Parotitis pathophysiology: Difference between revisions
m (Changes made per Mahshid's request) |
|||
(10 intermediate revisions by one other user not shown) | |||
Line 4: | Line 4: | ||
==Overview== | ==Overview== | ||
The pathophysiology of parotitis is dependent upon the cause. [[Viral]] parotitis is caused by the infiltration of [[respiratory]] droplets containing the [[mumps]] [[virus]]. The [[mumps]] HN and F [[glycoproteins]] reach the surface of the infected host [[cell]] through the [[Endoplasmic reticulum|endoplasmic reticulum]] and [[Golgi complex]]. [[Virions]] emerge from the infected [[cells]] due to the [[M protein]] facilitating the localization of the [[viral]] ribonucleic proteins onto the host [[cell]] [[membrane]]. Both HN and F [[glycoproteins]] mediate the fusion of [[virus]] and host [[cell]], as well as [[cell]] and [[cell]]-[[membrane]] fusion, to perpetuate the spread of the [[virus]] throughout the host. The [[virus]] replicates in the [[nasopharynx]] and regional [[lymph nodes]]. Upon replication, [[viremia]] occurs for three to five days, spreading to the [[salivary glands]]. Parotitis results from the [[inflammatory]] response tp the presence of [[mumps]] [[virus]] in the [[parotid]] [[salivary gland]]. [[Bacterial]] parotitis is most commonly caused by ''[[staphylococcus aureus]]''. | |||
==Pathogenesis== | ==Pathogenesis== | ||
===Viral Parotitis=== | ===Viral Parotitis=== | ||
*[[Viral]] parotitis is caused by the infiltration of [[respiratory]] droplets containing the [[mumps]] [[virus]].<ref name="pmid18923686">{{cite journal |vauthors=Conly J, Johnston B |title=Is mumps making a comeback? |journal=Can J Infect Dis Med Microbiol |volume=18 |issue=1 |pages=7–9 |year=2007 |pmid=18923686 |pmc=2542890 |doi= |url=}}</ref> | *[[Viral]] parotitis is caused by the infiltration of [[respiratory]] droplets containing the [[mumps]] [[virus]].<ref name="pmid18923686">{{cite journal |vauthors=Conly J, Johnston B |title=Is mumps making a comeback? |journal=Can J Infect Dis Med Microbiol |volume=18 |issue=1 |pages=7–9 |year=2007 |pmid=18923686 |pmc=2542890 |doi= |url=}}</ref> | ||
**[[Mumps]] [[virus]] is a member of the [[paramyoxoviridae]] family with a single-strand, negative-sense [[RNA]] [[molecule]]. | **[[Mumps]] [[virus]] is a member of the [[paramyxovirus|paramyoxoviridae]] family with a single-strand, negative-sense [[RNA]] [[molecule]]. | ||
**The [[mumps]] HN and F [[glycoproteins]] reach the surface of the infected host [[cell]] through the [[Endoplasmic reticulum|endoplasmic reticulum]] and [[Golgi complex]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | **The [[mumps]] HN and F [[glycoproteins]] reach the surface of the infected host [[cell]] through the [[Endoplasmic reticulum|endoplasmic reticulum]] and [[Golgi complex]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | ||
**[[Virions]] emerge from the infected [[cells]] due to the [[M protein]] facilitating the localization of the [[viral]] | **[[Virions]] emerge from the infected [[cells]] due to the [[M protein]] facilitating the localization of the [[viral]] ribonucleic proteins onto the host [[cell]] [[membrane]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | ||
**The [[virus]] binds with the neighboring host [[cell|cells]] via [[Sialic acids|sialic acid]] through HN [[glycoprotein]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | **The [[virus]] binds with the neighboring host [[cell|cells]] via [[Sialic acids|sialic acid]] through HN [[glycoprotein]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | ||
**Both HN and F [[glycoproteins]] mediate the fusion of virus and host [[cell]], as well as [[cell]] and [[cell]]-[[membrane]] fusion, to perpetuate the spread of the [[virus]] throughout the host.<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | **Both HN and F [[glycoproteins]] mediate the fusion of [[virus]] and host [[cell]], as well as [[cell]] and [[cell]]-[[membrane]] fusion, to perpetuate the spread of the [[virus]] throughout the host.<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | ||
*The [[virus]] replicates in the [[nasopharynx]] and regional [[lymph nodes]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | |||
*Upon replication, [[viremia]] occurs for three to five days, spreading to the [[salivary glands]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | |||
*The [[parotid]] [[gland]] particularly susceptible to parotitis due to the lower rate of [[secretion]].<ref name="pmid9389246">{{cite journal |vauthors=Chitre VV, Premchandra DJ |title=Recurrent parotitis |journal=Arch. Dis. Child. |volume=77 |issue=4 |pages=359–63 |year=1997 |pmid=9389246 |pmc=1717350 |doi= |url=}}</ref> | |||
