Parotitis pathophysiology: Difference between revisions

Jump to navigation Jump to search
(Created page with "{{Parotitis}} {{CMG}} ==Overview== Parotitis is an inflammatory disorder of the salivary gland, or sialadenitis. It is most commonly infectious in etiology but can be autoimm...")
 
m (Changes made per Mahshid's request)
 
(22 intermediate revisions by 4 users not shown)
Line 1: Line 1:
__NOTOC__
{{Parotitis}}
{{Parotitis}}
{{CMG}}
{{CMG}} {{AE}} {{LRO}}


==Overview==
==Overview==
Parotitis is an inflammatory disorder of the salivary gland, or sialadenitis. It is most commonly infectious in etiology but can be autoimmune or neoplastic.
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]]''.
==Pathophysiology==
Parotitis is a disease that occurs in debilitated patients. Dehydration and decreased salivary flow/stasis are the main risk factors for ascending infection through Stenson’s duct to the gland. Postoperative patients who are dehydrated and NPO with little salivary stimulation are at particular risk with an incidence estimated at 1 in 1000. Debilitating medical conditions such as [[Diabetes mellitus]], renal failure, [[HIV]] and [[Sjögrens’s syndrome]] are risk factors.


Patients with [[Anorexia]], [[Bulimia]], [[CF]] or those with salivary ductal dilation are also at risk. Ductal dilation is found in those with high intraoral pressure such as trumpet players and glass blowers. Medications with anticholinergic properties or diuretic effects
==Pathogenesis==
===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>
**[[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>
**[[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>
**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]].


The most common bacterial cause is S. aureus. S. pneumonia, S. pyogenes and H. influenza are also common. Less commonly gram negative rods (GNR) as well as anaerobes are found. M. tuberculosis and T. pallidum  have also been reported but are usually associated with chronic, painless infection.
===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.


Viral etiologies include paramyxovirus (particularly Mumps), influenza, parainfluenza, echovirus and coxsackie.  Cytomegalovirus (CMV) and adenovirus have been implicated in HIV patients.
==References==
 
Nonbacterial causes include Wegener’s granulomatosis and lymphoma. Cat-scratch and actinomycosis should be considered if the patient fails to respond to standard therapy. This predispose to parotitis. <ref>McQuone SJ. Acute Viral and Bacterial Infections of the Salivary Glands. Otolaryngologic Clinics of North America. 1999, 32:793-811. PMID 10477787</ref>
 
== References ==
{{Reflist}}
{{Reflist}}


Line 23: Line 33:


[[Category:Disease]]
[[Category:Disease]]
[[Category:Infectious disease]]
 
[[Category:Oncology]]
[[Category:Glands]]
[[Category:Rheumatology]]
[[Category:Inflammations]]
[[Category:Needs patient information]]

Latest revision as of 18:38, 18 September 2017

Parotitis Microchapters

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Parotitis from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

CT or MRI

Treatment

Medical Therapy

Surgery

Primary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Parotitis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Parotitis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Parotitis pathophysiology

CDC on Parotitis pathophysiology

Parotitis pathophysiology in the news

Blogs on Parotitis pathophysiology

Directions to Hospitals Treating Parotitis

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

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.

Template:WikiDoc Sources