Adenoiditis pathophysiology: Difference between revisions

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== Overview ==
== 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.<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 ==
== Pathophysiology ==
[[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>
* 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.


Oral cavity normal [[flora]] [[bacteria]] are found in adenoid flora as well, which include:
* Adenoids are developed from [[Lymphocyte|lymphocytes infiltration]] in subendothelium of nasopharynx during the 16th week of gestation.  
*[[Streptococcus|Alpha-hemolytic streptococci]]
*[[Enterococcus|Enterococci]]
*[[Corynebacterium]] species
*[[Coagulase-negative staphylococci]]
*[[Neisseria species]]
*[[Haemophilus|Haemophilus species]]
*[[Micrococcus|Micrococcus species]]
*Stomatococcus species
[[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.


==Overview==
* After the birth adenoids begin to enlarge.
Tonsillitis develops when the pathogen, [[viral]] or [[bacterial]], infects the [[tonsils]] and elicits an [[inflammatory]] response. It develops when the [[viruses]] infiltrate the tonsils and cause an [[inflammatory]] response of up-regulated [[cytokines]]. [[Bacterial]] tonsillitis considered acute is primarily caused by [[Group A streptococcal infection|group A β-hemolytic streptococcus (GABHS)]] ''[[streptococcus pyogenes]]'' infection. ''[[s. pyogenes]]'' and taxonomically-similar [[bacteria]] infiltrate the [[Tonsils|tonsillar]] [[epithelium]], successfully penetrating the protective [[mucosal]] films in the oral and nasal cavity. Recurrent [[bacterial]] tonsillitis is caused primarily by ''[[staphylococcus aureus]]''. Following invasion, ''[[S. aureus]]'' is internalized by non-[[phagocytic]] cells through [[fibronectin]]-binding [[protein]] and beta-[[integrins]]. Invasion of non-eukaryotic cells results in the up-regulation of [[cytokines]], resulting in tonsillitis. Tonsillitis is associated with conditions and diseases associated with its [[viral]] and [[bacterial]] pathogens.
* 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 adenoid development==
* Normal flora found in the mature adenoid tissue consists:
Adenoids are on the posterior nasopharynx, posterior to the nasal cavity. They are a component of the Waldeyer ring of lymphoid tissue, which is a ring of lymphoid tissue and include adenoids and tonsils.
** [[Streptococcus|Alpha-hemolytic streptococci]]
* Adenoids are developed from lymphocytes infiltration in subendothelium of nasopharynx in the 16th week of gestation.
**[[Enterococcus|Enterococci]]
 
**[[Corynebacterium]] species
* After the birth they begin to enlarge.
**[[Coagulase-negative staphylococci]]
**[[Neisseria species]]
**[[Haemophilus|Haemophilus species]]
**[[Micrococcus|Micrococcus species]]
**Stomatococcus species
* It is normal to find symptomatic adenoids in children aged 18-24 months.
* It is normal to find symptomatic adenoids in children aged 18-24 months.
* They continue their grow until individuals are aged 5-7 years.  
* They continue their grow until individuals are aged 5-7 years.  
Line 31: Line 27:
* 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.
At birth, the nasopharynx and, thus, the adenoids, are accessible to many organisms. The establishment of the upper respiratory tract is initiated at birth. By the time children are aged 6 months, lactobacilli, anaerobic streptococci, actinomycosis, Fusobacterium species, and Nocardia species are present. Normal flora found in the adenoid consists of alpha-hemolytic streptococci and enterococci, Corynebacterium species, coagulase-negative staphylococci, Neisseria species, Haemophilus species, Micrococcus species, and Stomatococcus species. The adenoids can become infected and harbor pathogenic bacteria, which may lead to the development of disease of the ears, nose, and sinuses.
== 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>
 
