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Tonsillitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2], Luke Rusowicz-Orazem, B.S.

Synonyms and keywords: Inflamed tonsils; tonsils inflamed

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]}Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]

Overview

Tonsillitis is the infection and inflammation of the tonsils. It usually presents as sore throat accompanied by fever.

Historical Perspective

Cornelius Caesus in A.D. 30 explained that tonsils are covered by a membrane and require to be separated and extracted by a process called tonsillectomy. This encyclopaedia was recovered in 1478 in Papal library, after being lost for 1400 years.[1]

Classification

The main types of tonsillitis are:

Pathophysiology

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.

Causes

The most common causes of tonsillitis are adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. It can also be caused by Epstein-Barr virus, herpes simplex virus, cytomegalovirus, or HIV. The second most common causes are bacterial which may be caused by group A streptococcal bacteria,[2] resulting in strep throat.[2]. Sometimes, tonsillitis is caused by a superinfection of spirochaeta and treponema, in this case called Vincent’s angina or Plaut-Vincent angina.[3]

Differentiating tonsillitis from other diseases

Tonsillitis must be differentiated from other diseases that present with edema and erythema of the tonsils and nasopharynx, lymphadenopathy, fever, dysphonia, and dysphagia.

Epidemiology and Demographics

The epidemiology of tonsillitis is not completely known. A research indicates that 15-30% of sore throats in children and 5-10% sore throats in adults are bacterial tonsillitis. Research on Norwegian twins indicates a prevalence of approximately 11,700 per 100,000 individuals, while a study on primary school children in Turkey indicated recurrent tonsillitis prevalence of approximately 12,100 per 100,000 individuals. Acute tonsillitis from S. pyogenes primarily affects children between 5 and 15 years old. Tonsillitis is more common in females than males. There is no racial or demographic predisposition to tonsillitis. The case fatality rate is unknown.

Risk Factors

Risk factors for tonsillitis involve increasing the risk of invasion by pathogenic viruses or bacteria, including environmental and systemic factors.

Natural history, complications and prognosis

Acute tonsillitis will usually present with erythema and edema of the tonsils rapidly upon infiltration of the pathogen. It is usually self-limited and symptoms will be resolved within 3-4 days. Recurrent tonsillitis will usually not resolve itself and will require antimicrobrial therapy or tonsillectomy when indicated. Complications of tonsillitis are caused by persistence and/or spread of the responsible pathogen – usually bacterial. The prognosis for acute tonsillitis without treatment is usually good, while the prognosis for untreated recurrent tonsillitis will vary based on presence of life-threatening complications. With treatment, the prognosis of acute and recurrent tonsillitis is usually good.

Diagnosis

History and Symptoms

Symptoms of tonsillitis include a severe sore throat (which may be experienced as referred pain to the ears), painful/ difficult swallowing, headache, fever and chills, and change in voice causing a “hot potato” voice.

Common symptoms of tonsillitis include localized pain in the head, neck, and throat, as well as coughing, headache, and systemic symptoms including fever, chills, and swollen lymph nodes in the neck. Less common symptoms include nausea, vomiting, furry tongue, bad breath (halitosis), and difficulty opening your mouth.

Physical Examination

Tonsillitis is mostly diagnosed clinically. Physical examination signs of tonsillitis include tonsillar erythema, edema, and exudate. Cervicular lymphadenopathy is present. along with fever and dysphonia. is characterized by signs of red, swollen tonsils which may have a purulent exudative coating of white patches (i.e. pus). In addition, there may be enlarged and tender neck cervical lymph nodes. Tonsillitis patients will usually present with malaise and lethargy, appearing ill, due to fever.[4]

Laboratory Findings

The diagnosis of GABHS tonsillitis is mostly clinical but it can be confirmed by culture. Samples are obtained by swabbing both tonsillar surfaces and the posterior pharyngeal wall are plated on sheep blood agar medium. The isolation rate can be increased by incubating the cultures under anaerobic conditions and using selective media.[4]

Treatment

Medical Therapy

The mainstay of therapy for tonsillitis includes antimicrobial therapy analgesics. Supportive therapy includes salt water gargles and lozenges. Antimicrobial therapy is usually penicillin, though alternative regimens include cephalosporins, clindamycin, azithromycin, clarithromycin, erythromycin, amoxicillin. Treatment of tonsillitis consists of pain management medications[5] and lozenges.[6] If the tonsillitis is caused by bacteria, then antibiotics are prescribed, with penicillin being most commonly used.[7] Erythromycin is used for patients allergic to penicillin. In many cases of tonsillitis, the pain caused by the inflamed tonsils warrants the prescription of topical anesthetics for temporary relief. Viscous lidocaine solutions are often prescribed for this purpose. Ibuprofen or other analgesics can help to decrease the edema and inflammation, which will ease the pain and allow the patient to swallow liquids sooner.[5] When tonsillitis is caused by a virus, the length of illness depends on which virus is involved. Usually, a complete recovery is made within one week; however, some rare infections may last for up to two weeks. Additionally, gargling with a solution of warm water and salt may reduce pain and swelling.

Surgery

Chronic cases may indicate tonsillectomy (surgical removal of tonsils) as a choice for treatment.[8]

Prevention

Primary Prevention

The most effective form of primary prevention consists of proper hygienic practices as well as avoiding individuals suffering from contagious infections that may result in tonsillitis.

