Otitis media pathophysiology
|
Otitis media Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Otitis media pathophysiology On the Web |
|
American Roentgen Ray Society Images of Otitis media pathophysiology |
|
Risk calculators and risk factors for Otitis media pathophysiology |
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
- Otitis media develops as a result of nasopharanx inflammation as a result of infections, such as viral upper respiratory infection and strep throat.[1]
- Nasopharyngitis is caused by the inhalation of respiratory droplets containing viral infection, usually rhinovirus or similar upper respiratory infection causing viruses.[3]
- The viruses penetrate through the epithelial cells in respiratory mucosa.
- The virus infiltrates histiocytes, lymphocytes, plasma cells, and neutrophils 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.[4]
- Nasopharyngitis results in eustachian tube dysfunction due to congestion from mucus production as a result of infection.[4]
- Pressure regulation in the inner ear is altered as the surrounding tissue absorbs trapped gas.[5]
- 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.[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]
- 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.[1]
- Associated conditions are also allergies-related, such as allergic rhinitis.
References
- ↑ 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.
- ↑ 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.
- ↑ Baron, Samuel (1996). Medical microbiology. Galveston, Tex: University of Texas Medical Branch at Galveston. ISBN 0963117211.
- ↑ 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.
- ↑ "Otitis media with effusion: MedlinePlus Medical Encyclopedia".
- ↑ 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.
- ↑ 7.0 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.