Tonsillitis medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Esther Lee, M.A. Luke Rusowicz-Orazem, B.S. Maliha Shakil, M.D. [2]

Overview

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. Supportive therapy includes salt water gargles and lozenges. There are noted challenges to antimicrobial therapy involving reduced or blocked efficacy of penicillin.

Medical Therapy

Antimicrobial therapy

Empiric Therapy

Challenges of Treatment

Despite in vitro efficacy, there is frequently reported inability of penicillin to fully resolve GABHS from patients with acute and relapsing tonsillitis.[6]

  • Over the past 50 years, the rate of penicillin failure has consistently increased from about 7% in 1950 to almost 40% in 2000.
  • There are several explanations for the failure of penicillin to eradicate GABHS tonsillitis:[7]
    • Poor penetration of penicillin into the tonsillar tissues, as well as the epithelial cells.[8]
    • Bacterial interactions between GABHS and the other members of the pharyngo-tonsillar bacterial flora.[9]
      • It is hypothesized that the enzyme beta-lactamase, secreted by beta-lactamase-producing aerobic and anaerobic bacteria that colonize the pharynx and tonsils, may “shield” GABHS from penicillin.
        • These organisms include S. aureus, Haemophillus influenzae, and Prevotella, Porphyromonas and Fusobacterium spp.[10] A recent increase was noted in the recovery of MRSA which was isolated from 16% of tonsils, making it more difficult to eradicate this and other beta-lactamase producing organisms.[11]
    • Coaggregation between Moraxella catarrhalis and GABHS, which can facilitate GABHS colonization.[12]
    • Absence of normal bacterial flora and resultant lack of interference on the growth of GABHS, makeing it easier for GABHS to colonize and invade the pharyngo-tonsillar area.[13][14][15]
    • Poor penetration of penicillin into the tonsillar cells and tonsillar surface fluid (allowing intracellular survival of GABHS)[8]
    • Resistance (i.e., erythromycin) or tolerance (i.e., penicillin) to the administered antibiotic
    • Inappropriate dose, duration of therapy, or choice of antibiotic

Symptomatic Treatment and Pain Management

References

  1. 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.
  2. Casey JR, Pichichero ME. Meta-analysis of cephalosporin versus penicillin treatment of group A streptococcal tonsillopharyngitis in children. Pediatrics 2004;113:866-882.
  3. Brook I (2009). "The role of beta-lactamase-producing-bacteria in mixed infections". BMC Infect Dis. 9: 202. doi:10.1186/1471-2334-9-202. PMC 2804585. PMID 20003454.
  4. Brook I (2007). "Microbiology and principles of antimicrobial therapy for head and neck infections". Infect Dis Clin North Am. 21 (2): 355–91. doi:10.1016/j.idc.2007.03.014. PMID 17561074.
  5. Gilbert, David (2015). The Sanford guide to antimicrobial therapy. Sperryville, Va: Antimicrobial Therapy. ISBN 978-1930808843.
  6. Casey JR, Pichichero ME (2007). "The evidence base for cephalosporin superiority over penicillin in streptococcal pharyngitis". Diagn. Microbiol. Infect. Dis. 57 (3 Suppl): 39S–45S. doi:10.1016/j.diagmicrobio.2006.12.020. PMID 17292576.
  7. Brook I, Foote PA (2005). "Efficacy of penicillin versus cefdinir in eradication of group A streptococci and tonsillar flora". Antimicrob. Agents Chemother. 49 (11): 4787–8. doi:10.1128/AAC.49.11.4787-4788.2005. PMC 1280135. PMID 16251332.
  8. 8.0 8.1 Kaplan EL, Chatwal GS, Rohde M. Reduced ability of penicillin to eradicate ingested Group A streptococci from epithelial cells: clinical and pathogenetic implications. Clin Infect Dis. 2006;43:1398-406.
  9. Brook I (1984). "The role of beta-lactamase-producing bacteria in the persistence of streptococcal tonsillar infection". Rev. Infect. Dis. 6 (5): 601–7. PMID 6390637.
  10. Brook I, Calhoun L, Yocum P (1980). "Beta-lactamase-producing isolates of Bacteroides species from children". Antimicrob. Agents Chemother. 18 (1): 164–6. PMC 283957. PMID 6968177.
  11. Brook I, Foote PA. Isolation of methicillin resistant Staphylococcus aureus from the surface and core of tonsils in children. Int J Pediatr Otorhinolaryngol. 2006 ;70:2099-102.
  12. Brook I, Gober AE (2006). "Increased recovery of Moraxella catarrhalis and Haemophilus influenzae in association with group A beta-haemolytic streptococci in healthy children and those with pharyngo-tonsillitis". J. Med. Microbiol. 55 (Pt 8): 989–92. doi:10.1099/jmm.0.46325-0. PMID 16849717.
  13. Grahn E, Holm SE (1983). "Bacterial interference in the throat flora during a streptococcal tonsillitis outbreak in an apartment house area". Zentralbl Bakteriol Mikrobiol Hyg A. 256 (1): 72–9. PMID 6362282.
  14. Brook I, Gober AE (1995). "Role of bacterial interference and beta-lactamase-producing bacteria in the failure of penicillin to eradicate group A streptococcal pharyngotonsillitis". Arch. Otolaryngol. Head Neck Surg. 121 (12): 1405–9. PMID 7488371.
  15. Brook I, Gober AE (1999). "Interference by aerobic and anaerobic bacteria in children with recurrent group A beta-hemolytic streptococcal tonsillitis". Arch. Otolaryngol. Head Neck Surg. 125 (5): 552–4. PMID 10326813.
  16. 16.0 16.1 16.2 Boureau, F; Pelen, F; Verriere, F; Paliwoda, A; Manfredi, R; Farhan, M; Wall, R (1999). "Evaluation of Ibuprofen vs Paracetamol Analgesic Activity Using a Sore Throat Pain Model". Clinical Drug Investigation. 17 (1): 1–8. doi:10.2165/00044011-199917010-00001. ISSN 1173-2563.
  17. "Tonsillitis - Treatment - NHS Choices".

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