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==Overview==
==Overview==
Poliovirus enters the body orally, and infects cells of the [[gastrointestinal]] tract, from the mouth to the [[ileum]] and [[mesenterium]]. After [[replication]], the virus may either be secreted in feces, contributing to the [[transmission]] of the disease, or reach the [[bloodstream]], and be transported to other cells of the body, such as those of the [[reticuloendothelial system]].  Although the precise mechanism of infection of [[CNS]] is not fully understood, the most supported hypothesis is the retrograde axonal transport, according to which the virus enters the [[axoplasm]] of a motor neuron, travels to its cell body, where it replicates, and leads to neuron death.  In the [[CNS]], [[poliovirus]] shows [[tropism]] for cells of the [[anterior horn]] of the [[spinal cord]], [[hypothalamus]], [[thalamus]], [[cerebellar vermis]], [[vestibular nuclei|vestibular]] and deep cerebral nuclei.  Death of the [[motor neuron]] is responsible for the [[paralysis]] often seen in poliomyelitis.  
The word poliomyelitis is derived from the Greek, where polio means grey and the work myelin means the marrow referring to the spinal cord. Polio myelitis primarily affects the spinal cord in turn leading to the manifestations. Poliovirus is a member of the enterovirus subgroup, family Picornaviridae. Poliovirus is primarily spread from the stools of the infected person and enters the body orally through contaminated water or food (feco-oral transmission), infecting the cells of the gastrointestinal tract, from the mouth to the ileum and mesentrium.   After [[replication]], the virus may either be secreted in feces, contributing to the [[transmission]] of the disease, or reach the [[bloodstream]], and be transported to other cells of the body, such as those of the [[reticuloendothelial system]].  Although the precise mechanism of infection of [[CNS]] is not fully understood, the most supported hypothesis is the retrograde axonal transport, according to which the virus enters the [[axoplasm]] of a motor neuron, travels to its cell body, where it replicates, and leads to neuron death.  In the [[CNS]], [[poliovirus]] shows [[tropism]] for cells of the [[anterior horn]] of the [[spinal cord]], [[hypothalamus]], [[thalamus]], [[cerebellar vermis]], [[vestibular nuclei|vestibular]] and deep cerebral nuclei.  Death of the [[motor neuron]] is responsible for the [[paralysis]] often seen in poliomyelitis.
==Case Definitions of Polio==
CDC has given a case definition of paralytic poliomyelitis for surveillance purposes
*“Acute onset of flaccid paralysis of one or more limbs with decreased or absent tendon reflex in the affected limbs, without other apparent causes, and without sensory or cognitive loss.”.<ref name="urlPoliomyelitis, Paralytic | 2010 Case Definition">{{cite web |url=https://wwwn.cdc.gov/nndss/conditions/poliomyelitis-paralytic/case-definition/2010/#:~:text=Confirmed-,Acute%20onset%20of%20a%20flaccid%20paralysis%20of%20one%20or%20more,onset%20of%20initial%20symptoms%3B%20OR |title=Poliomyelitis, Paralytic &#124; 2010 Case Definition |format= |work= |accessdate=}}</ref>
*A confirmed case requires persistence of neurological deficit for 60 days after the onset of the initial symptoms, fatal illness, or unknown follow-up status.<ref name="urlPoliomyelitis, Paralytic | 2010 Case Definition">{{cite web |url=https://wwwn.cdc.gov/nndss/conditions/poliomyelitis-paralytic/case-definition/2010/#:~:text=Confirmed-,Acute%20onset%20of%20a%20flaccid%20paralysis%20of%20one%20or%20more,onset%20of%20initial%20symptoms%3B%20OR |title=Poliomyelitis, Paralytic &#124; 2010 Case Definition |format= |work= |accessdate=}}</ref>
WHO case definition for a suspected case of poliomyelitis is:
*A suspected case is defined as a child under 15 years of age presenting with acute flaccid paralysis (AFP), or as any person at any age with paralytic illness if poliomyelitis is suspected<ref name="urlwww.who.int">{{cite web |url=https://www.who.int/ihr/Case_Definitions.pdf |title=www.who.int |format= |work= |accessdate=}}</ref>