  • Hygienic practices may be defined as the following:
  • Proper hand washing and hand antisepsis [9]
  • Proper selection of hand hygiene antimicrobial agents
  • Facial cleanliness
  • Proper dental hygiene [10]
  • Avoiding contact between hands, eyes, mouth, and infectious agents

Secondary Prevention

Secondary prevention involves usage of antibiotics to prevent recurrence of tonsillitis.[11]

References

  1. ↑ Template:McGuire, Neil G. “A method of guillotine tonsillectomy with an historical review.” The Journal of Laryngology & Otology 81.02 (1967): 187-196.
  2. ↑ 2.0 2.1 Putto A (1987). “Febrile exudative tonsillitis: viral or streptococcal?”. Pediatrics. 80 (1): 6–12. PMID 3601520.
  3. ↑ Van Cauwenberge P (1976). “[Significance of the fusospirillum complex (Plaut-Vincent angina)]”. Acta Otorhinolaryngol Belg (in Dutch; Flemish). 30 (3): 334–45. PMID 1015288. – fusospirillum complex (Plaut-Vincent angina) Van Cauwenberge studied the tonsils of 126 patients using direct microscope observation. The results showed that 40% of acute tonsillitis was caused by Vincent’s agina and 27% of chronic tonsillitis was caused by Spirochaeta
  4. ↑ 4.0 4.1 Template:Ruuskanen, Olli, et al. “Rapid diagnosis of adenoviral tonsillitis: A prospective clinical study.” The Journal of pediatrics 104.5 (1984): 725-728
  5. ↑ 5.0 5.1 Boureau, F.; et al. “Evaluation of Ibuprofen vs Paracetamol Analgesic Activity Using a Sore Throat Pain Model”. Clinical Drug Investigation. 17 year=1999: 1–8. – Boureau studied 113 patients who saw 19 physicians in France. Patients were give Ibuprofen 400mg or Paracetamol 1000mg randomly. Pain intensity, difficulty swallowing, and global pain relief were use to measure in hourly increments until 6 hours after patients first dose. The results showed that Ibuprofen better than Paracetamol in all three categories
  6. ↑ Praskash, T.; et al. (2001). “Koflet lozenges in the Treatment of Sore Throat”. The Antiseptic. 98: 124–127. – The efficacy of Koflet Lozenges was evaluated by symptomatic relief of pain. The 48 patients were examined by the Physicians and given a scale rating from 0-3. 0 stating no signs and symptoms and 3 being the worse. The results showed patients with pharyngitis 95% of the patient with positive feedbacks. Tonsillitis patients and patients with both symptoms gave 100% positive feedbacks
  7. ↑ Touw-Otten FW, Johansen KS (1992). “Diagnosis, antibiotic treatment and outcome of acute tonsillitis: report of a WHO Regional Office for Europe study in 17 European countries”. Fam Pract. 9 (3): 255–62. doi:10.1093/fampra/9.3.255. PMID 1459378. – 17 European Countries had a minimum of 10 physicians each that participated in a studied that involved 4094 patients that they had seen from Nov 1989 to May 1990. Sore throat, redness and swelling of tonsils, pus on tonsils, enlarge regional lymph nodes, or fever. Bacterial and serology test were performed to determined antibiotics usage. Antibiotics results had 2334 out of 3646 patient using penicillin. 343 out of the 3646 used amoxicillin and 554 out of 3646 used macrolides
  8. ↑ Paradise JL, Bluestone CD, Bachman RZ; et al. (1984). “Efficacy of tonsillectomy for recurrent throat infection in severely affected children. Results of parallel randomized and nonrandomized clinical trials”. N. Engl. J. Med. 310 (11): 674–83. PMID 6700642. – Paradise studied 187 children with tonsillectomy or tonsillectomy and adenoidectomy. 91 children were randomly put in surgical and non-surgical groups. The other 96 were place by parent’s choice. The results favored the surgical group on reoccurrence of throat infections during their initial and second year follow-up where the data was collected. While non-surgical groups did better in the long run. 13 out of the 95 surgical group encountered surgical complications after their second year follow up
  9. ↑ Centers for Disease Control and Prevention. Hand Hygiene. http://www.cdc.gov/handhygiene/providers/guideline.html. Accessed May 5th, 2016.
  10. ↑ Centers for Disease Control and Prevention. Topics for Body Hygiene. http://www.cdc.gov/healthywater/hygiene/body/. Accessed May 5th, 2016.
  11. ↑ Dagnelie CF, Bartelink ML, van der Graaf Y, Goessens W, de Melker RA (1998). “Towards a better diagnosis of throat infections (with group A beta-haemolytic streptococcus) in general practice”. Br J Gen Pract. 48 (427): 959–62. PMC 1409991. PMID 9624764.

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S., Usama Talib, BSc, MD [2]

Overview

Cornelius Caesus in A.D. 30 explained that tonsils are covered by a membrane and require to be separated and extracted by a process called tonsillectomy. This encyclopaedia was recovered in 1478 in Papal library, after being lost for 1400 years.[1]

Historical Perspective

  • Cornelius Caesus in A.D. 30 explained that tonsils are covered by a membrane and require to be separated and extracted by a process called tonsillectomy. This encyclopaedia was recovered in 1478 in Papal library, after being lost for 1400 years.[1]
  • In the sixth and seventh centuries Aetius and Paul described surgical treatment of tonsillitis, as one of the most ancient surgical procedures.[1]

References

  1. ↑ 1.0 1.1 1.2 Template:McGuire, Neil G. “A method of guillotine tonsillectomy with an historical review.” The Journal of Laryngology & Otology 81.02 (1967): 187-196.

