Adenoiditis pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
(Created page with "__NOTOC__ {{Adenoiditis}} {{CMG}};{{AE}}{{MIR}}")
 
No edit summary
Line 2: Line 2:
{{Adenoiditis}}
{{Adenoiditis}}
{{CMG}};{{AE}}{{MIR}}
{{CMG}};{{AE}}{{MIR}}
== Overview ==
== 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>
Oral cavity normal [[flora]] [[bacteria]] are found in adenoid flora as well, which include:
*[[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==
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.
==Normal adenoid development==
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.
* Adenoids are developed from lymphocytes infiltration in subendothelium of nasopharynx in the 16th week of gestation.
* After the birth they begin to enlarge.
* 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.
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.
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>
===Viral Tonsillitis===
*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>
**''[[S. aureus]]'' invades the [[tonsils]] 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>
**Invasion of non-eukaryotic cells results in the up-regulation of [[cytokines]], resulting in tonsillitis.
====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]]
[[GERD]]
|
|
|}

Revision as of 20:36, 31 May 2017

Adenoiditis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Adenoiditis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

Pathophysiology

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.[1]

Oral cavity normal flora bacteria are found in adenoid flora as well, which include:

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

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 β-hemolytic streptococcus (GABHS) streptococcus pyogenes infection. s. pyogenes and taxonomically-similar bacteria infiltrate the 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.

Normal adenoid development

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.

  • Adenoids are developed from lymphocytes infiltration in subendothelium of nasopharynx in the 16th week of gestation.
  • After the birth they begin to enlarge.
  • 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.

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.

Tonsillitis develops when the pathogen, viral or bacterial, infects the tonsils and elicits an inflammatory response.[2]

Viral Tonsillitis

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.[4][5][6]

Bacterial Tonsillitis

Bacterial tonsillitis develops upon infection of the tonsils with pathogenic bacteria.[7]

Acute Bacterial Tonsillitis

Recurrent Bacterial Tonsillitis

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 that can be caused due to allergies, asthma, GERD,that persists beyond 3 months.[4][5][6]
    • 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.[23]
Viral Tonsillitis
Acute Bacterial Tonsillitis
Recurrent Bacterial Tonsillitis Usually due to normal flora pathogen:
Chronic Bacterial Tonsillitis
Non-infectious Tonsillitis Allergies

Asthma

GERD

  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.
  2. ↑ 2.0 2.1 "Tonsillitis - Causes - NHS Choices".
  3. ↑ Endo LH, Ferreira D, Montenegro MC, Pinto GA, Altemani A, Bortoleto AE, Vassallo J (2001). "Detection of Epstein-Barr virus in tonsillar tissue of children and the relationship with recurrent tonsillitis". Int. J. Pediatr. Otorhinolaryngol. 58 (1): 9–15. PMID 11249975.
  4. ↑ 4.0 4.1 Sadeghi-Shabestari M, Jabbari Moghaddam Y, Ghaharri H (2011). "Is there any correlation between allergy and adenotonsillar tissue hypertrophy?". Int J Pediatr Otorhinolaryngol. 75 (4): 589–91. doi:10.1016/j.ijporl.2011.01.026. PMID 21377220.
  5. ↑ 5.0 5.1 Akcay A, Tamay Z, Dağdeviren E, Guler N, Ones U, Kara CO; et al. (2006). "Childhood asthma and its relationship with tonsillar tissue". Asian Pac J Allergy Immunol. 24 (2–3): 129–34. PMID 17136878.
  6. ↑ 6.0 6.1 Proenca-Modena JL, Pereira Valera FC, Jacob MG, Buzatto GP, Saturno TH, Lopes L; et al. (2012). "High rates of detection of respiratory viruses in tonsillar tissues from children with chronic adenotonsillar disease". PLoS One. 7 (8): e42136. doi:10.1371/journal.pone.0042136. PMC 3411673. PMID 22870291.
  7. ↑ 7.0 7.1 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.
  8. ↑ 8.0 8.1 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.
  9. ↑ Gibbons RJ (1989). "Bacterial adhesion to oral tissues: a model for infectious diseases". J. Dent. Res. 68 (5): 750–60. PMID 2654229.
  10. ↑ Cunningham, M. W. (2000). "Pathogenesis of Group A Streptococcal Infections". Clinical Microbiology Reviews. 13 (3): 470–511. doi:10.1128/CMR.13.3.470-511.2000. ISSN 0893-8512.
  11. ↑ Ellen RP, Gibbons RJ (1972). "M protein-associated adherence of Streptococcus pyogenes to epithelial surfaces: prerequisite for virulence". Infect. Immun. 5 (5): 826–30. PMC 422446. PMID 4564883.
  12. ↑ Courtney HS, Li Y, Dale JB, Hasty DL (1994). "Cloning, sequencing, and expression of a fibronectin/fibrinogen-binding protein from group A streptococci". Infect. Immun. 62 (9): 3937–46. PMC 303051. PMID 8063411.
  13. ↑ Hanski E, Caparon M (1992). "Protein F, a fibronectin-binding protein, is an adhesin of the group A streptococcus Streptococcus pyogenes". Proc. Natl. Acad. Sci. U.S.A. 89 (13): 6172–6. PMC 402144. PMID 1385871.
  14. ↑ Courtney, Harry S.; Hasty, David L.; Dale, James B.; Poirier, Thomas P. (1992). "A 28-kilodalton fibronectin-binding protein of group a streptococci". Current Microbiology. 25 (5): 245–250. doi:10.1007/BF01575856. ISSN 0343-8651.
  15. ↑ Winram SB, Lottenberg R (1996). "The plasmin-binding protein Plr of group A streptococci is identified as glyceraldehyde-3-phosphate dehydrogenase". Microbiology (Reading, Engl.). 142 ( Pt 8): 2311–20. doi:10.1099/13500872-142-8-2311. PMID 8760943.
  16. ↑ Walström, Torkel; Tylewska, Stanislawa (1982). "Glycoconjugates as possible receptors forStreptococcus pyogenes". Current Microbiology. 7 (6): 343–346. doi:10.1007/BF01572601. ISSN 0343-8651.
  17. ↑ Valentin-Weigand P, Grulich-Henn J, Chhatwal GS, Müller-Berghaus G, Blobel H, Preissner KT (1988). "Mediation of adherence of streptococci to human endothelial cells by complement S protein (vitronectin)". Infect. Immun. 56 (11): 2851–5. PMC 259660. PMID 2459063.
  18. ↑ Visai L, Bozzini S, Raucci G, Toniolo A, Speziale P (1995). "Isolation and characterization of a novel collagen-binding protein from Streptococcus pyogenes strain 6414". J. Biol. Chem. 270 (1): 347–53. PMID 7814395.
  19. ↑ Wessels MR, Bronze MS (1994). "Critical role of the group A streptococcal capsule in pharyngeal colonization and infection in mice". Proc. Natl. Acad. Sci. U.S.A. 91 (25): 12238–42. PMC 45412. PMID 7991612.
  20. ↑ 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.
  21. ↑ 21.0 21.1 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.
  22. ↑ 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.
  23. ↑ 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.
  24. ↑ 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.
Retrieved from "https://www.wikidoc.org/index.php?title=Adenoiditis_pathophysiology&oldid=1314746"