Croup pathophysiology
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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
- 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 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".