|
|
| (35 intermediate revisions by 7 users not shown) |
| Line 1: |
Line 1: |
| | __NOTOC__ |
| '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' | | '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' |
| {{DiseaseDisorder infobox |
| |
| Name = Poliomyelitis |
| |
| Image = Polio lores134.jpg|
| |
| Image caption = A man with an [[Atrophy|atrophied]] right leg due to poliomyelitis.|
| |
| ICD10 = {{ICD10|A|80||a|80}}, {{ICD10|B|91||b|90}} |
| |
| ICD9 = {{ICD9|045}}, {{ICD9|138}} |
| |
| DiseasesDB = 10209 |
| |
| MedlinePlus = 001402 |
| |
| MeshName = Poliomyelitis |
| |
| MeshNumber = C02.182.600.700 |
| |
| }}
| |
|
| |
| {{Polio}} | | {{Polio}} |
|
| |
|
| {{CMG}}; '''Associate Editor(s)-In-Chief:''' {{CZ}} | | {{CMG}};{{AE}} {{CZ}}; {{JS}} |
| | |
| == Overview ==
| |
| '''''Related Key Words and Synonyms:''''' Poliomyelitis
| |
| | |
| '''Poliomyelitis''', often called '''polio''' or '''infantile paralysis''', is an acute [[virus (biology)|viral]] [[infectious disease]] spread from person to person, primarily via the [[fecal-oral route]].<ref name=Harrison>{{cite book| author = Cohen JI| chapter = Chapter 175: Enteroviruses and Reoviruses| title = [[Harrison's Principles of Internal Medicine]]| editor = Kasper DL, Braunwald E, Fauci AS, ''et al'' (eds.)| edition = 16th ed.| publisher = McGraw-Hill Professional| year = 2004| pages = 1144| isbn = 0071402357 }}</ref> The term derives from the [[Greek language|Greek]] ''polio'' (πολίός), meaning "grey", ''myelon'' (µυελός), referring to the "[[spinal cord]]", and ''[[-itis]]'', which denotes [[inflammation]].<ref name=Chamberlin_2005>{{cite book | author = Chamberlin SL, Narins B (eds.) | title = The Gale Encyclopedia of Neurological Disorders | publisher = Thomson Gale | location = Detroit | year = 2005 | pages = 1859–70| isbn = 0-7876-9150-X}}</ref> Although around 90% of polio infections [[asymptomatic|have no symptoms at all]], effected individuals can exhibit a range of symptoms if the virus enters the [[Blood|blood stream]].<ref name=Sherris>{{cite book | author = Ryan KJ, Ray CG (eds.) | chapter = Enteroviruses | title = Sherris Medical Microbiology | edition = 4th ed. | pages = 535–7 | publisher = McGraw Hill | year = 2004 | id = ISBN 0-8385-8529-9 }}</ref> In fewer than 1% of cases the virus enters the [[central nervous system]], preferentially infecting and destroying [[motor neuron]]s, leading to muscle weakness and acute [[flaccid paralysis]]. Different types of paralysis may occur, depending on the nerves involved. Spinal polio is the most common form, characterized by asymmetric paralysis that most often involves the legs. Bulbar polio leads to weakness of muscles innervated by [[cranial nerves]]. Bulbospinal polio is a combination of bulbar and spinal paralysis.<ref name = PinkBook>{{cite book | author = Atkinson W, Hamborsky J, McIntyre L, Wolfe S (eds.) | chapter = Poliomyelitis | title = Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book) | edition = 10th ed. | pages = 101–14 | publisher = Public Health Foundation | location =Washington DC |year = 2007 | url = http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/polio.pdf | format = PDF}}</ref>
| |
|
| |
|
| Poliomyelitis was first recognized as a distinct condition by [[Jakob Heine]] in 1840.<ref name=Paul_1971>{{cite book| author = Paul JR| title=A History of Poliomyelitis| publisher=Yale University Press| location= New Haven, Conn| year=1971| pages=16–18| isbn= 0-300-01324-8| series= Yale studies in the history of science and medicine}}</ref> Its causative agent, [[poliovirus]], was identified in 1908 by [[Karl Landsteiner]].<ref name=Paul_1971/> Although major polio [[epidemic]]s were unknown before the 20th century, polio was one of the most dreaded childhood diseases of the 20th century in the United States. Polio epidemics have crippled thousands of people, mostly young children; the disease has caused paralysis and death for much of human history. Polio had existed for thousands of years quietly as an [[endemic (epidemiology)|endemic]] pathogen until the 1880s, when major epidemics began to occur in Europe; soon after, widespread epidemics appeared in the United States.<ref name = Trevelyan/> By 1910, much of the world experienced a dramatic increase in polio cases and frequent epidemics became regular events, primarily in cities during the summer months. These epidemics—which left thousands of children and adults paralyzed—provided the impetus for a "Great Race" towards the development of a [[vaccine]]. The [[polio vaccine]]s developed by [[Jonas Salk]] in 1952 and [[Albert Sabin]] in 1962 are credited with reducing the annual number of polio cases from many hundreds of thousands to around a thousand.<ref name=Aylward_2006>{{cite journal |author=Aylward R |title=Eradicating polio: today's challenges and tomorrow's legacy |journal=Ann Trop Med Parasitol |volume=100 |issue=5–6 |pages=401–13 |year=2006 |pmid=16899145}}</ref> Enhanced [[vaccination]] efforts led by the [[World Health Organization]], UNICEF and Rotary International could result in global eradication of the disease.<ref>{{cite journal |author=Heymann D |title=Global polio eradication initiative | url=http://www.scielosp.org/scielo.php?script=sci_arttext&pid=S0042-96862006000800006&lng=en&nrm=iso&tlng=en |journal=Bull. World Health Organ. |volume=84 |issue=8 |pages=595 |year=2006 |pmid=16917643 |doi=}}</ref>
| | {{SK}} Poliomyelitis; Heine-Medin disease. |
|
| |
|
| == History == | | ==[[Polio overview|Overview]]== |
| {{main|History of poliomyelitis}}
| |
| [[Image:Polio Egyptian Stele.jpg|thumb|left|An Egyptian stele thought to represent a polio victim, 18th Dynasty (1403–1365 BC)]] | |
|
| |
|
| The effects of polio have been known since prehistory; Ancient Egyptian paintings and carvings depict otherwise healthy people with withered limbs, and children walking with canes at a young age.<ref name=Paul_1971/> The first clinical description was provided by the British physician Michael Underwood in 1789, where he refers to polio as "a debility of the lower extremities".<ref name=Underwood_1789>{{cite book | last = Underwood | first = Michael | title = Debility of the lower extremities. ''In:'' A treatise on the diseases <nowiki>[sic]</nowiki> of children, with general directions for the management of infants from the birth (1789) | volume = 2 | publisher = Philadelphia: Printed by T. Dobson, no. 41, South Second-Street | year = 1793 | pages = pp. 254–6 | series = Early American Imprints, 1st series, no. 26291 (filmed); Copyright 2002 by the American Antiquarian Society | url=http://catalog.mwa.org/cgi-bin/Pwebrecon.cgi?v1=1&ti=1,1&Search%5FArg=Underwood%2C%20Michael&Search%5FCode=OPAU&CNT=10&PID=23682&SEQ=20070223225426&SID=1 | format = fee required | accessdate = 2007-02-23 }}</ref> The work of physicians [[Jakob Heine]] in 1840 and Karl Oskar Medin in 1890 led to it being known as ''Heine-Medin disease''.<ref name=Pearce_2005>{{cite journal |author=Pearce J |title=Poliomyelitis (Heine-Medin disease) |journal=J Neurol Neurosurg Psychiatry |volume=76 |issue=1 |pages=128 |year=2005 |url=http://jnnp.bmj.com/cgi/content/full/76/1/128 | format = free registration required | pmid=15608013}}</ref> The disease was later called ''infantile paralysis'', based on its propensity to affect children.