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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S., Usama Talib, BSc, MD [2]

Overview

Tonsillitis can be classified into acute, and recurrent forms. Acute tonsillitis is primarily caused by viral or bacterial infection; the former of which is usually self-limited. Bacterial acute tonsillitis will usually resolve with antimicrobial therapy. Recurrent tonsillitis is primarily caused by bacterial infection – usually group A streptococcus. Systemic symptoms, including fever, are usually absent due to their association with viral acute manifestations of tonsillitis. Tonsillectomy may be indicated for patients with recurrent tonsillitis if antimicrobial therapy is ineffective.

Classification

Tonsillitis can be classified into[1][2]

Acute Tonsillitis

Recurrent Tonsillitis

  • Tonsillitis that is recurrent is primarily caused by bacterial infection – usually group A streptococcus.[4]
  • Presents primarily with tonsillar erythema and edema, along with odynophagia, dysphonia, dyspnea, and dysphagia.
    • Systemic symptoms, including fever, are usually absent due to their association with viral acute manifestations of tonsillitis.
  • Tonsillectomy is indicated for patients with recurrent tonsillitis if the following criteria are met:[5]
    • 7 episodes of tonsillitis in a single year OR
    • 5 episodes in each of 2 consecutive years OR
    • 3 episodes in each of 3 consecutive years

Chronic Tonsillitis

Persistence of the infection for a duration over 3 months is known as chronic tonsillitis. The viruses usually stay and lead to chronic inflammation or it results from repeated allergies or GERD.[6][7][8]

References

  1. ↑ 1.0 1.1 Stelter K (2014). “Tonsillitis and sore throat in children”. GMS Curr Top Otorhinolaryngol Head Neck Surg. 13: Doc07. doi:10.3205/cto000110. PMC 4273168. PMID 25587367.
  2. ↑ Darrow DH, Siemens C (2002). “Indications for tonsillectomy and adenoidectomy”. Laryngoscope. 112 (8 Pt 2 Suppl 100): 6–10. doi:10.1002/lary.5541121404. PMID 12172229.
  3. ↑ “Tonsillitis – NHS Choices”.
  4. ↑ 4.0 4.1 4.2 Stuck BA, Götte K, Windfuhr JP, Genzwürker H, Schroten H, Tenenbaum T (2008). “Tonsillectomy in children”. Dtsch Arztebl Int. 105 (49): 852–60, quiz 860–1. doi:10.3238/arztebl.2008.0852. PMC 2689639. PMID 19561812.
  5. ↑ Paradise JL, Bluestone CD, Bachman RZ, Colborn DK, Bernard BS, Taylor FH, Rogers KD, Schwarzbach RH, Stool SE, Friday GA (1984). “Efficacy of tonsillectomy for recurrent throat infection in severely affected children. Results of parallel randomized and nonrandomized clinical trials”. N. Engl. J. Med. 310 (11): 674–83. doi:10.1056/NEJM198403153101102. PMID 6700642.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ 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.


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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S., Usama Talib, BSc, MD [2]

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

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.[3][4][5]

Bacterial Tonsillitis

Bacterial tonsillitis develops upon infection of the tonsils with pathogenic bacteria.[6]

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.[3][4][5]
    • 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.[22]

Associated conditions

Tonsillitis is associated with conditions and diseases associated with its viral and bacterial pathogens, including the following:

References

  1. ↑ 1.0 1.1 “Tonsillitis – Causes – NHS Choices”.
  2. ↑ 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. ↑ 3.0 3.1 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.
  4. ↑ 4.0 4.1 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.
  5. ↑ 5.0 5.1 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.
  6. ↑ 6.0 6.1 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.
  7. ↑ 7.0 7.1 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.
  8. ↑ Gibbons RJ (1989). “Bacterial adhesion to oral tissues: a model for infectious diseases”. J. Dent. Res. 68 (5): 750–60. PMID 2654229.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ Walström, Torkel; Tylewska, Stanislawa (1982). “Glycoconjugates as possible receptors forStreptococcus pyogenes”. Current Microbiology. 7 (6): 343–346. doi:10.1007/BF01572601. ISSN 0343-8651.
  16. ↑ 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.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ 20.0 20.1 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.
  21. ↑ 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.
  22. ↑ 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.
  23. ↑ 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.
  24. ↑ “Pharyngitis – sore throat: MedlinePlus Medical Encyclopedia”.
  25. ↑ “Flu: MedlinePlus Medical Encyclopedia”.
  26. ↑ “Common Cold: MedlinePlus”.
  27. ↑ “Group A Strep | Scarlet Fever | GAS | CDC”.
  28. ↑ “Rheumatic fever – NHS Choices”.
  29. ↑ 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.
  30. ↑ 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.


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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2] Luke Rusowicz-Orazem, B.S.