==Pathogenesis==
 
Poliovirus enters the body through the mouth and infects nearby [[cell]]s, such as those of the mouth, nose, and throat.  The most common course of [[infection]] is the replication of [[poliovirus]] in cells of the [[gastrointestinal]] tract, followed by viral shedding in feces.  The specific cells of the [[gastrointestinal]] tract, where poliovirus replicates, are not known, however, the virus was successfully isolated from [[lymphatic]] cells of the [[GI tract]], including:<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>  
==Pathophysiology==
===Transmission===
Poliovirus is mostly transmitted through the [[fecal-oral route]], by ingestion of contaminated food or water. In some instances, the oral-oral route may be relevant through [[pharyngeal]] secretions. <ref name="pmid20978089">{{cite journal| author=Nathanson N, Kew OM| title=From emergence to eradication: the epidemiology of poliomyelitis deconstructed. | journal=Am J Epidemiol | year= 2010 | volume= 172 | issue= 11 | pages= 1213-29 | pmid=20978089 | doi=10.1093/aje/kwq320 | pmc=PMC2991634 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20978089  }} </ref><ref name=CDC>{{cite web | title = Poliomyelitis | url = http://www.cdc.gov/vaccines/pubs/pinkbook/polio.html#epi }}</ref> Poliomyelitis is highly contagious and spreads easily through 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>  Viral particles are excreted in the [[feces]] for several weeks, after initial infection. 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]] can 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>
 
Poliovirus enters the body orally and most often infects nearby [[cell]]s, such as those of the mouth, nose, and throat. Poliovirus commonly targets specific tissues in the CNS such as:<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>
* [[Anterior horn]] cells of the [[spinal cord]] (in severe cases of the disease, the intermediate, intermediolateral and posterior gray columns may also be affected)
* [[Hypothalamus]]
* [[Thalamus]]
* [[Vestibular nuclei]]
* Deep cerebral nuclei
* [[Reticular formation]]
* [[Cerebellar vermis]]
===Pathogenesis===
It infects cells by binding to an immunoglobulin-like receptor known as CD155 on the cell surface.  The most common course of [[infection]] is the replication of [[poliovirus]] in cells of the [[gastrointestinal]] tract, followed by viral shedding in feces.  The specific cells of the [[gastrointestinal]] tract, where poliovirus replicates, are not known, however, the virus was successfully isolated from [[lymphatic]] cells of the [[GI tract]], including:<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>. Viral particles have been seen in:
* [[tonsils|Tonsillar]] cells
* [[tonsils|Tonsillar]] cells
* [[Peyer's patches]] of the [[ileum]]
* [[Peyer's patches]] of the [[ileum]]
* [[Lymph nodes]] of the [[mesenterium]]
* [[Lymph nodes]] of the [[mesenterium]]


The virus enters the [[bloodstream]] and migrates to the [[reticuloendothelial]] cells across the body.  [[Poliovirus]] is able to reach the [[central nervous system]] in a small fraction of the [[symptomatic]] patients.<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>  Not only isn't the disease a phase of the [[viral replication]] cycle, as it does not benefit the virus in any way.  The molecular mechanism behind the disease is not known.<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>
The virus enters the [[bloodstream]] and migrates to the [[reticuloendothelial]] cells across the body.  [[Poliovirus]] is able to reach the [[central nervous system]] in a small fraction of the [[symptomatic]] patients.<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>  Not only is the disease not a phase of the [[viral replication]] cycle, it also does not benefit the virus in any way.  The molecular mechanism behind this disease process is not known.<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>
 
[[Poliovirus]] replicates inside [[monocytes]], which allows for secondary hematogenous spread.  The pathological mechanism responsible for the clinical manifestations of CNS poliomyelitis is characterized by selective destruction of [[motor neurons]].  Depending of the involved site, motor neuron loss may lead to focal or generalized symptoms. Most commonly observed signs and symptoms include asymmetric limb paralysis in spinal polio and respiratory disturbance with cranial nerve defects in bulbar polio.
 
Although the mechanism of viral spread to the [[CNS]] is not fully understood, two main hypotheses have been proposed:<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>
# [[Poliovirus]] diffuses directly through the [[blood brain barrier]] from the [[bloodstream]] to the [[CNS]], regardless of cellular receptors.
# [[Poliovirus]] is transported from the peripheral [[muscles]] to the [[brain]] and [[spinal cord]], through retrograde axonal transport.  This hypothesis has been experimentally proven in mice, after [[CD155]] transformation.
Several recent findings supporting the retrograde axonal transport hypothesis have been reported:<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>.
** Detection of axonal poliovirus in patients with poliomyelitis.
** Interruption of a nerve connection between a site of multiple intramuscular injections and the spinal cord in mice with poliovirus viremia led to improved clinical course of infection. This supports the ''provocation poliomyelitis'' hypothesis which states that muscle injury in patients with poliovirus viremia triggers retrograde axonal transport of the virus. This phenomenon is seen in children receiving intramuscular vaccines in areas endemic for poliovirus.<ref name="pmid9573275">{{cite journal| author=Gromeier M, Wimmer E| title=Mechanism of injury-provoked poliomyelitis. | journal=J Virol | year= 1998 | volume= 72 | issue= 6 | pages= 5056-60 | pmid=9573275 | doi= | pmc=PMC110068 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9573275  }} </ref>
** In mice [[genetically]] transformed to express [[CD155]], injection of [[poliovirus]] in the left limb led to viral detection in the left anterior horn of the [[spinal cord]] only.  When the [[sciatic nerve]] was promptly sectioned after injection of the virus, the risk of paralysis in the injected limb was greatly reduced.
** [[Bulbar poliomyelitis]] following [[tonsillectomy]] may possibly be explained by the previously described mechanisms.
** Overexpression of [[CD155]] in the [[muscle fiber]]s of patients with paralytic poliomyelitis. To note, [[CD155]] directly interacts with the [[dynein]] retrograde complex through Tctex-1.<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>
<br>
The main explanation for increased susceptibility to retrograde axonal transport of poliovirus in areas of injured muscle has been explained. In a neuronal [[synapse]], the rate of [[endocytosis]] is related to the level of [[neuron]] activity.  Correspondingly, for a [[motor neuron]], the level of [[neuron]] activity and rate of endocytosis at the [[neuromuscular junction]] is related to the extent of [[muscle]] contraction.  This explains the connection between extreme exercise or muscle injury and development of poliomyelitis in patients with [[viremia]].  Also, since most of [[CD155]] receptors are transported back to the [[cell body]], the virus is carried along, supporting the retrograde transport hypothesis.<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>
 