| | ==[[Polio historical perspective|Historical Perspective]]== |
|
| |
|
| Before the 20th century, polio infections were rarely seen in infants before six months of age, most cases occurring in children six months to four years of age.<ref name=Robertson_1993>{{cite web | author = Robertson S | title = Module 6: Poliomyelitis | work = The Immunological Basis for Immunization Series| publisher = World Health Organization. Geneva, Switzerland. | url = http://www.who.int/vaccines-documents/DocsPDF-IBI-e/mod6_e.pdf | format = PDF | date = 1993 | accessdate = 2007-05-08}}</ref> Poorer [[sanitation]] of the time resulted in a constant exposure to the virus, which enhanced a natural [[immunity (medical)|immunity]] within the population. In developed countries during the late 19th and early 20th centuries, improvements were made in community sanitation, including better sewage disposal and clean water supplies. These changes drastically increased the proportion of children and adults at risk of paralytic polio infection, by reducing childhood exposure and immunity to the disease.
| | ==[[Polio classification|Classification]]== |
|
| |
|
| Small localized paralytic polio [[epidemic]]s began to appear in Europe and the United States around 1900.<ref name = Trevelyan>{{cite journal |author=Trevelyan B, Smallman-Raynor M, Cliff A |title=The Spatial Dynamics of Poliomyelitis in the United States: From Epidemic Emergence to Vaccine-Induced Retreat, 1910–1971| url= http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16741562 |journal=Ann Assoc Am Geogr |volume=95 |issue=2 |pages=269–293 |year=2005 |pmid=16741562}}</ref> 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.<ref name=Melnick_1990>{{cite book | author = Melnick JL | title = Poliomyelitis. In: Tropical and Geographical Medicine| edition = 2nd ed. | publisher = McGraw-Hill | year =1990 | pages = p. 558–76 | isbn = 007068328X }}</ref> Accordingly, the rate of paralysis and death due to polio infection also increased during this time.<ref name = Trevelyan/> In the United States, the 1952 polio epidemic became the worst outbreak in the nation's history. Of nearly 58,000 cases reported that year 3,145 died and 21,269 were left with mild to disabling paralysis.<ref name=Zamula>{{cite journal |author= Zamula E|title=A New Challenge for Former Polio Patients | url= http://www.fda.gov/bbs/topics/CONSUMER/CON00006.html |journal= FDA Consumer |volume = 25 |issue = 5 |pages = 21–5 |year=1991}}</ref>
| | ==[[Polio pathophysiology|Pathophysiology]]== |
|
| |
|
| The polio epidemics changed not only the lives of those who survived them, but also affected profound cultural changes; spurring grassroots fund-raising campaigns that would revolutionize medical philanthropy, and giving rise to the modern field of [[Physical therapy|rehabilitation therapy]]. As one of the largest disabled groups in the world polio survivors also helped to advance the modern [[disability rights movement]] through campaigns for the social and civil rights of the [[disabled]]. The World Health Organization estimates that there are 10 to 20 million polio survivors worldwide.<ref name= NewsDesk>{{cite web | title = After Effects of Polio Can Harm Survivors 40 Years Later | publisher = March of Dimes | url = http://www.marchofdimes.com/aboutus/791_1718.asp | date = [[2001-06-01]] | accessdate = 2007-08-07}}</ref> In 1977 there were 254,000 persons living in the United States who had been paralyzed by polio.<ref>{{cite journal | author = Frick NM, Bruno RL | title = Post-polio sequelae: physiological and psychological overview | journal = Rehabilitation literature | volume = 47 | issue = 5–6 | pages = 106–11 | year = 1986 | pmid = 3749588 | doi = | accessdate = 2007-06-04}}</ref> 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.<ref name= NewsDesk/> Many List of polio survivors|notable individuals have survived polio and often credit the prolonged immobility and residual paralysis associated with polio as a driving force in their lives and careers.<ref>{{cite book |author=Richard L. Bruno |title=The Polio Paradox: Understanding and Treating "Post-Polio Syndrome" and Chronic Fatigue |publisher=Warner Books |location=New York |year=2002 |pages= 105-6|isbn=0-446-69069-4 |oclc= |doi=}}</ref>
| | ==Causes== |
| | [[Poliovirus]] |
|
| |
|
| The disease was very well publicized during the polio epidemics of the 1950s, with extensive media coverage of any scientific advancements that might lead to a cure. Thus, the scientists working on polio became some of the most famous of the century. Fifteen scientists and two laymen who made important contributions to the knowledge and treatment of poliomyelitis are honored by the [[Polio Hall of Fame]] at the [[Roosevelt Warm Springs Institute for Rehabilitation]] in Warm Springs, Georgia, USA.
| | ==[[Polio differential diagnosis|Differentiating Polio from other Diseases]]== |
|
| |
|
| ==Cause== | | ==[[Polio epidemiology and demographics|Epidemiology and Demographics]]== |
|
| |
|
| [[Image:Polio EM PHIL 1875 lores.PNG|thumb|left|A [[Transmission electron microscopy|TEM]] [[micrograph]] of poliovirus]]
| | ==[[Polio risk factors|Risk Factors]]== |
| {{main|Poliovirus}}
| |
| Poliomyelitis is caused by infection with a member of the [[genus]] ''[[enterovirus]]'' known as [[poliovirus]] (PV). This group of [[RNA virus]]es prefers to inhabit the [[gastrointestinal tract]].<ref name=Harrison /> PV [[pathogen|infects and causes disease]] in humans alone.<ref name=Sherris /> Its [[Virus#Structure|structure]] is very simple, composed of a single [[sense (molecular biology)|(+) sense]] [[RNA]] [[genome]] enclosed in a protein shell called a [[capsid]].<ref name=Sherris /> In addition to protecting the virus’s genetic material, the capsid proteins enable poliovirus to infect certain types of cells. Three [[serovar|serotype]]s of poliovirus have been identified—poliovirus type 1 (PV1), type 2 (PV2), and type 3 (PV3)—each with a slightly different capsid protein.<ref>{{cite book |author=Katz, Samuel L.; Gershon, Anne A.; Krugman, Saul; Hotez, Peter J. |title=Krugman's infectious diseases of children |publisher=Mosby |location=St. Louis |year=2004 |pages=81–97 |isbn=0-323-01756-8 |oclc= |doi=}}</ref> All three are extremely [[virulence|virulent]] and produce the same disease symptoms.<ref name=Sherris /> PV1 is the most commonly encountered form, and the one most closely associated with paralysis.<ref name= Ohri/>
| |
|
| |
|
| Individuals who are exposed to the virus, either through infection or by [[immunization]] with polio vaccine, develop [[immunity (medical)|immunity]]. In immune individuals, [[IgA]] [[antibodies]] against poliovirus are present in the [[tonsil]]s and gastrointestinal tract and are able to block virus replication; [[IgG]] and [[IgM]] antibodies against PV can prevent the spread of the virus to motor neurons of the [[central nervous system]].<ref name=Kew_2005/> Infection or vaccination with one serotype of poliovirus does not provide immunity against the other serotypes, and full immunity requires exposure to each serotype.<ref name=Kew_2005/>
| | ==[[Polio natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
|
| |
|
| | ==Diagnosis== |
| | [[Polio history and symptoms|History and Symptoms]] | [[Polio physical examination|Physical Examination]] | [[Polio laboratory findings|Laboratory Findings]] |
|
| |
|
| == Classification == | | ==Treatment== |
|
| |
|
| The term ''poliomyelitis'' is used to identify the disease caused by any of the three [[Serovar|serotype]]s of poliovirus. Two basic patterns of polio infection are described: a minor illness which does not involve the [[central nervous system]] (CNS), sometimes called ''abortive poliomyelitis'', and a major illness involving the CNS, which may be paralytic or non-paralytic.<ref>{{cite journal |author=Falconer M, Bollenbach E |title=Late functional loss in nonparalytic polio |journal=American journal of physical medicine & rehabilitation / Association of Academic Physiatrists |volume=79 |issue=1 |pages=19–23 |year=2000 |pmid=10678598}}</ref> In most people with a [[immunocompetent|normal immune system]], a poliovirus infection is asymptomatic. Rarely the infection produces minor symptoms; these may include upper [[respiratory tract]] infection (sore throat and fever), [[gastrointestinal tract|gastrointestinal]] disturbances (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhea), and [[influenza]]-like illnesses.<ref name= PinkBook/>