Overview

The most common causes of tonsillitis are adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. It can also be caused by epstein-barr virus, herpes simplex virus, cytomegalovirus, or HIV. The second most common causes are bacterial which may be caused by group A streptococcal bacteria,[1] resulting in strep throat.[1]. Sometimes, tonsillitis is caused by a superinfection of spirochaeta and treponema, in this case called Vincent’s angina or Plaut-Vincent angina.[2]

Causes

Life-Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Causes by Organ System

Cardiovascular Obstructive sleep apnea
Chemical/Poisoning No underlying causes
Dental Pericoronitis, trench mouth, Vincent’s angina
Dermatologic Guttate psoriasis, hand-foot-and-mouth disease, neutrophilic dermatoses
Drug Side Effect Alemtuzumab, carglumic acid, cyclosporine, formoterol, fusidic acid (ophthalmic), human papillomavirus 9-valent vaccine, montelukast, natalizumab, pimecrolimus, secukinumab, tobramycin
Ear Nose Throat Angina tonsillaris, tonsil cancer, tonsillolith, trench mouth, Vincent’s angina
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic Gastroesophageal reflux disease
Genetic No underlying causes
Hematologic No underlying causes
Iatrogenic No underlying causes
Infectious Disease Adenovirus, bordetella pertussis, chlamydia pneumoniae, common cold, corynebacterium diphtheriae, cytomegalovirus,diphtheria, enteroviruses, Epstein-Barr virus, fusobacterium necrophorum, Group A streptococcal infection, guttate psoriasis,hand-foot-and-mouth disease, herpes simplex , herpes simplex virus, HIV, infectious mononucleosis, influenza , influenza virus, Lemierre’s syndrome, measles, mycoplasma pneumoniae, neisseria gonorrhoeae, parainfluenza viruses, plague, respiratory syncytial virus, rhinovirus, rubeola, staphylococcus aureus, streptococcus pneumoniae, streptococcus pyogenes, syphilis, trench mouth, treponema pallidum, tuberculosis, tularemia, Vincent’s angina, yersinia pestis infection
Musculoskeletal/Orthopedic No underlying causes
Neurologic Obstructive sleep apnea
Nutritional/Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic Malignancy, tonsil cancer
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary Asthma, bordetella pertussis, common cold, obstructive sleep apnea, tuberculosis
Renal/Electrolyte No underlying causes
Rheumatology/Immunology/Allergy Allergies
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous No underlying causes

Causes in Alphabetical Order

Causes

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Putto A (1987). “Febrile exudative tonsillitis: viral or streptococcal?”. Pediatrics. 80 (1): 6–12. PMID 3601520.
  2. ↑ Van Cauwenberge P (1976). “[Significance of the fusospirillum complex (Plaut-Vincent angina)]”. Acta Otorhinolaryngol Belg (in Dutch; Flemish). 30 (3): 334–45. PMID 1015288. – fusospirillum complex (Plaut-Vincent angina) Van Cauwenberge studied the tonsils of 126 patients using direct microscope observation. The results showed that 40% of acute tonsillitis was caused by Vincent’s agina and 27% of chronic tonsillitis was caused by Spirochaeta
  3. ↑ Brook, I.; Foote, P. A. (2006). “Isolation of methicillin resistant Staphylococcus aureus from the surface and core of tonsils in children”. Int J Pediatr Otorhinolaryngol. 70 (12): 2099–2102. doi:10.1016/j.ijporl.2006.08.004. PMID 16962178.
  4. ↑ Brook, I.; Gober, A. E. (2008). “Concurrent influenza A and group A beta-hemolytic streptococcal pharyngotonsillitis”. Ann Otol Rhinol Laryngol. 117 (4): 310–312. PMID 18478842.
  5. ↑ Brook, I. (2005). “The role of anaerobic bacteria in tonsillitis”. Int J Pediatr Otorhinolaryngol. 69 (1): 9–19. doi:10.1016/j.ijporl.2004.08.007. PMID 15627441.
  6. ↑ Renn CN, Straff W, Dorfmüller A, Al-Masaoudi T, Merk HF, Sachs B (2002). “Amoxicillin-induced exanthema in young adults with infectious mononucleosis: demonstration of drug-specific lymphocyte reactivity”. Br. J. Dermatol. 147 (6): 1166–70. doi:10.1046/j.1365-2133.2002.05021.x. PMID 12452866. -Renn studied 4 patients who where treated amoxicillin for throat infection and lymphadenopathy. Infectious mononucleosis was present in the patient’s blood due to trace of Epstein-Barr antibodies. The three tests performed where the patched test, intracutaneous test, and lymphocyte transformation test. The results of the patched test that pointed to amoxicillin as the caused of their rash were 1 out of 4 patients. The intracutaneous showed 2 out of 4 patients with positive results that pointed to amoxicillin. The LTT results showed 3 out of 4 that pointed to amoxicillin

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Differentiating Tonsillitis from other Diseases

Differentiating Tonsillitis from other Diseases

Overview

Tonsillitis is a bacterial or viral infection that causes inflammation and swelling of the tonsils. Most often, this infection is characterized by two distinct traits; sore throat and difficulty swallowing. However, other infections such as Scarlet fever and Epstein-Barr virus may present in a similar fashion. Thus prior to any treatment of the infection, it is important to perform diagnostic testing to identify the correct infection.