[[Poliovirus]] replicates inside [[monocytes]], which allows it to spread from the initially infected cells to the [[bloodstream]].  The [[pathogenesis]] behind the clinical manifestations of [[CNS infection]] results from the selective destruction of [[motor neurons]].  [[Motor neuron]] attack may lead to symptoms such as [[paralysis]], [[respiratory arrest]] and death.  Although the mechanism of viral spread to the [[CNS]] is not fully understood, two theories persist:<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840 }} </ref>
Once at the [[cell body]] of the [[neuron]], the change from [[axoplasm]] to [[cytoplasm]] is thought to interfere with the stability of the viral coat, leading to the exposure of the viral [[RNA]].  [[Viral replication]] interferes with [[neuron]] stability, killing the [[motor neuron]].  Death of a [[motor neuron]] paralyzes the respective [[muscle fiber]].
# [[Poliovirus]] diffuses directly through the [[blood brain barrier]], from the [[bloodstream]] to the [[CNS]], regardless of cellular receptors.
# [[Poliovirus]] is transported from the [[muscle]] to the [[brain]] and [[spinal cord]], through retrograde axonal transport.  This hypothesis has been experimentally proven in mice, after [[CD155]] transformation.


===Retrograde Axonal Transport Hypothesis===
===Course of Disease===
Recent discoveries supporting the second hypothesis have been reported:<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840 }} </ref>
''The pre- paralytic or non-paralytic course of the disease'' includes:-<ref name="pmidhttps://dx.doi.org/10.1136/pgmj.72.853.641">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=https://dx.doi.org/10.1136/pgmj.72.853.641 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10 }} </ref>
* Axonal presence of poliovirus, in patients with poliomyelitis, has been reported - This explains the "provocation poliomyelitis" phenomenon, in which muscle trauma, in the presence of [[viremia]], was associated with an higher risk of developing poliomyelitis.
*Headache
* In mice, [[genetically]] transformed to express [[CD155]], after injection of [[poliovirus]] in the left limb, [[viral replication]] was only noted in the left anterior horn of the [[spinal cord]].  [[Viral replication]] occurred 33 hours before onset of [[paralysis]].  When the [[sciatic nerve]] was promptly sectioned after injection of the virus, the predisposition of the implicated leg to be paralyzed was eliminated.
*Pharyngitis
* In the same mice, if [[poliovirus]] was injected [[intravenously]], poliomyelitis would manifest first in the [[limb]] that had been injured by multiple empty needle injections.  This leads to the idea that injured [[muscle]] opens a way for the [[virus]] to penetrate the terminal of the [[presynaptic]] [[motor neuron]].
*Myalgia
* [[Bulbar poliomyelitis]] following [[tonsillectomy]] may possibly be explained by the previously described mechanisms.
*Anorexia
* There is over expression of [[CD155]] on the [[muscle fiber]]s of patients with paralytic poliomyelitis.
*Nausea
* [[CD155]], directly interacts with the [[dynein]] retrograde complex, through Tctex-1.
*Vomiting
In non- paralytic illness, the symptoms go away within one or two weeks.


