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==Overview==
The pathogenesis of otitis media is directly connected to the pathogen responsible for [[nasopharyngitis]]. This includes infectious causes, such as [[viral]] [[upper respiratory infection]], as well as [[bacterial]] infection from ''[[Streptococcus pneumoniae]]'', ''[[Haemophilus influenzae]]'', ''[[Moraxella catarrhalis]]'', and ''[[Staphylococcus aureus]]''. [[Mucus]] in the [[middle ear]] causes congestion that results in dysfunction of the [[eustachian tube]]. Pressure regulation in the [[inner ear]] is altered, causing effusion of fluid into the [[tympanic cavity]] containing the pathogen of [[nasopharyngitis]]. Otitis media results from the [[inflammatory]] response to the infection. Otitis media is transmitted through [[respiratory]] droplets through saliva or mucus, as well as direct physical contact with a contaminated individual or physical surface. Otitis media is often associated with other [[upper respiratory]] conditions caused by the [[nasopharynx]] pathogen, as well as allergic conditions such as allergic [[rhinitis]]. There is evidence of genetic predisposition to otitis media, with statistically significant evidence that it has high heritability. The following genes have been identified as having having potential pathogenic qualities for otitis media: ''CAPN14'', ''GALNT14'', ''BPIFA3'', ''BPIFA1'', ''[[BMP5]]'', ''GALNT13'', ''[[NELL1]]'', ''TGFB3''. Up-regulation of the genes correlated to otitis media pathogenesis contribute to individual susecptibility to the disease.
 
==Pathophysiology==
===Pathogenesis===
*Otitis media develops as a result of [[nasopharanx]] [[inflammation]] as a result of [[infection|infections]], such as [[viral]] [[upper respiratory infection]] and [[strep throat]].<ref name="pmid24400296">{{cite journal |vauthors=Coticchia JM, Chen M, Sachdeva L, Mutchnick S |title=New paradigms in the pathogenesis of otitis media in children |journal=Front Pediatr |volume=1 |issue= |pages=52 |year=2013 |pmid=24400296 |pmc=3874850 |doi=10.3389/fped.2013.00052 |url=}}</ref>
**Rarely it can result as from symptoms of [[allergies]].<ref name="pmid15971648">{{cite journal |vauthors=Nguyen LH, Manoukian JJ, Tewfik TL, Sobol SE, Joubert P, Mazer BD, Schloss MD, Taha R, Hamid QA |title=Evidence of allergic inflammation in the middle ear and nasopharynx in atopic children with otitis media with effusion |journal=J Otolaryngol |volume=33 |issue=6 |pages=345–51 |year=2004 |pmid=15971648 |doi= |url=}}</ref>
*[[Nasopharyngitis]] is caused by the inhalation of [[respiratory]] droplets containing [[viral]] infection, usually [[rhinovirus]] or similar [[upper respiratory infection]] causing viruses.<ref name="MicroBio4">{{cite book | last = Baron | first = Samuel | title = Medical microbiology | publisher = University of Texas Medical Branch at Galveston | location = Galveston, Tex | year = 1996 | isbn = 0963117211 }}</ref>
**The viruses penetrate through the [[epithelial]] [[cells]] in respiratory [[mucosa]].
**The virus infiltrates [[histiocytes]], [[lymphocytes]], [[plasma cells]], and [[neutrophils]] [[White blood cells|white blood cells]].
**[[Inflammation]] is caused by the up-regulated production of [[cytokines]], localized in the [[nasopharynx]], evidenced by [[nasal]] secretions of [[proteins]] and [[immunoglobin]].
*[[Bacterial]] infections, including ''[[Streptococcus pneumoniae]]'', ''[[Haemophilus influenzae]]'', ''[[Moraxella catarrhalis]]'', and ''[[Staphylococcus aureus]]'' can also result in [[nasopharyngitis]].<ref name="pmid24453496">{{cite journal |vauthors=Qureishi A, Lee Y, Belfield K, Birchall JP, Daniel M |title=Update on otitis media - prevention and treatment |journal=Infect Drug Resist |volume=7 |issue= |pages=15–24 |year=2014 |pmid=24453496 |pmc=3894142 |doi=10.2147/IDR.S39637 |url=}}</ref>
*[[Nasopharyngitis]] results in [[eustachian tube]] dysfunction due to congestion from [[mucus]] production as a result of infection.<ref name="pmid24453496">{{cite journal |vauthors=Qureishi A, Lee Y, Belfield K, Birchall JP, Daniel M |title=Update on otitis media - prevention and treatment |journal=Infect Drug Resist |volume=7 |issue= |pages=15–24 |year=2014 |pmid=24453496 |pmc=3894142 |doi=10.2147/IDR.S39637 |url=}}</ref>
**Pressure regulation in the [[inner ear]] is altered as the surrounding tissue absorbs trapped gas.<ref name="urlOtitis media with effusion: MedlinePlus Medical Encyclopedia">{{cite web |url=https://www.nlm.nih.gov/medlineplus/ency/article/007010.htm |title=Otitis media with effusion: MedlinePlus Medical Encyclopedia |format= |work= |accessdate=}}</ref>
**Negative pressure results in middle-ear effusion of fluid into the [[tympanic cavity]].
*The fluid may contain the [[viral]] or [[bacterial]] [[pathogens]] for [[nasopharyngitis]], infecting the middle ear.
*Otitis media results from the [[inflammatory]] response to the middle ear infection.
 