| | [[Polio medical therapy|Medical Therapy]] | [[Polio prevention|Prevention]] | [[Polio future or investigational therapies|Future or Investigational Therapies]] |
|
| |
|
| The virus enters the central nervous system in about 3% of infections. Most patients with CNS involvement develop non-paralytic [[aseptic meningitis]], with symptoms of headache, neck, back, abdominal and extremity pain, fever, vomiting, [[lethargy]] and irritability.<ref name=Chamberlin_2005 /><ref name=Late>{{cite book | author=Leboeuf C | title=The late effects of Polio: Information For Health Care Providers. | url = http://www.health.qld.gov.au/polio/gp/GP_Manual.pdf| format=PDF | publisher=Commonwealth Department of Community Services and Health |year = 1992 |isbn=1-875412-05-0| accessdate=2007-11-10}}</ref> Approximately 1 in 200 to 1 in 1000 cases progress to [[paralytic]] disease, in which the muscles become weak, floppy and poorly-controlled, and finally completely paralyzed; this condition is known as [[Flaccid paralysis|acute flaccid paralysis]].<ref>Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment.. Philadelphia Davis, 79–101. OCLC 2078290</ref> Depending on the site of paralysis, paralytic poliomyelitis is classified as ''spinal'', ''bulbar'', or ''bulbospinal''. [[Encephalitis]], an infection of the brain tissue itself, can occur in rare cases and is usually restricted to infants. It is characterized by confusion, changes in mental status, headaches, fever, and less commonly [[seizure]]s and [[spastic paralysis]].<ref name= Encephalitis>{{cite book |author=Wood, Lawrence D. H.; Hall, Jesse B.; Schmidt, Gregory D. |title=Principles of Critical Care, Third Edition |publisher=McGraw-Hill Professional |location= |year=2005 |pages=870 |isbn=0-07-141640-4 |oclc= |doi=}}</ref>
| | ==Case Studies== |
| | | [[Polio case study one|Case #1]] |
| == Epidemiology and Demographics ==
| |
| | |
| ===Occurrence===
| |
| | |
| At one time poliovirus infection occurred throughout the world. Transmission of wild poliovirus was interrupted in the United States in 1979, or possibly earlier. A polio eradication program conducted by the Pan American Health Organization led to elimination of polio in the Western Hemisphere in 1991. The Global Polio Eradication Program has dramatically reduced poliovirus transmission throughout the world. In 2005, only 1,948 confirmed cases of polio were reported globally and polio was endemic in six countries.
| |
| | |
| Poliovirus infection typically peaks in the summer months in temperate climates. There is no seasonal pattern in tropical climates.
| |
| | |
| ===Transmission===
| |
| | |
| Person-to-person spread of poliovirus via the fecal-oral route is the most important route of transmission, although the
| |
| oral-oral route may account for some cases.
| |
| | |
| Poliomyelitis is highly contagious and spreads easily from human-to-human contact.<ref name=Kew_2005>{{cite journal |author=Kew O, Sutter R, de Gourville E, Dowdle W, Pallansch M |title=Vaccine-derived polioviruses and the endgame strategy for global polio eradication |journal=Annu Rev Microbiol |volume=59 |issue= |pages=587–635 |year=2005 |pmid=16153180}}</ref> In endemic areas, wild polioviruses can infect virtually the entire human population.<ref name=McGraw>{{cite book |author = Parker SP (ed.) | title = McGraw-Hill Concise Encyclopedia of Science & Technology |publisher=McGraw-Hill |location=New York |year=1998 | isbn=0-07-052659-1| page= 67}}</ref> It is seasonal in temperate climates, with peak transmission occurring in summer and autumn.<ref name=Kew_2005 /> These seasonal differences are far less pronounced in tropical areas.<ref name=McGraw /> The time between first exposure and first symptoms, known as the [[incubation period]], is usually 6 to 20 days, with a maximum range of 3 to 35 days.<ref name=Racaniello>{{cite journal |author=Racaniello V |title=One hundred years of poliovirus pathogenesis |journal=[[Virology (journal)|Virology]] |volume=344 |issue=1 |pages=9–16 |year=2006 |pmid = 16364730}}</ref> Virus particles are excreted in the [[feces]] for several weeks following initial infection.<ref name=Racaniello /> The disease is [[Transmission (medicine)|transmitted]] primarily via the [[fecal-oral route]], by ingesting contaminated food or water. It is occasionally transmitted via the oral-oral route,<ref name= Ohri>{{cite journal |last= Ohri |first=Linda K. |coauthors= Jonathan G. Marquess |year=1999 |title= Polio: Will We Soon Vanquish an Old Enemy? |journal= Drug Benefit Trends |volume= 11 |issue= 6|pages=41–54 |id= |url=http://www.medscape.com/viewarticle/416890 |accessdate= 2007-11-06 }} (Available free on [[Medscape]]; registration required.)</ref> a mode especially visible in areas with good sanitation and hygiene.<ref name=Kew_2005 /> Polio is most infectious between 7–10 days before and 7–10 days after the appearance of symptoms, but transmission is possible as long as the virus remains in the saliva or feces.<ref name= Ohri/>
| |
| | |
| Factors that increase the risk of polio infection or affect the severity of the disease include [[immune deficiency]],<ref>{{cite journal |author=Davis L, Bodian D, Price D, Butler I, Vickers J |title=Chronic progressive poliomyelitis secondary to vaccination of an immunodeficient child |journal=[[New England Journal of Medicine|N Engl J Med]] |volume=297 |issue=5 |pages=241–5 |year=1977 |pmid = 195206}}</ref> [[malnutrition]],<ref>{{cite journal |author=Chandra R |title=Reduced secretory antibody response to live attenuated measles and poliovirus vaccines in malnourished children| url= http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=1131622|journal=[[British Medical Journal|Br Med J]] |volume=2 |issue=5971 |pages=583–5 |year=1975 |pmid=1131622}}</ref> [[tonsillectomy]],<ref>{{cite journal |author=Miller A |title=Incidence of poliomyelitis; the effect of tonsillectomy and other operations on the nose and throat | url= http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12978882 |journal=Calif Med |volume=77 |issue=1 |pages=19–21 |year=1952 |pmid=12978882}}</ref> physical activity immediately following the onset of paralysis,<ref>{{cite journal |author=Horstmann D |title=Acute poliomyelitis relation of physical activity at the time of onset to the course of the disease |journal=[[Journal of the American Medical Association|J Am Med Assoc]] |volume=142 |issue=4 |pages=236–41 |year=1950 |pmid=15400610}}</ref> skeletal muscle injury due to [[intramuscular injection|injection]] of vaccines or therapeutic agents,<ref>{{cite journal |author=Gromeier M, Wimmer E |title=Mechanism of injury-provoked poliomyelitis |url= http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=9573275| journal=J. Virol. |volume=72 |issue=6 |pages=5056–60 |year=1998 |pmid=9573275 |doi=}}</ref> and [[pregnancy]].<ref name= Evans_1960>{{cite journal |author=Evans C |title=Factors influencing the occurrence of illness during naturally acquired poliomyelitis virus infections | url=http://mmbr.asm.org/cgi/reprint/24/4/341.pdf | format = PDF | journal=Bacteriol Rev |volume=24 |issue=4 |pages=341–52 |year=1960 |pmid=13697553}}</ref> Although the virus can cross the [[placenta]] during pregnancy, the fetus does not appear to be affected by either maternal infection or polio vaccination.<ref name=UK>{{cite book |author=Joint Committee on Vaccination and Immunisation (Salisbury A, Ramsay M, Noakes K (eds.) |title = Chapter 26:Poliomyelitis. ''in:'' Immunisation Against Infectious Disease, 2006 | url=http://www.immunisation.nhs.uk/files/GB_26_polio.pdf | format = PDF |publisher=Stationery Office |location=Edinburgh |year=2006 |pages = 313–29 |isbn = 0-11-322528-8}}</ref> Maternal antibodies also 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}}</ref>
| |
| | |
| ===Reservoir===
| |
| | |
| Humans are the only known reservoir of poliovirus, which is transmitted most frequently by persons with inapparent infections. There is no asymptomatic carrier state except in immune deficient persons.
