Parotitis pathophysiology: Difference between revisions

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==Overview==
==Overview==
Acute infection can occur in any [[salivary gland]] but the most commonly affected one is the parotid. This is thought to be due to a combination of anatomic and physiologic factors. The saliva from the parotid is less mucoid than that from the other salivary glands. [[IgA]], [[lysozyme]] and [[sialic acid]] are all found in smaller amounts in the more viscous parotid secretions. These substances are thought to help fight off ascending [[bacterial]] infection. Bacterial parotitis is generally unilateral in adults (75-90%), while [[viral]] is generally bilateral. Though 80-90% of salivary [[calculi]] occur in the Wharton’s duct of the [[submandibular gland]], the parotid remains the most common site of acute [[suppurative]] salivary infection. The secretions from the submandibular gland are more alkaline, thought to result in a higher concentration of insoluble calcium phosphate.
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]] [[RNP]] 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>
**[[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==
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[[Category:Disease]]
[[Category:Disease]]
[[Category:Infectious disease]]
 
[[Category:Glands]]
[[Category:Glands]]
[[Category:Inflammations]]
[[Category:Inflammations]]

Latest revision as of 18:38, 18 September 2017

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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

Bacterial Parotitis

References

  1. 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. 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.
  3. Chitre VV, Premchandra DJ (1997). "Recurrent parotitis". Arch. Dis. Child. 77 (4): 359–63. PMC 1717350. PMID 9389246.
  4. 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.

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