Adenoiditis pathophysiology: Difference between revisions
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== Overview == | == Overview == | ||
[[Adenoid|Adenoids]] are involved in the production of mostly secretory [[IgA]], which is transported to the surface | The pathogenesis of adenoiditis is characterized by its inflammation. This process is primarily due to an elevated rate of trafficking of lymphocytes into adenoid from the blood, exceeding the rate of outflow from the adenoid.<ref name="pmid24753638" /> [[Adenoid|Adenoids]] are involved in the production of mostly secretory [[IgA]], which is transported to the surface where it provides local [[immune]] protection. Adenoids can be infected by either [[bacterial]] and [[viral]] pathogens leading to adenoiditis.<ref name="pmid12117336" /> | ||
== | == Pathophysiology == | ||
* Adenoids are on the posterior nasopharynx, posterior to the nasal cavity. They are a component of the [[Waldeyer's ring]] of lymphoid tissue, which is a ring of lymphoid tissue and | * Adenoids are on the posterior nasopharynx, posterior to the nasal cavity. They are a component of the [[Waldeyer's ring]] of lymphoid tissue, which is a ring of lymphoid tissue and includes adenoids and tonsils. | ||
* Adenoids are developed from [[Lymphocyte|lymphocytes infiltration]] in subendothelium of nasopharynx | * Adenoids are developed from [[Lymphocyte|lymphocytes infiltration]] in subendothelium of nasopharynx during the 16th week of gestation. | ||
* After the birth | * After the birth adenoids begin to enlarge. | ||
* By the time children are aged 6 months, [[lactobacilli]], [[Anaerobic bacteria|anaerobic streptococci]], [[actinomycosis]], [[Fusobacterium species]], and [[Nocardia]] species are present. | * By the time children are aged 6 months, [[lactobacilli]], [[Anaerobic bacteria|anaerobic streptococci]], [[actinomycosis]], [[Fusobacterium species]], and [[Nocardia]] species are present in the mucosal flora. | ||
* Normal flora found in the mature adenoid tissue consists: | * Normal flora found in the mature adenoid tissue consists: | ||
** [[Streptococcus|Alpha-hemolytic streptococci]] | ** [[Streptococcus|Alpha-hemolytic streptococci]] | ||
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* Adenoids start to shrink by the age 6-7. | * Adenoids start to shrink by the age 6-7. | ||
* By the time children reach 10-12, the adenoids are usually small enough for the child to become asymptomatic. | * By the time children reach 10-12, the adenoids are usually small enough for the child to become asymptomatic. | ||
== | == Pathogenesis == | ||
* [[Adenoid|Adenoids]] are involved in the production of mostly secretory [[IgA]], which is transported to the surface providing local [[immune]] protection. Studies suggest that a reduction in [[IgA]] will happen postoperative of [[adenoidectomy]].<ref name="pmid12117336">{{cite journal |vauthors=Havas T, Lowinger D |title=Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy |journal=Arch. Otolaryngol. Head Neck Surg. |volume=128 |issue=7 |pages=789–91 |year=2002 |pmid=12117336 |doi= |url=}}</ref> | * [[Adenoid|Adenoids]] are involved in the production of mostly secretory [[IgA]], which is transported to the surface providing local [[immune]] protection. Studies suggest that a reduction in [[IgA]] will happen postoperative of [[adenoidectomy]].<ref name="pmid12117336">{{cite journal |vauthors=Havas T, Lowinger D |title=Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy |journal=Arch. Otolaryngol. Head Neck Surg. |volume=128 |issue=7 |pages=789–91 |year=2002 |pmid=12117336 |doi= |url=}}</ref> | ||
| Line 40: | Line 40: | ||