| |
| | |
| ===Secular Trends in the United States===
| |
| | |
| Before the 18th century, polioviruses probably circulated widely. Initial infections with at least one type probably occurred in early infancy, when transplacentally acquired maternal antibodies were high. Exposure throughout life probably provided continual boosting of immunity, and paralytic infections were probably rare. (This view has been recently challenged based on data from lameness studies in developing countries.)
| |
| | |
| In the immediate prevaccine era, improved sanitation allowed less frequent exposure and increased the age of primary infection. Boosting of immunity from natural exposure became more infrequent and the number of susceptible persons accumulated, ultimately resulting in the occurrence of epidemics, with 13,000 to 20,000 paralytic cases reported annually.
| |
| | |
| In the early vaccine era, the incidence dramatically decreased after the introduction of inactivated polio vaccine (IPV) in 1955. The decline continued following oral polio vaccine (OPV) introduction in 1961. In 1960, a total of 2,525 paralytic cases were reported, compared with 61 in 1965.
| |
| | |
| The last cases of paralytic poliomyelitis caused by endemic transmission of wild virus in the United States were in 1979, when an outbreak occurred among the Amish in several Midwest states. The virus was imported from the Netherlands. From 1980 through 1999, a total of 152 confirmed cases of paralytic poliomyelitis were reported, an average of 8 cases per year. Six cases were acquired outside the United States and imported. The last imported case was reported in 1993. Two cases were classified as indeterminant (no poliovirus isolated from samples obtained from the patients, and patients had no history of recent vaccination or direct contact with a vaccine recipient). The remaining 144 (95%) cases were vaccine-associated paralytic polio (VAPP) caused by live oral polio vaccine.
| |
| | |
| In order to eliminate VAPP from the United States, ACIP recommended in 2000 that IPV be used exclusively in the United States. The last case of VAPP acquired in the United States was reported in 1999. In 2005, an unvaccinated U.S. resident was infected with polio vaccine virus in Costa Rica and subsequently developed VAPP. Also in 2005, several asymptomatic infections with a vaccine-derived poliovirus were detected in unvaccinated children in Minnesota. The source of the vaccine virus has not been
| |
| determined, but it appeared to have been circulating among humans for at least 2 years based on genetic changes in the virus. No VAPP has been reported from this virus.
| |
| | |
| [[Image:Polio USA, 1950-2004.jpg|center|frame|Poliomyelitis in the U.S., 1950-2204]]
| |
| {{clr}}
| |
| | |
| [[Image:Polio USA, 1980-2004.jpg|center|frame|Poliomyelitis in the U.S., 1980-2204]]
| |
| {{clr}}
| |
| | |
| == Risk Factors ==
| |
| Poliovirus is highly infectious, with seroconversion rates among susceptible household contacts of children nearly 100%, and
| |
| greater than 90% among susceptible household contacts of adults. Persons infected with poliovirus are most infectious
| |
| from 7 to 10 days before and after the onset of symptoms, but poliovirus may be present in the stool from 3 to 6 weeks.
| |
| | |
| == Pathophysiology & Etiology==
| |
| | |
| {| class = "prettytable" style = "float:right; font-size:90%; margin-left:15px"
| |
| |+'''Outcomes of poliovirus infection'''
| |
| |-
| |
| ! style="background:#efefef;" | Outcome
| |
| ! style="background:#efefef" | Proportion of cases<ref name = PinkBook/>
| |
| |-
| |
| | Asymptomatic
| |
| | align="center" |90–95%
| |
| |-
| |
| | Minor illness
| |
| |align="center" |4–8%
| |
| |-
| |
| |Non-paralytic aseptic<br/> meningitis
| |
| | align="center" |1–2%
| |
| |-
| |
| |Paralytic poliomyelitis
| |
| | align="center" |0.1–0.5%
| |
| |-
| |
| |— Spinal polio
| |
| |align="center" |79% of paralytic cases
| |
| |-
| |
| |— Bulbospinal polio
| |
| |align="center" |19% of paralytic cases
| |
| |-
| |
| |— Bulbar polio
| |
| |align="center" |2% of paralytic cases
| |
| |}
| |
| | |
| ===Etiologic agent===
| |
| | |
| Poliovirus is a member of the enterovirus subgroup, family Picornaviridae. Enteroviruses are transient inhabitants of the gastrointestinal tract, and are stable at acid pH. Picornaviruses are small, ether-insensitive viruses with an RNA genome.
| |
| | |
| There are three poliovirus serotypes (P1, P2, and P3). There is minimal heterotypic immunity between the three serotypes. That is, immunity to one serotype does not produce significant immunity to the other serotypes. The poliovirus is rapidly inactivated by heat, formaldehyde, chlorine, and ultraviolet light.
| |
| | |
| ===Pathogenesis===
| |
| [[Image:Polio spine.png|thumb|left|A blockage of the [[lumbar]] anterior spinal cord [[artery]] due to polio (PV3)]]
| |
| 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. 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. In a small percentage of cases the virus spreads and replicates in other sites such as brown fat, the reticuloendothelial tissues, and muscle. 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. Penetration of the CNS provides no known benefit to the virus, and is quite possibly an "accidental" deviation of a normal gastrointestinal infection. 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.
| |
| | |
| ===Paralytic polio===
| |
| [[Image:Poliovirus Myotonic dystrophic.jpg|right|thumb|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. 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. Other changes associated with paralytic disease occur in the hypothalamus and thalamus. 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.
| |
| | |
| 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. 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. 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.