===Transmission===
*Otitis media is transmitted through [[respiratory]] droplets through saliva or mucus, as well as direct physical contact with a contaminated individual or physical surface.
**The pathogen responsible for the causative [[nasopharyngitis]] is also responsible for otitis media.<ref name="pmid24453496">{{cite journal |vauthors=Qureishi A, Lee Y, Belfield K, Birchall JP, Daniel M |title=Update on otitis media - prevention and treatment |journal=Infect Drug Resist |volume=7 |issue= |pages=15–24 |year=2014 |pmid=24453496 |pmc=3894142 |doi=10.2147/IDR.S39637 |url=}}</ref>
 
===Genetics===
*There is evidence of genetic predisposition to otitis media, with statistically significant evidence that it has high heritability.<ref name="pmid22018929">{{cite journal |vauthors=Hafrén L, Kentala E, Järvinen TM, Leinonen E, Onkamo P, Kere J, Mattila PS |title=Genetic background and the risk of otitis media |journal=Int. J. Pediatr. Otorhinolaryngol. |volume=76 |issue=1 |pages=41–4 |year=2012 |pmid=22018929 |doi=10.1016/j.ijporl.2011.09.026 |url=}}</ref>
**Hereditary factors comprising 45-75% of risk factors for otitis media, as revealed by heritability studies involving twins and triplets.<ref name="pmid23133572">{{cite journal |vauthors=Rye MS, Warrington NM, Scaman ES, Vijayasekaran S, Coates HL, Anderson D, Pennell CE, Blackwell JM, Jamieson SE |title=Genome-wide association study to identify the genetic determinants of otitis media susceptibility in childhood |journal=PLoS ONE |volume=7 |issue=10 |pages=e48215 |year=2012 |pmid=23133572 |pmc=3485007 |doi=10.1371/journal.pone.0048215 |url=}}</ref>
*The following genes have been identified as having having potential pathogenic qualities for otitis media:<ref name="pmid23133572">{{cite journal |vauthors=Rye MS, Warrington NM, Scaman ES, Vijayasekaran S, Coates HL, Anderson D, Pennell CE, Blackwell JM, Jamieson SE |title=Genome-wide association study to identify the genetic determinants of otitis media susceptibility in childhood |journal=PLoS ONE |volume=7 |issue=10 |pages=e48215 |year=2012 |pmid=23133572 |pmc=3485007 |doi=10.1371/journal.pone.0048215 |url=}}</ref>
**2p23.1
***''CAPN14''
***''GALNT14''
**20q11.21
***''BPIFA3''
***''BPIFA1''
**Those that interact with the [[TGFβ]] pathway:
***''[[BMP5]]''
***''GALNT13''
***''[[NELL1]]''
***''TGFB3''
*Up-regulation of the genes correlated to otitis media pathogenesis contribute to individual susceptibility to the disease.
 
==Associated Conditions==
*Otitis media is often associated with other [[upper respiratory]] conditions caused by the [[nasopharynx]] pathogen.<ref name="pmid24400296">{{cite journal |vauthors=Coticchia JM, Chen M, Sachdeva L, Mutchnick S |title=New paradigms in the pathogenesis of otitis media in children |journal=Front Pediatr |volume=1 |issue= |pages=52 |year=2013 |pmid=24400296 |pmc=3874850 |doi=10.3389/fped.2013.00052 |url=}}</ref>
**[[Common cold]]
**[[Strep throat]]
**[[Sinusitis]]
*Associated conditions are also allergies-related, such as allergic [[rhinitis]].