* [[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.<ref name="pmid11843928">{{cite journal |vauthors=Capper R, Canter RJ |title=Is the incidence of tonsillectomy influenced by the family medical or social history? |journal=Clin Otolaryngol Allied Sci |volume=26 |issue=6 |pages=484–7 |year=2001 |pmid=11843928 |doi= |url=}}</ref><ref name="KvestadKværner2005">{{cite journal|last1=Kvestad|first1=Ellen|last2=Kværner|first2=Kari Jorunn|last3=Røysamb|first3=Espen|last4=Tambs|first4=Kristian|last5=Harris|first5=Jennifer Ruth|last6=Magnus|first6=Per|title=Heritability of Recurrent Tonsillitis|journal=Archives of Otolaryngology–Head & Neck Surgery|volume=131|issue=5|year=2005|pages=383|issn=0886-4470|doi=10.1001/archotol.131.5.383}}</ref>
*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">{{cite journal |vauthors=Mohseni S, Shojaiefard A, Khorgami Z, Alinejad S, Ghorbani A, Ghafouri A |title=Peripheral lymphadenopathy: approach and diagnostic tools |journal=Iran J Med Sci |volume=39 |issue=2 Suppl |pages=158–70 |year=2014 |pmid=24753638 |pmc=3993046 |doi= |url=}}</ref>
*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 streptococcal infection|group A β-hemolytic streptococcus (GABHS)]] ''[[Streptococcus pyogenes]]'' infection.<ref name="pmid9804015">{{cite journal |vauthors=Lilja M, Räisänen S, Stenfors LE |title=Initial events in the pathogenesis of acute tonsillitis caused by Streptococcus pyogenes |journal=Int. J. Pediatr. Otorhinolaryngol. |volume=45 |issue=1 |pages=15–20 |year=1998 |pmid=9804015 |doi= |url=}}</ref>
**''[[S. pyogenes]]'' and taxonomically-similar [[bacteria]] infiltrate the adenoidal [[epithelium]], successfully penetrating the protective [[mucosal]] films in the oral and nasal cavity.<ref name="pmid3317744">{{cite journal |vauthors=Beachey EH, Courtney HS |title=Bacterial adherence: the attachment of group A streptococci to mucosal surfaces |journal=Rev. Infect. Dis. |volume=9 Suppl 5 |issue= |pages=S475–81 |year=1987 |pmid=3317744 |doi= |url=}}</ref><ref name="pmid2654229">{{cite journal |vauthors=Gibbons RJ |title=Bacterial adhesion to oral tissues: a model for infectious diseases |journal=J. Dent. Res. |volume=68 |issue=5 |pages=750–60 |year=1989 |pmid=2654229 |doi= |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).
 
== Gross pathology ==
*On gross pathology, characteristic findings of adenoiditis, include:
:*Enlarged adenoids
:*Soft greasy yellow areas within capsule