***Colonization begins when the [[bacteria]] adheres to the adenoid surface [[proteins]] through [[lipoteichoic acid]] (LTA), depositing [[fibronectin]] molecules that bind to the adenoidal [[epithelium]].<ref name="pmid3317744" /><ref name="pmid17426506">{{cite journal |vauthors=Zhang JM, An J |title=Cytokines, inflammation, and pain |journal=Int Anesthesiol Clin |volume=45 |issue=2 |pages=27–37 |year=2007 |pmid=17426506 |pmc=2785020 |doi=10.1097/AIA.0b013e318034194e |url=}}</ref> | ***Colonization begins when the [[bacteria]] adheres to the adenoid surface [[proteins]] through [[lipoteichoic acid]] (LTA), depositing [[fibronectin]] molecules that bind to the adenoidal [[epithelium]].<ref name="pmid3317744" /><ref name="pmid17426506">{{cite journal |vauthors=Zhang JM, An J |title=Cytokines, inflammation, and pain |journal=Int Anesthesiol Clin |volume=45 |issue=2 |pages=27–37 |year=2007 |pmid=17426506 |pmc=2785020 |doi=10.1097/AIA.0b013e318034194e |url=}}</ref> | ||
*Adenoid paracortex may also be enlarged secondarily as a result of the activation and proliferation of antigen-specific T and B cells (clonal expansion). | *Adenoid paracortex may also be enlarged secondarily as a result of the activation and proliferation of antigen-specific T and B cells (clonal expansion). | ||
== Gross pathology == | |||
*On gross pathology, characteristic findings of adenoiditis, include: | *On gross pathology, characteristic findings of adenoiditis, include: | ||
:*Enlarged adenoids | :*Enlarged adenoids | ||
:*Soft greasy yellow areas within capsule | :*Soft greasy yellow areas within capsule | ||
== Microscopic Pathology == | |||
*On microscopic histopathological analysis, characteristic findings of adenoiditis | *On microscopic histopathological analysis, characteristic findings of adenoiditis | ||
*Recurrent [[bacterial]] tonsillitis is caused primarily by ''[[Staphylococcus aureus]]''.<ref name="pmid20209109">{{cite journal |vauthors=Zautner AE, Krause M, Stropahl G, Holtfreter S, Frickmann H, Maletzki C, Kreikemeyer B, Pau HW, Podbielski A |title=Intracellular persisting Staphylococcus aureus is the major pathogen in recurrent tonsillitis |journal=PLoS ONE |volume=5 |issue=3 |pages=e9452 |year=2010 |pmid=20209109 |pmc=2830486 |doi=10.1371/journal.pone.0009452 |url=}}</ref> | *Recurrent [[bacterial]] tonsillitis is caused primarily by ''[[Staphylococcus aureus]]''.<ref name="pmid20209109">{{cite journal |vauthors=Zautner AE, Krause M, Stropahl G, Holtfreter S, Frickmann H, Maletzki C, Kreikemeyer B, Pau HW, Podbielski A |title=Intracellular persisting Staphylococcus aureus is the major pathogen in recurrent tonsillitis |journal=PLoS ONE |volume=5 |issue=3 |pages=e9452 |year=2010 |pmid=20209109 |pmc=2830486 |doi=10.1371/journal.pone.0009452 |url=}}</ref> | ||
| Line 48: | Line 52: | ||
**Following invasion, ''[[S. aureus]]'' is internalized by non-[[phagocytic]] cells through [[fibronectin]]-binding [[protein]] and beta-[[integrins]].<ref name="pmid11549002">{{cite journal |vauthors=Alexander EH, Hudson MC |title=Factors influencing the internalization of Staphylococcus aureus and impacts on the course of infections in humans |journal=Appl. Microbiol. Biotechnol. |volume=56 |issue=3-4 |pages=361–6 |year=2001 |pmid=11549002 |doi= |url=}}</ref> | **Following invasion, ''[[S. aureus]]'' is internalized by non-[[phagocytic]] cells through [[fibronectin]]-binding [[protein]] and beta-[[integrins]].<ref name="pmid11549002">{{cite journal |vauthors=Alexander EH, Hudson MC |title=Factors influencing the internalization of Staphylococcus aureus and impacts on the course of infections in humans |journal=Appl. Microbiol. Biotechnol. |volume=56 |issue=3-4 |pages=361–6 |year=2001 |pmid=11549002 |doi= |url=}}</ref> | ||
**Invasion of non-eukaryotic cells results in the up-regulation of [[cytokines]], resulting in adenoiditis | **Invasion of non-eukaryotic cells results in the up-regulation of [[cytokines]], resulting in adenoiditis | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Disease]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Otolaryngology]] | |||
[[Category:Pediatrics]] | |||