| |
| | |
| ===Spinal polio===
| |
| [[Image:Polio spinal diagram.jpg|right|thumb|The location of motor neurons in the anterior horn cells of the spinal column.]]
| |
| Spinal polio is the most common form of paralytic poliomyelitis; it results from viral invasion of the motor neurons of the [[Anterior horn (spinal cord)|anterior horn cells]], or the [[anatomical terms of location#Dorsal and ventral|ventral]] (front) [[gray matter]] section in the [[spinal column]], which are responsible for movement of the muscles, including those of the [[torso|trunk]], [[limb (anatomy)|limb]]s and the [[intercostal muscle]]s.<ref name= Henry1>{{cite book | author = Frauenthal HWA, Manning JVV | title = Manual of infantile paralysis, with modern methods of treatment.| publisher = Philadelphia Davis | year = 1914| pages= 79–101 |url= http://books.google.com/books?vid=029ZCFMPZ0giNI1KiG6E&id=piyLQnuT-1YC&printsec=titlepage | oclc= 2078290}}</ref> Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron [[ganglion|ganglia]]. When spinal neurons die, [[Wallerian degeneration]] takes place, leading to weakness of those muscles formerly [[innervate]]d by the now dead neurons.<ref name=ConoJ /> With the destruction of nerve cells, the muscles no longer receive signals from the brain or spinal cord; without nerve stimulation, the muscles [[atrophy]], becoming weak, floppy and poorly controlled, and finally completely paralyzed.<ref name=Henry1 /> Progression to maximum paralysis is rapid (two to four days), and is usually associated with fever and muscle pain.<ref name= ConoJ>{{cite book | author = Cono J, Alexander LN | chapter = Chapter 10, Poliomyelitis. | title = Vaccine Preventable Disease Surveillance Manual | edition = 3rd ed. | pages = p. 10–1 | publisher = Centers for Disease Control and Prevention | year = 2002 | url = http://www.cdc.gov/vaccines/pubs/surv-manual/downloads/chpt10_polio.pdf | format = PDF}}</ref> Deep [[tendon reflex|tendon]] [[reflex]]es are also affected, and are usually absent or diminished; [[sensation]] (the ability to feel) in the paralyzed limbs, however, is not affected.<ref name=ConoJ />
| |
| | |
| The extent of spinal paralysis depends on the region of the cord affected, which may be [[cervical]], [[thoracic]], or [[lumbar]].<ref name=Guide>{{cite book |author= |title=Professional Guide to Diseases (Professional Guide Series) |publisher=Lippincott Williams & Wilkins |location=Hagerstown, MD |year= 2005|pages=243–5 |isbn=1-58255-370-X |oclc= |doi=}}</ref> The virus may affect muscles on both sides of the body, but more often the paralysis is asymmetrical.<ref>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, e-text. ISBN 0-9631172-1-1</ref> Any [[Limb (anatomy)|limb]] or combination of limbs may be affected—one leg, one arm, or both legs and both arms. Paralysis is often more severe [[proximal]]ly (where the limb joins the body) than [[distal]]ly (the [[fingertip]]s and [[toe]]s). <ref>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, e-text. ISBN 0-9631172-1-1</ref>
| |
| | |
| ===Bulbar polio===
| |
| [[Image:Brain bulbar region.jpg|right|thumb|The location and anatomy of the bulbar region (in orange).]]
| |
| Comprising about 2% of cases of paralytic polio, bulbar polio occurs when poliovirus invades and destroys nerves within the [[bulbar]] region of the [[brain stem]].<ref name = PinkBook /> The bulbar region is a [[white matter]] pathway that connects the [[cerebral cortex]] to the brain stem. The destruction of these nerves weakens the muscles supplied by the [[cranial nerve]]s, producing symptoms of [[encephalitis]], and causes difficulty breathing, speaking and swallowing.<ref name=Late /> Critical nerves affected are the [[glossopharyngeal nerve]], which partially controls swallowing and functions in the throat, tongue movement and taste; the [[vagus nerve]], which sends signals to the heart, intestines, and lungs; and the [[accessory nerve]], which controls upper neck movement. Due to the effect on swallowing, secretions of [[mucus]] may build up in the airway causing suffocation. <ref>Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers, 12. ISBN 0-7660-1592-0.</ref> Other signs and symptoms include facial weakness, caused by destruction of the [[trigeminal nerve]] and [[facial nerve]], which innervate the cheeks, [[tear duct]]s, gums, and muscles of the face, among other structures; [[diplopia|double vision]]; difficulty in chewing; and abnormal respiratory rate, depth, and rhythm, which may lead to [[respiratory arrest]]. [[Pulmonary edema]] and [[Shock (medical)|shock]] are also possible, and may be fatal.<ref name=Guide/>
| |
| | |
| ==== Bulbospinal polio ====
| |
| Approximately 19% of all paralytic polio cases have both bulbar and spinal symptoms; this subtype is called ''respiratory polio'' or ''bulbospinal polio''.<ref name= PinkBook /> Here the virus affects the upper part of the [[Cervical vertebrae|cervical spinal cord]] (C3 through C5), and paralysis of the [[Thoracic diaphragm|diaphragm]] occurs. The critical nerves affected are the [[phrenic nerve]], which drives the diaphragm to inflate the [[lungs]], and those that drive the 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 [[medical ventilator|ventilator]]. It can lead to paralysis of the arms and legs and may also affect swallowing and heart functions.<ref name= Hoyt/>
| |
| | |
| == Natural History ==
| |
| Records from antiquity mention crippling diseases compatible with poliomyelitis. Michael Underwood first described a debility of the lower extremities in children that was recognizable as poliomyelitis in England in 1789. The first outbreaks in Europe were reported in the early 19th century, and outbreaks were first reported in the United States in 1843. For the next hundred years, epidemics of polio were reported from developed countries in the Northern Hemisphere each summer and fall. These epidemics became increasingly severe, and the average age of persons affected rose. The increasingly older age of persons with primary infection increased both the disease severity and number of deaths from polio. Polio reached a peak in the United States in 1952, with more than 21,000 paralytic cases. However, following introduction of effective vaccines, polio incidence declined rapidly. The last case of wild-virus polio acquired in the United States was in 1979, and global polio eradication may be achieved within the next decade.
| |
| | |
| ===Polio Eradication===
| |
| | |
| Following the widespread use of poliovirus vaccine in the mid-1950s, the incidence of poliomyelitis declined rapidly
| |
| in many industrialized countries. In the United States, the
| |
| number of cases of paralytic poliomyelitis reported annually
| |
| declined from more than 20,000 cases in 1952 to fewer than
| |
| 100 cases in the mid-1960s. The last documented indigenous
| |
| transmission of wild poliovirus in the United States was
| |
| in 1979.
| |
| | |
| In 1985, the member countries of the Pan American Health
| |
| Organization adopted the goal of eliminating poliomyelitis
| |
| from the Western Hemisphere by 1990. The strategy to
| |
| achieve this goal included increasing vaccination coverage;
| |
| enhancing surveillance for suspected cases (i.e., surveillance
| |
| for acute flaccid paralysis); and using supplemental
| |
| immunization strategies such as national immunization
| |
| days, house-to-house vaccination, and containment activities.
| |
| Since 1991, when the last wild-virus–associated indigenous
| |
| case was reported from Peru, no additional cases of poliomyelitis
| |
| have been confirmed despite intensive surveillance. In
| |
| September 1994, an international commission certified the
| |
| Western Hemisphere to be free of indigenous wild poliovirus.
| |
| The commission based its judgment on detailed reports from
| |
| national certification commissions that had been convened
| |
| in every country in the region.
