modern methods of treatment. Special Types of Poliomyelitis: p 179-183 | publisher = Philadelphia Davis | year = 1914| url= http://books.google.com/books?vid=029ZCFMPZ0giNI1KiG6E&id=piyLQnuT-1YC&printsec=titlepage | oclc= 2078290}}</ref> Even with [[intravenous]] [[antiviral]] therapy and intensive care the mortality rate for these cases is extremely high.

=== 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).<ref name=Cashman>{{cite journal |author=Trojan D, Cashman N |title=Post-poliomyelitis syndrome |journal=Muscle Nerve |volume=31 |issue=1 |pages=6-19 |year=2005 |id=PMID 15599928}}</ref> 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.<ref name= Annals>{{cite journal |author=Lin K, Lim Y |title=Post-poliomyelitis syndrome: case report and review of the literature| url= http://www.annals.edu.sg/pdf/34VolNo7200508/V34N7p447.pdf |journal=Ann Acad Med Singapore |volume=34 |issue=7 |pages=447-9 |year=2005 |id=PMID 16123820}}</ref> 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.<ref name=Cashman/> Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.<ref name=PinkPages/>


==Prognosis==
==Prognosis==

Revision as of 17:19, 8 May 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 which is spread from person-to-person via the fecal-oral route.[2] The majority of polio infections are asymptomatic. In about 1% of cases the virus enters the central nervous system (CNS) via the blood stream. Within the CNS, poliovirus preferentially infects and destroys motor neurons. The destruction of motor neurons causes muscle weakness and flaccid paralysis.

An ancient disease, polio was first recognized as a medical entity by Jakob Heine in 1840. In the early part of the twentieth century, the United States, and much of the world experienced a huge increase in the number of polio cases. The disease tended to strike white, affluent individuals, and hit 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 Dr. Jonas Salk and in 1962 by Dr. Albert Sabin, are credited with reducing of the annual number of polio cases from many hundreds of thousands to around a thousand. In recent years enhanced vaccination efforts led by Rotary International, UNICEF and the World Health Organization may soon result in global eradication of the disease.


Poliovirus

Main article: Poliovirus

Poliovirus, a small RNA enterovirus composed of an RNA genome enclosed in a non-enveloped capsid, is the causative agent of poliomyelitis.[3] Poliovirus is strictly a human pathogen, and it cannot naturally infect other species.[2] The genome of poliovirus is limited, and only large enough to encode about 10 genes which, in turn, encode the small number of viral proteins critical for invasion and replication of the virus within human cells.[4]

An Electron micrograph of poliovirus.

There are three different serotypes of poliovirus, poliovirus type 1 (PV1), poliovirus type 2 (PV2), and poliovirus type 3 (PV3); each with a slightly different capsid protein.[2] PV1 is the most common form encountered in nature, however all three forms are extremely infectious.

Pathogenesis

Polio is highly contagious, and spreads easily via human-to-human contact, usually through the mouth due to fecally contaminated water or food (fecal-oral transmission).[5] In endemic areas wild polioviruses can infect virtually the entire population.[6] In temperate climates polio is a seasonal disease, the period of peak transmission of polio is in the summer and autumn and transmission of the virus is reduced during winter.[5] In tropical areas seasonal differences in transmission are far less pronounced.[6]

Following an initial infection with poliovirus, virus particles are excreted in the feces for several weeks.[7] The infection is passed on to others when 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] 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]

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


Prognosis

Patients with abortive polio infections, or those that develop aseptic meningitis can be expected to recover completely.[15]

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

In many cases of paralytic polio, nearby surviving neurons sprout to reinnervate the muscles which have lost nerve input, by growing "superclustered" axons, to replace those that have died, and the paralysis is temporary.[16] Within a month, nerve impulses begin to return to the apparently paralyzed muscle, and recovery is usually complete within six to eight months.[15] 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.[15] If the nerve cells are completely destroyed, paralysis will be permanent.

Fifty percent of patients with spinal polio recover fully, 25% are left with a severe disability and 25% recover with mild disability.[17] 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.[18]

Up to 0.2% of all polio infections, but nearly 20% of paralytic polio cases result in respiratory paralysis and require mechanical ventilation of the patient during the acute stage. Without respiratory support, the bulbar form of paralytic poliomyelitis often results in death.[19] With mechanical ventilation the mortality rate of bulbar polio ranges from 25% to 75%, depending on the age of the patient.[18] Permanent quadriplegia and/or permanent respiratory paralysis occurs in only 0.01% (1 in 10,000) of all poliovirus infections.