[[Category:Pulmonology]] | |||
[[Category:Emergency medicine]] | |||
[[Category:Infectious disease]] | |||
[[Category:Surgery]] | |||
Latest revision as of 20:18, 29 July 2020
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Adenoiditis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]
Overview
The pathogenesis of adenoiditis is characterized by its inflammation. This process is primarily due to an elevated rate of trafficking of lymphocytes into adenoid from the blood, exceeding the rate of outflow from the adenoid.[1] Adenoids are involved in the production of mostly secretory IgA, which is transported to the surface where it provides local immune protection. Adenoids can be infected by either bacterial and viral pathogens leading to adenoiditis.[2]
Pathophysiology
- Adenoids are on the posterior nasopharynx, posterior to the nasal cavity. They are a component of the Waldeyer's ring of lymphoid tissue, which is a ring of lymphoid tissue and includes adenoids and tonsils.
- Adenoids are developed from lymphocytes infiltration in subendothelium of nasopharynx during the 16th week of gestation.
- After the birth adenoids begin to enlarge.
- By the time children are aged 6 months, lactobacilli, anaerobic streptococci, actinomycosis, Fusobacterium species, and Nocardia species are present in the mucosal flora.
- Normal flora found in the mature adenoid tissue consists:
- Alpha-hemolytic streptococci
- Enterococci
- Corynebacterium species
- Coagulase-negative staphylococci
- Neisseria species
- Haemophilus species
- Micrococcus species
- Stomatococcus species
- It is normal to find symptomatic adenoids in children aged 18-24 months.
- They continue their grow until individuals are aged 5-7 years.
- Adenoids start to shrink by the age 6-7.
- By the time children reach 10-12, the adenoids are usually small enough for the child to become asymptomatic.
Pathogenesis
- Adenoids are involved in the production of mostly secretory IgA, which is transported to the surface providing local immune protection. Studies suggest that a reduction in IgA will happen postoperative of adenoidectomy.[2]
- Adenoiditis can happen as a result of infection and harbor pathogenic bacterial activity, which may lead to the development of disease of the ears, nose, and sinuses. Adenoiditis can progress to chronic disease if remain untreated for a long term.
- Parental history of tonsillectomy and atopy hold significant predictive power in pediatric adenoiditis.[3][4]
- The pathogenesis of adenoiditis is characterized by its inflammation. This process is primarily due to an elevated rate of trafficking of lymphocytes into adenoid from the blood, exceeding the rate of outflow from the adenoid.[1]
- The persistence of tonsillitis beyond 3 months is known as chronic tonsillitis. In case of chronic bacterial tonsillitis the bacteria persist in the tonsils and lead to chronic inflammation. This persistent infection and inflammation leads to chronic tonsillitis. Manifestations appear whenever the patient has decline in immunity.
- The immune response between the antigen and lymphocyte that leads to cellular proliferation and enlargement of the adeoid especially in paracortex area which lead to excess enlargement of the adenoids.