| |
| | |
| In 1988, the World Health Assembly (the governing body
| |
| of the World Health Organization) adopted the goal of
| |
| global eradication of poliovirus by the year 2000. Although
| |
| this goal was not achieved, substantial progress has been
| |
| made. One type of poliovirus appears to have already been
| |
| eradicated. The last isolation of type 2 virus was in India in
| |
| October 1999.
| |
| | |
| The Americas were declared polio-free in 1994.<ref name=MMWR_1994>{{cite journal| author= | title = International Notes Certification of Poliomyelitis Eradication—the Americas, 1994 | journal = MMWR Morb Mortal Wkly Rep | publisher = Centers for Disease Control and Prevention | volume= 43 | issue= 39 | pages = 720–2 | year=1994 | url = http://www.cdc.gov/mmwr/preview/mmwrhtml/00032760.htm | pmid = 7522302 }}</ref> In 2000 polio was officially eradicated in 36 Western Pacific countries, including China and Australia.<ref name= Pacific>{{cite journal | author = | title = General News. Major Milestone reached in Global Polio Eradication: Western Pacific Region is certified Polio-Free | journal = Health Educ Res | year = 2001 | volume = 16 | issue = 1 | pages = p. 109 | url= http://her.oxfordjournals.org/cgi/reprint/16/1/109.pdf | format = PDF}}</ref><ref name="D'Souza_2002">{{cite journal |author=D'Souza R, Kennett M, Watson C |title=Australia declared polio free |journal=Commun Dis Intell |volume=26 |issue=2 |pages=253–60 |year=2002 |pmid=12206379}}</ref> [[Europe]] was declared polio-free in 2002.<ref name=WHO_Europe_2002>{{cite press release | title = Europe achieves historic milestone as Region is declared polio-free | publisher = European Region of the World Health Organization | date = [[2002-06-21]] | url = http://www.who.int/mediacentre/news/releases/releaseeuro02/en/index.html | accessdate = 2007-11-07 }}</ref> Today, polio remains [[Endemic (epidemiology)|endemic]] in only four countries: Nigeria, India, Pakistan, and Afghanistan.<ref>"Update on vaccine-derived polioviruses" (2006). MMWR Morb Mortal Wkly Rep 55 (40): 1093–7. PMID 17035927</ref>
| |
| | |
| == 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. 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. 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). For each reported case of paralytic polio caused by wild poliovirus, it is estimated that another 200 to 3,000 contagious asymptomatic carriers exist. Therefore, isolation of wild poliovirus constitutes a public health emergency, and appropriate efforts to control the spread of the disease must be initiated immediately.
| |
| | |
| === History and Symptoms ===
| |
| The incubation period for poliomyelitis is commonly 6 to 20
| |
| days with a range of 3 to 35 days.
| |
| | |
| The response to poliovirus infection is highly variable and
| |
| has been categorized on the basis of the severity of clinical
| |
| presentation.
| |
| | |
| Up to 95% of all polio infections are inapparent or
| |
| asymptomatic. Estimates of the ratio of inapparent to
| |
| paralytic illness vary from 50:1 to 1,000:1 (usually 200:1).
| |
| Infected persons without symptoms shed virus in the stool
| |
| and are able to transmit the virus to others.
| |
| | |
| Approximately 4%–8% of polio infections consist of a
| |
| minor, nonspecific illness without clinical or laboratory
| |
| evidence of central nervous system invasion. This clinical
| |
| presentation is known as abortive poliomyelitis, and is
| |
| characterized by complete recovery in less than a week.
| |
| Three syndromes observed with this form of poliovirus
| |
| infection are upper respiratory tract infection (sore throat
| |
| and [[fever]]), gastrointestinal disturbances ([[nausea]], [[vomiting]],
| |
| abdominal pain, [[constipation]] or, rarely, [[diarrhea]]), and
| |
| [[influenza]]-like illness. These syndromes are indistinguishable
| |
| from other viral illnesses.
| |
| | |
| Nonparalytic aseptic [[meningitis]] (symptoms of stiffness of
| |
| the neck, back, and/or legs), usually following several days
| |
| after a prodrome similar to that of minor illness, occurs in
| |
| 1%–2% of polio infections. Increased or abnormal sensations
| |
| can also occur. Typically these symptoms will last from 2 to
| |
| 10 days, followed by complete recovery.
| |
| | |
| Fewer than 1% of all polio infections result in flaccid
| |
| paralysis. Paralytic symptoms generally begin 1 to 10 days
| |
| after prodromal symptoms and progress for 2 to 3 days.
| |
| Generally, no further paralysis occurs after the temperature
| |
| returns to normal. The prodrome may be biphasic, especially
| |
| in children, with initial minor symptoms separated by a
| |
| 1- to 7-day period from more major symptoms. Additional
| |
| prodromal signs and symptoms can include a loss of superficial
| |
| reflexes, initially increased deep tendon reflexes and severe
| |
| muscle aches and spasms in the limbs or back. The illness
| |
| progresses to flaccid paralysis with diminished deep tendon
| |
| reflexes, reaches a plateau without change for days to weeks,
| |
| and is usually asymmetrical. Strength then begins to return.
| |
| Patients do not experience sensory losses or changes in cognition.
| |
| | |
| Many persons with paralytic poliomyelitis recover completely
| |
| and, in most, muscle function returns to some degree.
| |
| Weakness or paralysis still present 12 months after onset is
| |
| usually permanent.
| |
| | |
| Paralytic polio is classified into three types, depending on
| |
| the level of involvement. Spinal polio is most common, and
| |
| during 1969–1979, accounted for 79% of paralytic cases.
| |
| It is characterized by asymmetric paralysis that most often
| |
| involves the legs. Bulbar polio leads to weakness of muscles
| |
| innervated by cranial nerves and accounted for 2% of cases
| |
| during this period. Bulbospinal polio, a combination of
| |
| bulbar and spinal paralysis, accounted for 19% of cases.
| |
| | |
| The death-to-case ratio for paralytic polio is generally 2%–5%
| |
| among children and up to 15%–30% for adults (depending
| |
| on age). It increases to 25%–75% with bulbar involvement.
| |
| | |
| == Laboratory Findings ==
| |
| | |
| ===Viral Isolation===
| |
| | |
| Poliovirus may be recovered from the stool or pharynx of a person with poliomyelitis. Isolation of virus from the cerebrospinal
| |
| fluid (CSF) is diagnostic, but is rarely accomplished.
| |
| If poliovirus is isolated from a person with acute flaccid paralysis, it must be tested further, using oligonucleotide mapping (fingerprinting) or genomic sequencing, to determine if the virus is “wild type” (that is, the virus that causes polio
| |
| disease) or vaccine type (virus that could derive from a vaccine strain).
| |
| | |
| ===Serology===
| |
| | |
| Neutralizing antibodies appear early and may be at high levels by the time the patient is hospitalized; therefore, a fourfold rise in antibody titer may not be demonstrated.
| |
| | |
| ===Cerebrospinal Fluid===
| |
| | |
| In poliovirus infection, the CSF usually contains an increased number of white blood cells (10–200 cells/mm3,
| |
| primarily lymphocytes) and a mildly elevated protein (40–50 mg/100 mL).