Differential Diagnosis

  • There are two diseases that are distinguished to present similarly to Tonsillitis; they are Scarlet fever and Epstein Barr Virus.
Disease Definition
Scarlet Fever
  • Streptococcus pyogenes (group A strep) is responsible for scarlet fever. It can also cause simple angina, erysipelas and serious toxin-mediated syndromes like necrotizing fasciitis and the so-called streptococal toxic shock-like syndrome. The virulence of group A strep seems to be increasing lately. The exanthem of scarlatina is thought to be due to erythrogenic toxin production by specific streptococcal strains in a nonimmune patient. Along with erythrogenic toxins, the Group A strep produces several toxins and enzymes. Two of the most important are the streptolysins O and S. Streptolysin O, an hemolytic, thermolabile and immunogenic toxin, is the base of an assay for scarlatina and erysipelas – the anti-streptolysin O titer.
  • Early symptoms indicating the onset of scarlet fever can include:

[1] [2]

Rash

  • Characteristic rash, which:
  • is fine, red, and rough-textured; it blanches upon pressure
  • Pastia lines (where the rash becomes confluent in the arm pits and groins) appear and persist after the rash is gone
  • The rash begins to fade three to four days after onset and desquamation (peeling) begins. “This phase begins with flakes peeling from the face. Peeling from the palms and around the fingers occurs about a week later and can last up to a month.”[2] Peeling also occurs in axilla, groin, and tips of the fingers and toes.[1]
Epstein-Barr Virus

EBV is named after Michael Epstein and Yvonne Barr, who together with Bert Achong, discovered the virus in 1964.[3]

  • Epstein-Barr virus is ubiquitous across the globe and the strongest causative agent for the manifestation of infectious mononucleosis. Commonly, a person is first exposed to the virus during or after adolescence. Though once deemed “The Kissing Disease”, recent research has shown that transmission of mononucleosis not only occurs from intimate contact with infected saliva, but also from contact with the airborne virus.
  • Symptoms of infectious mononucleosis are:
  • Sometimes, a splenomegaly or hepatomegaly may develop. Heart problems or involvement of the central nervous system occurs only rarely, and infectious mononucleosis is almost never fatal. There are no known associations between active EBV infection and problems during pregnancy, such as miscarriages or birth defects. Although the symptoms of infectious mononucleosis usually resolve in 1 or 2 months, EBV remains dormant or latent in a few cells in the throat and blood for the rest of the person’s life. Periodically, the virus can reactivate and is commonly found in the saliva of infected persons. This reactivation usually occurs without symptoms of illness.

Tonsillitis must be differentiated from other causes of dysphagia and fever.

Variable Croup Epiglottitis Pharyngitis Bacterial tracheitis Tonsilitis Retropharyngeal abscess Subglottic stenosis
Presentation Cough ✔ — Sore throat, pain on swallowing, fever, headache, abdominal pain, nausea and vomiting Barking cough, stridor,

fever, chest pain,

ear pain, difficulty breathing, headache, dizziness.

Sore throat, pain on swallowing, fever, headache, cough Neck pain, stiff neck, torticollis

fever, malaise, stridor, and barking cough

Depends on severity. May have respiratory distress at birth, exercise-induced dyspnea, intermittent wheezing. Inspiratory stridor. [4]
Stridor ✔ ✔
Drooling — ✔
Others are Hoarseness, Difficulty breathing, symptoms of the common cold, Runny nose, Fever Other symptoms include difficulty breathing, fever, chills, difficulty swallowing, hoarseness of voice
Causes Parainfluenza virus H. influenza type b, beta-hemolytic streptococci, Staphylococcus aureus, fungi and viruses. Group A beta-hemolytic streptococcus. Staphylococcus aureus Most common cause is viral including adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. Second most common causes are bacterial; Group A streptococcal bacteria,[5]  Polymicrobial infection. Mostly; Streptococcus pyogenes, Staphylococcus aureus and respiratory anaerobes (example; Fusobacteria, Prevotella, and Veillonella species)[6][7][8][9][10][11] Congenital, trauma
Physical exams findings Suprasternal and intercostal indrawing,[12] Inspiratory stridor[13], expiratory wheezing,[13] Sternal wall retractions[14] Cyanosis, Cervical lymphadenopathy, Inflammed epiglottis Inflammed pharynx with or without exudate Subglottic narrowing with purulent secretions in the trachea[15][16] Fever, especially 100°F or higher.[17][18]Erythema, edema and Exudate of the tonsils.[19] cervical lymphadenopathy, Dysphonia.[20] Child may be unable to open the mouth widely. May have enlarged

cervical lymph nodes and neck mass.

Signs of respiratory distress, intermittent wheezing. Inspiratory stridor. [4]
Age commonly affected Mainly 6 months and 3 years old

rarely, adolescents and adults[21]

Used to be mostly found in

pediatric age group between 3 to 5 years,

however, recent trend favors adults

as most commonly affected individuals[22]

with a mean age of 44.94 years.

Mostly in children and young adults,

with 50% of cases identified

between the ages of 5 to 24 years.[23]

Mostly during the first six years of life Primarily affects children

between 5 and 15 years old.[24]