Complications of paralytic polio involve the lungs, kidneys and heart and may include: pulmonary edema, aspiration pneumonia, urinary tract infections, kidney stones, paralytic ileus, myocarditis and cor pulmonale.[20]

Diagnosis

Polio is a rare disease in much of the world, and few doctors have ever seen a case of polio. If polio is suspected, however, the usual follow-up test is a lumbar puncture, or "spinal tap", to collect the patient's cerebrospinal fluid (CSF). The CSF of individuals with polio contains an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level.[21]

A laboratory diagnosis of poliomyelitis is usually made based on recovery of poliovirus from the stool or pharynx. Detection of virus from the CSF is diagnostic of paralytic polio, but rarely occurs. Neutralizing antibodies to poliovirus appear in the blood of infected patients early in the course of infection.[18]

When poliovirus is isolated from a patient experiencing acute flaccid paralysis, it is then further tested, using oligonucleotide mapping (genetic fingerprinting), or more recently by by PCR amplification, to determine if the virus is “wild type” (that is, the virus encountered in nature) or vaccine type (is derived from a strain of poliovirus used to produce polio vaccine).[22] Isolation of wild poliovirus constitutes a public health emergency, and appropriate control efforts must be initiated immediately.[23]

Treatment

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, portable ventilators to support breathing, moderate exercise and a nutritious diet.[24]

In 1916, spurred by recent epidemics and experiencing little success in treating polio patients, researchers set out to find new and better treatments for the disease. Between 1917 and the early 1950s several therapies were explored in an effort to prevent deformities including hydrotherapy, electrotherapy and surgical treatments such as tendon lengthening and nerve grafting.[16] 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. [25] Massage, passive motion exercises, and vitamin C were also used to treat polio victims.[16] [26] [27] Most of these treatments provided little tangible therapeutic value. However, two effective supportive measures for the treatment of polio did emerge during this time, the iron lung and an anti-polio antibody serum.[28]

Iron lung

This iron lung was donated to the CDC by the family of Mr. Barton Hebert of Covington, Louisiana, who’d used the device from the late 1950s until his death in 2003.

An noninvasive negative-pressure ventilator (more commonly called an iron lung) is used to artificially maintain respiration during an acute polio infection, generally for about one to two weeks, or until a person can breathe independently.

The first iron lung used in the treatment of polio victims was invented by Philip Drinker, Louis Agassiz Shaw, and James Wilson at Harvard, and tested October 12, 1928 at Children’s Hospital, Boston.[29] The Drinker iron lung was powered by an electric motor attached to two vacuum cleaners, and worked by changing the pressure inside the machine, pulling air in and out of the lungs. The design of the iron lung was subsequently improved by John Haven Emerson in 1931.[29] The Emerson Iron Lung was produced until 1970.[30]

During the polio epidemics, the iron lung saved many thousands of lives, but the machine was large and cumbersome and the price of each machine was enormous,[31] in the 1930s, an iron lung cost about $1,500 - about the same price as the average home.[32] The cost of running the machine was also prohibitive, as patients were encased in the metal chambers for months, years and sometimes for life,[30] and even with an iron lung, the fatality rate for patients with bulbar polio exceeded 90%.[33]

These drawbacks led to the development of more modern positive-pressure ventilators and the use of positive-pressure ventilation by tracheostomy. Positive pressure ventilators, were first used to treat bulbar patients in Blegdamshospital, Copenhagen, Denmark during a polio outbreak in 1952,[33] and reduced mortality in bulbar patients from 90% to 20%.[34] The Copenhagen epidemic has been described as the start of intensive care, when large numbers of patients were ventilated by hand ("bagged") by medical students and anyone else on hand.[35] Today many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators that are worn over the chest and abdomen.[34]

Antibody serum

In 1950—three years before the arrival of the Salk vaccine—William Hammon at the University of Pittsburgh isolated serum from the blood of polio survivors.[28] The serum contained antibodies to poliovirus, and was used to prevent the spread of polio and to reduce the severity of disease in polio patients. The results of a large clinical trial were promising; the serum was shown to be about 80% effective in preventing the development of paralytic poliomyelitis, and protection was shown to last for 5 weeks if given under tightly controlled circumstances.[36] The serum was also shown to reduce the severity of the disease in patients that developed polio.[28]

