Croup pathophysiology: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Croup}} | {{Croup}} | ||
{{CMG}} {{AE}} {{LRO}} | {{CMG}} {{AE}} {{LRO}} | ||
==Overview== | ==Overview== | ||
The viral | Development of croup results from infiltration of [[white blood cells]] through the [[human parainfluenza virus]] (HPIV). HPIV expels its [[nucleocapsid]] into the recipient cell [[cytoplasm]]. The [[viral]] transcription then occurs through the HPIV [[RNA]]-dependent [[RNA polymerase]]. The [[viral]] [[Messenger RNA|mRNAs]] are translated into [[viral]] [[protein|proteins]], leading to the replication of the [[genome]] into the negative-sense [[RNA]] strand, which is then encapsidated by the [[nucleoprotein]] and used for further transcription and replication. The [[inflammation]] response to HPIV occurs from the up-regulation of [[cytokine|cytokines]] and the released [[Immunoglobulin E]] inhibiting [[histamine]]. The resultant swelling of the [[larynx]], [[trachea]], and large [[bronchi]] obstructs the airways, which leads to croup. | ||
==Pathogenesis== | ==Pathogenesis== | ||
*Development of [[Virus| | *Development of [[Virus|viral]] croup results from infiltration of [[histiocytes]], [[lymphocytes]], [[plasma cells]], and [[neutrophils]] [[White blood cells|white blood cells]] primarily by [[human parainfluenza viruses]] (HPIV).<ref name="Cherry2008">{{cite journal|last1=Cherry|first1=James D.|title=Croup|journal=New England Journal of Medicine|volume=358|issue=4|year=2008|pages=384–391|issn=0028-4793|doi=10.1056/NEJMcp072022}}</ref>. | ||
**HPIV fuses with the white blood cells through the [[glycoproteins]] [[hemagglutinin-neuraminidase]] and [[fusion protein]].<ref name="Henrickson2003">{{cite journal|last1=Henrickson|first1=K. J.|title=Parainfluenza Viruses|journal=Clinical Microbiology Reviews|volume=16|issue=2|year=2003|pages=242–264|issn=0893-8512|doi=10.1128/CMR.16.2.242-264.2003}}</ref> | **HPIV fuses with the [[white blood cells]] through the [[glycoproteins]] [[Hemagglutinin|hemagglutinin]]-[[Neuraminidase|neuraminidase]] and [[fusion protein]].<ref name="Henrickson2003">{{cite journal|last1=Henrickson|first1=K. J.|title=Parainfluenza Viruses|journal=Clinical Microbiology Reviews|volume=16|issue=2|year=2003|pages=242–264|issn=0893-8512|doi=10.1128/CMR.16.2.242-264.2003}}</ref> | ||
**Upon fusion, the HPIV [[nucleocapsid]] is expelled into the recipient cell [[cytoplasm]].<ref name="Henrickson2003">{{cite journal|last1=Henrickson|first1=K. J.|title=Parainfluenza Viruses|journal=Clinical Microbiology Reviews|volume=16|issue=2|year=2003|pages=242–264|issn=0893-8512|doi=10.1128/CMR.16.2.242-264.2003}}</ref> | **Upon fusion, the HPIV [[nucleocapsid]] is expelled into the recipient cell [[cytoplasm]].<ref name="Henrickson2003">{{cite journal|last1=Henrickson|first1=K. J.|title=Parainfluenza Viruses|journal=Clinical Microbiology Reviews|volume=16|issue=2|year=2003|pages=242–264|issn=0893-8512|doi=10.1128/CMR.16.2.242-264.2003}}</ref> | ||
**Viral transcription occurs through virus-specific [[RNA]]-dependent [[ | **Viral transcription occurs through virus-specific [[RNA]]-dependent [[RNA polymerase]].<ref name="Henrickson2003">{{cite journal|last1=Henrickson|first1=K. J.|title=Parainfluenza Viruses|journal=Clinical Microbiology Reviews|volume=16|issue=2|year=2003|pages=242–264|issn=0893-8512|doi=10.1128/CMR.16.2.242-264.2003}}</ref> | ||
**The viral mRNAs are translated into viral proteins, leading to the replication of genome into the following:<ref name="Henrickson2003">{{cite journal|last1=Henrickson|first1=K. J.|title=Parainfluenza Viruses|journal=Clinical Microbiology Reviews|volume=16|issue=2|year=2003|pages=242–264|issn=0893-8512|doi=10.1128/CMR.16.2.242-264.2003}}</ref> | **The viral [[Messenger RNA|mRNAs]] are translated into [[viral]] [[protein|proteins]], leading to the replication of the [[genome]] into the following:<ref name="Henrickson2003">{{cite journal|last1=Henrickson|first1=K. J.