Mostly between 2-4 years, but can occur in other age groups.[25][26] May be congenital congenital or acquired. Mean age in acquired is 54.1 years[27]
Imaging finding Steeple sign on neck X-ray Thumbprint sign on neck x-ray — Lateral neck xray shows intraluminal membranes and tracheal wall irregularity. Intraoral or transcutaneous USG may show an abscess making CT scan unnecessary.[28][29][30] On CT scan, a mass impinging on the posterior pharyngeal wall with rim enhancement is seen[31][32] Bronchoscopy reveals subglottic stenosis. Computed tomography may reveal a concentric stenotic tracheal segment.[33]
Treatment Dexamethasone and nebulised epinephrine Airway maintenance, parenteral Cefotaxime or Ceftriaxone in combination with Vancomycin. Adjuvant therapy includes corticosteroids and racemic Epinephrine.[34][35] Antimicrobial therapy mainly penicillin-based and analgesics. Airway maintenance and antibiotics Antimicrobial therapy mainly penicillin-based and analgesics with tonsilectomy in selected cases. Immediate surgical drainage and antimicrobial therapy. emperic therapy involves; ampicillin-sulbactam or clindamycin. Endoscopic balloon dilation for patients with low-grade subglottic stenosis,[36] glucocorticoid injections, and resection.[37]

Differentiating between Common Misdiagnosis

Scarlet Fever

  • Scarlet fever may be ruled out in testing for specific bacteria that produce the erythrogenic toxin.
  • This toxin is ultimately the underlying cause of Scarlet fever.
  • In its absence, Scarlet fever would only present as purulent tonsillitis.

Epstein-Barr

  • Differentiated based on clinical manifestations.
  • May be responsible for prolonged fatigue.
  • Tonsillectomy may lead to further complications including an increased risk of hemorrhaging.

References

  1. ↑ 1.0 1.1 Balentine J and Kessler D (March 7, 2006). “Scarlet Fever”. eMedicine. emerg/518.
  2. ↑ 2.0 2.1 Dyne P and McCartan K (October 19, 2005). “Pediatrics, Scarlet Fever”. eMedicine. emerg/402.
  3. ↑ Epstein MA, Achong BG, Barr YM (1964). “Virus particles in cultured lymphblasts from Burkitt’s Lymphoma”. Lancet. 1: 702–3. PMID 14107961.
  4. ↑ 4.0 4.1 Nussbaumer-Ochsner Y, Thurnheer R (2015). “IMAGES IN CLINICAL MEDICINE. Subglottic Stenosis”. N Engl J Med. 373 (1): 73. doi:10.1056/NEJMicm1404785. PMID 26132943.
  5. ↑ Putto A (1987). “Febrile exudative tonsillitis: viral or streptococcal?”. Pediatrics. 80 (1): 6–12. PMID 3601520.
  6. ↑ Cheng J, Elden L (2013). “Children with deep space neck infections: our experience with 178 children”. Otolaryngol Head Neck Surg. 148 (6): 1037–42. doi:10.1177/0194599813482292. PMID 23520072.
  7. ↑ Abdel-Haq N, Quezada M, Asmar BI (2012). “Retropharyngeal abscess in children: the rising incidence of methicillin-resistant Staphylococcus aureus”. Pediatr Infect Dis J. 31 (7): 696–9. doi:10.1097/INF.0b013e318256fff0. PMID 22481424.
  8. ↑ Inman JC, Rowe M, Ghostine M, Fleck T (2008). “Pediatric neck abscesses: changing organisms and empiric therapies”. Laryngoscope. 118 (12): 2111–4. doi:10.1097/MLG.0b013e318182a4fb. PMID 18948832.
  9. ↑ Brook I (2004). “Microbiology and management of peritonsillar, retropharyngeal, and parapharyngeal abscesses”. J Oral Maxillofac Surg. 62 (12): 1545–50. PMID 15573356.
  10. ↑ Wright CT, Stocks RM, Armstrong DL, Arnold SR, Gould HJ (2008). “Pediatric mediastinitis as a complication of methicillin-resistant Staphylococcus aureus retropharyngeal abscess”. Arch Otolaryngol Head Neck Surg. 134 (4): 408–13. doi:10.1001/archotol.134.4.408. PMID 18427007.
  11. ↑ Asmar BI (1990). “Bacteriology of retropharyngeal abscess in children”. Pediatr Infect Dis J. 9 (8): 595–7. PMID 2235179.
  12. ↑ Johnson D (2009). “Croup”. BMJ Clin Evid. 2009. PMC 2907784. PMID 19445760.
  13. ↑ 13.0 13.1 Cherry, James D. (2008). “Croup”. New England Journal of Medicine. 358 (4): 384–391. doi:10.1056/NEJMcp072022. ISSN 0028-4793.
  14. ↑ Johnson D (2009). “Croup”. BMJ Clin Evid. 2009. PMC 2907784. PMID 19445760.
  15. ↑ Liston SL, Gehrz RC, Siegel LG, Tilelli J (1983). “Bacterial tracheitis”. Am J Dis Child. 137 (8): 764–7. PMID 6869336.
  16. ↑ Liston SL, Gehrz RC, Jarvis CW (1981). “Bacterial tracheitis”. Arch Otolaryngol. 107 (9): 561–4. PMID 7271556.
  17. ↑ Tonsillitis. Medline Plus. https://www.nlm.nih.gov/medlineplus/ency/article/001043.htm. Accessed May 2nd, 2016.
  18. ↑ “Tonsillitis – NHS Choices”.
  19. ↑ Stelter K (2014). “Tonsillitis and sore throat in children”. GMS Curr Top Otorhinolaryngol Head Neck Surg. 13: Doc07. doi:10.3205/cto000110. PMC 4273168. PMID 25587367.
  20. ↑ “Tonsillitis – Symptoms – NHS Choices”.
  21. ↑ Tong MC, Chu MC, Leighton SE, van Hasselt CA (1996). “Adult croup”. Chest. 109 (6): 1659–62. PMID 8769531.
  22. ↑ Lichtor JL, Roche Rodriguez M, Aaronson NL, Spock T, Goodman TR, Baum ED (2016). “Epiglottitis: It Hasn’t Gone Away”. Anesthesiology. 124 (6): 1404–7. doi:10.1097/ALN.0000000000001125. PMID 27031010.
  23. ↑ Bennett, John (2015). Mandell, Douglas, and Bennett’s principles and practice of infectious diseases. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1455748013.
  24. ↑ Sharav, Yair; Benoliel, Rafael (2008). Orofacial Pain and Headache. Elsevier. ISBN 0723434123.
  25. ↑ Craig FW, Schunk JE (2003). “Retropharyngeal abscess in children: clinical presentation, utility of imaging, and current management”. Pediatrics. 111 (6 Pt 1): 1394–8. PMID 12777558.
  26. ↑ Coulthard M, Isaacs D (1991). “Neonatal retropharyngeal abscess”. Pediatr Infect Dis J. 10 (7): 547–9. PMID 1876473.
  27. ↑ Nicolli EA, Carey RM, Farquhar D, Haft S, Alfonso KP, Mirza N (2017). “Risk factors for adult acquired subglottic stenosis”. J Laryngol Otol. 131 (3): 264–267. doi:10.1017/S0022215116009798. PMID 28007041.
  28. ↑ Kawabata M, Umakoshi M, Makise T, Miyashita K, Harada M, Nagano H; et al. (2016). “Clinical classification of peritonsillar abscess based on CT and indications for immediate abscess tonsillectomy”. Auris Nasus Larynx. 43 (2): 182–6. doi:10.1016/j.anl.2015.09.014. PMID 26527518.
  29. ↑ Nogan S, Jandali D, Cipolla M, DeSilva B (2015). “The use of ultrasound imaging in evaluation of peritonsillar infections”. Laryngoscope. 125 (11): 2604–7. doi:10.1002/lary.25313. PMID 25946659.
  30. ↑ Fordham MT, Rock AN, Bandarkar A, Preciado D, Levy M, Cohen J; et al. (2015). “Transcervical ultrasonography in the diagnosis of pediatric peritonsillar abscess”. Laryngoscope. 125 (12): 2799–804. doi:10.1002/lary.25354. PMID 25945805.
  31. ↑ Philpott CM, Selvadurai D, Banerjee AR (2004). “Paediatric retropharyngeal abscess”. J Laryngol Otol. 118 (12): 919–26. PMID 15667676.
  32. ↑ Vural C, Gungor A, Comerci S (2003). “Accuracy of computerized tomography in deep neck infections in the pediatric population”. Am J Otolaryngol. 24 (3): 143–8. PMID 12761699.
  33. ↑ Nussbaumer-Ochsner Y, Thurnheer R (2015). “IMAGES IN CLINICAL MEDICINE. Subglottic Stenosis”. N Engl J Med. 373 (1): 73. doi:10.1056/NEJMicm1404785. PMID 26132943.
  34. ↑ Nickas BJ (2005). “A 60-year-old man with stridor, drooling, and “tripoding” following a nasal polypectomy”. J Emerg Nurs. 31 (3): 234–5, quiz 321. doi:10.1016/j.jen.2004.10.015. PMID 15983574.
  35. ↑ Wick F, Ballmer PE, Haller A (2002). “Acute epiglottis in adults”. Swiss Med Wkly. 132 (37–38): 541–7. PMID 12557859.
  36. ↑ Cui PC, Luo JS, Zhao DQ, Guo ZH, Ma RN (2016). “[Management of subglottic stenosis in children with endoscopic balloon dilation]”. Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 51 (4): 286–8. doi:10.3760/cma.j.issn.1673-0860.2016.04.009. PMID 27095722.
  37. ↑ Nussbaumer-Ochsner Y, Thurnheer R (2015). “IMAGES IN CLINICAL MEDICINE. Subglottic Stenosis”. N Engl J Med. 373 (1): 73. doi:10.1056/NEJMicm1404785. PMID 26132943.