The large scale use of antibody serum to prevent and treat polio had a number of drawbacks, however, including the observation that the immunity provided by the serum did not last long, and the protection offered by the antibody was incomplete, that reinjection was required during each epidemic outbreak, and that the optimal time frame for administration was unknown.[37] The antibody serum was widely administered, but obtaining the serum was an expensive and time-consuming process, and the focus of the medical community soon shifted to the development of a polio vaccine.[38]

  1. ^ a b Stacey L. Chamberlin (Editor), Brigham Narins (Editor). The Gale Encyclopedia of Neurological Disorders. Detroit: Thomson Gale. ISBN 0-7876-9150-X. {{cite book}}: |author= has generic name (help)
  2. ^ a b c Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. pp. pp. 535–7. ISBN 0838585299. {{cite book}}: |author= has generic name (help); |edition= has extra text (help); |pages= has extra text (help)CS1 maint: multiple names: authors list (link)
  3. ^ Cite error: The named reference Chan was invoked but never defined (see the help page).
  4. ^ Goodsell DS (1998). The machinery of life. New York: Copernicus. ISBN 0-387-98273-6.
  5. ^ a b Kew O, Sutter R, de Gourville E, Dowdle W, Pallansch M. "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, David Salisbury (Editor), Mary Ramsay (Editor), Karen Noakes (Editor). Immunisation Against Infectious Disease 2006 Chapter 26:Poliomyelitis (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. ^ 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.
  16. ^ a b c Cite error: The named reference Henry1 was invoked but never defined (see the help page).
  17. ^ 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)
  18. ^ a b c Cite error: The named reference PinkPages was invoked but never defined (see the help page).
  19. ^ Cite error: The named reference Mayo was invoked but never defined (see the help page).
  20. ^ Mayo Clinic Staff (2005-05-19). "Polio: Complications". Mayo Foundation for Medical Education and Research (MFMER). Retrieved 2007-02-26.
  21. ^ Mayo Clinic Staff (2005-05-19). "Polio: Screening and diagnosis". Mayo Foundation for Medical Education and Research (MFMER). Retrieved 2007-02-26.
  22. ^ Chezzi C (1996). "Rapid diagnosis of poliovirus infection by PCR amplification". J Clin Microbiol. 34 (7): 1722–5. PMID 8784577.
  23. ^ Cite error: The named reference Cono was invoked but never defined (see the help page).
  24. ^ Mayo Clinic Staff (2005-05-19). "Polio: Treatment". Mayo Foundation for Medical Education and Research (MFMER). Retrieved 2007-02-26.
  25. ^ Oppewal S (1997). "Sister Elizabeth Kenny, an Australian nurse, and treatment of poliomyelitis victims". Image J Nurs Sch. 29 (1): 83–7. PMID 9127546.
  26. ^ Klenner, Fred R. (July 1949). "The Treatment of Poliomyelitis and Other Virus Diseases with Vitamin C". Southern Medicine & Surgery. 111 (7).
  27. ^ Jungeblut, Claus Washington (October 1935). "Inactivation of poliomyelitis virus by crystalline vitamin C". Journal of Experimental Medicine. 62: 517–521.
  28. ^ a b c Hammon W. "Passive immunization against poliomyelitis". Monogr Ser World Health Organ. 26: 357–70. PMID 14374581.
  29. ^ a b Branson, RD (1998). "A Tribute to John H. Emerson. Jack Emerson: Notes on his life and contributions to respiratory care" (PDF). Respiratory Care. 43 (7): 567–71.
  30. ^ a b Roxanne Nelson. (September 2004) On Borrowed Time The last iron lung users face a future without repair service. AARP Bulletin. Accessed 07-02-07.
  31. ^ Wilson D (2005). "Braces, wheelchairs, and iron lungs: the paralyzed body and the machinery of rehabilitation in the polio epidemics". J Med Humanit. 26 (2–3): 173–90. PMID 15877198.
  32. ^ Staff of the National Museum of American History, Behring Center. "Whatever Happened to Polio?". Retrieved 2007-03-09.
  33. ^ a b West J (2005). "The physiological challenges of the 1952 Copenhagen poliomyelitis epidemic and a renaissance in clinical respiratory physiology". J Appl Physiol. 99 (2): 424–32. PMID 16020437.
  34. ^ a b Cite error: The named reference Goldberg was invoked but never defined (see the help page).
  35. ^ Ger Wackers (1994). "Constructivist Medicine" (html). Retrieved 2007-02-02. {{cite journal}}: Cite journal requires |journal= (help)
  36. ^ 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)
  37. ^ 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.
  38. ^ 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)
Retrieved from "https://en.wikipedia.org/w/index.php?title=Polio&oldid=129287293"