|title=Parainfluenza Viruses|journal=Clinical Microbiology Reviews|volume=16|issue=2|year=2003|pages=242–264|issn=0893-8512|doi=10.1128/CMR.16.2.242-264.2003}}</ref> | ||
***Positive-[[ | ***Positive-sense [[RNA]] strand | ||
***Negative-[[ | ***Negative-sense [[RNA]] strand | ||
**The negative-sense RNA strand is encapsidated by [[nucleoprotein]] and is then used for further transcription and replication. | **The negative-sense RNA strand is encapsidated by [[nucleoprotein]] and is then used for further transcription and replication. | ||
*HPIV infection usually begins at the [[epithelium]] in the [[Upper respiratory tract|upper respiratory tract]], spreading to the [[paranasal sinus|paranasal sinuses]], [[larynx]] and [[bronchi]].<ref name="SchomackerSchaap-Nutt2012">{{cite journal|last1=Schomacker|first1=Henrick|last2=Schaap-Nutt|first2=Anne|last3=Collins|first3=Peter L|last4=Schmidt|first4=Alexander C|title=Pathogenesis of acute respiratory illness caused by human parainfluenza viruses|journal=Current Opinion in Virology|volume=2|issue=3|year=2012|pages=294–299|issn=18796257|doi=10.1016/j.coviro.2012.02.001}}</ref> | |||
*HPIV infection usually begins at the [[epithelium]] in the [[Upper | |||
*The infiltration from HPIV causes [[inflammation]] by the up-regulated production of [[cytokines]], localized in the [[trachea]].<ref name="Schaap-NuttLiesman2012">{{cite journal|last1=Schaap-Nutt|first1=Anne|last2=Liesman|first2=Rachael|last3=Bartlett|first3=Emmalene J.|last4=Scull|first4=Margaret A.|last5=Collins|first5=Peter L.|last6=Pickles|first6=Raymond J.|last7=Schmidt|first7=Alexander C.|title=Human parainfluenza virus serotypes differ in their kinetics of replication and cytokine secretion in human tracheobronchial airway epithelium|journal=Virology|volume=433|issue=2|year=2012|pages=320–328|issn=00426822|doi=10.1016/j.virol.2012.08.027}}</ref> | *The infiltration from HPIV causes [[inflammation]] by the up-regulated production of [[cytokines]], localized in the [[trachea]].<ref name="Schaap-NuttLiesman2012">{{cite journal|last1=Schaap-Nutt|first1=Anne|last2=Liesman|first2=Rachael|last3=Bartlett|first3=Emmalene J.|last4=Scull|first4=Margaret A.|last5=Collins|first5=Peter L.|last6=Pickles|first6=Raymond J.|last7=Schmidt|first7=Alexander C.|title=Human parainfluenza virus serotypes differ in their kinetics of replication and cytokine secretion in human tracheobronchial airway epithelium|journal=Virology|volume=433|issue=2|year=2012|pages=320–328|issn=00426822|doi=10.1016/j.virol.2012.08.027}}</ref> | ||
*Additionally, HPIV-response [[Immunoglobulin E]] (IgE) release has been found to inhibit [[histamine]], contributing to the inflammation that causes croup.<ref name ="HistaCroup">{{cite journal |vauthors=Welliver RC, Sun M, Rinaldo D |title=Defective regulation of immune responses in croup due to parainfluenza virus |journal=Pediatr. Res. |volume=19 |issue=7 |pages=716–20 |year=1985 |pmid=2991841 |doi=10.1203/00006450-198507000-00016 |url=}}</ref> | |||
*Of the four different [[serotype|serotypes]], HPIV-1 and HPIV-2 are the serotypes that cause croup.<ref name ="CroupType">{{cite book | last = Baron | first = Samuel | title = Medical microbiology | publisher = University of Texas Medical Branch at Galveston | location = Galveston, Tex | year = 1996 | isbn = 0-9631172-1-1 }}</ref> | |||
==Transmission== | ==Transmission== | ||
*Croup may develop after [[ | *Croup may develop after [[human parainfluenza virus]] is transmitted primarily by [[cough|coughing]], releasing infected secretions through respiratory droplets or contaminated surfaces or objects.<ref name="CDCPath">{{cite web |url=http://www.cdc.gov/parainfluenza/hcp/clinical.html |title=Human Parainfluenza Viruses | Clinical Overview of HPIVs | CDC |format= |work= |accessdate=}}</ref> | ||
==References== | ==References== | ||
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{{WikiDoc Sources}} | {{WikiDoc Sources}} | ||
[[Category:Pediatrics]] | [[Category:Pediatrics]] | ||
[[Category:Pulmonology]] | [[Category:Pulmonology]] | ||
[[Category:Emergency medicine]] | [[Category:Emergency medicine]] | ||
[[Category:Disease]] | [[Category:Disease]] | ||
Latest revision as of 17:30, 18 September 2017
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Croup pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.