In a neuronal [[synapse]], the rate of [[endocytosis]] is related to the level of [[neuron]] activity.  For the [[motor neuron]], the level of [[neuron]] activity at the [[neuromuscular junction]] is associated with [[muscle]] contraction, therefore, increased [[muscle]] activity is related to increased rate of [[endocytosis]].  This explains the connection between extreme exercise activity and development of poliomyelitis in patients with [[viremia]], since there is greater probability of viral uptake.  Also, since most of [[CD155]] receptors are transported back to the [[cell body]], the virus is carried along, supporting the retrograde transport hypothesis.<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840 }} </ref>
''Paralytic Poliomyelitis'': <ref name="pmidhttps://dx.doi.org/10.1136/pgmj.72.853.641">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=https://dx.doi.org/10.1136/pgmj.72.853.641 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10 }} </ref>
After the meningitis phase, the spinal form of poliomyelitis occurs which consists of:
*Muscle pain
*Muscle spasms
*Fasciculations


Once at the [[cell body]] of the [[neuron]], the change from [[axoplasm]] to [[cytoplasm]] is thought to interfere with the stability of the viral coat, leading to the exposure of the viral [[RNA]]. [[Viral replication]] interferes with [[neuron]] stability, killing the [[motor neuron]].  Death of the [[motor neuron]] paralyzes the respective [[muscle fiber]]. Spread of the [[virus]] to nearby [[neuron]]s will be responsible for the death of these cells.
Weakness is asymmetrical affecting the lower limbs more than the upper limbs. The weakness usually becomes maximum within 48hrs, especially in children. In some, the weakness may further increase after a period of stability but no further weakness occurs once the fever subsides. Muscle tone is flaccid and the reflexes are absent along with paraesthesia. Any cranial nerve may be involved but most frequently leads to dysphasia, dysphasia, and respiratory failure<ref name="pmid13636523">{{cite journal| author=PLUM F, SWANSON AG| title=Central neurogenic hyperventilation in man. | journal=AMA Arch Neurol Psychiatry | year= 1959 | volume= 81 | issue= 5 | pages= 535-49 | pmid=13636523 | doi=10.1001/archneurpsyc.1959.02340170001001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13636523 }} </ref>. Vasomotor involvement such as hypertension, hypotension, and circulatory collapse lead to mortality in patients.


In the [[CNS]], poliovirus shows [[tropism]] for certain pathways and tissues:<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840  }} </ref>
* [[Anterior horn]] cells of the [[spinal cord]] (in severe cases of the disease, the intermediate, intermediolateral and posterior gray columns may also be affected)
* [[Hypothalamus]]
* [[Thalamus]]
* [[Vestibular nuclei]]
* Deep cerebral nuclei
* [[Reticular formation]]
* [[Cerebellar vermis]]


Lesion distribution in paralytic and non-paralytic cases is the same. Additionally, [[inflammation]] can be detected in any affected area of the [[CNS]], supporting the idea that in order to produce clinical manifestations, severe [[neuron]] damage must occur.  The different clinical forms of [[poliomyelitis]] will depend on the most affected area of the [[CNS]].  Individual host factors and the neuropathogenicity of the [[virus]] influence the severity of the lesions.<ref name="pmid15885840">{{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 | year= 2005 | volume= 111 | issue= 2 | pages= 175-93 | pmid=15885840 | doi=10.1016/j.virusres.2005.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15885840 }} </ref>
''Bulbar form'':<ref name="pmid13174358">{{cite journal| author=ANDERSON GW, RONDEAU JL| title=Absence of tonsils as a factor in the development of bulbar poliomyelitis. | journal=J Am Med Assoc | year= 1954 | volume= 155 | issue= 13 | pages= 1123-30 | pmid=13174358 | doi=10.1001/jama.1954.03690310001001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13174358 }} </ref>
Seen more in children in which tonsils and adenoids have been removed.


==Transmission==
==Vaccine mediated polio infection==
Poliovirus is mostly transmitted through the [[fecal-oral route]], by ingestion of contaminated food or water, and through [[pharyngeal]] secretions. In some instances, the oral-oral route may account for some cases. <ref name="pmid20978089">{{cite journal| author=Nathanson N, Kew OM| title=From emergence to eradication: the epidemiology of poliomyelitis deconstructed. | journal=Am J Epidemiol | year= 2010 | volume= 172 | issue= 11 | pages= 1213-29 | pmid=20978089 | doi=10.1093/aje/kwq320 | pmc=PMC2991634 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20978089  }} </ref><ref name=CDC>{{cite web | title = Poliomyelitis | url = http://www.cdc.gov/vaccines/pubs/pinkbook/polio.html#epi }}</ref>
[[Polio vaccine|Oral polio vaccine (OPV)]] is one of the safest and most effective vaccination programs that prevented millions of cases of [[polio]]  not only through direct [[immunization]] but also through [[herd immunity]]. In rare occasions, the [[vaccine]] is associated with [[Polio|paralytic polio]].  
There are two subtypes of paralytic polio related to [[Polio vaccine|OPV]] vaccine: vaccine associated paralytic polio and vaccine derived paralytic polio.