**[[Salivary]] flow rate is reduced due to the [[inflammation]] response. | |||
**Reduced [[saliva]] flow rate in the [[parotid]] [[gland]] leads to a reduction in the [[salivary]] defense [[proteins]] IgA (sIgA) and IgG, increasing vulnerability of the [[parotid]] [[gland]] to infection.<ref name="pmid22605979">{{cite journal |vauthors=Fábián TK, Hermann P, Beck A, Fejérdy P, Fábián G |title=Salivary defense proteins: their network and role in innate and acquired oral immunity |journal=Int J Mol Sci |volume=13 |issue=4 |pages=4295–320 |year=2012 |pmid=22605979 |pmc=3344215 |doi=10.3390/ijms13044295 |url=}}</ref> | |||
*Parotitis results from the [[inflammatory]] response to the presence of [[mumps]] [[virus]] in the [[parotid]] [[salivary gland]]. | |||
===Bacterial Parotitis=== | |||
*[[Bacterial]] parotitis is most commonly caused by ''[[staphylococcus aureus]]'', a gram-positive [[coccal]] bacterium often found in the [[respiratory tract]]. | |||
*''[[Staphylococcus aureus]]'' infects the host through skin to skin or skin to surface contact with an infected individual or object. | |||
==References== | ==References== | ||
Line 23: | Line 33: | ||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category:Glands]] | [[Category:Glands]] | ||
[[Category:Inflammations]] | [[Category:Inflammations]] |
Latest revision as of 18:38, 18 September 2017
Parotitis Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Parotitis pathophysiology On the Web |
American Roentgen Ray Society Images of Parotitis pathophysiology |
Risk calculators and risk factors for Parotitis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.
Overview
The pathophysiology of parotitis is dependent upon the cause. Viral parotitis is caused by the infiltration of respiratory droplets containing the mumps virus. The mumps HN and F glycoproteins reach the surface of the infected host cell through the endoplasmic reticulum and Golgi complex. Virions emerge from the infected cells due to the M protein facilitating the localization of the viral ribonucleic proteins onto the host cell membrane. Both HN and F glycoproteins mediate the fusion of virus and host cell, as well as cell and cell-membrane fusion, to perpetuate the spread of the virus throughout the host. The virus replicates in the nasopharynx and regional lymph nodes. Upon replication, viremia occurs for three to five days, spreading to the salivary glands. Parotitis results from the inflammatory response tp the presence of mumps virus in the parotid salivary gland. Bacterial parotitis is most commonly caused by staphylococcus aureus.
Pathogenesis
Viral Parotitis
- Viral parotitis is caused by the infiltration of respiratory droplets containing the mumps virus.[1]
- Mumps virus is a member of the paramyoxoviridae family with a single-strand, negative-sense RNA molecule.
- The mumps HN and F glycoproteins reach the surface of the infected host cell through the endoplasmic reticulum and Golgi complex.[2]
- Virions emerge from the infected cells due to the M protein facilitating the localization of the viral ribonucleic proteins onto the host cell membrane.[2]
- The virus binds with the neighboring host cells via sialic acid through HN glycoprotein.[2]
- Both HN and F glycoproteins mediate the fusion of virus and host cell, as well as cell and cell-membrane fusion, to perpetuate the spread of the virus throughout the host.[2]
- The virus replicates in the nasopharynx and regional lymph nodes.[2]
- Upon replication, viremia occurs for three to five days, spreading to the salivary glands.[2]
- The parotid gland particularly susceptible to parotitis due to the lower rate of secretion.[3]
- Parotitis results from the inflammatory response to the presence of mumps virus in the parotid salivary gland.
Bacterial Parotitis
- Bacterial parotitis is most commonly caused by staphylococcus aureus, a gram-positive coccal bacterium often found in the respiratory tract.
- Staphylococcus aureus infects the host through skin to skin or skin to surface contact with an infected individual or object.
References
- ↑ Conly J, Johnston B (2007). "Is mumps making a comeback?". Can J Infect Dis Med Microbiol. 18 (1): 7–9. PMC 2542890. PMID 18923686.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP (2015). "Molecular biology, pathogenesis and pathology of mumps virus". J. Pathol. 235 (2): 242–52. doi:10.1002/path.4445. PMC 4268314. PMID 25229387.
- ↑ Chitre VV, Premchandra DJ (1997). "Recurrent parotitis". Arch. Dis. Child. 77 (4): 359–63. PMC 1717350. PMID 9389246.
- ↑ Fábián TK, Hermann P, Beck A, Fejérdy P, Fábián G (2012). "Salivary defense proteins: their network and role in innate and acquired oral immunity". Int J Mol Sci. 13 (4): 4295–320. doi:10.3390/ijms13044295. PMC 3344215. PMID 22605979.