| |
| | |
| == Risk Stratification==
| |
| After an interval of 30–40 years, 25%–40% of persons who contracted paralytic poliomyelitis in childhood experience new muscle pain and exacerbation of existing weakness, or develop new weakness or paralysis. This disease entity is referred to as postpolio syndrome. Factors that increase the risk of postpolio syndrome include increasing length of time since acute poliovirus infection, presence of permanent residual impairment after recovery from the acute illness, and female sex. The pathogenesis of postpolio syndrome is thought to involve the failure of oversized motor units created during the recovery process of paralytic poliomyelitis. Postpolio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.
| |
| | |
| == Treatment ==
| |
| [[Image:Womanonsideinlung.jpg|thumb|left|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. Treatment of polio also often requires long-term rehabilitation including physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery.
| |
| | |
| 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.
| |
| | |
| Other historical treatments for polio have included hydrotherapy, electrotherapy and surgical treatments such as tendon lengthening and nerve grafting. 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. Massage, passive motion exercises, and vitamin C were also used to treat polio victims, with varying degrees of success.
| |
| | |
| == Primary Prevention ==
| |
| | |
| === Passive immunization ===
| |
| | |
| In 1950, [[William Hammon]] at the University of Pittsburgh purified the [[gamma globulin]] component of the [[blood plasma]] of polio survivors.<ref name=Hammon_1955>{{cite journal |author=Hammon W |title=Passive immunization against poliomyelitis |journal=Monogr Ser World Health Organ |volume=26 |issue= |pages=357–70 |year = 1955 |pmid=14374581}}</ref> Hammon proposed that the gamma globulin, 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 gamma globulin was shown to be about 80% effective in preventing the development of paralytic poliomyelitis.<ref>{{cite journal |author=Hammon W, Coriell L, Ludwig E, ''et al'' |title=Evaluation of Red Cross gamma globulin as a prophylactic agent for poliomyelitis. 5. Reanalysis of results based on laboratory-confirmed cases |journal=J Am Med Assoc |volume=156 |issue=1 |pages=21–7 |year=1954 |pmid=13183798}}</ref> It was also shown to reduce the severity of the disease in patients that developed polio.<ref name=Hammon_1955 /> The gamma globulin 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.<ref name=Rinaldo>{{cite journal |author=Rinaldo C |title=Passive immunization against poliomyelitis: the Hammon gamma globulin field trials, 1951–1953 |journal=[[American Journal of Public Health|Am J Public Health]] |volume=95 |issue=5 |pages=790–9 |year=2005 |pmid=15855454}}</ref>
| |
| | |
| [[Image:Poliodrops.jpg|thumb|right|A child receives oral polio vaccine]]
| |
| | |
| ===Antibody serum===
| |
| | |
| In 1950 William Hammon at the University of Pittsburgh isolated a serum from the blood of polio survivors. 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. The serum was also shown to reduce the severity of the disease in patients that developed polio. 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.
| |
| | |
| ===Vaccine===
| |
| | |
| [[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 (so-called herd immunity).
| |
| | |
| 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. 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. 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. 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. 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. OPV produces excellent immunity in the intestine, which helps prevent infection with wild virus in areas where the virus is endemic. 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.
| |
| | |
| ==Prognosis==
| |
| | |
| Patients with abortive polio infections recover completely. In those that develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery.<ref name=Neumann/> In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; cells that are not destroyed but lose function temporarily may recover within four to six weeks after onset.<ref name=Neumann>{{cite journal |author=Neumann D |title=Polio: its impact on the people of the United States and the emerging profession of physical therapy |url= http://www.post-polio.org/edu/hpros/Aug04HistPersNeumann.pdf | format = PDF | journal=The Journal of orthopaedic and sports physical therapy |volume=34 |issue=8 |pages=479–92 |year=2004 |pmid=15373011}} Reproduced online with permission by Post-Polio Health International; retrieved on [[2007-11-10]].</ref> Half the patients with spinal polio recover fully, one quarter recover with mild disability and the remaining quarter are left with severe disability.<ref>{{cite book |author=Cuccurullo SJ |title=Physical Medicine and Rehabilitation Board Review |url= http://www.ncbi.nlm.nih.gov/books/bv.fcgi?&rid=physmedrehab.table.8357 | publisher=Demos Medical Publishing | year = 2004 |isbn=1-888799-45-5}}</ref> The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of [[viremia]], and inversely proportional to the degree of [[immunity (medical)|immunity]].<ref>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</ref>. Spinal polio is rarely fatal.<ref>Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers, 12. ISBN 0-7660-1592-0.</ref>
| |
| | |
| [[Image:Polio sequelle.jpg|thumb|A child with a deformity of her right leg due to polio]]
| |
| | |
| Without respiratory support, consequences of poliomyelitis with [[Respiration (physiology)|respiratory]] involvement include [[suffocation]] or [[aspiration pneumonia|pneumonia from aspiration of secretions]].<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 (journal)|Chest]] |volume=121 |issue=2 |pages=321–4 |year=2002 |id=PMID 11834636}}</ref> 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.<ref name= PinkBook /> Bulbar polio often causes death if respiratory support is not provided;<ref name= Hoyt /> with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient.<ref name=PinkBook /><ref>{{cite journal |author=Miller AH, Buck LS |title=Tracheotomy in bulbar poliomyelitis |url= http://www.pubmedcentral.nih.gov/pagerender.fcgi?artid=1520308&pageindex=1#page |journal=California medicine |volume=72 |issue=1 |pages=34–6 |year=1950 |pmid=15398892 |doi=}}</ref> When positive pressure ventilators are available, the mortality can be reduced to 15%.<ref name=Wackers>{{cite paper| author = Wackers, G.| title = Constructivist Medicine| version = PhD-thesis| publisher = Maastricht: Universitaire Pers Maastricht| date = 1994| url = http://www.fdcw.unimaas.nl/personal/WebSitesMWT/Wackers/proefschrift.html#h4| format = [[web]]| accessdate = 2008-01-04 }}</ref>
| |
| | |
| ===Recovery===
| |
| | |
| Many cases of poliomyelitis result in only temporary paralysis.<ref>Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment.. Philadelphia Davis, 79–101. OCLC 2078290</ref> Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months.<ref name=Neumann /> The [[neurophysiology|neurophysiological]] processes involved in recovery following acute paralytic poliomyelitis are quite effective; muscles are able to retain normal strength even if half the original motor neurons have been lost.<ref>{{cite journal |author=Sandberg A, Hansson B, Stålberg E |title=Comparison between concentric needle EMG and macro EMG in patients with a history of polio |journal=Clinical Neurophysiology |volume=110 |issue=11 |pages=1900–8 |year=1999 |pmid=10576485}}</ref> Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.<ref name=Neumann />
| |
| | |