Poliomyelitis is highly contagious and spreads easily through 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> Viral particles are excreted in the [[feces]] for several weeks, following initial infection.
===Vaccine associated paralytic polio===
*Vaccine associated paralytic polio (VAPP) occurs when the [[Attenuated virus|attenuated strain]] used in the [[vaccine]] reverts inside the intestine into more [[virulent]] form.<ref name="urlwww.who.int">{{cite web |url=http://www.who.int/immunization/diseases/poliomyelitis/endgame_objective2/oral_polio_vaccine/VAPPandcVDPVFactSheet-Feb2015.pdf |title=www.who.int |format= |work= |accessdate=}}</ref><ref name="pmid3029445">{{cite journal |vauthors=Nkowane BM, Wassilak SG, Orenstein WA, Bart KJ, Schonberger LB, Hinman AR, Kew OM |title=Vaccine-associated paralytic poliomyelitis. United States: 1973 through 1984 |journal=JAMA |volume=257 |issue=10 |pages=1335–40 |year=1987 |pmid=3029445 |doi= |url=}}</ref><ref name="pmid7476613">{{cite journal |vauthors=Sullivan AA, Boyle RS, Whitby RM |title=Vaccine-associated paralytic poliomyelitis |journal=Med. J. Aust. |volume=163 |issue=8 |pages=423–4 |year=1995 |pmid=7476613 |doi= |url=}}</ref>
*The more virulent form is capable of causing the disease only in the vaccinated child or a close susceptible contact. Therfore, no outbreaks are associated with VAPP.
*The [[prevalence]] of (VAPP) is 1 in 2.7 million doses of the vaccine.
*In developed countries, the risk of VAPP is increased with the first dose of the vaccine while in developed countries, It’s increased with subsequent doses.


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]] can 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>
===Vaccine derived paralytic polio===
*Vaccine derived paralytic polio (VDPP) is caused by very rare [[mutation]] of the original strain of polio in the vaccine.<ref name="urlwww.who.int">{{cite web |url=http://www.who.int/immunization/diseases/poliomyelitis/endgame_objective2/oral_polio_vaccine/VAPPandcVDPVFactSheet-Feb2015.pdf |title=www.who.int |format= |work= |accessdate=}}</ref><ref name="pmid14673763">{{cite journal |vauthors=Khetsuriani N, Prevots DR, Quick L, Elder ME, Pallansch M, Kew O, Sutter RW |title=Persistence of vaccine-derived polioviruses among immunodeficient persons with vaccine-associated paralytic poliomyelitis |journal=J. Infect. Dis. |volume=188 |issue=12 |pages=1845–52 |year=2003 |pmid=14673763 |doi=10.1086/379791 |url=}}</ref>
*VDPP has the ability to cause the disease in any non immune person whether the vaccinated person or a contact, therefore it has the ability to cause [[Outbreak|outbreaks]] or even [[epidemics]] especially in communities that are not properly covered with the [[vaccination]] program.
*When it causes [[outbreaks]], VDPP is called circulating vaccine derived paralytic polio (cVDPP).
*In the last 10 years, 24 VDPP reported [[outbreaks]] happened in 21 countries causing 750 cases of [[Polio|paralytic polio.]]
*The management of VDPP is conducting extensive vaccination campaigns in the affected community aiming for vaccinating every child and thus preventing the spread of the [[infection]].


==Gallery==
==Microscopic Pathology Images==
<gallery>
<gallery>
Image:Poliomyelitis1.png|A photomicrograph of skeletal muscle tissue revealing myotonic dystrophic changes as a result of Polio Type III.<SMALL><SMALL>''[http://phil.cdc.gov/phil/  Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.]''<ref name="PHIL">{{Cite web | title = Public Health Image Library (PHIL), Centers for Disease Control and Prevention | url = http://phil.cdc.gov/phil/}}</ref></SMALL></SMALL>
Image:Poliomyelitis1.png|A photomicrograph of skeletal muscle tissue revealing myotonic dystrophic changes as a result of Polio Type III.<SMALL><SMALL>''[http://phil.cdc.gov/phil/  Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.]''<ref name="PHIL">{{Cite web | title = Public Health Image Library (PHIL), Centers for Disease Control and Prevention | url = http://phil.cdc.gov/phil/}}</ref></SMALL></SMALL>
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Image:Polio9.jpg|A photomicrograph of the cervical spinal cord in the region of the anterior horn revealing Polio Type III degenerative changes.<SMALL><SMALL>''[http://phil.cdc.gov/phil/  Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.]''<ref name="PHIL">{{Cite web | title = Public Health Image Library (PHIL), Centers for Disease Control and Prevention | url = http://phil.cdc.gov/phil/}}</ref></SMALL></SMALL>
Image:Polio9.jpg|A photomicrograph of the cervical spinal cord in the region of the anterior horn revealing Polio Type III degenerative changes.<SMALL><SMALL>''[http://phil.cdc.gov/phil/  Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.]''<ref name="PHIL">{{Cite web | title = Public Health Image Library (PHIL), Centers for Disease Control and Prevention | url = http://phil.cdc.gov/phil/}}</ref></SMALL></SMALL>