Overview
Development of croup results from infiltration of white blood cells through the human parainfluenza virus (HPIV). HPIV expels its nucleocapsid into the recipient cell cytoplasm. The viral transcription then occurs through the HPIV RNA-dependent RNA polymerase. The viral mRNAs are translated into viral proteins, leading to the replication of the genome into the negative-sense RNA strand, which is then encapsidated by the nucleoprotein and used for further transcription and replication. The inflammation response to HPIV occurs from the up-regulation of cytokines and the released Immunoglobulin E inhibiting histamine. The resultant swelling of the larynx, trachea, and large bronchi obstructs the airways, which leads to croup.
Pathogenesis
- Development of viral croup results from infiltration of histiocytes, lymphocytes, plasma cells, and neutrophils white blood cells primarily by human parainfluenza viruses (HPIV).[1].
- HPIV fuses with the white blood cells through the glycoproteins hemagglutinin-neuraminidase and fusion protein.[2]
- Upon fusion, the HPIV nucleocapsid is expelled into the recipient cell cytoplasm.[2]
- Viral transcription occurs through virus-specific RNA-dependent RNA polymerase.[2]
- The viral mRNAs are translated into viral proteins, leading to the replication of the genome into the following:[2]
- The negative-sense RNA strand is encapsidated by nucleoprotein and is then used for further transcription and replication.
- HPIV infection usually begins at the epithelium in the upper respiratory tract, spreading to the paranasal sinuses, larynx and bronchi.[3]
- The infiltration from HPIV causes inflammation by the up-regulated production of cytokines, localized in the trachea.[4]
- Additionally, HPIV-response Immunoglobulin E (IgE) release has been found to inhibit histamine, contributing to the inflammation that causes croup.[5]
- Of the four different serotypes, HPIV-1 and HPIV-2 are the serotypes that cause croup.[6]
Transmission
- Croup may develop after human parainfluenza virus is transmitted primarily by coughing, releasing infected secretions through respiratory droplets or contaminated surfaces or objects.[7]
References
- ↑ Cherry, James D. (2008). "Croup". New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.
- ↑ 2.0 2.1 2.2 2.3 Henrickson, K. J. (2003). "Parainfluenza Viruses". Clinical Microbiology Reviews. 16 (2): 242–264. doi:10.1128/CMR.16.2.242-264.2003. ISSN 0893-8512.
- ↑ Schomacker, Henrick; Schaap-Nutt, Anne; Collins, Peter L; Schmidt, Alexander C (2012). "Pathogenesis of acute respiratory illness caused by human parainfluenza viruses". Current Opinion in Virology. 2 (3): 294–299. doi:10.1016/j.coviro.2012.02.001. ISSN 1879-6257.
- ↑ Schaap-Nutt, Anne; Liesman, Rachael; Bartlett, Emmalene J.; Scull, Margaret A.; Collins, Peter L.; Pickles, Raymond J.; Schmidt, Alexander C. (2012). "Human parainfluenza virus serotypes differ in their kinetics of replication and cytokine secretion in human tracheobronchial airway epithelium". Virology. 433 (2): 320–328. doi:10.1016/j.virol.2012.08.027. ISSN 0042-6822.
- ↑ Welliver RC, Sun M, Rinaldo D (1985). "Defective regulation of immune responses in croup due to parainfluenza virus". Pediatr. Res. 19 (7): 716–20. doi:10.1203/00006450-198507000-00016. PMID 2991841.
- ↑ Baron, Samuel (1996). Medical microbiology. Galveston, Tex: University of Texas Medical Branch at Galveston. ISBN 0-9631172-1-1.
- ↑ "Human Parainfluenza Viruses | Clinical Overview of HPIVs | CDC".