Tonsillitis develops when the pathogen, [[viral]] or [[bacterial]], infects the [[tonsils]] and elicits an [[inflammatory]] response.<ref name="urlTonsillitis - Causes - NHS Choices">{{cite web |url=http://www.nhs.uk/Conditions/Tonsillitis/Pages/Causes.aspx |title=Tonsillitis - Causes - NHS Choices |format= |work= |accessdate=}}</ref>
== Microscopic Pathology ==
===Viral Tonsillitis===
*On microscopic histopathological analysis, characteristic findings of adenoiditis
*Viral tonsillitis is usually caused by the following viruses:<ref name="urlTonsillitis - Causes - NHS Choices" />
**[[Rhinovirus]]
**[[Influenza]]
**[[Parainfluenza virus]]
**[[Adenovirus]]
**[[Measles|Rubeola virus]]
**[[Epstein Barr virus|Epstein barr virus]]<ref name="pmid11249975">{{cite journal |vauthors=Endo LH, Ferreira D, Montenegro MC, Pinto GA, Altemani A, Bortoleto AE, Vassallo J |title=Detection of Epstein-Barr virus in tonsillar tissue of children and the relationship with recurrent tonsillitis |journal=Int. J. Pediatr. Otorhinolaryngol. |volume=58 |issue=1 |pages=9–15 |year=2001 |pmid=11249975 |doi= |url=}}</ref>
*Tonsillitis develops when the [[viruses]] infiltrate the tonsils and cause an [[inflammatory]] response of up-regulated [[cytokines]].
====Chronic Viral Tonsillitis====
The persistence of tonsillitis beyond 3 months is known as chronic tonsillitis. In case of chronic viral  tonsillitis the virus persist in the tonsils and lead to chronic inflammation. This persistent infection and [[inflammation]] leads to chronic tonsillitis. The most common involved [[viruses]] is [[EBV]].<ref name="pmid21377220">{{cite journal| author=Sadeghi-Shabestari M, Jabbari Moghaddam Y, Ghaharri H| title=Is there any correlation between allergy and adenotonsillar tissue hypertrophy? | journal=Int J Pediatr Otorhinolaryngol | year= 2011 | volume= 75 | issue= 4 | pages= 589-91 | pmid=21377220 | doi=10.1016/j.ijporl.2011.01.026 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21377220  }}</ref><ref name="pmid17136878">{{cite journal| author=Akcay A, Tamay Z, Dağdeviren E, Guler N, Ones U, Kara CO et al.| title=Childhood asthma and its relationship with tonsillar tissue. | journal=Asian Pac J Allergy Immunol | year= 2006 | volume= 24 | issue= 2-3 | pages= 129-34 | pmid=17136878 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17136878  }}</ref><ref name="pmid22870291">{{cite journal| author=Proenca-Modena JL, Pereira Valera FC, Jacob MG, Buzatto GP, Saturno TH, Lopes L et al.| title=High rates of detection of respiratory viruses in tonsillar tissues from children with chronic adenotonsillar disease. | journal=PLoS One | year= 2012 | volume= 7 | issue= 8 | pages= e42136 | pmid=22870291 | doi=10.1371/journal.pone.0042136 | pmc=3411673 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22870291  }}</ref>
===Bacterial Tonsillitis===
[[Bacterial]] tonsillitis develops upon infection of the [[tonsils]] with pathogenic [[bacteria]].<ref name="pmid9804015">{{cite journal |vauthors=Lilja M, Räisänen S, Stenfors LE |title=Initial events in the pathogenesis of acute tonsillitis caused by Streptococcus pyogenes |journal=Int. J. Pediatr. Otorhinolaryngol. |volume=45 |issue=1 |pages=15–20 |year=1998 |pmid=9804015 |doi= |url=}}</ref>
====Acute Bacterial Tonsillitis====
*[[Bacterial]] tonsillitis considered acute is primarily caused by [[Group A streptococcal infection|group A β-hemolytic streptococcus (GABHS)]] ''[[Streptococcus pyogenes]]'' infection.<ref name="pmid9804015" />
**''[[S. pyogenes]]'' and taxonomically-similar [[bacteria]] infiltrate the [[Tonsils|tonsillar]] [[epithelium]], successfully penetrating the protective [[mucosal]] films in the oral and nasal cavity.<ref name="pmid3317744">{{cite journal |vauthors=Beachey EH, Courtney HS |title=Bacterial adherence: the attachment of group A streptococci to mucosal surfaces |journal=Rev. Infect. Dis. |volume=9 Suppl 5 |issue= |pages=S475–81 |year=1987 |pmid=3317744 |doi= |url=}}</ref><ref name="pmid2654229">{{cite journal |vauthors=Gibbons RJ |title=Bacterial adhesion to oral tissues: a model for infectious diseases |journal=J. Dent. Res. |volume=68 |issue=5 |pages=750–60 |year=1989 |pmid=2654229 |doi= |url=}}</ref>
***Colonization begins when the [[bacteria]] adheres to the [[tonsillar]] surface [[proteins]] through [[lipoteichoic acid]] (LTA), depositing [[fibronectin]] molecules that bind to the [[tonsillar]] [[epithelium]].<ref name="pmid3317744" />
***The following [[virulence factors]] contribute to ''[[S. pyogenes]]'' adhesion to the [[tonsils]]:<ref name="Cunningham2000">{{cite journal|last1=Cunningham|first1=M. W.