| One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or ''axonal sprouts''.<ref>{{cite journal |author=Cashman NR, Covault J, Wollman RL, Sanes JR |title=Neural cell adhesion molecule in normal, denervated, and myopathic human muscle |journal=Ann. Neurol. |volume=21 |issue=5 |pages=481–9 |year=1987 |pmid=3296947}}</ref> These sprouts can [[reinnervate]] orphaned muscle fibers that have been denervated by acute polio infection,<ref name=Agre>{{cite journal |author=Agre JC, Rodríquez AA, Tafel JA |title=Late effects of polio: critical review of the literature on neuromuscular function |journal=Archives of physical medicine and rehabilitation |volume=72 |issue=11 |pages=923–31 |year=1991 |pmid=1929813}}</ref> restoring the fibers' capacity to contract and improving strength.<ref>{{cite journal |author=Trojan DA, Cashman NR |title=Post-poliomyelitis syndrome |journal=Muscle Nerve |volume=31 |issue=1 |pages=6–19 |year=2005 |pmid=15599928}}</ref> Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units: <ref>Gawne AC, Halstead LS (1995). "Post-polio syndrome: pathophysiology and clinical management". Critical Review in Physical Medicine and Rehabilitation 7: 147–88. Reproduced online with permission by Lincolnshire Post-Polio Library; retrieved on 2007-11-10.</ref> 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 [[muscle hypertrophy|myofiber hypertrophy]]—enlargement of muscle fibers through exercise and activity—and transformation of [[Muscle fiber#Type II|type II muscle fibers]] to [[Muscle fiber#Type I| type I muscle fibers]].<ref name=Agre /><ref name = Grimby_1989>{{cite journal |author=Grimby G, Einarsson G, Hedberg M, Aniansson A |title=Muscle adaptive changes in post-polio subjects |journal=Scandinavian journal of rehabilitation medicine |volume=21 |issue=1 |pages=19–26 |year=1989 |pmid=2711135}}</ref>
| |
| | |
| In addition to these physiological processes, the body possesses a number of compensatory mechanisms to maintain function in the presence of residual paralysis. These include the use of weaker muscles at a higher than usual intensity relative to the [[Muscle contraction#Contractions, by muscle type|muscle's maximal capacity]], enhancing athletic development of previously little-used muscles, and using [[ligament]]s for stability, which enables greater mobility.<ref name = Grimby_1989 />
| |
| | |
| ==Complications==
| |
| | |
| Residual complications of paralytic polio often occur following the initial recovery process. <ref>Leboeuf C (1992). The late effects of Polio: Information For Health Care Providers. (PDF), Commonwealth Department of Community Services and Health. ISBN 1-875412-05-0. Retrieved on 2007-11-10.</ref> 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 develops when the muscles that pull the toes downward are working, but those that pull it upward are not, and the foot naturally tends to drop toward the ground. If the problem is left untreated, the [[Achilles tendon]]s 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.<ref name= Aftereffects>{{cite web | author = Sanofi Pasteur | title = Poliomyelitis virus (picornavirus, enterovirus), after-effects of the polio, paralysis, deformations | work = Polio Eradication | url = http://www.polio.info/polio-eradication/front/index.jsp?siteCode=POLIO&lang=EN&codeRubrique=14 | accessdate = 2007-07-31}}</ref> 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]]).<ref name= Aftereffects /> [[Osteoporosis]] and increased likelihood of [[bone fracture]]s may occur. Extended use of braces or wheelchairs may cause compression [[neuropathy]], as well as a loss of proper function of the [[vein]]s in the legs, due to pooling of blood in paralyzed lower limbs.<ref name=MayoComps>{{cite web |author = Mayo Clinic Staff | date=[[2005-05-19]] | url = http://www.mayoclinic.com/health/polio/DS00572/DSECTION=7 | title = Polio: Complications| publisher = Mayo Foundation for Medical Education and Research (MFMER)| accessdate=2007-02-26}}</ref><ref name= Hoyt>{{cite book |author=Hoyt, William Graves; Miller, Neil; Walsh, Frank |title=Walsh and Hoyt's clinical neuro-ophthalmology |publisher=Lippincott Williams & Wilkins |location=Hagerstown, MD |year=2005 |pages=3264–65 |isbn=0-7817-4814-3 |oclc= |doi=}}</ref> Complications from prolonged immobility involving the [[lungs]], [[kidney]]s and [[heart]] include [[pulmonary edema]], [[aspiration pneumonia]], [[urinary tract infection]]s, [[kidney stone]]s, [[paralytic ileus]], [[myocarditis]] and [[cor pulmonale]].<ref name=MayoComps /><ref name= Hoyt/>
| |
| | |
| === Post-polio syndrome ===
| |
| {{main|Post-polio syndrome}}
| |
| Around a quarter of individuals who survive paralytic polio in childhood develop additional symptoms decades after recovering from the acute infection, notably muscle weakness, extreme fatigue, or paralysis. This condition is known 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 |pmid = 15599928}}</ref> The symptoms of PPS are thought to involve a failure of the over-sized motor units created during recovery from paralytic disease.<ref name=Ramlow_1992>{{cite journal |author=Ramlow J, Alexander M, LaPorte R, Kaufmann C, Kuller L |title=Epidemiology of the post-polio syndrome |journal=Am. J. Epidemiol. |volume=136 |issue=7 |pages=769–86 |year=1992 |pmid=1442743}}</ref><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 | format = PDF |journal=Ann Acad Med Singapore |volume=34 |issue=7 |pages=447–9 |year=2005 |pmid = 16123820}}</ref> Factors that increase the risk of PPS include the length of time since acute poliovirus infection, the presence of permanent residual impairment after recovery from the acute illness, and both 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=PinkBook />
| |
| | |
| ==References==
| |
| {{Reflist|2}}
| |
| | |
| | |
| == Further reading ==
| |
| <div class="references-small" style="-moz-column-count:2; column-count:2;">
| |
| *{{cite book | author = Frauenthal HWA, Manning JVV | title = Manual of infantile paralysis, with modern methods of treatment: Pathology. | publisher = Davis | location = Philadelphia| year = 1914| url= http://books.google.com/books?vid=029ZCFMPZ0giNI1KiG6E&id=piyLQnuT-1YC&printsec=titlepage | pages = pp. 79–101 | oclc = 2078290}} (Full text available from Google Books, with hundreds of pictures.)
| |
| * {{cite book |author = Huckstep RL |title=Poliomyelitis: a guide for developing countries - including appliances and rehabilitation for the disabled |url= http://www.worldortho.com/index.php?option=com_content&task=view&id=522&Itemid=267 |publisher=Churchill Livingstone |location=Edinburgh |year=1975 |pages= |isbn=0443013128 |oclc= |doi=}} (A look at the modern polio patient and polio treatment techniques.)
| |
| * http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/polio.pdf
| |
| * http://en.wikipedia.org/wiki/Poliomyelitis
| |
| * {{dmoz|Health/Conditions_and_Diseases/Infectious_Diseases/Viral/Poliomyelitis/}}
| |
| * [http://www.scq.ubc.ca/?p=45 Polio: A Virus' Struggle] – an amusing yet educational graphic novella from the ''Science Creative Quarterly'' (co-published by the University of British Columbia, in PDF format).
| |
| * [http://www.paho.org/English/DPI/Number2_article8.htm Fermín: Making Polio History] An article about Luis Fermín Tenorio Cortez, the last case of polio reported in the Americas.
| |
| * [http://www.johnprestwich.btinternet.co.uk/40-years-a-layabout.htm A UK Polio survivor] – An account of John Prestwich, who lived 50 years in an iron lung.
| |
| </div>
| |
| | |
| == Acknowledgements ==
| |
| The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.
| |
| | |
| ----
| |
|
| |
|
| {{Viral diseases}} | | {{Viral diseases}} |
|
| |
| {{SIB}}
| |
|
| |
|
| [[ar:شلل أطفال]] | | [[ar:شلل أطفال]] |
| Line 405: |
Line 68: |
| [[uk:Поліомієліт]] | | [[uk:Поліомієліт]] |
| [[zh:脊髓灰質炎]] | | [[zh:脊髓灰質炎]] |
| | | [[pl:Choroba Heinego-Medina]] |
| {{WH}} | | {{WH}} |
| {{WS}} | | {{WS}} |
| [[pl:Choroba Heinego-Medina]]
| |
|
| |
|
| [[Category:Disease]] | | [[Category:Disease]] |
| [[Category:Infectious disease]]
| |
| [[Category:Overview complete]]
| |