Image:Polio10.jpg|Under a low magnification of 40X, this photomicrograph of a brain tissue specimen, specifically from the pontine region (pons), revealed histopathologic changes in a confirmed polio, or poliomyelitis patient. This tissue section was extracted from the pons at the level of the cranial nerve VI (CN VI) nucleus, which is also known as the abducens nerve.<SMALL><SMALL>''[http://phil.cdc.gov/phil/  Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.]''<ref name="PHIL">{{Cite web | title = Public Health Image Library (PHIL), Centers for Disease Control and Prevention | url = http://phil.cdc.gov/phil/}}</ref></SMALL></SMALL>
Image:Polio10.jpg|Under a low magnification, this photomicrograph of pontine tissue at the level of abducens nucleus reveals histopathologic changes in a poliomyelitis patient.<SMALL><SMALL>''[http://phil.cdc.gov/phil/  Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.]''<ref name="PHIL">{{Cite web | title = Public Health Image Library (PHIL), Centers for Disease Control and Prevention | url = http://phil.cdc.gov/phil/}}</ref></SMALL></SMALL>


Image:Polio11.jpg|Photomicrograph of the Cervical Spinal Cord Affected by Polio Type III Virus<SMALL><SMALL>''[http://phil.cdc.gov/phil/  Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.]''<ref name="PHIL">{{Cite web | title = Public Health Image Library (PHIL), Centers for Disease Control and Prevention | url = http://phil.cdc.gov/phil/}}</ref></SMALL></SMALL>
Image:Polio11.jpg|Photomicrograph of the Cervical Spinal Cord Affected by Polio Type III Virus<SMALL><SMALL>''[http://phil.cdc.gov/phil/  Adapted from Public Health Image Library (PHIL), Centers for Disease Control and Prevention.]''<ref name="PHIL">{{Cite web | title = Public Health Image Library (PHIL), Centers for Disease Control and Prevention | url = http://phil.cdc.gov/phil/}}</ref></SMALL></SMALL>
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==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
[[Category:Primary care]]
[[Category:Disease]]
[[Category:Infectious disease]]
{{WH}}
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{{WS}}
{{WS}}
[[Category:Disease]]

Latest revision as of 01:33, 16 October 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]Gurmandeep Singh Sandhu,M.B.B.S.[3]

Overview

The word poliomyelitis is derived from the Greek, where polio means grey and the work myelin means the marrow referring to the spinal cord. Polio myelitis primarily affects the spinal cord in turn leading to the manifestations. Poliovirus is a member of the enterovirus subgroup, family Picornaviridae. Poliovirus is primarily spread from the stools of the infected person and enters the body orally through contaminated water or food (feco-oral transmission), infecting the cells of the gastrointestinal tract, from the mouth to the ileum and mesentrium. After replication, the virus may either be secreted in feces, contributing to the transmission of the disease, or reach the bloodstream, and be transported to other cells of the body, such as those of the reticuloendothelial system. Although the precise mechanism of infection of CNS is not fully understood, the most supported hypothesis is the retrograde axonal transport, according to which the virus enters the axoplasm of a motor neuron, travels to its cell body, where it replicates, and leads to neuron death. In the CNS, poliovirus shows tropism for cells of the anterior horn of the spinal cord, hypothalamus, thalamus, cerebellar vermis, vestibular and deep cerebral nuclei. Death of the motor neuron is responsible for the paralysis often seen in poliomyelitis.

Case Definitions of Polio

CDC has given a case definition of paralytic poliomyelitis for surveillance purposes

  • “Acute onset of flaccid paralysis of one or more limbs with decreased or absent tendon reflex in the affected limbs, without other apparent causes, and without sensory or cognitive loss.”.[1]
  • A confirmed case requires persistence of neurological deficit for 60 days after the onset of the initial symptoms, fatal illness, or unknown follow-up status.[1]

WHO case definition for a suspected case of poliomyelitis is:

  • A suspected case is defined as a child under 15 years of age presenting with acute flaccid paralysis (AFP), or as any person at any age with paralytic illness if poliomyelitis is suspected[2]


Pathophysiology

Transmission

Poliovirus is mostly transmitted through the fecal-oral route, by ingestion of contaminated food or water. In some instances, the oral-oral route may be relevant through pharyngeal secretions. [3][4] Poliomyelitis is highly contagious and spreads easily through human-to-human contact.[5] In endemic areas, wild polioviruses can infect virtually the entire human population.[6] Viral particles are excreted in the feces for several weeks, after initial infection. Although the virus can cross the placenta during pregnancy, the fetus does not appear to be affected by either maternal infection, or polio vaccination.[7] Maternal antibodies can also cross the placenta, providing passive immunity that protects the infant from polio infection during the first few months of life.[8]