|title=Pathogenesis of Group A Streptococcal Infections|journal=Clinical Microbiology Reviews|volume=13|issue=3|year=2000|pages=470–511|issn=0893-8512|doi=10.1128/CMR.13.3.470-511.2000}}</ref>
****Containing [[M protein]], allowing colonization<ref name="pmid4564883">{{cite journal |vauthors=Ellen RP, Gibbons RJ |title=M protein-associated adherence of Streptococcus pyogenes to epithelial surfaces: prerequisite for virulence |journal=Infect. Immun. |volume=5 |issue=5 |pages=826–30 |year=1972 |pmid=4564883 |pmc=422446 |doi= |url=}}</ref>
****Lipotechoic acid (LTA): Binds with [[fibronectin]] or [[fibrinogen]], causing adhesion of the bacteria to the [[dermis]]<ref name="pmid8063411">{{cite journal |vauthors=Courtney HS, Li Y, Dale JB, Hasty DL |title=Cloning, sequencing, and expression of a fibronectin/fibrinogen-binding protein from group A streptococci |journal=Infect. Immun. |volume=62 |issue=9 |pages=3937–46 |year=1994 |pmid=8063411 |pmc=303051 |doi= |url=}}</ref>
****[[Protein]] F: Binds with [[fibronectin]] to mediate adhesion<ref name="pmid1385871">{{cite journal |vauthors=Hanski E, Caparon M |title=Protein F, a fibronectin-binding protein, is an adhesin of the group A streptococcus Streptococcus pyogenes |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=89 |issue=13 |pages=6172–6 |year=1992 |pmid=1385871 |pmc=402144 |doi= |url=}}</ref>
****29-kDa [[fibronectin]]-binding [[protein]]<ref name="CourtneyHasty1992">{{cite journal|last1=Courtney|first1=Harry S.|last2=Hasty|first2=David L.|last3=Dale|first3=James B.|last4=Poirier|first4=Thomas P.|title=A 28-kilodalton fibronectin-binding protein of group a streptococci|journal=Current Microbiology|volume=25|issue=5|year=1992|pages=245–250|issn=0343-8651|doi=10.1007/BF01575856}}</ref>
****[[Glyceraldehyde 3-phosphate dehydrogenase]]<ref name="pmid8760943">{{cite journal |vauthors=Winram SB, Lottenberg R |title=The plasmin-binding protein Plr of group A streptococci is identified as glyceraldehyde-3-phosphate dehydrogenase |journal=Microbiology (Reading, Engl.) |volume=142 ( Pt 8) |issue= |pages=2311–20 |year=1996 |pmid=8760943 |doi=10.1099/13500872-142-8-2311 |url=}}</ref>
****70-kDa [[galactose]]-binding [[protein]]<ref name="WalströmTylewska1982">{{cite journal|last1=Walström|first1=Torkel|last2=Tylewska|first2=Stanislawa|title=Glycoconjugates as possible receptors forStreptococcus pyogenes|journal=Current Microbiology|volume=7|issue=6|year=1982|pages=343–346|issn=0343-8651|doi=10.1007/BF01572601}}</ref>
****[[Vitronectin]]-binding S [[protein]]<ref name="pmid2459063">{{cite journal |vauthors=Valentin-Weigand P, Grulich-Henn J, Chhatwal GS, Müller-Berghaus G, Blobel H, Preissner KT |title=Mediation of adherence of streptococci to human endothelial cells by complement S protein (vitronectin) |journal=Infect. Immun. |volume=56 |issue=11 |pages=2851–5 |year=1988 |pmid=2459063 |pmc=259660 |doi= |url=}}</ref>
****[[Collagen]]-binding protein<ref name="pmid7814395">{{cite journal |vauthors=Visai L, Bozzini S, Raucci G, Toniolo A, Speziale P |title=Isolation and characterization of a novel collagen-binding protein from Streptococcus pyogenes strain 6414 |journal=J. Biol. Chem. |volume=270 |issue=1 |pages=347–53 |year=1995 |pmid=7814395 |doi= |url=}}</ref>
****[[Serum]] opacity factor
****[[Hyaluronate]] capsule<ref name="pmid7991612">{{cite journal |vauthors=Wessels MR, Bronze MS |title=Critical role of the group A streptococcal capsule in pharyngeal colonization and infection in mice |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=91 |issue=25 |pages=12238–42 |year=1994 |pmid=7991612 |pmc=45412 |doi= |url=}}</ref>
**This results in an [[inflammatory]] response of up-regulated [[cytokines]], leading to tonsillitis.<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>
====Recurrent Bacterial Tonsillitis====
*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>
**''[[S. aureus]]'' invades the [[tonsils]] through microbial surface components recognizing adhesive matrix molecules ([[MSCRAMM]]<nowiki/>s)<ref name="pmid20209109" />
**''[[S. aureus]]'' invades the adenoids through microbial surface components recognizing adhesive matrix molecules ([[MSCRAMM]]<nowiki/>s)<ref name="pmid20209109" />
**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 tonsillitis.
**Invasion of non-eukaryotic cells results in the up-regulation of [[cytokines]], resulting in adenoiditis
====Chronic Bacterial Tonsillitis====
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.
===Non-infectious Tonsillitis===
*It is a type of [[Chronic (medicine)|chronic]] that can be caused due to allergies, [[asthma]], [[GERD]],that persists beyond 3 months.<ref name="pmid21377220" /><ref name="pmid17136878" /><ref name="pmid22870291" />
**Recurrent [[GERD]] or [[allergies]] or [[astma]] can cause repeated irritation of the tonsils leading to chronic tonsillitis.
==Genetics==
*White not fully understood, there is quantitative evidence of recurrent tonsillitis heritability.<ref name="KvestadKværner2005">{{cite journal|last1=Kvestad|first1=Ellen|last2=Kværner|first2=Kari Jorunn|last3=Røysamb|first3=Espen|last4=Tambs|first4=Kristian|last5=Harris|first5=Jennifer Ruth|last6=Magnus|first6=Per|title=Heritability of Recurrent Tonsillitis|journal=Archives of Otolaryngology–Head & Neck Surgery|volume=131|issue=5|year=2005|pages=383|issn=0886-4470|doi=10.1001/archotol.131.5.383}}</ref>
**Parental history of [[tonsillectomy]] and [[atopy]] hold significant predictive power in pediatric tonsillitis.<ref name="pmid11843928">{{cite journal |vauthors=Capper R, Canter RJ |title=Is the incidence of tonsillectomy influenced by the family medical or social history? |journal=Clin Otolaryngol Allied Sci |volume=26 |issue=6 |pages=484–7 |year=2001 |pmid=11843928 |doi= |url=}}</ref>
 
