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 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.
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]
- Tonsillitis develops when the viruses infiltrate the tonsils and cause an inflammatory response of up-regulated cytokines.
Bacterial Tonsillitis
Bacterial tonsillitis develops upon infection of the tonsils with pathogenic bacteria.[3]
Acute Bacterial Tonsillitis
- Bacterial tonsillitis considered acute is primarily caused by group A β-hemolytic streptococcus (GABHS) Streptococcus pyogenes infection.[3]
- S. pyogenes and taxonomically-similar bacteria infiltrate the tonsillar epithelium, successfully penetrating the protective mucosal films in the oral and nasal cavity.[4][5]
- Colonization begins when the bacteria adheres to the tonsillar surface proteins through lipoteichoic acid (LTA), depositing fibronectin molecules that bind to the tonsillar epithelium.[4]
- The following virulence factors contribute to S. pyogenes adhesion to the tonsils:[6]
- Containing M protein, allowing colonization[7]
- Lipotechoic acid (LTA): binds with fibronectin or fibrinogen, causing adhesion of the bacteria to the dermis[8]
- Protein F: binds with fibronectin to mediate adhesion[9]
- 29-kDa fibronectin-binding protein[10]
- Glyceraldehyde 3-phosphate dehydrogenase[11]
- 70-kDa galactose-binding protein[12]
- Vitronectin-binding S protein[13]
- Collagen-binding protein[14]
- Serum opacity factor
- Hyaluronate capsule[15]
- This results in an inflammatory response of up-regulated cytokines, leading to tonsillitis.[16]
- S. pyogenes and taxonomically-similar bacteria infiltrate the tonsillar epithelium, successfully penetrating the protective mucosal films in the oral and nasal cavity.[4][5]
Recurrent Bacterial Tonsillitis
- Recurrent bacterial tonsillitis is caused primarily by Staphylococcus aureus.[17]
- S. aureus invades the tonsils through microbial surface components recognizing adhesive matrix molecules (MSCRAMMS)[17]
- Following invasion, S. aureus is internalized by non-phagocytic cells through fibronectin-binding protein and beta-integrins.[18]
- Invasion of non-eukaryotic cells results in the up-regulation of cytokines, resulting in tonsillitis.
Chronic Tonsillitis
- chronic can be due to allergies, asthma, GERD, viruses like EBV or bacterial that persists beyond 3 months.[19][20][21]
Genetics
- White not fully understood, there is quantitative evidence of recurrent tonsillitis' heritability.[22]
- Parental history of tonsillectomy and atopy hold significant predictive power in pediatric tonsillitis.[23]
Associated conditions
Tonsillitis is associated with conditions and diseases associated with its viral and bacterial pathogens, including the following:
- Streptococcal pharyngitis[24]
- Influenza[25]
- Common cold[26]
- Scarlet fever[27]
- Rheumatic fever[28]
- Acute glomerulonephritis[29]
- Peritonsillar abscess[30]
References
- ↑ 1.0 1.1 "Tonsillitis - Causes - NHS Choices".
- ↑ 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.
- ↑ 3.0 3.1 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.
- ↑ 4.0 4.1 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.
- ↑ 17.0 17.1 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ "Pharyngitis - sore throat: MedlinePlus Medical Encyclopedia".
- ↑ "Flu: MedlinePlus Medical Encyclopedia".
- ↑ "Common Cold: MedlinePlus".
- ↑ "Group A Strep | Scarlet Fever | GAS | CDC".
- ↑ "Rheumatic fever - NHS Choices".
- ↑ Almroth G, Lindell A, Aselius H, Sörén L, Svensson L, Hultman P, Eribe ER, Olsen I (2005). "Acute glomerulonephritis associated with streptococcus pyogenes with concomitant spread of streptococcus constellatus in four rural families". Ups. J. Med. Sci. 110 (3): 217–31. PMID 16454159.
- ↑ Klug TE, Rusan M, Fuursted K, Ovesen T (2016). "Peritonsillar Abscess: Complication of Acute Tonsillitis or Weber's Glands Infection?". Otolaryngol Head Neck Surg. 155 (2): 199–207. doi:10.1177/0194599816639551. PMID 27026737.