Adenoiditis pathophysiology
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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
Adenoids are involved in the production of mostly secretory IgA, which is transported to the surface providing local immune protection. They can be infected by either bacterial and viral pathogens and develop to adenoiditis.[1]
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.
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:
- Alpha-hemolytic streptococci
- Enterococci
- Corynebacterium species
- Coagulase-negative staphylococci
- Neisseria species
- Haemophilus species
- 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.
- 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.[2]
- 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.
- Adenoid paracortex may also be enlarged secondarily as a result of the activation and proliferation of antigen-specific T and B cells (clonal expansion).
- On gross pathology, characteristic findings of adenoiditis, include:
- Enlarged adenoids
- Soft greasy yellow areas within capsule
- On microscopic histopathological analysis, characteristic findings of adenoiditis
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.
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.[3]
Adenoiditis is an inflammation of the lymphoid tissue at the back of the roof of the mouth (the adenoids). Adenoiditis, or enlarged adenoids (adenoid hypertrophy), is unusual in adults because the adenoids normally shrink and almost disappear as the individual reaches adolescence. Hypertrophy of the adenoids occurs naturally or is caused by chronic inflammation. Chronic adenoid inflammation may cause nose-breathing problems due to their location.
Tonsillitis and adenoiditis may occur at the same time in children.
Viral Tonsillitis
- Viral tonsillitis is usually caused by the following viruses:[3]
- 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.[5][6][7]
Bacterial Tonsillitis
Bacterial tonsillitis develops upon infection of the tonsils with pathogenic bacteria.[8]
Acute Bacterial Tonsillitis
- Bacterial tonsillitis considered acute is primarily caused by group A β-hemolytic streptococcus (GABHS) Streptococcus pyogenes infection.[8]
- S. pyogenes and taxonomically-similar bacteria infiltrate the tonsillar epithelium, successfully penetrating the protective mucosal films in the oral and nasal cavity.[9][10]
- Colonization begins when the bacteria adheres to the tonsillar surface proteins through lipoteichoic acid (LTA), depositing fibronectin molecules that bind to the tonsillar epithelium.[9]
- The following virulence factors contribute to S. pyogenes adhesion to the tonsils:[11]
- Containing M protein, allowing colonization[12]
- Lipotechoic acid (LTA): Binds with fibronectin or fibrinogen, causing adhesion of the bacteria to the dermis[13]
- Protein F: Binds with fibronectin to mediate adhesion[14]
- 29-kDa fibronectin-binding protein[15]
- Glyceraldehyde 3-phosphate dehydrogenase[16]
- 70-kDa galactose-binding protein[17]
- Vitronectin-binding S protein[18]
- Collagen-binding protein[19]
- Serum opacity factor
- Hyaluronate capsule[20]
- This results in an inflammatory response of up-regulated cytokines, leading to tonsillitis.[21]
- S. pyogenes and taxonomically-similar bacteria infiltrate the tonsillar epithelium, successfully penetrating the protective mucosal films in the oral and nasal cavity.[9][10]
Recurrent Bacterial Tonsillitis
- Recurrent bacterial tonsillitis is caused primarily by Staphylococcus aureus.[22]
- S. aureus invades the tonsils through microbial surface components recognizing adhesive matrix molecules (MSCRAMMs)[22]
- Following invasion, S. aureus is internalized by non-phagocytic cells through fibronectin-binding protein and beta-integrins.[23]
- 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 that can be caused due to allergies, asthma, GERD,that persists beyond 3 months.[5][6][7]
Genetics
- White not fully understood, there is quantitative evidence of recurrent tonsillitis heritability.[24]
- Parental history of tonsillectomy and atopy hold significant predictive power in pediatric tonsillitis.[25]
| Viral Tonsillitis | |||
| Acute Bacterial Tonsillitis | |||
| Recurrent Bacterial Tonsillitis | Usually due to normal flora pathogen: | ||
| Chronic Bacterial Tonsillitis | |||
| Non-infectious Tonsillitis | Allergies |
- ↑ 1.0 1.1 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.
- ↑ 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.
- ↑ 3.0 3.1 "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.
- ↑ 5.0 5.1 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.
- ↑ 6.0 6.1 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.
- ↑ 7.0 7.1 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.
- ↑ 8.0 8.1 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.
- ↑ 9.0 9.1 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.
- ↑ 22.0 22.1 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.
- ↑ 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.