==References==
==References==
{{reflist|2}}
{{reflist|2}}
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[[Category:Needs content]]
[[Category:Primary care]]
[[Category:Disease]]
[[Category:Disease]]
[[Category:Infectious disease]]
[[Category:Inflammations]]
[[Category:Inflammations]]
[[Category:Otolaryngology]]
[[Category:Otolaryngology]]
[[Category:Otology]]
[[Category:Otology]]
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Latest revision as of 23:30, 29 July 2020

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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.

Overview

The pathogenesis of otitis media is directly connected to the pathogen responsible for nasopharyngitis. This includes infectious causes, such as viral upper respiratory infection, as well as bacterial infection from Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Staphylococcus aureus. Mucus in the middle ear causes congestion that results in dysfunction of the eustachian tube. Pressure regulation in the inner ear is altered, causing effusion of fluid into the tympanic cavity containing the pathogen of nasopharyngitis. Otitis media results from the inflammatory response to the infection. Otitis media is transmitted through respiratory droplets through saliva or mucus, as well as direct physical contact with a contaminated individual or physical surface. Otitis media is often associated with other upper respiratory conditions caused by the nasopharynx pathogen, as well as allergic conditions such as allergic rhinitis. There is evidence of genetic predisposition to otitis media, with statistically significant evidence that it has high heritability. The following genes have been identified as having having potential pathogenic qualities for otitis media: CAPN14, GALNT14, BPIFA3, BPIFA1, BMP5, GALNT13, NELL1, TGFB3. Up-regulation of the genes correlated to otitis media pathogenesis contribute to individual susecptibility to the disease.

Pathophysiology

Pathogenesis

Transmission

  • Otitis media is transmitted through respiratory droplets through saliva or mucus, as well as direct physical contact with a contaminated individual or physical surface.
    • The pathogen responsible for the causative nasopharyngitis is also responsible for otitis media.[4]

Genetics

  • There is evidence of genetic predisposition to otitis media, with statistically significant evidence that it has high heritability.[6]
    • Hereditary factors comprising 45-75% of risk factors for otitis media, as revealed by heritability studies involving twins and triplets.[7]
  • The following genes have been identified as having having potential pathogenic qualities for otitis media:[7]
    • 2p23.1
      • CAPN14
      • GALNT14
    • 20q11.21
      • BPIFA3
      • BPIFA1
    • Those that interact with the TGFβ pathway:
  • Up-regulation of the genes correlated to otitis media pathogenesis contribute to individual susceptibility to the disease.

Associated Conditions

References

  1. 1.0 1.1 Coticchia JM, Chen M, Sachdeva L, Mutchnick S (2013). "New paradigms in the pathogenesis of otitis media in children". Front Pediatr. 1: 52. doi:10.3389/fped.2013.00052. PMC 3874850. PMID 24400296.
  2. Nguyen LH, Manoukian JJ, Tewfik TL, Sobol SE, Joubert P, Mazer BD, Schloss MD, Taha R, Hamid QA (2004). "Evidence of allergic inflammation in the middle ear and nasopharynx in atopic children with otitis media with effusion". J Otolaryngol. 33 (6): 345–51. PMID 15971648.
  3. Baron, Samuel (1996). Medical microbiology. Galveston, Tex: University of Texas Medical Branch at Galveston. ISBN 0963117211.
  4. 4.0 4.1 4.2 Qureishi A, Lee Y, Belfield K, Birchall JP, Daniel M (2014). "Update on otitis media - prevention and treatment". Infect Drug Resist. 7: 15–24. doi:10.2147/IDR.S39637. PMC 3894142. PMID 24453496.
  5. "Otitis media with effusion: MedlinePlus Medical Encyclopedia".
  6. Hafrén L, Kentala E, Järvinen TM, Leinonen E, Onkamo P, Kere J, Mattila PS (2012). "Genetic background and the risk of otitis media". Int. J. Pediatr. Otorhinolaryngol. 76 (1): 41–4. doi:10.1016/j.ijporl.2011.09.026. PMID 22018929.
  7. 7.0 7.1 Rye MS, Warrington NM, Scaman ES, Vijayasekaran S, Coates HL, Anderson D, Pennell CE, Blackwell JM, Jamieson SE (2012). "Genome-wide association study to identify the genetic determinants of otitis media susceptibility in childhood". PLoS ONE. 7 (10): e48215. doi:10.1371/journal.pone.0048215. PMC 3485007. PMID 23133572.

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