Sandbox:Tonsillitis pathophysiology
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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
Tonsillitis is associated with infection, it is currently unknown if the swelling and other symptoms are caused by the infectious agents themselves, or by the host immune response to these agents. Tonsillitis may be a result of aberrant immune responses to the normal bacterial flora of the nasopharynx.
Pathogenesis
Tonsillitis develops when the pathogen, viral or bacterial, infects the tonsils and elicits an inflammatory response.[1]
Viral Tonsillitis
Viral tonsillitis is usually caused by the following viruses:[1]
Bacterial Tonsillitis
Bacterial tonsillitis develops upon infection of the tonsils with pathogenic bacteria.[2]
Acute Bacterial Tonsillitis
- Bacterial tonsillitis considered acute is primarily caused by group A β-hemolytic streptococcus (GABHS) Streptococcus pyogenes infection.[2]
- S. pyogenes and taxonomically-similar bacteria infiltrate the tonsillar epithelium, successfully penetrating the protective mucosal films in the oral and nasal cavity.[3][4]
- Colonization begins when the bacteria adheres to the tonsillar surface proteins through lipoteichoic acid (LTA), depositing fibronectin molecules that bind to the tonsillar epithelium.[3]
- The following virulence factors contribute to S. pyogenes adhesion to the tonsils:[5]
- Containing M protein, allowing colonization[6]
- Lipotechoic acid (LTA): binds with fibronectin or fibrinogen, causing adhesion of the bacteria to the dermis[7]
- Protein F: binds with fibronectin to mediate adhesion[8]
- 29-kDa fibronectin-binding protein[9]
- Glyceraldehyde 3-phosphate dehydrogenase[10]
- 70-kDa galactose-binding protein[11]
- Vitronectin-binding S protein[12]
- Collagen-binding protein[13]
- Serum opacity factor
- Hyaluronate capsule[14]
- This results in an inflammatory response of up-regulated cytokines, leading to tonsillitis.[15]
- S. pyogenes and taxonomically-similar bacteria infiltrate the tonsillar epithelium, successfully penetrating the protective mucosal films in the oral and nasal cavity.[3][4]
Recurrent Bacterial Tonsillitis
- Recurrent bacterial tonsillitis is caused primarily by Staphylococcus aureus.[16]
- S. aureus invades the tonsils through microbial surface components recognizing adhesive matrix molecules (MSCRAMMS)[16]
- Following invasion, S. aureus is internalized by non-phagocytic cells through fibronectin-binding protein and beta-integrins.[17]
- Invasion of non-eukaryotic cells results in the up-regulation of cytokines, resulting in tonsillitis.
Pathophysiology
- Under normal circumstances, as viruses and bacteria enter the body through the nose and mouth, they are filtered in the tonsils.[18][19]
- Acute tonsillitis may occur as a result of a Streptococcus pyogenes infection.
- S. pyogenes may be identified within the mucous layer that covers the tonsils as well as the surface of epithelial cells.
- The progression of the infection begins with penetration of infectious bacteria into the mucous barrier.
- Further progression results in the attachment of the infectious bacteria to the surfaces of epithelial cells. .
- Infection may then spread from cell to cell with the appearance of long chains of coccus-bacteria, encroaching on the border of the epithelial cells.
- Spread of infection may lead to the penetration of infectious bacteria into the outermost layers of epithelial cells - resulting in inflammation of the tonsils.
- Within the tonsils, white blood cells of the immune system mount an attack that helps destroy the viruses or bacteria by producing inflammatory cytokines like Phospholipase A2, [20] which also lead to fever.[18][19]
- Infection also provokes the production of cytokines and the activation of a complement immune response - both of which contribute to the overall inflammation of the tonsils.
References
- ↑ 1.0 1.1 "Tonsillitis - Causes - NHS Choices".
- ↑ 2.0 2.1 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.
- ↑ 3.0 3.1 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Walström, Torkel; Tylewska, Stanislawa (1982). "Glycoconjugates as possible receptors forStreptococcus pyogenes". Current Microbiology. 7 (6): 343–346. doi:10.1007/BF01572601. ISSN 0343-8651.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 16.0 16.1 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.
- ↑ 18.0 18.1 van Kempen MJ, Rijkers GT, Van Cauwenberge PB (2000). "The immune response in adenoids and tonsils". Int. Arch. Allergy Immunol. 122 (1): 8–19. doi:10.1159/000024354. PMID 10859465. Unknown parameter
|month=ignored (help) - ↑ 19.0 19.1 Perry M, Whyte A (1998). "Immunology of the tonsils". Immunology Today. 19 (9): 414–21. doi:10.1016/S0167-5699(98)01307-3. PMID 9745205. Unknown parameter
|month=ignored (help) - ↑ "Circulating phospholipase-A2 activity in obstructive sleep apnea". International Journal of Pediatric Otorhinolaryngology. 2012. doi:10.1016/j.ijporl.2011.12.026. PMID 22297210.
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