Poliovirus enters the body orally and most often infects nearby cells, such as those of the mouth, nose, and throat. Poliovirus commonly targets specific tissues in the CNS such as:[9]

Pathogenesis

It infects cells by binding to an immunoglobulin-like receptor known as CD155 on the cell surface. The most common course of infection is the replication of poliovirus in cells of the gastrointestinal tract, followed by viral shedding in feces. The specific cells of the gastrointestinal tract, where poliovirus replicates, are not known, however, the virus was successfully isolated from lymphatic cells of the GI tract, including:[9]. Viral particles have been seen in:

The virus enters the bloodstream and migrates to the reticuloendothelial cells across the body. Poliovirus is able to reach the central nervous system in a small fraction of the symptomatic patients.[9] Not only is the disease not a phase of the viral replication cycle, it also does not benefit the virus in any way. The molecular mechanism behind this disease process is not known.[9]

Poliovirus replicates inside monocytes, which allows for secondary hematogenous spread. The pathological mechanism responsible for the clinical manifestations of CNS poliomyelitis is characterized by selective destruction of motor neurons. Depending of the involved site, motor neuron loss may lead to focal or generalized symptoms. Most commonly observed signs and symptoms include asymmetric limb paralysis in spinal polio and respiratory disturbance with cranial nerve defects in bulbar polio.

Although the mechanism of viral spread to the CNS is not fully understood, two main hypotheses have been proposed:[9]

  1. Poliovirus diffuses directly through the blood brain barrier from the bloodstream to the CNS, regardless of cellular receptors.
  2. Poliovirus is transported from the peripheral muscles to the brain and spinal cord, through retrograde axonal transport. This hypothesis has been experimentally proven in mice, after CD155 transformation.

Several recent findings supporting the retrograde axonal transport hypothesis have been reported:[9].

    • Detection of axonal poliovirus in patients with poliomyelitis.
    • Interruption of a nerve connection between a site of multiple intramuscular injections and the spinal cord in mice with poliovirus viremia led to improved clinical course of infection. This supports the provocation poliomyelitis hypothesis which states that muscle injury in patients with poliovirus viremia triggers retrograde axonal transport of the virus. This phenomenon is seen in children receiving intramuscular vaccines in areas endemic for poliovirus.[10]
    • In mice genetically transformed to express CD155, injection of poliovirus in the left limb led to viral detection in the left anterior horn of the spinal cord only. When the sciatic nerve was promptly sectioned after injection of the virus, the risk of paralysis in the injected limb was greatly reduced.
    • Bulbar poliomyelitis following tonsillectomy may possibly be explained by the previously described mechanisms.
    • Overexpression of CD155 in the muscle fibers of patients with paralytic poliomyelitis. To note, CD155 directly interacts with the dynein retrograde complex through Tctex-1.[9]


The main explanation for increased susceptibility to retrograde axonal transport of poliovirus in areas of injured muscle has been explained. In a neuronal synapse, the rate of endocytosis is related to the level of neuron activity. Correspondingly, for a motor neuron, the level of neuron activity and rate of endocytosis at the neuromuscular junction is related to the extent of muscle contraction. This explains the connection between extreme exercise or muscle injury and development of poliomyelitis in patients with viremia. Also, since most of CD155 receptors are transported back to the cell body, the virus is carried along, supporting the retrograde transport hypothesis.[9]


Once at the cell body of the neuron, the change from axoplasm to cytoplasm is thought to interfere with the stability of the viral coat, leading to the exposure of the viral RNA. Viral replication interferes with neuron stability, killing the motor neuron. Death of a motor neuron paralyzes the respective muscle fiber.

Course of Disease

The pre- paralytic or non-paralytic course of the disease includes:-[11]

  • Headache
  • Pharyngitis
  • Myalgia
  • Anorexia
  • Nausea
  • Vomiting

In non- paralytic illness, the symptoms go away within one or two weeks.

Paralytic Poliomyelitis: [11] After the meningitis phase, the spinal form of poliomyelitis occurs which consists of:

  • Muscle pain
  • Muscle spasms
  • Fasciculations

Weakness is asymmetrical affecting the lower limbs more than the upper limbs. The weakness usually becomes maximum within 48hrs, especially in children. In some, the weakness may further increase after a period of stability but no further weakness occurs once the fever subsides. Muscle tone is flaccid and the reflexes are absent along with paraesthesia. Any cranial nerve may be involved but most frequently leads to dysphasia, dysphasia, and respiratory failure[12]. Vasomotor involvement such as hypertension, hypotension, and circulatory collapse lead to mortality in patients.


Bulbar form:[13] Seen more in children in which tonsils and adenoids have been removed.

Vaccine mediated polio infection

Oral polio vaccine (OPV) is one of the safest and most effective vaccination programs that prevented millions of cases of polio not only through direct immunization but also through herd immunity. In rare occasions, the vaccine is associated with paralytic polio. There are two subtypes of paralytic polio related to OPV vaccine: vaccine associated paralytic polio and vaccine derived paralytic polio.