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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

The epidemiology of adenoiditis is not completely known. There is research that indicates 15-30% of sore throats in children and 5-10% sore throats in adults are bacterial adenotonsillitis. Research on Norwegian twins indicates a prevalence of approximately 11,700 per 100,000 individuals, while a study on primary school children in Turkey indicated recurrent tonsillitis prevalence of approximately 12,100 per 100,000 individuals.

Epidemiology and Demographics

Incidence

  • The incidence of tonsillitis is not completely known, research indicates that 15-30% of sore throats in children and 5-10% sore throats in adults are bacterial tonsillitis.[1][2][3]

Prevalence

  • The prevalence of tonsillitis is not completely known.
    • Research on Norwegian twins indicates recurrent tonsillitis prevalence of approximately 11,700 per 100,000 individuals.[4]
    • A study on primary school children in Turkey indicated recurrent tonsillitis prevalence of approximately 12,100 per 100,000 individuals.[5]

Case Fatality Rate

The case fatality rate of tonsillitis is unknown.

Age

  • Acute tonsillitis from S. pyogenes primarily affects children between 5 and 15 years old.[6]

Gender

  • Research on tonsillitis patients evidences that it is more common in females than males.[4][7]

Race

There is no racial predisposition to tonsillitis.

Developing and Developed Countries

There is no geographic predisposition to tonsillitis.