*
{| class="wikitable"
!
!
!
!
|-
|Viral Tonsillitis
|
* [[Epstein Barr virus|Epstein-barr virus]] (EBV)
* [[Adeno virus|Human adenovirus]]
* [[Enterovirus]]
* [[Rhinovirus]]
* [[Respiratory syncytial virus]]
* [[Mononucleosis]]
* [[Cytomegalovirus|Cytomegalovirus (CMV)]]
* [[Toxoplasmosis]]
* [[Herpes virus]]
|
|
|-
|Acute Bacterial Tonsillitis
|
* [[Haemophilus influenzae]]
* [[Streptococcus|Group A β-hemolytic streptococcus]]
* [[Staphylococcus aureus]]
 
* [[Moraxella catarrhalis]]
* [[Streptococcus pneumoniae]]
|
|
|-
|Recurrent Bacterial Tonsillitis
| rowspan="2" |Usually due to normal flora pathogen:
* [[Staphylococcus aureus]]
* [[Streptococcus|Group A β-hemolytic streptococcus]]
|
|
|-
|Chronic Bacterial Tonsillitis
|
|
|-
|Non-infectious Tonsillitis
|Allergies


[[Asthma]]
==References==
{{Reflist|2}}


[[GERD]]
[[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

Adenoiditis Microchapters

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Future or Investigational Therapies

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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.
  • 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]
  • 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

References

  1. ↑ 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. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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. ↑ 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.
  7. ↑ Gibbons RJ (1989). "Bacterial adhesion to oral tissues: a model for infectious diseases". J. Dent. Res. 68 (5): 750–60. PMID 2654229.
  8. ↑ 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. ↑ 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.
  10. ↑ 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.
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