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==Pathogenesis==
==Pathogenesis==
*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>.
*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|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 [[RNA Polymerase|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>
**Viral transcription occurs through virus-specific [[RNA]]-dependent [[RNA Polymerase|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>
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***Negative-[[sense]] RNA strand
***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 is transmitted by contact with infected secretions through respiratory droplets or contaminated surfaces or objects.
*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 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>
*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>

Revision as of 20:53, 26 January 2016

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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. Ujjwal Rastogi, MBBS [2]

Overview

The viral infection that causes croup leads to swelling of the larynx, trachea, and large bronchi due to infiltration of white blood cells (especially histiocytes, lymphocytes, plasma cells, and neutrophils). Swelling produces airway obstruction which, when significant, leads to dramatically increased work of breathing and the characteristic turbulent, noisy airflow known as stridor.

Pathogenesis

Transmission

  • Croup may develop after Human parainfluenza virus is transmitted primarily by coughing, releasing infected secretions through respiratory droplets or contaminated surfaces or objects.[5]

References

  1. Cherry, James D. (2008). "Croup". New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.
  2. 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.
  3. 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.
  4. 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.
  5. "Human Parainfluenza Viruses | Clinical Overview of HPIVs | CDC".


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