Vaccine associated paralytic polio

  • Vaccine associated paralytic polio (VAPP) occurs when the attenuated strain used in the vaccine reverts inside the intestine into more virulent form.[2][14][15]
  • The more virulent form is capable of causing the disease only in the vaccinated child or a close susceptible contact. Therfore, no outbreaks are associated with VAPP.
  • The prevalence of (VAPP) is 1 in 2.7 million doses of the vaccine.
  • In developed countries, the risk of VAPP is increased with the first dose of the vaccine while in developed countries, It’s increased with subsequent doses.

Vaccine derived paralytic polio

  • Vaccine derived paralytic polio (VDPP) is caused by very rare mutation of the original strain of polio in the vaccine.[2][16]
  • VDPP has the ability to cause the disease in any non immune person whether the vaccinated person or a contact, therefore it has the ability to cause outbreaks or even epidemics especially in communities that are not properly covered with the vaccination program.
  • When it causes outbreaks, VDPP is called circulating vaccine derived paralytic polio (cVDPP).
  • In the last 10 years, 24 VDPP reported outbreaks happened in 21 countries causing 750 cases of paralytic polio.
  • The management of VDPP is conducting extensive vaccination campaigns in the affected community aiming for vaccinating every child and thus preventing the spread of the infection.

Microscopic Pathology Images

References

  1. ↑ 1.0 1.1 "Poliomyelitis, Paralytic | 2010 Case Definition".
  2. ↑ 2.0 2.1 2.2 "www.who.int" (PDF).
  3. ↑ Nathanson N, Kew OM (2010). "From emergence to eradication: the epidemiology of poliomyelitis deconstructed". Am J Epidemiol. 172 (11): 1213–29. doi:10.1093/aje/kwq320. PMC 2991634. PMID 20978089.
  4. ↑ "Poliomyelitis".
  5. ↑ Kew O, Sutter R, de Gourville E, Dowdle W, Pallansch M (2005). "Vaccine-derived polioviruses and the endgame strategy for global polio eradication". Annu Rev Microbiol. 59: 587–635. PMID 16153180.
  6. ↑ Parker SP (ed.) (1998). McGraw-Hill Concise Encyclopedia of Science & Technology. New York: McGraw-Hill. p. 67. ISBN 0-07-052659-1.
  7. ↑ Joint Committee on Vaccination and Immunisation (Salisbury A, Ramsay M, Noakes K (eds.) (2006). Chapter 26:Poliomyelitis. in: Immunisation Against Infectious Disease, 2006 (PDF). Edinburgh: Stationery Office. pp. 313–29. ISBN 0-11-322528-8.
  8. ↑ 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.
  9. ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 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. doi:10.1016/j.virusres.2005.04.008. PMID 15885840.
  10. ↑ Gromeier M, Wimmer E (1998). "Mechanism of injury-provoked poliomyelitis". J Virol. 72 (6): 5056–60. PMC 110068. PMID 9573275.
  11. ↑ 11.0 11.1 Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID https://dx.doi.org/10.1136/pgmj.72.853.641 Check |pmid= value (help).
  12. ↑ PLUM F, SWANSON AG (1959). "Central neurogenic hyperventilation in man". AMA Arch Neurol Psychiatry. 81 (5): 535–49. doi:10.1001/archneurpsyc.1959.02340170001001. PMID 13636523.
  13. ↑ ANDERSON GW, RONDEAU JL (1954). "Absence of tonsils as a factor in the development of bulbar poliomyelitis". J Am Med Assoc. 155 (13): 1123–30. doi:10.1001/jama.1954.03690310001001. PMID 13174358.
  14. ↑ Nkowane BM, Wassilak SG, Orenstein WA, Bart KJ, Schonberger LB, Hinman AR, Kew OM (1987). "Vaccine-associated paralytic poliomyelitis. United States: 1973 through 1984". JAMA. 257 (10): 1335–40. PMID 3029445.
  15. ↑ Sullivan AA, Boyle RS, Whitby RM (1995). "Vaccine-associated paralytic poliomyelitis". Med. J. Aust. 163 (8): 423–4. PMID 7476613.
  16. ↑ Khetsuriani N, Prevots DR, Quick L, Elder ME, Pallansch M, Kew O, Sutter RW (2003). "Persistence of vaccine-derived polioviruses among immunodeficient persons with vaccine-associated paralytic poliomyelitis". J. Infect. Dis. 188 (12): 1845–52. doi:10.1086/379791. PMID 14673763.
  17. ↑ 17.00 17.01 17.02 17.03 17.04 17.05 17.06 17.07 17.08 17.09 17.10 "Public Health Image Library (PHIL), Centers for Disease Control and Prevention".

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