- Bacterial adenoiditis is primarily caused by group A β-hemolytic streptococcus (GABHS) Streptococcus pyogenes infection.[5]
- S. pyogenes and taxonomically-similar bacteria infiltrate the adenoidal epithelium, successfully penetrating the protective mucosal films in the oral and nasal cavity.[6][7]
- Colonization begins when the bacteria adheres to the adenoid surface proteins through lipoteichoic acid (LTA), depositing fibronectin molecules that bind to the adenoidal epithelium.[6][8]
- S. pyogenes and taxonomically-similar bacteria infiltrate the adenoidal epithelium, successfully penetrating the protective mucosal films in the oral and nasal cavity.[6][7]
- Adenoid paracortex may also be enlarged secondarily as a result of the activation and proliferation of antigen-specific T and B cells (clonal expansion).
Gross pathology
- On gross pathology, characteristic findings of adenoiditis, include:
- Enlarged adenoids
- Soft greasy yellow areas within capsule
Microscopic Pathology
- On microscopic histopathological analysis, characteristic findings of adenoiditis
- Recurrent bacterial tonsillitis is caused primarily by Staphylococcus aureus.[9]
- S. aureus invades the adenoids through microbial surface components recognizing adhesive matrix molecules (MSCRAMMs)[9]
- Following invasion, S. aureus is internalized by non-phagocytic cells through fibronectin-binding protein and beta-integrins.[10]
- Invasion of non-eukaryotic cells results in the up-regulation of cytokines, resulting in adenoiditis
References
- ↑ 1.0 1.1 Mohseni S, Shojaiefard A, Khorgami Z, Alinejad S, Ghorbani A, Ghafouri A (2014). "Peripheral lymphadenopathy: approach and diagnostic tools". Iran J Med Sci. 39 (2 Suppl): 158–70. PMC 3993046. PMID 24753638.
- ↑ 2.0 2.1 Havas T, Lowinger D (2002). "Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy". Arch. Otolaryngol. Head Neck Surg. 128 (7): 789–91. PMID 12117336.
- ↑ Capper R, Canter RJ (2001). "Is the incidence of tonsillectomy influenced by the family medical or social history?". Clin Otolaryngol Allied Sci. 26 (6): 484–7. PMID 11843928.
- ↑ Kvestad, Ellen; Kværner, Kari Jorunn; Røysamb, Espen; Tambs, Kristian; Harris, Jennifer Ruth; Magnus, Per (2005). "Heritability of Recurrent Tonsillitis". Archives of Otolaryngology–Head & Neck Surgery. 131 (5): 383. doi:10.1001/archotol.131.5.383. ISSN 0886-4470.
- ↑ Lilja M, Räisänen S, Stenfors LE (1998). "Initial events in the pathogenesis of acute tonsillitis caused by Streptococcus pyogenes". Int. J. Pediatr. Otorhinolaryngol. 45 (1): 15–20. PMID 9804015.
- ↑ 6.0 6.1 Beachey EH, Courtney HS (1987). "Bacterial adherence: the attachment of group A streptococci to mucosal surfaces". Rev. Infect. Dis. 9 Suppl 5: S475–81. PMID 3317744.
- ↑ Gibbons RJ (1989). "Bacterial adhesion to oral tissues: a model for infectious diseases". J. Dent. Res. 68 (5): 750–60. PMID 2654229.
- ↑ Zhang JM, An J (2007). "Cytokines, inflammation, and pain". Int Anesthesiol Clin. 45 (2): 27–37. doi:10.1097/AIA.0b013e318034194e. PMC 2785020. PMID 17426506.
- ↑ 9.0 9.1 Zautner AE, Krause M, Stropahl G, Holtfreter S, Frickmann H, Maletzki C, Kreikemeyer B, Pau HW, Podbielski A (2010). "Intracellular persisting Staphylococcus aureus is the major pathogen in recurrent tonsillitis". PLoS ONE. 5 (3): e9452. doi:10.1371/journal.pone.0009452. PMC 2830486. PMID 20209109.
- ↑ Alexander EH, Hudson MC (2001). "Factors influencing the internalization of Staphylococcus aureus and impacts on the course of infections in humans". Appl. Microbiol. Biotechnol. 56 (3–4): 361–6. PMID 11549002.