Polio pathophysiology: Difference between revisions

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* Physical activity during the period of [[viremia]]<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>  
* Physical activity during the period of [[viremia]]<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>
* [[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>
* [[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>  
* [[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 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>
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>


==Gallery==
==Gallery==

Revision as of 22:11, 31 August 2014

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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]

Overview

Pathogenesis

Poliovirus enters the body through the mouth and infects nearby cells, 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:[1]

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.[1] 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.[1]

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:[1]

  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 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

Recent discoveries supporting the second hypothesis have been reported:[1]

  • 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.
  • 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.
  • 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.
  • Bulbar poliomyelitis following tonsillectomy may possibly be explained by the previously described mechanisms.
  • There is over expression of CD155 on the muscle fibers of patients with paralytic poliomyelitis.
  • CD155, directly interacts with the dynein retrograde complex, through Tctex-1.

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.[1]

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 neurons will be responsible for the death of these cells.

In the CNS, poliovirus shows tropism for certain pathways and tissues:[1]

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.[1]

Transmission

Poliovirus is transmitted through the fecal-oral route and through pharyngeal secretions.[2]

Poliomyelitis is highly contagious and spreads easily through human-to-human contact.[3] In endemic areas, wild polioviruses can infect virtually the entire human population.[4] It is a seasonal disease in temperate climates, with peak transmission occurring during summer and autumn months. These seasonal differences are far less pronounced in tropical areas. The incubation period is usually 6 to 20 days, with a maximal range of 3 to 35 days.[5] Viral particles are excreted in the feces for several weeks, following initial infection. The disease is transmitted primarily via the fecal-oral route, by ingestion of contaminated food or water. It is occasionally transmitted via the oral-oral route,[6] a mode especially visible in areas with good sanitation and hygiene.

Factors that increase the risk of infection or affect the severity of the disease include:

Although the virus can cross the placenta during pregnancy, the fetus does not appear to be affected by either maternal infection, or polio vaccination.[13] Maternal antibodies can also cross the placenta, providing passive immunity that protects the infant from polio infection during the first few months of life.[14]

Gallery

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 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.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ Parker SP (ed.) (1998). McGraw-Hill Concise Encyclopedia of Science & Technology. New York: McGraw-Hill. p. 67. ISBN 0-07-052659-1.
  5. ↑ Racaniello V (2006). "One hundred years of poliovirus pathogenesis". Virology. 344 (1): 9–16. PMID 16364730.
  6. ↑ Ohri, Linda K. (1999). "Polio: Will We Soon Vanquish an Old Enemy?". Drug Benefit Trends. 11 (6): 41–54. Retrieved 2007-11-06. Unknown parameter |coauthors= ignored (help) (Available free on Medscape; registration required.)
  7. ↑ Davis L, Bodian D, Price D, Butler I, Vickers J (1977). "Chronic progressive poliomyelitis secondary to vaccination of an immunodeficient child". N Engl J Med. 297 (5): 241–5. PMID 195206.
  8. ↑ Chandra R (1975). "Reduced secretory antibody response to live attenuated measles and poliovirus vaccines in malnourished children". Br Med J. 2 (5971): 583–5. PMID 1131622.
  9. ↑ Miller A (1952). "Incidence of poliomyelitis; the effect of tonsillectomy and other operations on the nose and throat". Calif Med. 77 (1): 19–21. PMID 12978882.
  10. ↑ Horstmann D (1950). "Acute poliomyelitis relation of physical activity at the time of onset to the course of the disease". J Am Med Assoc. 142 (4): 236–41. PMID 15400610.
  11. ↑ Gromeier M, Wimmer E (1998). "Mechanism of injury-provoked poliomyelitis". J. Virol. 72 (6): 5056–60. PMID 9573275.
  12. ↑ Evans C (1960). "Factors influencing the occurrence of illness during naturally acquired poliomyelitis virus infections" (PDF). Bacteriol Rev. 24 (4): 341–52. PMID 13697553.
  13. ↑ 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.
  14. ↑ Sauerbrei A, Groh A, Bischoff A, Prager J, Wutzler P (2002). "Antibodies against vaccine-preventable diseases in pregnant women and their offspring in the eastern part of Germany". Med Microbiol Immunol. 190 (4): 167–72. PMID 12005329.
  15. ↑ 15.00 15.01 15.02 15.03 15.04 15.05 15.06 15.07 15.08 15.09 15.10 "Public Health Image Library (PHIL), Centers for Disease Control and Prevention".

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