References

  1. ↑ Komaroff AL, Pass TM, Aronson MD, Ervin CT, Cretin S, Winickoff RN, Branch WT (1986). “The prediction of streptococcal pharyngitis in adults”. J Gen Intern Med. 1 (1): 1–7. PMID 3534166.
  2. ↑ Kaplan EL, Top FH, Dudding BA, Wannamaker LW (1971). “Diagnosis of streptococcal pharyngitis: differentiation of active infection from the carrier state in the symptomatic child”. J. Infect. Dis. 123 (5): 490–501. PMID 5115179.
  3. ↑ Schroeder BM (2003). “Diagnosis and management of group A streptococcal pharyngitis”. Am Fam Physician. 67 (4): 880, 883–4. PMID 12613739.
  4. ↑ 4.0 4.1 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. ↑ Kara CO, Ergin H, Koçak G, Kiliç I, Yurdakul M (2002). “Prevalence of tonsillar hypertrophy and associated oropharyngeal symptoms in primary school children in Denizli, Turkey”. Int. J. Pediatr. Otorhinolaryngol. 66 (2): 175–9. PMID 12393253.
  6. ↑ Sharav, Yair; Benoliel, Rafael (2008). Orofacial Pain and Headache. Elsevier. ISBN 0723434123.
  7. ↑ Thorp MA, Isaacs S, Sellars SL (2000). “Tonsillectomy and tonsillitis in Cape Town–age and sex of patients”. S Afr J Surg. 38 (3): 62–4. PMID 11392200.

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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Risk factors for tonsillitis involve increasing the risk of invasion by pathogenic viruses or bacteria, including environmental and systemic factors.

Risk Factors

Risk factors for tonsillitis involve increasing the risk of invasion by pathogenic viruses or bacteria.[1][2][3]

References

  1. ↑ 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.
  2. ↑ “Stopping the Spread of Germs at Home, Work & School | Seasonal Influenza (Flu) | CDC”.
  3. ↑ Graham NM (1990). “The epidemiology of acute respiratory infections in children and adults: a global perspective”. Epidemiol Rev. 12: 149–78. PMID 2286216.
  4. ↑ Erling V, Jalil F, Hanson LA, Zaman S (1999). “The impact of climate on the prevalence of respiratory tract infections in early childhood in Lahore, Pakistan”. J Public Health Med. 21 (3): 331–9. PMID 10528962.
  5. ↑ Factor SH, Levine OS, Schwartz B, Harrison LH, Farley MM, McGeer A, Schuchat A (2003). “Invasive group A streptococcal disease: risk factors for adults”. Emerging Infect. Dis. 9 (8): 970–7. doi:10.3201/eid0908.020745. PMC 3020599. PMID 12967496.
  6. ↑ Early GJ, Seifried SE (2012). “Risk factors for community-associated Staphylococcus aureus skin infection in children of Maui”. Hawaii J Med Public Health. 71 (8): 218–23. PMC 3419822. PMID 22900237.


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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Acute tonsillitis will usually present with erythema and edema of the tonsils rapidly upon infiltration of the pathogen. It is usually self-limited and symptoms will be resolved within 3-4 days. Recurrent tonsillitis will usually not resolve itself and will require antimicrobrial therapy or tonsillectomy when indicated. Complications of tonsillitis are caused by persistence and/or spread of the responsible pathogen – usually bacterial. The prognosis for acute tonsillitis without treatment is usually good, while the prognosis for untreated recurrent tonsillitis will vary based on presence of life-threatening complications. With treatment, the prognosis of acute and recurrent tonsillitis is usually good.

Natural History

  • Acute tonsillitis will usually present with erythema and edema of the tonsils rapidly upon infiltration of the pathogen.[1]
    • Symptoms, including fever and sore throat, will usually manifest within 24 hours of infection.
  • Acute tonsillitis is usually self-limited and will be resolved within 3-4 days.
  • Recurrent tonsillitis will usually not resolve itself and will require antimicrobrial therapy or tonsillectomy when indicated.[2]
    • Left untreated, recurrent tonsillitis may persist and recur over periods of time and can lead to infectious complications.

Complications

Complications of tonsillitis are caused by persistence and/or spread of the responsible pathogen – usually bacterial – and include the following:[1]

Prognosis

  • The prognosis for acute tonsillitis without treatment is usually good; the disease is usually self-limited and will resolve itself within 3-4 days.[1]
  • The prognosis for recurrent tonsillitis varies based on the presence of life-threatening complications.[4]
  • With treatment, the prognosis of acute and recurrent tonsillitis is usually good.

References

  1. ↑ 1.0 1.1 1.2 “Tonsillitis – NHS Choices”.
  2. ↑ Stuck BA, Götte K, Windfuhr JP, Genzwürker H, Schroten H, Tenenbaum T (2008). “Tonsillectomy in children”. Dtsch Arztebl Int. 105 (49): 852–60, quiz 860–1. doi:10.3238/arztebl.2008.0852. PMC 2689639. PMID 19561812.
  3. ↑ Rio AC, Franchi-Teixeira AR, Nicola EM (2008). “Relationship between the presence of tonsilloliths and halitosis in patients with chronic caseous tonsillitis”. Br Dent J. 204 (2): E4. doi:10.1038/bdj.2007.1106. PMID 18037821.
  4. ↑ “Rheumatic fever: MedlinePlus Medical Encyclopedia”.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | X Ray | CT | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

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